**1.4 Intakes of trans-fatty acids in people of US and Japan**

Allison et al. [27] used food intake data from1989 to 1991 Continuing Survey of Food Intakes by Individuals (CSFII) and the trans-fatty acid contents of specific foods, which were calculated from a data base of the US Department of Agriculture. These data show the mean levels of trans-fatty acids intakes of US population.

The average percentage of energy ingested as trans-fatty acids was 2.6%, and the average percentage of total fat ingested as trans-fatty acids was 7.4%. Across all age and gender groups examined, estimates ranged from 2.6 to 2.8% and 7.1 to 7.9%, respectively [27].

In Japan, mean total fat and trans-fatty acid intake was 56.9 g/day (27.7% total energy) and 1.7 g/day (0.8% total energy), respectively, for women and 66.8 g/day (25.5% total energy) and 1.7 g/day (0.7% total energy) for men [28].

Recent studies indicate that the average trans-fatty acids intake was estimated to be 0.92–0.96 g/day, which was 0.44–0.47% of total daily energy intakes [29].

These data indicate that Japanese take far less amounts of trans-fatty acids compared with American.

#### **1.5 Omega fatty acids**

Intakes of long-chain ω-3 fatty acids (eicosapentaenoic acid (EPA), docosa pentaenoic acid (DPA), and docosahexanoic acid (DHA)) found in fish, and fish oils has been shown to be related to the low incidence of coronary heart disease in the Inuit people of Greenland [30].

We do not review roles of such fatty acids in health and disease in details. **Figure 3** summarizes roles of EPA in causing various dysfunctions of the body.

**103**

**Figure 4.**

**Figure 3.**

*Roles of Trans and ω Fatty Acids in Health; Special References to Their Differences…*

*Roles of EPA in the prevention of cell damage, inflammation, or thrombosis.*

Arachidonic acid (n-6 polyunsaturated fatty acid "PUFA") is converted to PGH2 (prostaglandin H2, which is converted to prostaglandin E2, inflammatory mediator) or to TXA2 (thromboxane A2), causing thrombosis. AA is also converted to LTA4

(leukotriene A2), then to leukotriene B4, inflammatory mediator [31]. Cells produce TNF-α or interleukin (IL)-1β, which case cell damages.

*Function of G-protein-coupled receptor 120 as a receptor of DHA and EPA.*

*DOI: http://dx.doi.org/10.5772/intechopen.89551*

*Roles of Trans and ω Fatty Acids in Health; Special References to Their Differences… DOI: http://dx.doi.org/10.5772/intechopen.89551*

**Figure 3.**

*Visions of Cardiomyocyte - Fundamental Concepts of Heart Life and Disease*

cholesteryl ester transfer protein (CETP) (upper left panel). In adipocytes, transfatty acids change fatty acid metabolism and, possibly, inflammatory responses. When trans fats are taken, nitric acid-dependent endothelial dysfunction is observed and circulating adhesion molecules increase. Trans fat modulates monocyte and macrophage function (lower left panel). Membrane receptors may affect subcellular mechanisms. These receptors localize with and are influenced by specific membrane phospholipids (upper right panel) such as endothelia nitric oxide synthetase or toll-like receptors. Trans-fatty acids may bind to nuclear receptors-

Trans-fatty acids may increase the risks of coronary heart disease (CHD). In a meta-analysis of four prospective cohort studies, a 2% increase in energy intake from trans-fatty acids was shown to be associated with a 23% increase in the

There are many papers showing increased risks of CHD in patients with high fatty acids levels [22–25]. These data are obtained using cohorts of Western

Koba et al. [26] recently reported using Japanese adult males that total transfatty acids levels were similar between acute coronary syndrome (ACS) and control subjects. Palmitelaidic acid levels were lower in ACS patients and were significantly directly associated with HDL cholesterol (HDL-C) and n-3 polyunsaturated FA (n-3 PUFA). Linoleic trans isomers (total C18:2 TFA) and primary industrially produced TFA (IP-TFAs) were significantly higher in ACS patients. Total trans-C18:1

Allison et al. [27] used food intake data from1989 to 1991 Continuing Survey of Food Intakes by Individuals (CSFII) and the trans-fatty acid contents of specific foods, which were calculated from a data base of the US Department of Agriculture. These data show the mean levels of trans-fatty acids intakes of US population. The average percentage of energy ingested as trans-fatty acids was 2.6%, and the average percentage of total fat ingested as trans-fatty acids was 7.4%. Across all age and gender groups examined, estimates ranged from 2.6 to 2.8% and 7.1 to 7.9%,

In Japan, mean total fat and trans-fatty acid intake was 56.9 g/day (27.7% total energy) and 1.7 g/day (0.8% total energy), respectively, for women and 66.8 g/day

Recent studies indicate that the average trans-fatty acids intake was estimated to

(25.5% total energy) and 1.7 g/day (0.7% total energy) for men [28].

be 0.92–0.96 g/day, which was 0.44–0.47% of total daily energy intakes [29]. These data indicate that Japanese take far less amounts of trans-fatty acids

Intakes of long-chain ω-3 fatty acids (eicosapentaenoic acid (EPA), docosa pentaenoic acid (DPA), and docosahexanoic acid (DHA)) found in fish, and fish oils has been shown to be related to the low incidence of coronary heart disease in

We do not review roles of such fatty acids in health and disease in details. **Figure 3** summarizes roles of EPA in causing various dysfunctions of the body.

regulating gene transcription such as liver X receptor (lower left panel).

**1.3 Effects on cardiovascular diseases**

isomers were comparable between ACS and control.

**1.4 Intakes of trans-fatty acids in people of US and Japan**

incidence of CHD [18–21].

populations.

respectively [27].

compared with American.

the Inuit people of Greenland [30].

**1.5 Omega fatty acids**

**102**

*Roles of EPA in the prevention of cell damage, inflammation, or thrombosis.*

#### **Figure 4.**

*Function of G-protein-coupled receptor 120 as a receptor of DHA and EPA.*

Arachidonic acid (n-6 polyunsaturated fatty acid "PUFA") is converted to PGH2 (prostaglandin H2, which is converted to prostaglandin E2, inflammatory mediator) or to TXA2 (thromboxane A2), causing thrombosis. AA is also converted to LTA4 (leukotriene A2), then to leukotriene B4, inflammatory mediator [31].

Cells produce TNF-α or interleukin (IL)-1β, which case cell damages.

EPA inhibits such processes, preventing cell damages, inflammation, and thrombosis. DHA may work in the similar ways as EPA.
