Okay, a little more on the subject. ALL essential oils are good for you even ALA. So if you are taking your Atkins Essential Oils, no worries. However, if you would like to make a slight improvement then change to taking your Omega-3 as fish oil.

Reasons:
1. Flaxseed oil (linseed oil) is made from the seed of the flax plant however it is the Omega-3 fish oil has been shown to decrease heart disease in societies and peoples that eat mainly fish.

2. Both ALA and LA as well as EPA and DHA all lower risk of heart disease and are all "essential" to the human diet. Which Omega-3 you take doesn't matter in this respect.

3. However, when it gets down to eicosanoid production (the microhormones), ALA inhibits eicosanoid production. (see abstract below) If your body is producing mostly series two (bad) eicosanoids, then it isn't so bad to shut down production. But the better method is to leave eicosanoid production intact because it can also do good things and shift to an increase in series one (the good guys) eicosanoids. So when you run out of your Atkins Essential Fatty Acids, you can switch to Omega-3 from fish oil.

Lipids 1989 Apr;24(4):305-11

Modulation of eicosanoid production and cell-mediated cytotoxicity by dietary alpha-linolenic acid in BALB/c mice.

Fritsche KL, Johnston PV.

Department of Food Science, University of Illinois, Urbana-Champaign.

The effects of dietary alpha-linolenic acid (18:3n-3) on fatty acid composition, eicosanoid production, and cell-mediated cytotoxic activity of immune cells before and after challenge with virus or poly I-C from BALB/c mice were studied. Weanling BALB/c mice were fed purified diets containing either 10%-by-weight corn oil or linseed oil providing a ratio of 18:3n-3 to 18:2n-6 of 1/32 or 2/1, respectively, for 6-10 weeks. Fatty acid analysis of splenocyte phospholipids showed an appreciable increase in the percentage of n-3, and a decrease in n-6, fatty acids in splenocytes from mice fed the linseed oil diet. Splenocyte prostaglandin E and peritoneal exudate cell leukotriene C production was significantly lower in the linseed oil-fed mice. In general, cell-mediated cytotoxic activity was similar for immune cells from linseed oil and corn oil-fed mice. However, 6 days after the viral challenge, splenocyte cell-mediated cytotoxic activity was significantly higher in linseed oil mice. This higher activity was associated with nonspecific cytotoxicity rather than that of viral-specific cytotoxic T-lymphocytes. Cell yields from the spleen and peritoneum were frequently significantly higher in linseed oil mice. Interactions between dietary 18:3n-3, eicosanoid production, and immune cell proliferation and/or migration are discussed. In summary, feeding mice a diet rich in 18:3n-3 elevates immune cell n-3 fatty acid content, reduces eicosanoid synthesis and, to a limited extent, enhances the cell-mediated cytotoxic response to a viral challenge.

Lipids 1993 Jun;28(6):517-23 Related Articles, Books, LinkOut


Effect of age and alpha-linolenic acid deficiency on delta 6 desaturase activity and liver lipids in rats.

Dinh TK, Bourre JM, Durand G.

Laboratoire de Nutrition et de Securite Alimentaire, INRA 78352 Jouy-en-Josas, France.

The combined effects of age and of diet deficient in n-3 fatty acids on delta 6 desaturation of linoleic acid and on lipid fatty acid composition were studied in the liver of the rat at 2, 6, 12, 18 and 24 mon of age. The profiles of delta 6 desaturase activity and fatty acid composition were studied in the deficient rats refed, at these different ages, either with 18:3n-3 (mixture of peanut and rapeseed oils) or with 20:5n-3 + 22:6n-3 (fish oil) diets for 2, 4, 8 or 12 wk. Results showed that the liver delta 6 desaturation activity in the control rats remained high at 2 and 6 mon, decreased by 30% from 6 to 12 mon, and then remained stable from 12 to 24 mon. In the deficient rats, this activity remained high during the entire period studied. Thus, the profile of liver delta 6 desaturase activity after puberty was not related to age only; it also depended on the polyunsaturated fatty acid (PUFA) n-6 and n-3 balance in the diet. In the controls, in parallel with the delta 6 desaturase activity, PUFA metabolism could be divided into three periods: a "young" period, and "old age" period, separated by a period of transition between 6 and 12 mon. Recovery from PUFA n-3 deficiency occurred at all ages but in a different manner depending on whether the rats were "young" or "old". Recovery was faster if long-chain n-3 PUFA rather than alpha-linolenic acid were supplied in the diet.