StudyRepo

Three methods of preparing french fries were compared: - 15 minutes air fried @ 200°C (manufacturer's recommendation) - 10 minutes deep fried in sunflower oil @ 180°C (legal limit in Turkey) - 15 minutes oven fried @ 200°C Both the air fried and oven fried fries had 2tbsp per 250g of sunflower oil spread on them before frying. Visible oil was wiped off after frying. Acrylamide formation was highest in the air fryer, then the deep fryer, then the oven, although the differences were not statistically significant.

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.

4,663 Danes were analyzed for adipose tissue linoleic acid content (buttocks) and followed for 21 years in the median. The median adipose LA content was 10.6%. They found a slight inverse relationship between higher LA content and all-cause mortality.

L.A. veterans were given a high-linoleic diet. Over the course of 4-5 years, the linoleic acid % in their body fat grew asymptotically to approach the linoleic acid % in the diet, minus a few % due to de novo lipogenesis.

Rodents were split into chow (low-fat) and "high-fat" (53% fat, 6% corn oil, 47% lard) groups. They were subjected to an artificial 6h "jet lag." Adaptation time was measured. The "high-fat" rodents took nearly 2x as long to advance phase, but were slightly faster at delaying phase. I.e. the "high-fat" PUFA diet turned them into night owls.

2x2 study design; obese vs lean rats and soybean oil vs. butter (both at 30%E). Obese phenotypes became more obese, lean ones did not.

Rats were fed 1%E linoleic acid, 8%E, and 8%E + 1% EPA/DHA. The 1% mice were the leanest, 8% most obese. In the 8% + EPA/DHA mice, the obesogenic effect was somewhat milder.

Food catering companies in the area of Navarro, Spain, were asked to self-report their practices for changing deep fryer oil. Subsequently, some of the kitchens were visited and the information was verified as best as possible by measuring total polar compounds in the fryer oil after frying. Policies for changing fryer oil ranged from "every 5 days" via "every 2 months" to "no defined frequency."

Rats were fed one of 3 diets: Normal fat (1.27% linoleic acid), high (hydrogenated) vegetable fat (3.85% LA), high lard fat (11.37% LA). The higher the LA content of the diet, the more the rats ate and the more obese they became.

Mice were put on high-fat diets containing coconut oil, coconut + soybean oil, fructose + coconut oil, and fructose + soybean + coconut oil. The soybean oil diets contained 10%E linoleic acid, the others only 2.2%. There was also a lower-fat control group with 1.2% LA. Weight wise, control mice did the best, followed by coconut oil mice and then fructose mice. Soybean mice actually did slightly worse than even soybean + fructose mice.

Mice were fed 1%E linoleic vs. 8%E in low-fat and medium-fat diets. The 8% LA mice had higher levels of LA oxidation products, higher serum leptin, increased liver endocannabinoids, and gained more weight when compared isocalorically to the 1% mice.

Palm, olive, and soybean oil were compared in a simulated deep-frying kitchen. Exhausted gases were examined. Palm oil released the most total particulate matter, whereas soybean oil released the most aldehydes. Olive oil had the least toxic emissions.

Fats and oils were exposed to high temperature at 145°C for 80 h with frying steamed noodles, and the polar compounds were determined. Fats examined were: Palm oil, vegetable shortening, soybean oil, beef tallow. After 80h of heating and repeated frying of steamed noodles, all fats except soybean oil reached around 30% of polar compounds. Soybean oil reached about 15%.

Salmon was cooked in various ways to study how it would impact fatty acid oxidation: boiling, pan-frying, and baking. MDA, TBARS, and peroxides were tested. Boiling did not increase peroxidation or MDA significantly. Baking increased perixodation, and pan-frying both peroxidation and MDA. Lipid peroxidation products 4-HNE and 4-HHE were significantly increased in baking, and even more in pan frying.

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 %.

Obese men were put on a calorie restricted diet (1,000kcal/day deficit) and exercise program for 16 weeks. Weight loss was 13 +- 4.9kg. Only up to 30% fat were allowed on the diet. Before and after weight loss, adipose biopsies and blood samples were taken. They also took full-body MRIs. Adipose linoleic acid changed from 12.7 ± 1.6 to 12.0 ± 1.3.

Meta-analysis reviewing studies that compare dietary fats to adipose fats in humans. It concludes that the half-life of fatty acid tissue is about 600 days, and it takes about 800-900 days to entirely replace the adipose tissue of an adult human (nearly 3 years). It mentions that very low fat diets seem to dilute the dietary fat via de novo lipogenesis, and the adipose fat will therefore not reflect the dietary fat closely. It also mentions that rapid fat loss/gain might influence the speed, the experiments were apparently largely done in weight stable people.

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.

The authors had previously shown that SFAs are preferentially shuttled into oxidation pathways compared to PUFAs. But this was only in an oxidative (catabolic?) state. With this study, they wanted to test the same thing in a state with de novo lipogenesis (DNL) upregulated. To test this, they fed 20 healthy volunteers a high-carbohydrate diet and then gave them either palmitate or linoleate. The two fats were tested 2 weeks apart. During the DNL state, linoleate was preferentially oxidized vs. palmitate.

200 individuals from Costa Rica were asked about their food intake to determine estimated fatty acid profiles, had adipose tissue samples taken, as well as whole-blood and plasma (which excludes e.g. red blood cells). Correlations were then compared between these sources. As expected, adipose fatty acids pretty closely resembled (estimated) dietary intake the closest. For linoleic acid in particular, the correlation between plasma and whole-blood was pretty strong too. Average whole-blood LA (22.38%) was higher than adipose (15.71%) and estimated diet (18.87%), and plasma was even higher (28.09%). Arachidonic acid, on the other hand, seemed strongly controlled: despite extremely low intakes and adipose levels (<1%), plasma (6%) and whole-blood levels (9%) were quite high.