Re: [CR] Good fats and health

[Guest guest]

Hi Al:

So another study seems to confirm many of our previous suspicions

but, as you note, not as regards SFA.

If I read it right, as previously noted, olive oil is neutral;

safflower oil is EXCELLENT to get what you need, LA, with the fewest

calories; and the CVD benefit of ALA is less than that of LA.

Another reason to avoid canola and soybean oils.

This now makes me wonder if there is any cancer risk (from aflatoxin,

possibly) associated with LA. If not then our options seem pretty

clear.

Rodney.

--- In , " old542000 " <apater@m...>

wrote:

>

> Hi All,

>

> Eating polyunsaturated fatty acid (PUFA) is considered

> to be better than the alternative bad fats, cholesterol and

> saturated or trans-fats. Trans-fats are not considered,

> but the new pdf-available below appears to suggest

> that what matters most for heart disease and all death

> risks are alpha-linoleic acid (LA) and total PUFA is

> more important than most other fats. Surprisingly,

> total or saturated fat did not matter.

>

> The below for simplicity does not show the data of

> Table 1-3, but did include the legend of Table 3 to

> clarify the confounders corrected for to derive the Model 4

> results.

>

> Table 1 examined the baseline characteristics and showed

> that the factors associated with all-cause death at significance

> level p<0.001 were age, smoking alcohol, socioeconomic status,

> and C-reactive protein. For p<0.01, there were systolic blood

> pressure and exercise. For p<0.05, there was diastolic

> blood pressure, BMI and fasting insulin level.

>

> Table 2 respective numbers were blood

> LA that was esterified and nonesterified,

> LA, alpha-linolenic acid (ALA), PUFA,

> alpha-tocopherol and ascorbic

> acid for p<0.001; diet % of energy PUFA and LA; and fiber, LA,

> ALA and % of energy ALA; but not statistically

> different were calories, fat, monounsaturated fat and nonesterified

> PUFAs.

>

> Table 3 showed the follow-up cardiovascular deaths in thirds

> of increasing levels to be related to LA, p<0.03; ALA, 0.18; and

> PUFA, p<0.02 for the levels in the diet.

>

> Arch Intern Med. 2005 Jan 24;165(2):193-9.

> Prediction of Cardiovascular Mortality in Middle-aged Men by

> Dietary and Serum

> Linoleic and Polyunsaturated Fatty Acids.

> Laaksonen DE, Nyyssonen K, Niskanen L, Rissanen TH, Salonen JT.

> PMID: 15668366 [PubMed - in process]

>

> BACKGROUND: Substitution of dietary polyunsaturated for

saturated

> fat has long

> been recommended for the primary prevention of cardiovascular

disease

> (CVD), but

> only a few prospective cohort studies have provided support for

this

> advice.

> METHODS: We assessed the association of dietary linoleic and total

> polyunsaturated fatty acid (PUFA) intake with cardiovascular and

> overall

> mortality in a population-based cohort of 1551 middle-aged men.

> Dietary fat

> composition was estimated with a 4-day food record and serum fatty

> acid

> composition. RESULTS: During the 15-year follow-up, 78 men died of

> CVD and 225

> of any cause. Total fat intake was not related to CVD or overall

> mortality. Men

> with an energy-adjusted dietary intake of linoleic acid (relative

> risk [RR]

> 0.39; 95% confidence interval [CI], 0.21-0.71) and PUFA (RR, 0.38;

> 95% CI,

> 0.20-0.70) in the upper third were less likely to die of CVD than

men

> with

> intake in the lower third after adjustment for age. Multivariate

> adjustment

> weakened the association somewhat. Mortality from CVD was also

lower

> for men

> with proportions of serum esterified linoleic acid (RR, 0.42; 95%

CI,

> 0.21-0.80)

> and PUFA (RR, 0.25; 95% CI, 0.12-0.50) in the upper vs lower third,

> with some

> attenuation in multivariate analyses. Serum and to a lesser extent

> dietary

> linoleic acid and PUFA were also inversely associated with overall

> mortality.

> CONCLUSIONS: Dietary polyunsaturated and more specifically linoleic

> fatty acid

> intake may have a substantial cardioprotective benefit that is also

> reflected in

> overall mortality. Dietary fat quality seems more important than

fat

> quantity in

> the reduction of cardiovascular mortality in men.

> PMID: 15668366 [PubMed - in process]

>

> INTRODUCTION

> Substitution of dietary polyunsaturated for saturated fat has

been

> recommended for

> several decades in the primary prevention of cardiovascular disease

> (CVD), but only a few

> prospective cohort studies have provided support for this advice.1-

4

> A biological basis has

> been provided by metabolic studies showing that polyunsaturated fat

> lowers, but saturated

> fat increases, serum low-density lipoprotein cholesterol (LDL-C)

> concentration.5 In

> contrast, evidence for reduction of total fat intake without

> modification of fat quality in

> the prevention of CVD is weak.6-7

> Trials in institutionalized patients have suggested that

> substitution of

> polyunsaturated for saturated fat may reduce coronary heart disease

> (CHD) or CVD.8-9 A few prospective

> cohort studies have indicated that increased polyunsaturated fat

> intake,1-4 a higher

> polyunsaturated-saturated fat ratio,4 or Keys score1-2 may decrease

> incident CHD1-2,4 or

> overall mortality,3 but more cohort studies have shown no

> association.6 The discrepancies may

> be due to small study size, imprecise dietary assessment, and

> insufficient control of

> confounding.7

> Experimental and in vitro studies have suggested that n-3 fatty

> acids such as

> -linolenic acid and fish oils have anti-inflammatory,

antithrombotic,

> and antiarrhythmic

> properties10-11 and improve insulin sensitivity.12 In contrast, n-6

> fatty acids such as linoleic

> and arachidonic acid have even been purported to promote

> inflammation, thrombosis, and

> insulin resistance.11-13 In a review of the evidence, however,

> linoleic acid also appears

> to decrease thrombosis,10 and may also decrease arrhythmias14 and

> improve insulin

> sensitivity.15 Only a few prospective studies have supported a role

> of dietary linoleic16 or

> -linolenic acid17 in primary CVD prevention.

> Of the few cohort studies showing an inverse association of

> dietary polyunsaturated

> fatty acid (PUFA) intake with CVD, none has been population based,

> and only 1 study has

> found an association with overall mortality.3 None of these studies

> has supported their

> findings with serum biomarkers. The aim of the present study was to

> assess the association of

> dietary fat quantity and quality, specifically linoleic and -

> linolenic acid, with CVD and

> overall mortality during a 15-year follow-up in a population-based

> cohort of 1551

> middle-aged men who were free of CVD, cancer, and diabetes at

> baseline.

>

> METHODS

> The Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study is a

> prospective

> population-based study.15, 18-22 The study population comprised a

> random age-stratified sample of

> 2682 men living in eastern Finland who were 42, 48, 54, or 60 years

> old at baseline

> between 1984 and 1989. The University of Kuopio Research Ethics

> Committee approved the study.

> All participants gave their written informed consent.

> For the present study, all men with a history of CVD, diabetes,

or

> cancer at baseline

> (n = 1123) were excluded. Men with missing data for both dietary

and

> serum fatty acids

> were also excluded, leaving 1551 men for the analyses.

> ... saturated (SAFA), monounsaturated (MUFA), and linoleic and -

> linolenic fatty acids

> was assessed with 4-day food records.23 The consumption of foods

was

> assessed at the time

> of blood sampling at baseline. The dietary records were collected

on

> 3 workdays and 1

> weekend day. Data collection was carried out year-round, except for

> July, when most Finns

> are on vacation. The participants were instructed on the use of

> household measures to

> quantitatively record their food intake during the 4 days of data

> collection. A nutritionist

> gave the instructions and checked the completed food intake

records.

> Dietary intake of

> nutrients and foods was calculated using NUTRICA software (version

> 2.5; National Public

> Health Institute, Turku, Finland). The software is based on mainly

> Finnish values of nutrient

> composition of foods. The nutrient compositions of foods in NUTRICA

> software version 2.5

> have been analyzed mainly in the 1990s. For the assessment of

dietary

> fatty acids, an

> earlier vers

> ion

> (1.0) was used because of the changes in fatty acid contents of

> margarines in Finland

> during the last 15 years. In all, the database contains

comprehensive

> data for 1300 food

> items and dishes and 30 nutrients. Intake of fatty acids and fiber

> was calculated in grams

> per day.

>

> ... RESULTS

> The median follow-up for the cohort of 1551 men was 14.6 years

> (range, 0.8-17.8

> years), thus representing 22 645 person-years. During this time, 78

> men died of CVD and 225

> died of any cause. Because some men with dietary measures of fat

> intake had missing serum

> fatty acid measures and vice versa, there were 78 deaths from CVD

and

> 220 deaths from any

> cause in analyses with dietary measures of fat intake.

Corresponding

> numbers for analyses

> with serum fatty acid composition were 69 and 202, respectively.

> Smoking, blood pressure,

> BMI, and C-reactive protein were positively associated with CVD or

> overall mortality

> (Table 1), and socioeconomic status, plasma vitamin E, plasma

> ascorbic acid, and dietary

> fiber intake were inversely associated. In analyses with continuous

> variables, men with a

> lower dietary intake of linoleic and -linolenic acid and PUFA had a

> higher cardiovascular

> and overall mortality after adjustment for age and year of

> examination (P<.01 to P<.05;

> Table 2). Pro

> portions

> of esterified linoleic and -linolenic acid and total PUFA and

> proportions of

> nonesterified linoleic acid were also inversely associated with

death

> from CVD or any cause (P<.001

> to P<.05; Table 2). Intake of total fat, SAFA, MUFA, and

cholesterol

> were not associated

> with CVD.

> ... *Data are given as relative risk (95% confidence interval)

of

> cardiovascular death

> (n = 78). proportional hazards regression analyses: model 1,

> adjusted for

> age and year of examination; model 2, adjusted for age, year of

> examination, smoking,

> alcohol consumption, adult socioeconomic status and moderate to

> vigorous leisure-time physical activity; model 3, adjusted for

model

> 2 and plasma

> lipid-standardized -tocopherol levels, plasma ascorbic acid, and

> dietary total

> energy and energy-adjusted saturated fat and fiber intake; and

model

> 4, adjusted for

> model 3 and low-density lipoprotein cholesterol concentrations,

> systolic

> blood pressure, blood pressure medication, family history of

ischemic

> heart disease,

> C-reactive protein concentrations, fasting concentrations of

insulin

> and

> nonesterified fatty acids, and body mass index.

>

> Table 4. Relative Risks of Cardiovascular Death According to

Serum

> Fatty Acid

> Proportions Categorized Into Thirds*

> --------------------------------------------------------------------

--

> ----------------------------------

> Serum Fatty Acid Proportion in Thirds, Median (Range), % Model 1

> Model 2 Model 3 Model 4

> --------------------------------------------------------------------

--

> -----------------------------------

> Esterified linoleic acid proportions

> 24 (11-26) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> (Referent)

> 28 (26-30) 0.82 (0.48-1.41) 0.95 (0.54-1.65) 1.00 (0.56-1.72) 1.20

> (0.66-2.10)

> 32 (30-43) 0.42 (0.21-0.80) 0.48 (0.24-0.93) 0.51 (0.24-1.04) 0.59

> (0.28-1.23)

> P for trend .01 .04 .08 .22

> Esterified n-6 fatty acid proportions

> 31 (16-33) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> (Referent)

> 35 (33-36) 0.64 (0.37-1.10) 0.74 (0.42-1.32) 0.79 (0.44-1.42) 0.99

> (0.55-1.80)

> 38 (36-49) 0.37 (0.19-0.72) 0.42 (0.22-0.83) 0.46 (0.23-0.95) 0.51

> (0.25-1.07)

> P for trend .003 .01 .04 .10

> Esterified -linolenic acid proportions

> 0.6 (0.0-0.7) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> (Referent)

> 0.8 (0.7-0.9) 0.52 (0.28-0.97) 0.52 (0.28-0.97) 0.53 (0.28-0.99)

0.66

> (0.34-1.28)

> 1.0 (0.9-1.7) 0.77 (0.44-1.37) 0.84 (0.47-1.50) 0.86 (0.47-1.55)

1.19

> (0.63-2.26)

> P for trend .49 .52 .57 .61

> Esterified polyunsaturated fatty acid proportions

> 37 (22-39) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> (Referent)

> 40 (39-42) 0.56 (0.32-0.96) 0.66 (0.38-1.17) 0.72 (0.40-1.30) 0.84

> (0.45-1.54)

> 44 (42-54) 0.25 (0.12-0.50) 0.30 (0.15-0.62) 0.32 (0.15-0.70) 0.36

> (0.16-0.79)

> P for trend .001 .001 .004 .01

> *Data are given as relative risk (95% confidence interval) of

> cardiovascular death (n =

> 69). See Table 3 for an explanation of the models.

>

> FATTY ACID CORRELATIONS

> Dietary linoleic acid intake was correlated with nonesterified

(r

> = 0.34) and

> esterified (r = 0.49) linoleic acid proportions. Total PUFA intake

> was composed of, on average,

> 77% dietary linoleic acid and was highly correlated with total PUFA

> intake (r = 0.95).

> Dietary PUFA and SAFA intake were inversely correlated (r = –0.34).

> Dietary PUFA intake and

> serum PUFA esterified proportions were also correlated (r = 0.50).

> These correlations

> were highly significant (P<.001).

> Nonesterified and esterified linoleic acid and PUFA proportions

> were also inversely

> associated with BMI and fasting insulin and glucose concentrations,

> whereas the

> corresponding fatty acids estimated from food records were not or

> were only weakly associated. In

> multivariate linear regression analyses, the determinants of serum

> esterified linoleic acid

> proportions were dietary linoleic acid intake ( = .51), alcohol

> intake ( = –.17), BMI ( =

> –.11), blood glucose concentrations ( = –.07), serum insulin

> concentrations ( = –.05),

> and age ( = –.02). The corresponding determinants of esterified

PUFA

> proportions were

> dietary PUFA intake ( = .51), alcohol intake ( = –.10), BMI ( = –

> .03), glucose ( = –.09),

> insulin ( = –.05), and age ( = –.06).

>

> DIETARY FATTY ACIDS AND CARDIOVASCULAR MORTALITY

> Men with dietary linoleic acid intake in the upper third were up

> to 61% less likely to

> die of CVD than their counterparts whose intake was in the lower

> third after adjustment

> for age and year of examination (Table 3). Men whose -linolenic

acid

> intake was in the

> upper third were 30% to 42% less likely to die of CVD than men

whose

> intake was in the lower

> third, but the associations were not significant. When using

dietary -

> linolenic acid

> intake as a natural log–transformed continuous variable, the

> association was statistically

> significant in all models: model 1: relative risk (RR), 0.37 (95%

> confidence interval [CI],

> 0.18-0.77); model 2: RR, 0.43 (95% CI, 0.20-0.90); model 3: RR,

0.41

> (95% CI, 0.18-0.91);

> and model 4: RR, 0.42 (95% CI, 0.18-0.95).

> Esterified -linolenic acid proportions were not associated with

> CVD mortality (Table

> 4). The linoleic/-linolenic acid ratio (upper vs lower third, model

> 1: RR, 0.80 [95% CI,

> 0.46-1.40]), n-6/n-3 ratio (upper vs lower third, model 1: RR, 0.80

> [95% CI, 0.45-1.43]),

> n-3 fatty acids (upper vs lower third, model 1: RR, 0.88, 95% CI,

> 0.43-1.80), or long

> chain PUFA (upper vs lower third, model 1: RR, 1.19 [95% CI, 0.67-

> 2.09]) were not

> significantly associated with CVD mortality. Nonesterified linoleic

> acid proportions were also

> associated with CVD mortality, but the gradient was nonlinear, with

> the lowest risk in the

> middle third (middle vs lower third, model 1: RR, 0.40 [95% CI,

0.22-

> 0.75]). Adjustment for

> confounding or mediating variables (models 2-4) weakened the

> association (data not

> shown).

>

> SERUM FATTY ACIDS AND OVERALL MORTALITY

> Esterified linoleic acids proportions were or tended to be

> associated with a lower

> overall mortality (upper vs lower third, model 1: RR, 0.44 [95% CI,

> 0.30-0.67], P for trend,

> <.001; model 2: RR, 0.59 [95% CI, 0.40-0.86], P for trend, .005;

> model 3: RR, 0.66 [95%

> CI, 0.43-0.97], P for trend, .03; model 4: RR, 0.69 [95% CI, 0.41-

> 1.03], P for trend,

> .08). The inverse associations for proportions of n-6 fatty acids

and

> especially PUFA were

> even stronger and significant in all models (data not shown; P for

> trend, <.001 to.02). The

> serum PUFA/SAFA ratio was also associated with overall mortality

> (upper vs lower third,

> model 1: RR, 0.44 [95% CI, 0.30-0.64]; model 2: RR, 0.57 [95% CI,

> 0.39-0.84]; model 3: RR,

> 0.60 [95% CI, 0.40-0.90]; and model 4: RR, 0.65 [95% CI, 0.43-

1.00]).

> Esterified

> -linolenic acid proportions had a borderline association with

overall

> mortality after adjustment

> for age and year of examination (upper vs lower third, model 1: RR,

> 0.72 [95% CI,

> 0.51-1.03], P f

> or

> trend, .05), but not after adjustment for potential confounding or

> mediating variables

> (data not shown).

>

> COMMENT

> Middle-aged men with proportions of serum linoleic acid, n-6

fatty

> acids, and

> especially PUFA in the upper third were up to 3 times less likely

to

> die of CVD than men with

> proportions in the lower third. Dietary intake of linoleic acid and

> total PUFA as assessed

> with a 4-day food record was also inversely associated with CVD,

but

> total fat intake was

> not. Importantly, both serum and dietary fatty acid composition

were

> assessed in this

> study.

> Men with energy-adjusted dietary PUFA intake in the upper third

> had less than half the

> risk of premature CVD mortality as men with intake in the lower

> third, even after

> multivariate adjustment. The inverse correlations of dietary PUFA

and

> SAFA intake indicate that

> the apparent benefit of PUFA intake probably comes about in part

> through substitution of

> PUFA for SAFA intake (in these men, by substitution of margarine

for

> butter).27 This,

> coupled with the inverse association of the dietary PUFA/SAFA ratio

> with CVD mortality,

> provides support for increasing PUFA intake at the expense of SAFA

> intake in the primary

> prevention of CVD and underscores the importance of dietary fat

> quality over quantity. These

> findings agree with those from the Western Electric Study, in which

> coronary death was

> the outcome,1 and the Nurses Health Study, in which myocardial

> infarction was the outcome.4

> Monounsaturated fatty acid intake was not associated with CVD or

> overall mortality.

> Possible benef

> icial

> effects in our study may be obscured by the high collinearity of

> MUFA intake with SAFA

> intake.

> Serum esterified PUFA proportions were even more strongly

> associated with CVD

> mortality than dietary PUFA intake. Fasting insulin and glucose

> levels, BMI, smoking, and alcohol

> intake were also associated with serum fatty acid composition,

> probably, at least in

> part, independently of dietary fatty acid intake.28 Although

> attenuated somewhat, the inverse

> association of especially serum PUFA proportions with CVD mortality

> remained significant

> even when adjusting for these variables.

> After adjustment for lipids, the Pearson correlation of serum

> esterified linoleic acid

> proportions measured from whole serum with the energy-adjusted

> dietary intake of linoleic

> acid from the 4-day food diary was 0.50, much higher than that of

> serum cholesterol ester

> linoleic acid proportions with linoleic acid intake (r = 0.28), as

> estimated by a

> semiquantitative food frequency questionnaire in the

Atherosclerosis

> Risk in Communities

> Study.28 The correlation of serum linoleic acid proportions

measured

> 4 years later with dietary

> linoleic acid intake at baseline in 895 men participating in the

KIHD

> Study 4-year

> follow-up was 0.36 (data not shown). Serum esterified fatty acid

> proportions are thus a good

> measure of habitual dietary fat composition. Saturated fat intake

in

> Finland has decreased

> since the mid-1980s27 when the KIHD Study began, but our data

> indicate that the relative

> ranking of these men with respect to dietary fat quality may be

> stabile, at least during

> the firs

> t 4

> years of follow-up.

> Nonesterified linoleic acid proportions in the fasting state

also

> reflect adipose and

> dietary fatty acid composition.29 Men with higher nonesterified

> linoleic acid proportions

> seemed to have a lower CVD mortality, but the lowest mortality was

in

> the middle third.

> The imprecision and low sensitivity of the measurement of

> nonesterified fatty acids in our

> study (coefficient of variation, 15%) may explain the discrepancy

in

> results between

> nonesterified and esterified linoleic acid proportions.

> Men with dietary intake of linoleic acid in the upper third were

> less than half as

> likely to die of CVD than men with intake in the lower third.

> Findings for serum proportions

> of linoleic acid and especially total n-6 fatty acids were similar,

> although some

> attenuation was seen in multivariate models. Because linoleic acid

> (18:2n-6) is elongated to

> arachidonic acid (20:4n-6) in the metabolism of serum fatty acids,

n-

> 6 fatty acid

> proportions are also an index of linoleic acid intake. The Nurses

> Health Study also found an

> inverse association of dietary linoleic acid intake with incident

> CHD.4 Serum linoleic acid

> proportions have also been inversely associated with incident CHD30-

> 31 and stroke32 in

> nested case-control30, 32 and cohort31 studies. For serum linoleic

> and n-6 fatty acids and

> total PUFA proportions, this apparent protective benefit carried

over

> to lower overall

> mortality. Because CVD deaths made up only about one third of total

> deaths, this implies that

> n-6 fatty

> acids

> may also tend to decrease non-CVD mortality.

> We found a nonsignificant trend for an inverse association of

> dietary and serum

> -linolenic acid, but not serum fish oils, with CVD and overall

> mortality. The Lyon Heart

> Study,33 with increased -linolenic acid intake as one of the

dietary

> interventions, and the

> Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto

> miocardico

> (GISSI)-Prevenzione trial,34 which focused on fish oil supplements,

> show that n-3 fatty acids reduce risk

> in secondary CHD prevention. In the present study, -linolenic acid

> intake at baseline was

> low. Furthermore, in this cohort fish oils, which were inversely

> associated with acute

> coronary events,20 come mainly from nonfatty lake fish. In Finland,

> lake fish are also a

> major dietary source of mercury, which was positively associated

with

> coronary events.20

> Total PUFA intake was low in these middle-aged Finnish men, but

> the n-6/n-3 ratio was

> high (6.5 ± 1.8). We found no association of the serum n-6/n-3

ratio

> with CVD or overall

> mortality. Some in vitro, animal, and cross-sectional studies have

> suggested that a high

> n-6/n-3 ratio may increase the risk of CVD, but the evidence

> suggesting that it may have

> a clinical or public health relevance is weak6 and inconsistent

with

> the present

> findings.

> Strengths of this study include its longitudinal population-

based

> design, detailed

> assessment of potential confounding and mediating factors, and

> assessment of dietary fat

> composition with both food records and serum biomarkers. The

> consistency of the associations

> of dietary intake of linoleic acid and PUFA and corresponding serum

> proportions,

> especially with CVD mortality, lends further validity to the

> findings. The main findings

> suggesting that increased linoleic acid or PUFA intake or

> substitution of polyunsaturated for

> saturated fat decreases CVD mortality furthermore agree with those

of

> the Nurses Health

> Study.4 Nonetheless, these associations may not apply to high

> polyunsaturated fat and low

> saturated fat diets or to other ethnic groups.

> We found strong inverse associations of dietary and serum

linoleic

> acid and PUFA, but

> no association of dietary total fat intake, with CVD mortality.

> Dietary fat quality thus

> seems more important than fat quantity in the reduction of CVD

> mortality in middle-aged

> men. Carrying out recommendations to replace saturated fat with

> polyunsaturated fat in the

> primary prevention of cardiovascular disease may substantially

> decrease CVD and to a

> lesser degree overall mortality.

>

>

> Cheers, Alan Pater

[Guest guest]

Hi folks:

Talk of the devil. Linoleic acid REDUCES the incidence of cancer in

men, just out:

http://www.newstarget.com/001741.html

Safflower looks better and better.

Rodney.

> >

> > Hi All,

> >

> > Eating polyunsaturated fatty acid (PUFA) is considered

> > to be better than the alternative bad fats, cholesterol and

> > saturated or trans-fats. Trans-fats are not considered,

> > but the new pdf-available below appears to suggest

> > that what matters most for heart disease and all death

> > risks are alpha-linoleic acid (LA) and total PUFA is

> > more important than most other fats. Surprisingly,

> > total or saturated fat did not matter.

> >

> > The below for simplicity does not show the data of

> > Table 1-3, but did include the legend of Table 3 to

> > clarify the confounders corrected for to derive the Model 4

> > results.

> >

> > Table 1 examined the baseline characteristics and showed

> > that the factors associated with all-cause death at significance

> > level p<0.001 were age, smoking alcohol, socioeconomic status,

> > and C-reactive protein. For p<0.01, there were systolic blood

> > pressure and exercise. For p<0.05, there was diastolic

> > blood pressure, BMI and fasting insulin level.

> >

> > Table 2 respective numbers were blood

> > LA that was esterified and nonesterified,

> > LA, alpha-linolenic acid (ALA), PUFA,

> > alpha-tocopherol and ascorbic

> > acid for p<0.001; diet % of energy PUFA and LA; and fiber, LA,

> > ALA and % of energy ALA; but not statistically

> > different were calories, fat, monounsaturated fat and

nonesterified

> > PUFAs.

> >

> > Table 3 showed the follow-up cardiovascular deaths in thirds

> > of increasing levels to be related to LA, p<0.03; ALA, 0.18; and

> > PUFA, p<0.02 for the levels in the diet.

> >

> > Arch Intern Med. 2005 Jan 24;165(2):193-9.

> > Prediction of Cardiovascular Mortality in Middle-aged Men by

> > Dietary and Serum

> > Linoleic and Polyunsaturated Fatty Acids.

> > Laaksonen DE, Nyyssonen K, Niskanen L, Rissanen TH, Salonen JT.

> > PMID: 15668366 [PubMed - in process]

> >

> > BACKGROUND: Substitution of dietary polyunsaturated for

> saturated

> > fat has long

> > been recommended for the primary prevention of cardiovascular

> disease

> > (CVD), but

> > only a few prospective cohort studies have provided support for

> this

> > advice.

> > METHODS: We assessed the association of dietary linoleic and total

> > polyunsaturated fatty acid (PUFA) intake with cardiovascular and

> > overall

> > mortality in a population-based cohort of 1551 middle-aged men.

> > Dietary fat

> > composition was estimated with a 4-day food record and serum

fatty

> > acid

> > composition. RESULTS: During the 15-year follow-up, 78 men died

of

> > CVD and 225

> > of any cause. Total fat intake was not related to CVD or overall

> > mortality. Men

> > with an energy-adjusted dietary intake of linoleic acid (relative

> > risk [RR]

> > 0.39; 95% confidence interval [CI], 0.21-0.71) and PUFA (RR,

0.38;

> > 95% CI,

> > 0.20-0.70) in the upper third were less likely to die of CVD than

> men

> > with

> > intake in the lower third after adjustment for age. Multivariate

> > adjustment

> > weakened the association somewhat. Mortality from CVD was also

> lower

> > for men

> > with proportions of serum esterified linoleic acid (RR, 0.42; 95%

> CI,

> > 0.21-0.80)

> > and PUFA (RR, 0.25; 95% CI, 0.12-0.50) in the upper vs lower

third,

> > with some

> > attenuation in multivariate analyses. Serum and to a lesser

extent

> > dietary

> > linoleic acid and PUFA were also inversely associated with

overall

> > mortality.

> > CONCLUSIONS: Dietary polyunsaturated and more specifically

linoleic

> > fatty acid

> > intake may have a substantial cardioprotective benefit that is

also

> > reflected in

> > overall mortality. Dietary fat quality seems more important than

> fat

> > quantity in

> > the reduction of cardiovascular mortality in men.

> > PMID: 15668366 [PubMed - in process]

> >

> > INTRODUCTION

> > Substitution of dietary polyunsaturated for saturated fat has

> been

> > recommended for

> > several decades in the primary prevention of cardiovascular

disease

> > (CVD), but only a few

> > prospective cohort studies have provided support for this

advice.1-

> 4

> > A biological basis has

> > been provided by metabolic studies showing that polyunsaturated

fat

> > lowers, but saturated

> > fat increases, serum low-density lipoprotein cholesterol (LDL-C)

> > concentration.5 In

> > contrast, evidence for reduction of total fat intake without

> > modification of fat quality in

> > the prevention of CVD is weak.6-7

> > Trials in institutionalized patients have suggested that

> > substitution of

> > polyunsaturated for saturated fat may reduce coronary heart

disease

> > (CHD) or CVD.8-9 A few prospective

> > cohort studies have indicated that increased polyunsaturated fat

> > intake,1-4 a higher

> > polyunsaturated-saturated fat ratio,4 or Keys score1-2 may

decrease

> > incident CHD1-2,4 or

> > overall mortality,3 but more cohort studies have shown no

> > association.6 The discrepancies may

> > be due to small study size, imprecise dietary assessment, and

> > insufficient control of

> > confounding.7

> > Experimental and in vitro studies have suggested that n-3

fatty

> > acids such as

> > -linolenic acid and fish oils have anti-inflammatory,

> antithrombotic,

> > and antiarrhythmic

> > properties10-11 and improve insulin sensitivity.12 In contrast, n-

6

> > fatty acids such as linoleic

> > and arachidonic acid have even been purported to promote

> > inflammation, thrombosis, and

> > insulin resistance.11-13 In a review of the evidence, however,

> > linoleic acid also appears

> > to decrease thrombosis,10 and may also decrease arrhythmias14 and

> > improve insulin

> > sensitivity.15 Only a few prospective studies have supported a

role

> > of dietary linoleic16 or

> > -linolenic acid17 in primary CVD prevention.

> > Of the few cohort studies showing an inverse association of

> > dietary polyunsaturated

> > fatty acid (PUFA) intake with CVD, none has been population

based,

> > and only 1 study has

> > found an association with overall mortality.3 None of these

studies

> > has supported their

> > findings with serum biomarkers. The aim of the present study was

to

> > assess the association of

> > dietary fat quantity and quality, specifically linoleic and -

> > linolenic acid, with CVD and

> > overall mortality during a 15-year follow-up in a population-

based

> > cohort of 1551

> > middle-aged men who were free of CVD, cancer, and diabetes at

> > baseline.

> >

> > METHODS

> > The Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study is

a

> > prospective

> > population-based study.15, 18-22 The study population comprised a

> > random age-stratified sample of

> > 2682 men living in eastern Finland who were 42, 48, 54, or 60

years

> > old at baseline

> > between 1984 and 1989. The University of Kuopio Research Ethics

> > Committee approved the study.

> > All participants gave their written informed consent.

> > For the present study, all men with a history of CVD,

diabetes,

> or

> > cancer at baseline

> > (n = 1123) were excluded. Men with missing data for both dietary

> and

> > serum fatty acids

> > were also excluded, leaving 1551 men for the analyses.

> > ... saturated (SAFA), monounsaturated (MUFA), and linoleic

and -

> > linolenic fatty acids

> > was assessed with 4-day food records.23 The consumption of foods

> was

> > assessed at the time

> > of blood sampling at baseline. The dietary records were collected

> on

> > 3 workdays and 1

> > weekend day. Data collection was carried out year-round, except

for

> > July, when most Finns

> > are on vacation. The participants were instructed on the use of

> > household measures to

> > quantitatively record their food intake during the 4 days of data

> > collection. A nutritionist

> > gave the instructions and checked the completed food intake

> records.

> > Dietary intake of

> > nutrients and foods was calculated using NUTRICA software

(version

> > 2.5; National Public

> > Health Institute, Turku, Finland). The software is based on

mainly

> > Finnish values of nutrient

> > composition of foods. The nutrient compositions of foods in

NUTRICA

> > software version 2.5

> > have been analyzed mainly in the 1990s. For the assessment of

> dietary

> > fatty acids, an

> > earlier vers

> > ion

> > (1.0) was used because of the changes in fatty acid contents of

> > margarines in Finland

> > during the last 15 years. In all, the database contains

> comprehensive

> > data for 1300 food

> > items and dishes and 30 nutrients. Intake of fatty acids and

fiber

> > was calculated in grams

> > per day.

> >

> > ... RESULTS

> > The median follow-up for the cohort of 1551 men was 14.6 years

> > (range, 0.8-17.8

> > years), thus representing 22 645 person-years. During this time,

78

> > men died of CVD and 225

> > died of any cause. Because some men with dietary measures of fat

> > intake had missing serum

> > fatty acid measures and vice versa, there were 78 deaths from CVD

> and

> > 220 deaths from any

> > cause in analyses with dietary measures of fat intake.

> Corresponding

> > numbers for analyses

> > with serum fatty acid composition were 69 and 202, respectively.

> > Smoking, blood pressure,

> > BMI, and C-reactive protein were positively associated with CVD

or

> > overall mortality

> > (Table 1), and socioeconomic status, plasma vitamin E, plasma

> > ascorbic acid, and dietary

> > fiber intake were inversely associated. In analyses with

continuous

> > variables, men with a

> > lower dietary intake of linoleic and -linolenic acid and PUFA had

a

> > higher cardiovascular

> > and overall mortality after adjustment for age and year of

> > examination (P<.01 to P<.05;

> > Table 2). Pro

> > portions

> > of esterified linoleic and -linolenic acid and total PUFA and

> > proportions of

> > nonesterified linoleic acid were also inversely associated with

> death

> > from CVD or any cause (P<.001

> > to P<.05; Table 2). Intake of total fat, SAFA, MUFA, and

> cholesterol

> > were not associated

> > with CVD.

> > ... *Data are given as relative risk (95% confidence interval)

> of

> > cardiovascular death

> > (n = 78). proportional hazards regression analyses: model 1,

> > adjusted for

> > age and year of examination; model 2, adjusted for age, year of

> > examination, smoking,

> > alcohol consumption, adult socioeconomic status and moderate to

> > vigorous leisure-time physical activity; model 3, adjusted for

> model

> > 2 and plasma

> > lipid-standardized -tocopherol levels, plasma ascorbic acid, and

> > dietary total

> > energy and energy-adjusted saturated fat and fiber intake; and

> model

> > 4, adjusted for

> > model 3 and low-density lipoprotein cholesterol concentrations,

> > systolic

> > blood pressure, blood pressure medication, family history of

> ischemic

> > heart disease,

> > C-reactive protein concentrations, fasting concentrations of

> insulin

> > and

> > nonesterified fatty acids, and body mass index.

> >

> > Table 4. Relative Risks of Cardiovascular Death According to

> Serum

> > Fatty Acid

> > Proportions Categorized Into Thirds*

> > ------------------------------------------------------------------

--

> --

> > ----------------------------------

> > Serum Fatty Acid Proportion in Thirds, Median (Range), % Model 1

> > Model 2 Model 3 Model 4

> > ------------------------------------------------------------------

--

> --

> > -----------------------------------

> > Esterified linoleic acid proportions

> > 24 (11-26) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> > (Referent)

> > 28 (26-30) 0.82 (0.48-1.41) 0.95 (0.54-1.65) 1.00 (0.56-1.72)

1.20

> > (0.66-2.10)

> > 32 (30-43) 0.42 (0.21-0.80) 0.48 (0.24-0.93) 0.51 (0.24-1.04)

0.59

> > (0.28-1.23)

> > P for trend .01 .04 .08 .22

> > Esterified n-6 fatty acid proportions

> > 31 (16-33) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> > (Referent)

> > 35 (33-36) 0.64 (0.37-1.10) 0.74 (0.42-1.32) 0.79 (0.44-1.42)

0.99

> > (0.55-1.80)

> > 38 (36-49) 0.37 (0.19-0.72) 0.42 (0.22-0.83) 0.46 (0.23-0.95)

0.51

> > (0.25-1.07)

> > P for trend .003 .01 .04 .10

> > Esterified -linolenic acid proportions

> > 0.6 (0.0-0.7) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent)

1.00

> > (Referent)

> > 0.8 (0.7-0.9) 0.52 (0.28-0.97) 0.52 (0.28-0.97) 0.53 (0.28-0.99)

> 0.66

> > (0.34-1.28)

> > 1.0 (0.9-1.7) 0.77 (0.44-1.37) 0.84 (0.47-1.50) 0.86 (0.47-1.55)

> 1.19

> > (0.63-2.26)

> > P for trend .49 .52 .57 .61

> > Esterified polyunsaturated fatty acid proportions

> > 37 (22-39) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> > (Referent)

> > 40 (39-42) 0.56 (0.32-0.96) 0.66 (0.38-1.17) 0.72 (0.40-1.30)

0.84

> > (0.45-1.54)

> > 44 (42-54) 0.25 (0.12-0.50) 0.30 (0.15-0.62) 0.32 (0.15-0.70)

0.36

> > (0.16-0.79)

> > P for trend .001 .001 .004 .01

> > *Data are given as relative risk (95% confidence interval) of

> > cardiovascular death (n =

> > 69). See Table 3 for an explanation of the models.

> >

> > FATTY ACID CORRELATIONS

> > Dietary linoleic acid intake was correlated with nonesterified

> (r

> > = 0.34) and

> > esterified (r = 0.49) linoleic acid proportions. Total PUFA

intake

> > was composed of, on average,

> > 77% dietary linoleic acid and was highly correlated with total

PUFA

> > intake (r = 0.95).

> > Dietary PUFA and SAFA intake were inversely correlated (r = –

0.34).

> > Dietary PUFA intake and

> > serum PUFA esterified proportions were also correlated (r =

0.50).

> > These correlations

> > were highly significant (P<.001).

> > Nonesterified and esterified linoleic acid and PUFA

proportions

> > were also inversely

> > associated with BMI and fasting insulin and glucose

concentrations,

> > whereas the

> > corresponding fatty acids estimated from food records were not or

> > were only weakly associated. In

> > multivariate linear regression analyses, the determinants of

serum

> > esterified linoleic acid

> > proportions were dietary linoleic acid intake ( = .51), alcohol

> > intake ( = –.17), BMI ( =

> > –.11), blood glucose concentrations ( = –.07), serum insulin

> > concentrations ( = –.05),

> > and age ( = –.02). The corresponding determinants of esterified

> PUFA

> > proportions were

> > dietary PUFA intake ( = .51), alcohol intake ( = –.10), BMI ( = –

> > .03), glucose ( = –.09),

> > insulin ( = –.05), and age ( = –.06).

> >

> > DIETARY FATTY ACIDS AND CARDIOVASCULAR MORTALITY

> > Men with dietary linoleic acid intake in the upper third were

up

> > to 61% less likely to

> > die of CVD than their counterparts whose intake was in the lower

> > third after adjustment

> > for age and year of examination (Table 3). Men whose -linolenic

> acid

> > intake was in the

> > upper third were 30% to 42% less likely to die of CVD than men

> whose

> > intake was in the lower

> > third, but the associations were not significant. When using

> dietary -

> > linolenic acid

> > intake as a natural log–transformed continuous variable, the

> > association was statistically

> > significant in all models: model 1: relative risk (RR), 0.37 (95%

> > confidence interval [CI],

> > 0.18-0.77); model 2: RR, 0.43 (95% CI, 0.20-0.90); model 3: RR,

> 0.41

> > (95% CI, 0.18-0.91);

> > and model 4: RR, 0.42 (95% CI, 0.18-0.95).

> > Esterified -linolenic acid proportions were not associated

with

> > CVD mortality (Table

> > 4). The linoleic/-linolenic acid ratio (upper vs lower third,

model

> > 1: RR, 0.80 [95% CI,

> > 0.46-1.40]), n-6/n-3 ratio (upper vs lower third, model 1: RR,

0.80

> > [95% CI, 0.45-1.43]),

> > n-3 fatty acids (upper vs lower third, model 1: RR, 0.88, 95% CI,

> > 0.43-1.80), or long

> > chain PUFA (upper vs lower third, model 1: RR, 1.19 [95% CI, 0.67-

> > 2.09]) were not

> > significantly associated with CVD mortality. Nonesterified

linoleic

> > acid proportions were also

> > associated with CVD mortality, but the gradient was nonlinear,

with

> > the lowest risk in the

> > middle third (middle vs lower third, model 1: RR, 0.40 [95% CI,

> 0.22-

> > 0.75]). Adjustment for

> > confounding or mediating variables (models 2-4) weakened the

> > association (data not

> > shown).

> >

> > SERUM FATTY ACIDS AND OVERALL MORTALITY

> > Esterified linoleic acids proportions were or tended to be

> > associated with a lower

> > overall mortality (upper vs lower third, model 1: RR, 0.44 [95%

CI,

> > 0.30-0.67], P for trend,

> > <.001; model 2: RR, 0.59 [95% CI, 0.40-0.86], P for trend, .005;

> > model 3: RR, 0.66 [95%

> > CI, 0.43-0.97], P for trend, .03; model 4: RR, 0.69 [95% CI, 0.41-

> > 1.03], P for trend,

> > .08). The inverse associations for proportions of n-6 fatty acids

> and

> > especially PUFA were

> > even stronger and significant in all models (data not shown; P

for

> > trend, <.001 to.02). The

> > serum PUFA/SAFA ratio was also associated with overall mortality

> > (upper vs lower third,

> > model 1: RR, 0.44 [95% CI, 0.30-0.64]; model 2: RR, 0.57 [95% CI,

> > 0.39-0.84]; model 3: RR,

> > 0.60 [95% CI, 0.40-0.90]; and model 4: RR, 0.65 [95% CI, 0.43-

> 1.00]).

> > Esterified

> > -linolenic acid proportions had a borderline association with

> overall

> > mortality after adjustment

> > for age and year of examination (upper vs lower third, model 1:

RR,

> > 0.72 [95% CI,

> > 0.51-1.03], P f

> > or

> > trend, .05), but not after adjustment for potential confounding

or

> > mediating variables

> > (data not shown).

> >

> > COMMENT

> > Middle-aged men with proportions of serum linoleic acid, n-6

> fatty

> > acids, and

> > especially PUFA in the upper third were up to 3 times less likely

> to

> > die of CVD than men with

> > proportions in the lower third. Dietary intake of linoleic acid

and

> > total PUFA as assessed

> > with a 4-day food record was also inversely associated with CVD,

> but

> > total fat intake was

> > not. Importantly, both serum and dietary fatty acid composition

> were

> > assessed in this

> > study.

> > Men with energy-adjusted dietary PUFA intake in the upper

third

> > had less than half the

> > risk of premature CVD mortality as men with intake in the lower

> > third, even after

> > multivariate adjustment. The inverse correlations of dietary PUFA

> and

> > SAFA intake indicate that

> > the apparent benefit of PUFA intake probably comes about in part

> > through substitution of

> > PUFA for SAFA intake (in these men, by substitution of margarine

> for

> > butter).27 This,

> > coupled with the inverse association of the dietary PUFA/SAFA

ratio

> > with CVD mortality,

> > provides support for increasing PUFA intake at the expense of

SAFA

> > intake in the primary

> > prevention of CVD and underscores the importance of dietary fat

> > quality over quantity. These

> > findings agree with those from the Western Electric Study, in

which

> > coronary death was

> > the outcome,1 and the Nurses Health Study, in which myocardial

> > infarction was the outcome.4

> > Monounsaturated fatty acid intake was not associated with CVD or

> > overall mortality.

> > Possible benef

> > icial

> > effects in our study may be obscured by the high collinearity of

> > MUFA intake with SAFA

> > intake.

> > Serum esterified PUFA proportions were even more strongly

> > associated with CVD

> > mortality than dietary PUFA intake. Fasting insulin and glucose

> > levels, BMI, smoking, and alcohol

> > intake were also associated with serum fatty acid composition,

> > probably, at least in

> > part, independently of dietary fatty acid intake.28 Although

> > attenuated somewhat, the inverse

> > association of especially serum PUFA proportions with CVD

mortality

> > remained significant

> > even when adjusting for these variables.

> > After adjustment for lipids, the Pearson correlation of serum

> > esterified linoleic acid

> > proportions measured from whole serum with the energy-adjusted

> > dietary intake of linoleic

> > acid from the 4-day food diary was 0.50, much higher than that of

> > serum cholesterol ester

> > linoleic acid proportions with linoleic acid intake (r = 0.28),

as

> > estimated by a

> > semiquantitative food frequency questionnaire in the

> Atherosclerosis

> > Risk in Communities

> > Study.28 The correlation of serum linoleic acid proportions

> measured

> > 4 years later with dietary

> > linoleic acid intake at baseline in 895 men participating in the

> KIHD

> > Study 4-year

> > follow-up was 0.36 (data not shown). Serum esterified fatty acid

> > proportions are thus a good

> > measure of habitual dietary fat composition. Saturated fat intake

> in

> > Finland has decreased

> > since the mid-1980s27 when the KIHD Study began, but our data

> > indicate that the relative

> > ranking of these men with respect to dietary fat quality may be

> > stabile, at least during

> > the firs

> > t 4

> > years of follow-up.

> > Nonesterified linoleic acid proportions in the fasting state

> also

> > reflect adipose and

> > dietary fatty acid composition.29 Men with higher nonesterified

> > linoleic acid proportions

> > seemed to have a lower CVD mortality, but the lowest mortality

was

> in

> > the middle third.

> > The imprecision and low sensitivity of the measurement of

> > nonesterified fatty acids in our

> > study (coefficient of variation, 15%) may explain the discrepancy

> in

> > results between

> > nonesterified and esterified linoleic acid proportions.

> > Men with dietary intake of linoleic acid in the upper third

were

> > less than half as

> > likely to die of CVD than men with intake in the lower third.

> > Findings for serum proportions

> > of linoleic acid and especially total n-6 fatty acids were

similar,

> > although some

> > attenuation was seen in multivariate models. Because linoleic

acid

> > (18:2n-6) is elongated to

> > arachidonic acid (20:4n-6) in the metabolism of serum fatty

acids,

> n-

> > 6 fatty acid

> > proportions are also an index of linoleic acid intake. The Nurses

> > Health Study also found an

> > inverse association of dietary linoleic acid intake with incident

> > CHD.4 Serum linoleic acid

> > proportions have also been inversely associated with incident

CHD30-

> > 31 and stroke32 in

> > nested case-control30, 32 and cohort31 studies. For serum

linoleic

> > and n-6 fatty acids and

> > total PUFA proportions, this apparent protective benefit carried

> over

> > to lower overall

> > mortality. Because CVD deaths made up only about one third of

total

> > deaths, this implies that

> > n-6 fatty

> > acids

> > may also tend to decrease non-CVD mortality.

> > We found a nonsignificant trend for an inverse association of

> > dietary and serum

> > -linolenic acid, but not serum fish oils, with CVD and overall

> > mortality. The Lyon Heart

> > Study,33 with increased -linolenic acid intake as one of the

> dietary

> > interventions, and the

> > Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto

> > miocardico

> > (GISSI)-Prevenzione trial,34 which focused on fish oil

supplements,

> > show that n-3 fatty acids reduce risk

> > in secondary CHD prevention. In the present study, -linolenic

acid

> > intake at baseline was

> > low. Furthermore, in this cohort fish oils, which were inversely

> > associated with acute

> > coronary events,20 come mainly from nonfatty lake fish. In

Finland,

> > lake fish are also a

> > major dietary source of mercury, which was positively associated

> with

> > coronary events.20

> > Total PUFA intake was low in these middle-aged Finnish men,

but

> > the n-6/n-3 ratio was

> > high (6.5 ± 1.8). We found no association of the serum n-6/n-3

> ratio

> > with CVD or overall

> > mortality. Some in vitro, animal, and cross-sectional studies

have

> > suggested that a high

> > n-6/n-3 ratio may increase the risk of CVD, but the evidence

> > suggesting that it may have

> > a clinical or public health relevance is weak6 and inconsistent

> with

> > the present

> > findings.

> > Strengths of this study include its longitudinal population-

> based

> > design, detailed

> > assessment of potential confounding and mediating factors, and

> > assessment of dietary fat

> > composition with both food records and serum biomarkers. The

> > consistency of the associations

> > of dietary intake of linoleic acid and PUFA and corresponding

serum

> > proportions,

> > especially with CVD mortality, lends further validity to the

> > findings. The main findings

> > suggesting that increased linoleic acid or PUFA intake or

> > substitution of polyunsaturated for

> > saturated fat decreases CVD mortality furthermore agree with

those

> of

> > the Nurses Health

> > Study.4 Nonetheless, these associations may not apply to high

> > polyunsaturated fat and low

> > saturated fat diets or to other ethnic groups.

> > We found strong inverse associations of dietary and serum

> linoleic

> > acid and PUFA, but

> > no association of dietary total fat intake, with CVD mortality.

> > Dietary fat quality thus

> > seems more important than fat quantity in the reduction of CVD

> > mortality in middle-aged

> > men. Carrying out recommendations to replace saturated fat with

> > polyunsaturated fat in the

> > primary prevention of cardiovascular disease may substantially

> > decrease CVD and to a

> > lesser degree overall mortality.

> >

> >

> > Cheers, Alan Pater

[Guest guest]

Hi folks:

And another new study from an entirely different population coming to

a similar conclusion regarding LA protecting against cancer.

In addition this study found, again, that starch increases cancer

risk.

Rodney.

> >

> > Hi All,

> >

> > Eating polyunsaturated fatty acid (PUFA) is considered

> > to be better than the alternative bad fats, cholesterol and

> > saturated or trans-fats. Trans-fats are not considered,

> > but the new pdf-available below appears to suggest

> > that what matters most for heart disease and all death

> > risks are alpha-linoleic acid (LA) and total PUFA is

> > more important than most other fats. Surprisingly,

> > total or saturated fat did not matter.

> >

> > The below for simplicity does not show the data of

> > Table 1-3, but did include the legend of Table 3 to

> > clarify the confounders corrected for to derive the Model 4

> > results.

> >

> > Table 1 examined the baseline characteristics and showed

> > that the factors associated with all-cause death at significance

> > level p<0.001 were age, smoking alcohol, socioeconomic status,

> > and C-reactive protein. For p<0.01, there were systolic blood

> > pressure and exercise. For p<0.05, there was diastolic

> > blood pressure, BMI and fasting insulin level.

> >

> > Table 2 respective numbers were blood

> > LA that was esterified and nonesterified,

> > LA, alpha-linolenic acid (ALA), PUFA,

> > alpha-tocopherol and ascorbic

> > acid for p<0.001; diet % of energy PUFA and LA; and fiber, LA,

> > ALA and % of energy ALA; but not statistically

> > different were calories, fat, monounsaturated fat and

nonesterified

> > PUFAs.

> >

> > Table 3 showed the follow-up cardiovascular deaths in thirds

> > of increasing levels to be related to LA, p<0.03; ALA, 0.18; and

> > PUFA, p<0.02 for the levels in the diet.

> >

> > Arch Intern Med. 2005 Jan 24;165(2):193-9.

> > Prediction of Cardiovascular Mortality in Middle-aged Men by

> > Dietary and Serum

> > Linoleic and Polyunsaturated Fatty Acids.

> > Laaksonen DE, Nyyssonen K, Niskanen L, Rissanen TH, Salonen JT.

> > PMID: 15668366 [PubMed - in process]

> >

> > BACKGROUND: Substitution of dietary polyunsaturated for

> saturated

> > fat has long

> > been recommended for the primary prevention of cardiovascular

> disease

> > (CVD), but

> > only a few prospective cohort studies have provided support for

> this

> > advice.

> > METHODS: We assessed the association of dietary linoleic and total

> > polyunsaturated fatty acid (PUFA) intake with cardiovascular and

> > overall

> > mortality in a population-based cohort of 1551 middle-aged men.

> > Dietary fat

> > composition was estimated with a 4-day food record and serum

fatty

> > acid

> > composition. RESULTS: During the 15-year follow-up, 78 men died

of

> > CVD and 225

> > of any cause. Total fat intake was not related to CVD or overall

> > mortality. Men

> > with an energy-adjusted dietary intake of linoleic acid (relative

> > risk [RR]

> > 0.39; 95% confidence interval [CI], 0.21-0.71) and PUFA (RR,

0.38;

> > 95% CI,

> > 0.20-0.70) in the upper third were less likely to die of CVD than

> men

> > with

> > intake in the lower third after adjustment for age. Multivariate

> > adjustment

> > weakened the association somewhat. Mortality from CVD was also

> lower

> > for men

> > with proportions of serum esterified linoleic acid (RR, 0.42; 95%

> CI,

> > 0.21-0.80)

> > and PUFA (RR, 0.25; 95% CI, 0.12-0.50) in the upper vs lower

third,

> > with some

> > attenuation in multivariate analyses. Serum and to a lesser

extent

> > dietary

> > linoleic acid and PUFA were also inversely associated with

overall

> > mortality.

> > CONCLUSIONS: Dietary polyunsaturated and more specifically

linoleic

> > fatty acid

> > intake may have a substantial cardioprotective benefit that is

also

> > reflected in

> > overall mortality. Dietary fat quality seems more important than

> fat

> > quantity in

> > the reduction of cardiovascular mortality in men.

> > PMID: 15668366 [PubMed - in process]

> >

> > INTRODUCTION

> > Substitution of dietary polyunsaturated for saturated fat has

> been

> > recommended for

> > several decades in the primary prevention of cardiovascular

disease

> > (CVD), but only a few

> > prospective cohort studies have provided support for this

advice.1-

> 4

> > A biological basis has

> > been provided by metabolic studies showing that polyunsaturated

fat

> > lowers, but saturated

> > fat increases, serum low-density lipoprotein cholesterol (LDL-C)

> > concentration.5 In

> > contrast, evidence for reduction of total fat intake without

> > modification of fat quality in

> > the prevention of CVD is weak.6-7

> > Trials in institutionalized patients have suggested that

> > substitution of

> > polyunsaturated for saturated fat may reduce coronary heart

disease

> > (CHD) or CVD.8-9 A few prospective

> > cohort studies have indicated that increased polyunsaturated fat

> > intake,1-4 a higher

> > polyunsaturated-saturated fat ratio,4 or Keys score1-2 may

decrease

> > incident CHD1-2,4 or

> > overall mortality,3 but more cohort studies have shown no

> > association.6 The discrepancies may

> > be due to small study size, imprecise dietary assessment, and

> > insufficient control of

> > confounding.7

> > Experimental and in vitro studies have suggested that n-3

fatty

> > acids such as

> > -linolenic acid and fish oils have anti-inflammatory,

> antithrombotic,

> > and antiarrhythmic

> > properties10-11 and improve insulin sensitivity.12 In contrast, n-

6

> > fatty acids such as linoleic

> > and arachidonic acid have even been purported to promote

> > inflammation, thrombosis, and

> > insulin resistance.11-13 In a review of the evidence, however,

> > linoleic acid also appears

> > to decrease thrombosis,10 and may also decrease arrhythmias14 and

> > improve insulin

> > sensitivity.15 Only a few prospective studies have supported a

role

> > of dietary linoleic16 or

> > -linolenic acid17 in primary CVD prevention.

> > Of the few cohort studies showing an inverse association of

> > dietary polyunsaturated

> > fatty acid (PUFA) intake with CVD, none has been population

based,

> > and only 1 study has

> > found an association with overall mortality.3 None of these

studies

> > has supported their

> > findings with serum biomarkers. The aim of the present study was

to

> > assess the association of

> > dietary fat quantity and quality, specifically linoleic and -

> > linolenic acid, with CVD and

> > overall mortality during a 15-year follow-up in a population-

based

> > cohort of 1551

> > middle-aged men who were free of CVD, cancer, and diabetes at

> > baseline.

> >

> > METHODS

> > The Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study is

a

> > prospective

> > population-based study.15, 18-22 The study population comprised a

> > random age-stratified sample of

> > 2682 men living in eastern Finland who were 42, 48, 54, or 60

years

> > old at baseline

> > between 1984 and 1989. The University of Kuopio Research Ethics

> > Committee approved the study.

> > All participants gave their written informed consent.

> > For the present study, all men with a history of CVD,

diabetes,

> or

> > cancer at baseline

> > (n = 1123) were excluded. Men with missing data for both dietary

> and

> > serum fatty acids

> > were also excluded, leaving 1551 men for the analyses.

> > ... saturated (SAFA), monounsaturated (MUFA), and linoleic

and -

> > linolenic fatty acids

> > was assessed with 4-day food records.23 The consumption of foods

> was

> > assessed at the time

> > of blood sampling at baseline. The dietary records were collected

> on

> > 3 workdays and 1

> > weekend day. Data collection was carried out year-round, except

for

> > July, when most Finns

> > are on vacation. The participants were instructed on the use of

> > household measures to

> > quantitatively record their food intake during the 4 days of data

> > collection. A nutritionist

> > gave the instructions and checked the completed food intake

> records.

> > Dietary intake of

> > nutrients and foods was calculated using NUTRICA software

(version

> > 2.5; National Public

> > Health Institute, Turku, Finland). The software is based on

mainly

> > Finnish values of nutrient

> > composition of foods. The nutrient compositions of foods in

NUTRICA

> > software version 2.5

> > have been analyzed mainly in the 1990s. For the assessment of

> dietary

> > fatty acids, an

> > earlier vers

> > ion

> > (1.0) was used because of the changes in fatty acid contents of

> > margarines in Finland

> > during the last 15 years. In all, the database contains

> comprehensive

> > data for 1300 food

> > items and dishes and 30 nutrients. Intake of fatty acids and

fiber

> > was calculated in grams

> > per day.

> >

> > ... RESULTS

> > The median follow-up for the cohort of 1551 men was 14.6 years

> > (range, 0.8-17.8

> > years), thus representing 22 645 person-years. During this time,

78

> > men died of CVD and 225

> > died of any cause. Because some men with dietary measures of fat

> > intake had missing serum

> > fatty acid measures and vice versa, there were 78 deaths from CVD

> and

> > 220 deaths from any

> > cause in analyses with dietary measures of fat intake.

> Corresponding

> > numbers for analyses

> > with serum fatty acid composition were 69 and 202, respectively.

> > Smoking, blood pressure,

> > BMI, and C-reactive protein were positively associated with CVD

or

> > overall mortality

> > (Table 1), and socioeconomic status, plasma vitamin E, plasma

> > ascorbic acid, and dietary

> > fiber intake were inversely associated. In analyses with

continuous

> > variables, men with a

> > lower dietary intake of linoleic and -linolenic acid and PUFA had

a

> > higher cardiovascular

> > and overall mortality after adjustment for age and year of

> > examination (P<.01 to P<.05;

> > Table 2). Pro

> > portions

> > of esterified linoleic and -linolenic acid and total PUFA and

> > proportions of

> > nonesterified linoleic acid were also inversely associated with

> death

> > from CVD or any cause (P<.001

> > to P<.05; Table 2). Intake of total fat, SAFA, MUFA, and

> cholesterol

> > were not associated

> > with CVD.

> > ... *Data are given as relative risk (95% confidence interval)

> of

> > cardiovascular death

> > (n = 78). proportional hazards regression analyses: model 1,

> > adjusted for

> > age and year of examination; model 2, adjusted for age, year of

> > examination, smoking,

> > alcohol consumption, adult socioeconomic status and moderate to

> > vigorous leisure-time physical activity; model 3, adjusted for

> model

> > 2 and plasma

> > lipid-standardized -tocopherol levels, plasma ascorbic acid, and

> > dietary total

> > energy and energy-adjusted saturated fat and fiber intake; and

> model

> > 4, adjusted for

> > model 3 and low-density lipoprotein cholesterol concentrations,

> > systolic

> > blood pressure, blood pressure medication, family history of

> ischemic

> > heart disease,

> > C-reactive protein concentrations, fasting concentrations of

> insulin

> > and

> > nonesterified fatty acids, and body mass index.

> >

> > Table 4. Relative Risks of Cardiovascular Death According to

> Serum

> > Fatty Acid

> > Proportions Categorized Into Thirds*

> > ------------------------------------------------------------------

--

> --

> > ----------------------------------

> > Serum Fatty Acid Proportion in Thirds, Median (Range), % Model 1

> > Model 2 Model 3 Model 4

> > ------------------------------------------------------------------

--

> --

> > -----------------------------------

> > Esterified linoleic acid proportions

> > 24 (11-26) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> > (Referent)

> > 28 (26-30) 0.82 (0.48-1.41) 0.95 (0.54-1.65) 1.00 (0.56-1.72)

1.20

> > (0.66-2.10)

> > 32 (30-43) 0.42 (0.21-0.80) 0.48 (0.24-0.93) 0.51 (0.24-1.04)

0.59

> > (0.28-1.23)

> > P for trend .01 .04 .08 .22

> > Esterified n-6 fatty acid proportions

> > 31 (16-33) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> > (Referent)

> > 35 (33-36) 0.64 (0.37-1.10) 0.74 (0.42-1.32) 0.79 (0.44-1.42)

0.99

> > (0.55-1.80)

> > 38 (36-49) 0.37 (0.19-0.72) 0.42 (0.22-0.83) 0.46 (0.23-0.95)

0.51

> > (0.25-1.07)

> > P for trend .003 .01 .04 .10

> > Esterified -linolenic acid proportions

> > 0.6 (0.0-0.7) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent)

1.00

> > (Referent)

> > 0.8 (0.7-0.9) 0.52 (0.28-0.97) 0.52 (0.28-0.97) 0.53 (0.28-0.99)

> 0.66

> > (0.34-1.28)

> > 1.0 (0.9-1.7) 0.77 (0.44-1.37) 0.84 (0.47-1.50) 0.86 (0.47-1.55)

> 1.19

> > (0.63-2.26)

> > P for trend .49 .52 .57 .61

> > Esterified polyunsaturated fatty acid proportions

> > 37 (22-39) 1.00 (Referent) 1.00 (Referent) 1.00 (Referent) 1.00

> > (Referent)

> > 40 (39-42) 0.56 (0.32-0.96) 0.66 (0.38-1.17) 0.72 (0.40-1.30)

0.84

> > (0.45-1.54)

> > 44 (42-54) 0.25 (0.12-0.50) 0.30 (0.15-0.62) 0.32 (0.15-0.70)

0.36

> > (0.16-0.79)

> > P for trend .001 .001 .004 .01

> > *Data are given as relative risk (95% confidence interval) of

> > cardiovascular death (n =

> > 69). See Table 3 for an explanation of the models.

> >

> > FATTY ACID CORRELATIONS

> > Dietary linoleic acid intake was correlated with nonesterified

> (r

> > = 0.34) and

> > esterified (r = 0.49) linoleic acid proportions. Total PUFA

intake

> > was composed of, on average,

> > 77% dietary linoleic acid and was highly correlated with total

PUFA

> > intake (r = 0.95).

> > Dietary PUFA and SAFA intake were inversely correlated (r = –

0.34).

> > Dietary PUFA intake and

> > serum PUFA esterified proportions were also correlated (r =

0.50).

> > These correlations

> > were highly significant (P<.001).

> > Nonesterified and esterified linoleic acid and PUFA

proportions

> > were also inversely

> > associated with BMI and fasting insulin and glucose

concentrations,

> > whereas the

> > corresponding fatty acids estimated from food records were not or

> > were only weakly associated. In

> > multivariate linear regression analyses, the determinants of

serum

> > esterified linoleic acid

> > proportions were dietary linoleic acid intake ( = .51), alcohol

> > intake ( = –.17), BMI ( =

> > –.11), blood glucose concentrations ( = –.07), serum insulin

> > concentrations ( = –.05),

> > and age ( = –.02). The corresponding determinants of esterified

> PUFA

> > proportions were

> > dietary PUFA intake ( = .51), alcohol intake ( = –.10), BMI ( = –

> > .03), glucose ( = –.09),

> > insulin ( = –.05), and age ( = –.06).

> >

> > DIETARY FATTY ACIDS AND CARDIOVASCULAR MORTALITY

> > Men with dietary linoleic acid intake in the upper third were

up

> > to 61% less likely to

> > die of CVD than their counterparts whose intake was in the lower

> > third after adjustment

> > for age and year of examination (Table 3). Men whose -linolenic

> acid

> > intake was in the

> > upper third were 30% to 42% less likely to die of CVD than men

> whose

> > intake was in the lower

> > third, but the associations were not significant. When using

> dietary -

> > linolenic acid

> > intake as a natural log–transformed continuous variable, the

> > association was statistically

> > significant in all models: model 1: relative risk (RR), 0.37 (95%

> > confidence interval [CI],

> > 0.18-0.77); model 2: RR, 0.43 (95% CI, 0.20-0.90); model 3: RR,

> 0.41

> > (95% CI, 0.18-0.91);

> > and model 4: RR, 0.42 (95% CI, 0.18-0.95).

> > Esterified -linolenic acid proportions were not associated

with

> > CVD mortality (Table

> > 4). The linoleic/-linolenic acid ratio (upper vs lower third,

model

> > 1: RR, 0.80 [95% CI,

> > 0.46-1.40]), n-6/n-3 ratio (upper vs lower third, model 1: RR,

0.80

> > [95% CI, 0.45-1.43]),

> > n-3 fatty acids (upper vs lower third, model 1: RR, 0.88, 95% CI,

> > 0.43-1.80), or long

> > chain PUFA (upper vs lower third, model 1: RR, 1.19 [95% CI, 0.67-

> > 2.09]) were not

> > significantly associated with CVD mortality. Nonesterified

linoleic

> > acid proportions were also

> > associated with CVD mortality, but the gradient was nonlinear,

with

> > the lowest risk in the

> > middle third (middle vs lower third, model 1: RR, 0.40 [95% CI,

> 0.22-

> > 0.75]). Adjustment for

> > confounding or mediating variables (models 2-4) weakened the

> > association (data not

> > shown).

> >

> > SERUM FATTY ACIDS AND OVERALL MORTALITY

> > Esterified linoleic acids proportions were or tended to be

> > associated with a lower

> > overall mortality (upper vs lower third, model 1: RR, 0.44 [95%

CI,

> > 0.30-0.67], P for trend,

> > <.001; model 2: RR, 0.59 [95% CI, 0.40-0.86], P for trend, .005;

> > model 3: RR, 0.66 [95%

> > CI, 0.43-0.97], P for trend, .03; model 4: RR, 0.69 [95% CI, 0.41-

> > 1.03], P for trend,

> > .08). The inverse associations for proportions of n-6 fatty acids

> and

> > especially PUFA were

> > even stronger and significant in all models (data not shown; P

for

> > trend, <.001 to.02). The

> > serum PUFA/SAFA ratio was also associated with overall mortality

> > (upper vs lower third,

> > model 1: RR, 0.44 [95% CI, 0.30-0.64]; model 2: RR, 0.57 [95% CI,

> > 0.39-0.84]; model 3: RR,

> > 0.60 [95% CI, 0.40-0.90]; and model 4: RR, 0.65 [95% CI, 0.43-

> 1.00]).

> > Esterified

> > -linolenic acid proportions had a borderline association with

> overall

> > mortality after adjustment

> > for age and year of examination (upper vs lower third, model 1:

RR,

> > 0.72 [95% CI,

> > 0.51-1.03], P f

> > or

> > trend, .05), but not after adjustment for potential confounding

or

> > mediating variables

> > (data not shown).

> >

> > COMMENT

> > Middle-aged men with proportions of serum linoleic acid, n-6

> fatty

> > acids, and

> > especially PUFA in the upper third were up to 3 times less likely

> to

> > die of CVD than men with

> > proportions in the lower third. Dietary intake of linoleic acid

and

> > total PUFA as assessed

> > with a 4-day food record was also inversely associated with CVD,

> but

> > total fat intake was

> > not. Importantly, both serum and dietary fatty acid composition

> were

> > assessed in this

> > study.

> > Men with energy-adjusted dietary PUFA intake in the upper

third

> > had less than half the

> > risk of premature CVD mortality as men with intake in the lower

> > third, even after

> > multivariate adjustment. The inverse correlations of dietary PUFA

> and

> > SAFA intake indicate that

> > the apparent benefit of PUFA intake probably comes about in part

> > through substitution of

> > PUFA for SAFA intake (in these men, by substitution of margarine

> for

> > butter).27 This,

> > coupled with the inverse association of the dietary PUFA/SAFA

ratio

> > with CVD mortality,

> > provides support for increasing PUFA intake at the expense of

SAFA

> > intake in the primary

> > prevention of CVD and underscores the importance of dietary fat

> > quality over quantity. These

> > findings agree with those from the Western Electric Study, in

which

> > coronary death was

> > the outcome,1 and the Nurses Health Study, in which myocardial

> > infarction was the outcome.4

> > Monounsaturated fatty acid intake was not associated with CVD or

> > overall mortality.

> > Possible benef

> > icial

> > effects in our study may be obscured by the high collinearity of

> > MUFA intake with SAFA

> > intake.

> > Serum esterified PUFA proportions were even more strongly

> > associated with CVD

> > mortality than dietary PUFA intake. Fasting insulin and glucose

> > levels, BMI, smoking, and alcohol

> > intake were also associated with serum fatty acid composition,

> > probably, at least in

> > part, independently of dietary fatty acid intake.28 Although

> > attenuated somewhat, the inverse

> > association of especially serum PUFA proportions with CVD

mortality

> > remained significant

> > even when adjusting for these variables.

> > After adjustment for lipids, the Pearson correlation of serum

> > esterified linoleic acid

> > proportions measured from whole serum with the energy-adjusted

> > dietary intake of linoleic

> > acid from the 4-day food diary was 0.50, much higher than that of

> > serum cholesterol ester

> > linoleic acid proportions with linoleic acid intake (r = 0.28),

as

> > estimated by a

> > semiquantitative food frequency questionnaire in the

> Atherosclerosis

> > Risk in Communities

> > Study.28 The correlation of serum linoleic acid proportions

> measured

> > 4 years later with dietary

> > linoleic acid intake at baseline in 895 men participating in the

> KIHD

> > Study 4-year

> > follow-up was 0.36 (data not shown). Serum esterified fatty acid

> > proportions are thus a good

> > measure of habitual dietary fat composition. Saturated fat intake

> in

> > Finland has decreased

> > since the mid-1980s27 when the KIHD Study began, but our data

> > indicate that the relative

> > ranking of these men with respect to dietary fat quality may be

> > stabile, at least during

> > the firs

> > t 4

> > years of follow-up.

> > Nonesterified linoleic acid proportions in the fasting state

> also

> > reflect adipose and

> > dietary fatty acid composition.29 Men with higher nonesterified

> > linoleic acid proportions

> > seemed to have a lower CVD mortality, but the lowest mortality

was

> in

> > the middle third.

> > The imprecision and low sensitivity of the measurement of

> > nonesterified fatty acids in our

> > study (coefficient of variation, 15%) may explain the discrepancy

> in

> > results between

> > nonesterified and esterified linoleic acid proportions.

> > Men with dietary intake of linoleic acid in the upper third

were

> > less than half as

> > likely to die of CVD than men with intake in the lower third.

> > Findings for serum proportions

> > of linoleic acid and especially total n-6 fatty acids were

similar,

> > although some

> > attenuation was seen in multivariate models. Because linoleic

acid

> > (18:2n-6) is elongated to

> > arachidonic acid (20:4n-6) in the metabolism of serum fatty

acids,

> n-

> > 6 fatty acid

> > proportions are also an index of linoleic acid intake. The Nurses

> > Health Study also found an

> > inverse association of dietary linoleic acid intake with incident

> > CHD.4 Serum linoleic acid

> > proportions have also been inversely associated with incident

CHD30-

> > 31 and stroke32 in

> > nested case-control30, 32 and cohort31 studies. For serum

linoleic

> > and n-6 fatty acids and

> > total PUFA proportions, this apparent protective benefit carried

> over

> > to lower overall

> > mortality. Because CVD deaths made up only about one third of

total

> > deaths, this implies that

> > n-6 fatty

> > acids

> > may also tend to decrease non-CVD mortality.

> > We found a nonsignificant trend for an inverse association of

> > dietary and serum

> > -linolenic acid, but not serum fish oils, with CVD and overall

> > mortality. The Lyon Heart

> > Study,33 with increased -linolenic acid intake as one of the

> dietary

> > interventions, and the

> > Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto

> > miocardico

> > (GISSI)-Prevenzione trial,34 which focused on fish oil

supplements,

> > show that n-3 fatty acids reduce risk

> > in secondary CHD prevention. In the present study, -linolenic

acid

> > intake at baseline was

> > low. Furthermore, in this cohort fish oils, which were inversely

> > associated with acute

> > coronary events,20 come mainly from nonfatty lake fish. In

Finland,

> > lake fish are also a

> > major dietary source of mercury, which was positively associated

> with

> > coronary events.20

> > Total PUFA intake was low in these middle-aged Finnish men,

but

> > the n-6/n-3 ratio was

> > high (6.5 ± 1.8). We found no association of the serum n-6/n-3

> ratio

> > with CVD or overall

> > mortality. Some in vitro, animal, and cross-sectional studies

have

> > suggested that a high

> > n-6/n-3 ratio may increase the risk of CVD, but the evidence

> > suggesting that it may have

> > a clinical or public health relevance is weak6 and inconsistent

> with

> > the present

> > findings.

> > Strengths of this study include its longitudinal population-

> based

> > design, detailed

> > assessment of potential confounding and mediating factors, and

> > assessment of dietary fat

> > composition with both food records and serum biomarkers. The

> > consistency of the associations

> > of dietary intake of linoleic acid and PUFA and corresponding

serum

> > proportions,

> > especially with CVD mortality, lends further validity to the

> > findings. The main findings

> > suggesting that increased linoleic acid or PUFA intake or

> > substitution of polyunsaturated for

> > saturated fat decreases CVD mortality furthermore agree with

those

> of

> > the Nurses Health

> > Study.4 Nonetheless, these associations may not apply to high

> > polyunsaturated fat and low

> > saturated fat diets or to other ethnic groups.

> > We found strong inverse associations of dietary and serum

> linoleic

> > acid and PUFA, but

> > no association of dietary total fat intake, with CVD mortality.

> > Dietary fat quality thus

> > seems more important than fat quantity in the reduction of CVD

> > mortality in middle-aged

> > men. Carrying out recommendations to replace saturated fat with

> > polyunsaturated fat in the

> > primary prevention of cardiovascular disease may substantially

> > decrease CVD and to a

> > lesser degree overall mortality.

> >

> >

> > Cheers, Alan Pater

[Guest guest]

DUH!!!! Sorry. Here are relevant abstract excerpts:

" ............. linoleic acid (OR = 0.8; 95% CI: 0.6-1.0) were

inversely related to prostate cancer. " , and

" CONCLUSIONS: Starch and monounsaturated fatty acids were directly

associated with prostate cancer risk ................ " .

Here is the abstract:

" Macronutrients, fatty acids, cholesterol and prostate cancer risk.

Bidoli E, Talamini R, Bosetti C, Negri E, Maruzzi D, Montella M,

Franceschi S, La Vecchia C.

Servizio di Epidemiologia e Biostatistica, Centro di Riferimento

Oncologico, Aviano (PN).

BACKGROUND: The role of selected macronutrients, fatty acids and

cholesterol in the etiology of prostate cancer was analyzed using

data from a case-control study carried out in five Italian areas

between 1991 and 2002. PATIENTS AND METHODS: Cases were 1294 men with

incident, histologically confirmed prostate cancer, and admitted to

the major teaching and general hospitals of study areas. Controls

were 1451 men admitted for acute, non-neoplastic conditions to the

same hospital network. Information on dietary habits was elicited

using a validated food frequency questionnaire including 78 food

groups and recipes. Odds ratios (OR) and 95% confidence intervals

(CI) were estimated for increasing levels of nutrient intake.

RESULTS: A direct association with prostate cancer was found for

starch intake (OR = 1.4 in the highest versus the lowest quintile of

intake; 95% CI: 1.1-1.8), whereas an inverse association emerged for

polyunsaturated fatty acids (OR = 0.8; 95% CI: 0.6-1.0). Among

polyunsaturated fatty acids, linolenic acid (OR = 0.7; 95% CI: 0.6-

0.9) and linoleic acid (OR = 0.8; 95% CI: 0.6-1.0) were inversely

related to prostate cancer. When the six major macronutrients were

included in the same model, the adverse effect of high intake of

starch and monounsaturated fatty acids was statistically significant

together with the protective effect of polyunsaturated fatty acids.

Results were consistent in separate strata of age, body mass index

and family history of prostate cancer. CONCLUSIONS: Starch and

monounsaturated fatty acids were directly associated with prostate

cancer risk and polyunsaturated fatty acids were inversely associated.

PMID: 15598953 [PubMed - in process] "

Rodney.

>

> > Hi folks:

> >

> > And another new study from an entirely different population

coming to

> > a similar conclusion regarding LA protecting against cancer.

> >

> > In addition this study found, again, that starch increases cancer

> > risk.

> >

> > Rodney.

[Guest guest]

Hi JW:

Am I confused? It seems to me that these studies appear to be saying

that LA is protective against both CVD and some forms of cancer.

Rodney.

> >

[Guest guest]

Hi Francesca:

I suspect it was not the ALA molecule that caused the advanced

prostate cancer in the PHS but, rather, ALA was a 'marker' for

aflatoxin.

Perhaps similarly, starch may be a marker for something else.

Nevertheless, if so, eating the starch necessarily entails increasing

the chances of eating the marker that causes the cancer. And starch,

corn starch for example, is a concentrated source of calories with

negligible micronutrients.

EAT THE BRAN!!! And the germ too, if you want.

'Just my take' .............

Rodney.

>

> > Hi Rodney,

> > I have a feeling that anything that provides nutrition to the

cells also

> > provides nutrition to the carcinomas.

> > LA IS the one proven essential fatty acid.

> > Maybe in excess LA is bad, but so is everything else.

> >

> > Regards.

[Guest guest]

Hi All,

This was not a prospective study. It found that adjustment allowed

only the polyunsaturated level to be associated with lower prstate

cancer risk. ALA helped better than LA.

Cheers, Al Pater.

--- In , " Rodney " <perspect1111@y...>

wrote:

>

> DUH!!!! Sorry. Here are relevant abstract excerpts:

>

> " ............. linoleic acid (OR = 0.8; 95% CI: 0.6-1.0) were

> inversely related to prostate cancer. " , and

>

> " CONCLUSIONS: Starch and monounsaturated fatty acids were directly

> associated with prostate cancer risk ................ " .

>

> Here is the abstract:

>

> " Macronutrients, fatty acids, cholesterol and prostate cancer risk.

>

> Bidoli E, Talamini R, Bosetti C, Negri E, Maruzzi D, Montella M,

> Franceschi S, La Vecchia C.

>

> Servizio di Epidemiologia e Biostatistica, Centro di Riferimento

> Oncologico, Aviano (PN).

>

> BACKGROUND: The role of selected macronutrients, fatty acids and

> cholesterol in the etiology of prostate cancer was analyzed using

> data from a case-control study carried out in five Italian areas

> between 1991 and 2002. PATIENTS AND METHODS: Cases were 1294 men

with

> incident, histologically confirmed prostate cancer, and admitted to

> the major teaching and general hospitals of study areas. Controls

> were 1451 men admitted for acute, non-neoplastic conditions to the

> same hospital network. Information on dietary habits was elicited

> using a validated food frequency questionnaire including 78 food

> groups and recipes. Odds ratios (OR) and 95% confidence intervals

> (CI) were estimated for increasing levels of nutrient intake.

> RESULTS: A direct association with prostate cancer was found for

> starch intake (OR = 1.4 in the highest versus the lowest quintile

of

> intake; 95% CI: 1.1-1.8), whereas an inverse association emerged

for

> polyunsaturated fatty acids (OR = 0.8; 95% CI: 0.6-1.0). Among

> polyunsaturated fatty acids, linolenic acid (OR = 0.7; 95% CI: 0.6-

> 0.9) and linoleic acid (OR = 0.8; 95% CI: 0.6-1.0) were inversely

> related to prostate cancer. When the six major macronutrients were

> included in the same model, the adverse effect of high intake of

> starch and monounsaturated fatty acids was statistically

significant

> together with the protective effect of polyunsaturated fatty acids.

> Results were consistent in separate strata of age, body mass index

> and family history of prostate cancer. CONCLUSIONS: Starch and

> monounsaturated fatty acids were directly associated with prostate

> cancer risk and polyunsaturated fatty acids were inversely

associated.

>

> PMID: 15598953 [PubMed - in process] "

>

> Rodney.

>

>