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Table 6.2 Stearic acid substituted for other fatty acids: effects on plasma lipids1

High-18:0 diet

Reference

Zock and Katan (27)

18:0 sub stituted for

FA°%e0f (%) (%) (%) (%) (%) (%) (%) (mg/d) (%) (%) (%) (%) (%)

energy)

Tholstrup et 12:0 +

Tholstrup et 16:0

Bonanome 16:0

Bonanome 18:1

Comparison diet Percentage change

12:0 14:0 16:0 18:0 18:1 18:2«-6 Fat Chol 12:0 14:0 16:0 18:0 18:1 18:2«-6 Fat Chol TC LDL-C HDL-C TG

18:2n-6

  1. 04 0.04 1.6 16.9 18.0
  2. 04 0.04 1.6 16.9 18.0

NR 0.04 3.3 17.2 15.8

  1. 5 1.0 5.7 11.8 15.4
  2. 6 40 216 12.0
  1. 7 1.2 16.0
  2. 6 40 216 0.3 0.5 17.3 1.9 15.3 3.2 40 <100 NR 0.4 18.0 1.9 15.5
  3. 2 40 <100 NR 0.04 2.2 0.9 31.9
  4. 9 40 388 0.7 0.9

1 FA fatty acid; Chol = cholesterol; TC = total cholesterol; LDL-C = low-density lipoprotein cholesterol; HDL-C = high-density lipoprotein cholesterol; TG = triglycerol; NR = nor reported.

* Significant difference between treatments (P <0.05).

  1. 2 40 212 22.1* 26.4* 13.1* 4.1 3.8 40 <100 14.4* 21.5* 5.5 0.7
  2. 8 40 <100 4.5 7.5 8.8 5.8
  3. 0 40 402 3.2* 6.0*

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(28) or only slightly less absorption (29, 30) compared with other fatty acids. Even in the studies that show differences, greater than 90% of stearic acid is absorbed. Other evidence suggests that hypercholesterolemic SFAs suppress LDL receptor activity whereas stearic acid does not (31). It also has been postulated that stearic acid may be neutral because it is rapidly metabolized to oleic acid; but results obtained by stable-isotope tracer methods have shown that less than 20% of stearic acid is converted to oleic acid (32, 33).

Of interest are the results from recent studies which suggest that, compared to other SFAs (e.g. palmitic acid), stearic acid is preferentially incorporated into phospholipids instead of cholesteryl esters and triglycerides (32). This may account, in part, for its lack of a cholesterolemic effect. Other still unidentified mechanism(s) also may contribute to the uniqueness of stearic acid.

Effects of Stearic Acid on Thrombosis Epidemiological Studies

There is epidemiological evidence that populations with a high intake of SFAs have increased platelet reactivity. This association, however, is based primarily on results from studies of ex vivo platelet aggregation in small groups of farmers living in Europe (34). Significant differences for in vitro platelet reactivity were observed among small groups of farmers from France, the UK, and Belgium. These results were attributed to differences in dietary SFA consumption; the stearic acid content of the diet, in particular, was shown to be most strongly associated with enhanced platelet reactivity. Of interest, however, is that in these studies the intake of SFA was high in all farmers, and the difference in stearic acid intakes between groups was small (<1% of energy).

A more recent and very comprehensive examination of the effects of diet and thrombosis/coagulation factors comes from the Atherosclerosis Risk in Communities (ARIC) study (35). Analysis of food intake data showed that, after controlling for common CHD risk factors, a high intake of total fat, cholesterol and SFA (from animal sources) was found to be associated with higher levels of fibrinogen and factor VII (which could increase thrombosis tendency). This study was, however, unable to identify a relationship of any individual SFA with coagulation factors.

Epidemiological studies have shown that a high intake of PUFA and omega-3 fatty acids, principally from fish, was associated with a reduced CHD risk and thrombosis tendency. In the ARIC study, a higher intake of fish was associated with lower levels of two coagulation factors (fibrinogen and factor VII).

Clinical and Animal Studies

Since the 1960s, scientists have been studying the potential relationship between dietary SFA and thrombosis tendency (36). These early studies, conducted

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