@ZackVegas
Did you read the two EFAD studies on human I cited above? They were on Vitamin, Mineral and Amino rich regimen: fat-free, intravenous hyperalimentation fluids and fat regimen total parenteral nutrition (TPN). Yet they developed skin conditions and reversed with EFA. The person (32-year-old man presented with history of anorexia) receiving TPN already having EFA and they had to increase the amount of fat he receives.
There's plenty of studies on TPN regimen and EFAD development:
Essential fatty acid deficiency during total parenteral nutrition
Essential fatty acid (EFA) deficiency has become a clinical problem since the advent of fat-free total parenteral nutrition (TPN). The following study was done to determine the minimum fat requirements for patients receiving continuous TPN solution. Seventy-seven patients who had 97 courses of TPN of at least 14 days duration were prospectively studied. The following fat supplementation was given: a) none, b) 10% soybean oil emulsion intravenously at fixed dosage, c) fat from an oral diet, or d) intravenous and oral fat. No patient was EFA deficient before the onset of TPN. EFA deficiency was prevented when at least 3.2% of total calories were given as intravenous fat or at least 15% as oral fat. Lesser amounts of fat decreased the rate of EFA deficiency development but did not prevent it from occurring. The 7.7 g/day of linoleic acid provided in 1000 ml per week of 10% soybean oil emulsion provides adequate fat to prevent EFA deficiency.
https://pubmed.ncbi.nlm.nih.gov/6782957/
Essential fatty acid deficiency in adults receiving total parenteral nutrition
In seven adult patients receiving fat-free total parenteral nutrition (TPN) for 4 to 8 weeks, weekly determinations of plasma fatty acids and total plasma tocopherols were made. Four patients were deficient in essential fatty acids, as defined by triene:tetraene ratio >0.4, at the end of the second week of TPN. Six patients were deficient by the end of the third week and all seven were deficient by the end of the fifth week of TPN treatment. One patient who was deficient in both essential fatty acids and zinc developed a scaling, eczemoid dermatitis that disappeared within 3 weeks after cessation of TPN and resumption of oral feedings containing both fat and zinc. After resumption of oral feedings by three patients, the triene:tetraene ratio returned to normal within 2 weeks. The mean of total plasma tocopherols fell over a period of 7 weeks and in three individuals, reached levels generally associated with deficiency. There were not any obvious clinical manifestations of vitamin E deficiency.
https://www.sciencedirect.com/science/article/abs/pii/S0002916523341066
Serum lipids and fatty acids composition of tissues in rats on total parenteral nutrition (TPN)
The modulating effect of energy and exogenous triglyceride supply on serum lipids and fatty acid composition of liver, tibialis anterior muscle, subcutaneous and peri-epididymal fat was assessed in rats using Total Parenteral Nutrition (TPN). Nutrients were infused continuously for 10 days through a central vein catheter. Four levels of fat were tested: No fat, Low fat (6% non-protein calories), Medium fat (30%) and High fat (60%), at 2 energy levels (270 kcal and 350 kcal/kg X day). An isonitrogenous supply was given to all groups as 0.9 g N/kg X day. At the highest level of fat intake (20.4 g/kg) at the high energy level triglycerides, cholesterol and phospholipids of serum were elevated. Biochemical signs of essential fatty acid (EFA) deficiency were observed as rising levels of eicosatrienoic acid and lowered concentrations of linoleic and arachidonic acid, mostly in the liver and the muscle in the No fat groups. EFA levels were reduced significantly in the No fat and Low fat groups and more pronounced at the high energy level. In conclusion, our study suggests that when energy intake is increased the EFA status becomes more critical. It seems evident that more EFA is required in absolute values when hypercaloric diets are given.
https://pubmed.ncbi.nlm.nih.gov/6438428/
Medium-chain triglyceride supplementation in infants with biliary atresia: a review of the evidence for impacts on fat absorption, growth, nutritional status and clinical outcomes.
Biliary atresia is a rare bile duct disease resulting in intestinal bile salt depletion due to poor bile flow. Medium-chain triglyceride (MCT) supplementation is widely recommended and used as the main dietary management in infants, however evidence for its use is limited and there is uncertainty regarding the optimal percentage (proportion of total fat that is MCT) and dose (grams/kilogram/day, g/kg/d). The aim was to review the evidence for the impact of MCT on fat absorption, growth, nutritional status and clinical outcomes in infants with biliary atresia and the optimal nutrition profile of MCT supplementation. A scoping review found that the mostly observational, historic evidence for MCT supplementation pointed to greater fat absorption during MCT supplementation compared to no supplementation, but also some evidence of a risk of essential fatty acid deficiency with very high MCT percentage. Only six studies have investigated MCT percentages and only three reported MCT dose. One analysis of MCT in the largest cohort of biliary atresia patients ever presented (n = 200), found no association between MCT percentage with growth, nutritional status or clinical outcomes. Counterintuitively, there was an unexpected inverse association between MCT dose and growth. A possible interpretation was that increased MCT was a consequence of poor growth rather than a cause, as infants either drank more or dietitians prescribed more MCT as fat malabsorption worsened. In conclusion, MCT is widely recommended, however, the evidence for its use is lacking and there remains uncertainty about the optimum percentage and dose for infants with biliary atresia.
https://europepmc.org/article/MED/41502374
Essential fatty acid deficiency in total parenteral nutrition. Detection by changes in intraocular pressure
Essential fatty acid deficiency (EFAD) has been commonly and readily diagnosed during fat-free total parenteral nutrition (TPN), with only vague awareness of possible functional and clinical derangements secondary to essential fatty acid deficiency. Arachidonic acid is known to be a precursor for prostaglandin (PG) synthesis. Prostaglandins are known to be intermediaries between stimulus and cellular response in a variety of physiologic and pathologic processes; one would suspect therefore that EFAD would result in PG deficiency with resultant multiple derangements in functions regulated by PG. We tested this hypothesis by serially measuring intraocular pressure (IOP) in patients before and during fat-free TPN and after supplementing these patients with fat. In the eye as well as in various other organs PG are believed to act as mediators of adrenergic neurotransmission by a negative feedback mechanism. As catecholamines are potent ocular hypotensive agents, decreased levels of PG due to EFAD will cause increase in catecholamine turnover with a reduction in IOP. Two groups of patients matched as to their age, sex, nutritional status and diseases were studied. One group (control) was receiving a normal diet or fat-containing TPN while the other group was receiving fat-free TPN. IOP in the fat-free TPN group dropped from 13.7 +/- 0.4 mmHg pre-TPN to 9.3 +/- 0.5 mmHg during the first week of fat-free TPN. Within two weeks after supplementation of fat or return to normal oral diet IOP returned to 13.9 +/- 0.3 mmHg. Prostaglandin levels, which were 0.025 +/- 0.004 ng/ml pre-TPN or in control patients decreased to 0.012 +/- 0.002 ng/ml (p < 0.001) during fat-free TPN, to return to normal after fat was added to TPN regime or patients returned to normal oral diet. During fat-free TPN linoleic acid levels decreased to 40% of its initial value with a mild increase upon the addition of fat, while eicosatrienoic acid and the triene:tetraene ratio increased to 6.5 times their initial values. Arachidonic acid levels did not change during fat-free TPN or after repletion with fat. Intraocular pressure determination seem to be a simple, harmless, inexpensive, reliable and sensitive indicator of EFAD. Moreover, IOP determination represent a functional derangement which in a clinical setting lends functional credence to the biochemical changes of EFAD whose entire significance has not yet been determined. Similarly, serial IOP determinations are sensitive in detecting adequate functional repletion of EFAD. As PG are known to act as intermediaries in a variety of physiological processes it seems reasonable to assume that the change in IOP is only one of many different changes and derangements to occur as a result of PG and EFA deficiency.
https://pubmed.ncbi.nlm.nih.gov/223507/
Essential fatty acid deficiency and home total parenteral nutrition patients
The requirements for essential fatty acids in patients on home parenteral nutrition are not well described. We therefore studied the needs of 12 patients receiving parenteral nutrition for at least 4 mo (range: 4 mo-17.3 yr; mean 7.0 ± 5.2 yr). Prior to the study, each patient had been receiving intravenous lipids either weekly or biweekly and had a triene to tetraene ratio (TTR) on plasma phospholipids performed at least annually. A TTR ≥ 0.2 was considered diagnostic for essential fatty acid deficiency (EFAD). The purpose of this study was to determine the required intravenous lipid supplementation in patients on home total parenteral nutrition (HTPN). Patients with an initial TTR of <0.2 had their intravenous lipid stopped and changes in their serum phospholipid fatty acids were followed every 3–4 wk. Nine of 12 patients had TTRs > 0.2 at some point in the study. Phase I consisted of patients who at initiation of the study had normal TTRs and were taken off lipid supplementation until their TTR became abnormal. Phases II, III, IV, and V consisted of lipid delivered in total nutrient admixtures in biweekly doses of 0.6, 1.2, 1.8, and 2.4 g of fat/kg bodyweight, respectively. Eight patients normalized their TTRs on the biweekly lipid regimens; one patient expired before his ratio normalized; and three patients could not be made deficient in essential fatty acids after 26 or more wk of fat-free parenteral nutrition. Most patients required 1.2 to 2.4 g of lipid/kg bodyweight/biweekly to correct serologic EFAD. The clinical background, as well as the length of small bowel remaining, did not seem to identify those patients who required lipid supplementation nor the final dose of lipid needed to normalize their TTRs.
https://www.sciencedirect.com/science/article/abs/pii/S0899900796908503
