StudyRepo

Literature review of essential fatty acids, their required amounts, and how they can be modified & used in the body. Recommends a linoleic acid intake of 7-10g/day because of the possible connection to heart disease. They detail the various changes in food intake that have been recorded as manipulating the conversion of PUFAs in the body via D5D and D6D, including protein, salt, other fats, fasting, and more.

Linoleic acid deficiency was induced in mice, and the enzymes responsible for synthesizing fatty acids were measured in the liver. Fatty acid synthesis enzymes were activated 5 to 10-fold in mice on a fat free diet. Saturated fat (coconut oil) was reintroduced to the diet, but did not bring down the enzyme levels. Meanwhile, reintroducing linoleic acid (via corn oil) did, over an 8 day period. This indicates that linoleic acid (or downstream, eg. ARA) deficiency is what activates the fatty acid synthesis enzymes. Only a few days were needed to dramatically deplete the linoleic acid in the mices' livers. Feeding a starved animal with a fat-free diet initiated liver linoleate depletion within 8 hours. Fatty acid synthesis hormones were observed as quickly as 5 days into the fat-free diet. When fatty acid synthesis was activated, increased levels of palmitoleic acid and oleic acid were observed. Stearic, linoleic, and arachidonic acid dropped. Palmitic acid remained about the same. Mead acid (omega-9 PUFA) was endogenously synthesized from oleic acid. Mice maintained on a fat-free or a linoleate-free diet developed fatty livers, which was reversed when linoleic acid was reintroduced to the diet.

One of the study authors, a healthy adult man, went on a "fat-free" diet (<2g fat/day) for 6 months. The diet was created equivalent to one deemed deficient in essential fatty acids in rats, which the rats developed health issues on and eventually got severely sick. The human subject remained well throughout the entire period, and did not even get a common cold. He had no skin issues and did not even get tired of the food. In fact, the subject reported less fatigue and a disappearance of migraines he'd had since childhood. He lost a moderate amount of weight (14lbs) and blood pressure decreased slightly. Arachidonic and linoleic acid were tested in serum before and during the diet. Arachidonic was 3.2% before, and 1.87% during the fat-free diet. Linoleic was 5.7% before and 3.2% during. This study was done in 1933, which explains the very low (for current day) linoleic acid %.

Rats were put on a 4x repeated 24h fast / 3 day feast cycle to see if this would deplete their body stores of essential PUFA fatty acids LA and ALA. The diet was 3% LA of kcals. Fatty acid profiles were obtained during each fast/feast cycle. It was observed that PUFAs were accumulated in body fat at much lower rates than MUFAs + SFAs when compared with a control (ad-lib fed) group. "Apparent" oxidation was calculated by the difference between intake and accumulation + excretion.

The aim of this study was to determine the effect of chain length, degree of unsaturation, and stereoisomeric effects of unsaturation on the oxidation of individual fatty acids in normal-weight men. For the carboxyl-labeled fatty acids, the order of oxidation from lowest to highest was as follows: laurate > linolenate > elaidate > linoleate > oleate > palmitate > stearate. When the average of the carboxyl and methyl data were used, the order was laurate > linolenate > elaidate > oleate > linoleate > palmitate > stearate.

This opinion paper explains why the term "essential fatty acid" is confusing and inconsistently applied.