Diet, heart and diversity

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Hi All,

Diet, heart and diversity in the response to three different diets for heart

health

risks seem to be well discussed in the below. The pdf is available.

M Ordovas

Diet-heart hypothesis: will diversity bring reconciliation?

Am J Clin Nutr 2005 82: 919-920.

.... In this issue of the Journal, Lefevre et al (8) present some results that

may

not soothe the above indicated controversy. However, the title and the opening

statement of the manuscript contain the words that may hold the clue to

reconciling

the lingering polemic: " Individual variability in response. " Lefevre et al's

study

design fulfills many of the expectations of a well-conducted dietary

intervention

study, namely, a randomized, double-blind, 3-period crossover controlled feeding

design. In addition, these investigators take multiple measurements per dietary

phase, which reduces the confounding of intraindividual variability. Moreover,

they

chemically measured the menus provided, thereby connecting the calculated with

the

actual composition of the diets. The composition of the diets was conventional:

the

average American diet (38% of energy as fat and 14% of energy as saturated fatty

acids), the Step I diet (30% fat; 9% saturated fatty acids), and the Step II

diet

(25% fat; 6% saturated fatty acids); the fat content was adjusted by adding or

removing milk fat. The diets were fed for 6 wk each to 86 free-living, healthy

men

aged 22–64 y. Although the biochemical variables presented in the article are

basic,

these are also the variables used by health professionals to ascertain dietary

therapeutic success. Compared with the average American diet, the Step I and

Step II

diets lowered LDL-cholesterol concentrations by 7% and 12%, respectively.

However,

the bad news was that plasma HDL-cholesterol concentrations decreased on a

similar

magnitude, whereas plasma triacylglycerols increased by 14% and 16%,

respectively.

These results were, on average, similar to those from many previous studies that

used similar experimental designs and diets. As in previous studies, the

magnitude

of individual variability in the response of plasma lipids to dietary

intervention

was astonishing. The investigators studied the potential influence of certain

baseline variables as modulators of dietary response. Their analyses showed

significantly smaller reductions in the LDL-cholesterol response to a Step II

diet

with an increase in percentage body fat, body mass index, or insulin

concentrations.

However, it is important to emphasize that the correlations were in the range of

0.2–0.3 and that the effect was far from specific. In fact, there were persons

in

the higher end of the body mass index distribution who had identical responses

to

those in the middle and lower ranges. Therefore, these data in isolation may not

raise too many expectations regarding the influence of anthropometric variables

on

plasma lipid responses to dietary manipulation. Nevertheless, this study joins

other

articles that support the notion that the benefits of a hypocholesterolemic diet

may

not reach their maximum performance in subjects who are overweight or obese (9,

10)

or who, as shown here (8), are insulin resistant. ...

The other relevant outcome of the study relates to the results obtained for the

ratio of total to HDL cholesterol, also known as the atherogenic ratio. Higher

values have been associated with an increased CVD risk. Therefore, the

elevations

observed after the Step I and II diets cast some concerns about the efficacy of

these low-fat diets to reduce CVD risk. However, experimental design may have

been

the driving force for the increased ratio of total to HDL cholesterol and

triacylglycerol concentrations observed after the low-fat diets. We need to keep

in

mind that the persons were maintained at constant weights throughout the

experiment

by adjustments to their dietary intake. However, when low-fat diets are provided

ad

libitum and result in weight loss, they have the positive effect of reducing

LDL-cholesterol concentrations without the potential downsides of decreasing

HDL-cholesterol concentrations and increasing triacylglycerol concentrations

(11).

Moreover, despite the indisputable epidemiologic evidence regarding the

protective

role of HDL cholesterol, what really matters is the efficacy of reverse

cholesterol

transport efficiency rather than HDL-cholesterol concentrations (12). Whether

the

lowered HDL-cholesterol concentrations that result from low-fat diets are

associated

with functional impairment remains to be elucidated, especially in those

situations

in which the decrease is not accompanied by increased triacylglycerol

concentrations. Therefore, deciding the suitability of a specific diet to reduce

CVD

risk based exclusively on its effects on the ratio of total to HDL cholesterol

may

be too vague ...

In summary, the study was carried out in a sound manner and the results

presented

are consistent with previous literature. However, the data reflect the

experimental

design, which was conceived to minimize confounders rather than to reflect real

life. It would be unfortunate if somebody decides to interpret from these

findings

that the best diet therapy for overweight or obese people to decrease CVD risk

would

be a high-fat diet consisting of milk products, and the authors judiciously

avoid

making this an explicit conclusion. Rather, they focus on the dramatic

variability

in the interindividual plasma lipid responses to diet even under a highly

controlled

environment and try to gain additional understanding about how factors such as

body

mass index and insulin sensitivity drive this variability. On the basis of the

data,

one may think about a hierarchical structure to dietary prevention or therapy

for

CVD. Thus, if the individual has insulin resistance or is obese, the primary

emphasis should be in normalizing those conditions to achieve the maximum

benefit of

the hypocholesterolemic diets. Whether insulin, body mass index, or waist

circumference are better determinants of impaired dietary responses cannot be

assessed from the present study because multiple stepwise regression analyses

are

not advisable when using such highly correlated variables. Moreover, many other

factors influence responses, including age, sex, physical activity, alcohol,

smoking, and genetics. Their combined and thoughtful use should help in the

identification of vulnerable populations or persons that will benefit from a

variety

of more personalized and mechanistic-based dietary recommendations. This

potential

for better prevention and therapy can and needs to be developed within the

context

of nutritional genomics (13) that, as part of systems biology, may provide the

tools

to achieve the holy grail of dietary prevention and therapy of CVDs. This

approach

will break with the traditional public health approach of one size fits all. In

this

regard, the first baby steps can be seen already in the most current version of

the

US Department of Agriculture pyramid (www.mypyramid.gov). Perhaps at some time

in

the future, the current controversies will be put to rest. We will be able to

identify those persons for whom diet plays no major role in their risk of CVD

and

this should appease those who defend the diet-heart null hypothesis (4, 5). The

same

tools will identify those persons who may benefit more from one of the many

potentially beneficial diets currently proposed (7).

Lefevre, M Champagne, T Tulley, C Rood, and

M Most

Individual variability in cardiovascular disease risk factor responses to

low-fat

and low-saturated-fat diets in men: body mass index, adiposity, and insulin

resistance predict changes in LDL cholesterol

Am J Clin Nutr 2005 82: 957-963.

ABSTRACT

.... average American diet (AAD) ... A randomized, double-blind, 3-period

crossover

controlled feeding design was used to examine the effects on plasma lipids of 3

diets that differed in total fat: the AAD [designed to contain 38% fat and 14%

saturated fatty acids (SFAs)], the Step I diet (30% fat with 9% SFAs), and the

Step

II diet (25% fat with 6% SFAs). The diets were fed for 6 wk each to 86

free-living,

healthy men aged 22–64 y at levels designed to maintain weight.

Results: Compared with the AAD, the Step I and Step II diets lowered LDL

cholesterol

by 6.8% and 11.7%, lowered HDL cholesterol by 7.5% and 11.2%, and raised

triacylglycerols by 14.3% and 16.2%, respectively. The Step II diet response

showed

significant positive correlations between changes in both LDL cholesterol and

the

ratio of total to HDL cholesterol and baseline percentage body fat, body mass

index,

and insulin. These associations were largely due to smaller reductions in LDL

cholesterol with increasing percentage body fat, body mass index, or insulin

concentrations. Subdivision of the study population showed that the participants

in

the upper one-half of fasting insulin concentrations averaged only 57% of the

reduction in LDL cholesterol with the Step II diet of the participants in the

lower

half.

Conclusion: Persons who are insulin resistant respond less favorably to Step II

diets than do those who are insulin sensitive.

TABLE 3 Effect of diets on lipid and lipoprotein concentrations1

--------------------------------------------------------------------------------

AAD Step I diet Step II diet

--------------------------------------------------------------------------------

Total cholesterol (mmol/L) 4.82±0.69 4.59±0.6^2 4.39±0.66^2,3

Triacylglycerol (mmol/L)4 1.06±0.65 1.20±0.76^2 1.22±0.80^2

LDL cholesterol (mmol/L) 3.25±0.58 3.03±0.56^2 2.87±0.52^2,3

HDL cholesterol (mmol/L) 1.07±0.23 0.99±0.22^2 0.95±0.22^2,3

Apolipoprotein A-I (g/L) 1.23±0.14 1.17±0.13^2 1.15±0.12^2,3

Apolipoprotein B (g/L) 0.97±0.19 0.93±0.20^2 0.90±0.18^2,3

Total:HDL cholesterol 4.70±1.08 4.84±1.18^2 4.85±1.26^2

--------------------------------------------------------------------------------

1 All values are ± SD; n = 86. AAD, average American diet.

2 Significantly different from AAD, P < 0.05 (ANOVA with Bonferroni

corrections).

3 Significantly different from Step I diet, P < 0.05 (ANOVA with Bonferroni

corrections).

4 Values were log transformed before statistical analyses.

TABLE 4 Correlation coefficients between selected screening parameters and

changes

in lipid endpoints1

--------------------------------------------------------------------------------

Endpoint BMI Waist diameter Percentage body fat Glucose ln Insulin ln HOMA

-------------------------------------------------------------------------------

TC

Step I-AAD 0.19 0.14 0.19 0.21 0.22^2 0.23^2

Step II-AAD 0.26^2 0.24^2 0.24^2 0.16 0.34^3 0.33^3

LDL cholesterol

Step I-AAD 0.15 0.14 0.16 0.25^2 0.21 0.23^2

Step II-AAD 0.22^2 0.22^2 0.22^2 0.12 0.26^2 0.26^2

HDL cholesterol

Step I-AAD 0.07 0.07 0.12 0.03 0.00 0.01

Step II-AAD –0.02 0.03 0.01 0.02 0.02 0.02

ln Triacylglycerol

Step I-AAD 0.11 –0.01 0.05 0.15 0.15 0.15

Step II-AAD 0.19 0.13 0.11 0.22^2 0.22^2 0.23^2

ln TC:HDL-C

Step I-AAD 0.13 0.10 0.11 0.28^4 0.29^4 0.30^3

Step II-AAD 0.29^4 0.26^2 0.28^4 0.20 0.32^3 0.32^3

--------------------------------------------------------------------------------

1 n = 86 participants. HOMA, homeostasis model assessment; TC, total

cholesterol;

AAD, average American diet; HDL-C, HDL cholesterol.

2 P < 0.05.

3 P < 0.005.

4 P < 0.01.

Supported by a grant from the National Dairy Council.

Al Pater, PhD; email: old542000@...

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