Tags

Type your tag names separated by a space and hit enter

Change in saturated fat intake is associated with progression of carotid and femoral intima-media thickness, and with levels of soluble intercellular adhesion molecule-1.

Abstract

BACKGROUND

A high saturated fat (SFA) intake may stimulate progression of atherosclerosis, and may be positively associated with expression of adhesion molecules.

METHODS

In moderately hypercholesterolaemic participants of a dietary intervention study (n=103; 55+/-10 years), we examined associations between reported changes in SFA intake and changes in carotid and femoral intima-media thickness (IMT) and soluble intercellular adhesion molecule-1 (sICAM-1) levels after 2 years. The carotid and femoral IMT was assessed by high-resolution B-mode ultrasound images.

RESULTS

After 2 years, dietary intake of SFA decreased with 1.8+/-2.6% of energy (P<0.01). In the lowest quintile of change in SFA intake (-5.9+/-1.4% of energy), changes in carotid and femoral IMT were +0.03 mm (SEM 0.03) and -0.09 mm (SEM 0.07), respectively, versus +0.10 mm (SEM 0.03), +0.17 mm (SEM 0.07) in the top quintile (+1.6+/-0.7% of energy) (P linear trend 0.07 (carotis), 0.02 (femoralis)). Changes in sICAM-1 were -19.0 ng/nl (SEM 5.6) in the lowest quintile, versus +8.6 ng/ml (SEM 5.3) in the top quintile (P linear trend <0.001), adjusted for baseline level, SFA intake, body mass index, age, changes in intake of fruit, polyunsaturated fat, and dietary cholesterol. Adjustments for changes in established risk factors did not alter these results.

CONCLUSIONS

Decreased SFA intake may reduce progression of atherosclerosis, as assessed by IMT, and is associated with reduced levels of sICAM-1 after 2 years. Further research using randomised placebo-controlled trials is necessary to exclude potential confounding variables and to confirm causality.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of General Practice, University of Groningen, Anton Deusinglaan 4, 9713 AW, Groningen, The Netherlands. w.bemelmans@med.rug.nl

    , , , , ,

    Source

    Atherosclerosis 163:1 2002 Jul pg 113-20

    MeSH

    Aged
    Analysis of Variance
    Arteriosclerosis
    Carotid Arteries
    Cholesterol, Dietary
    Diet
    Disease Progression
    Fatty Acids
    Female
    Femoral Artery
    Humans
    Intercellular Adhesion Molecule-1
    Male
    Middle Aged
    Predictive Value of Tests
    Probability
    Prospective Studies
    Risk Assessment
    Sensitivity and Specificity
    Solubility
    Time Factors
    Tunica Intima
    Tunica Media

    Pub Type(s)

    Clinical Trial
    Comparative Study
    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    12048128

    Citation

    Bemelmans, Wanda J E., et al. "Change in Saturated Fat Intake Is Associated With Progression of Carotid and Femoral Intima-media Thickness, and With Levels of Soluble Intercellular Adhesion Molecule-1." Atherosclerosis, vol. 163, no. 1, 2002, pp. 113-20.
    Bemelmans WJ, Lefrandt JD, Feskens EJ, et al. Change in saturated fat intake is associated with progression of carotid and femoral intima-media thickness, and with levels of soluble intercellular adhesion molecule-1. Atherosclerosis. 2002;163(1):113-20.
    Bemelmans, W. J., Lefrandt, J. D., Feskens, E. J., Broer, J., Tervaert, J. W., May, J. F., & Smit, A. J. (2002). Change in saturated fat intake is associated with progression of carotid and femoral intima-media thickness, and with levels of soluble intercellular adhesion molecule-1. Atherosclerosis, 163(1), pp. 113-20.
    Bemelmans WJ, et al. Change in Saturated Fat Intake Is Associated With Progression of Carotid and Femoral Intima-media Thickness, and With Levels of Soluble Intercellular Adhesion Molecule-1. Atherosclerosis. 2002;163(1):113-20. PubMed PMID: 12048128.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Change in saturated fat intake is associated with progression of carotid and femoral intima-media thickness, and with levels of soluble intercellular adhesion molecule-1. AU - Bemelmans,Wanda J E, AU - Lefrandt,Johan D, AU - Feskens,Edith J M, AU - Broer,Jan, AU - Tervaert,Jan Willem Cohen, AU - May,Johan F, AU - Smit,Andries J, PY - 2002/6/6/pubmed PY - 2002/12/6/medline PY - 2002/6/6/entrez SP - 113 EP - 20 JF - Atherosclerosis JO - Atherosclerosis VL - 163 IS - 1 N2 - BACKGROUND: A high saturated fat (SFA) intake may stimulate progression of atherosclerosis, and may be positively associated with expression of adhesion molecules. METHODS: In moderately hypercholesterolaemic participants of a dietary intervention study (n=103; 55+/-10 years), we examined associations between reported changes in SFA intake and changes in carotid and femoral intima-media thickness (IMT) and soluble intercellular adhesion molecule-1 (sICAM-1) levels after 2 years. The carotid and femoral IMT was assessed by high-resolution B-mode ultrasound images. RESULTS: After 2 years, dietary intake of SFA decreased with 1.8+/-2.6% of energy (P<0.01). In the lowest quintile of change in SFA intake (-5.9+/-1.4% of energy), changes in carotid and femoral IMT were +0.03 mm (SEM 0.03) and -0.09 mm (SEM 0.07), respectively, versus +0.10 mm (SEM 0.03), +0.17 mm (SEM 0.07) in the top quintile (+1.6+/-0.7% of energy) (P linear trend 0.07 (carotis), 0.02 (femoralis)). Changes in sICAM-1 were -19.0 ng/nl (SEM 5.6) in the lowest quintile, versus +8.6 ng/ml (SEM 5.3) in the top quintile (P linear trend <0.001), adjusted for baseline level, SFA intake, body mass index, age, changes in intake of fruit, polyunsaturated fat, and dietary cholesterol. Adjustments for changes in established risk factors did not alter these results. CONCLUSIONS: Decreased SFA intake may reduce progression of atherosclerosis, as assessed by IMT, and is associated with reduced levels of sICAM-1 after 2 years. Further research using randomised placebo-controlled trials is necessary to exclude potential confounding variables and to confirm causality. SN - 0021-9150 UR - https://www.unboundmedicine.com/medline/citation/12048128/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0021-9150(01)00747-X DB - PRIME DP - Unbound Medicine ER -