Plant Profiler

Safflower (Carthamus tinctorius)


Synonyms / Common Names / Related Terms
18:2, American saffron, Asteraceae (family), bastard saffron, Carthamus tinctorius , Carthamus tinctorius L., Compositae (family), dyer's saffron, EH0202, fake saffron, false saffron, high oleic acid safflower oil, hing hua, honghua, Intralipid®, kinobeon A, linoleate, linoleic acid, Liposyn®, Liposyn® II, Modified Liposyn®, Microlipid®, monounsaturated fatty acids, MUFA, n-6, n-6 polyunsaturated fatty acid, n-6 rich vegetable oils, non-esterified fatty acid (NEFA), notoginseny cream, N-(p-coumaroyl) serotonin, oleate, omega 6, polyunsaturated fat, polyunsaturated fatty acids, PSF, PUFA, SAF, safflower injection, safflower meal, safflower oil, safflower oil cake, safflower oil emulsion, safflower oil esters, safflower oil-based lipid emulsion (TPN + L group), safflower petals, safflower seeds, safflower yellow, safloroil, Safola®, tocopherols, triglyceride, US, zaffer, zafran.





Mechanism of Action
Pharmacology:
  • Constituents: The safflower plant (Carthamus tinctorius, L.) contains safflower yellow, chalconoid compounds, safflomin A64 and the pigment kinobeon A.
  • Safflower seeds contain N-(p-coumaroyl) serotonin.65,66
  • Constituents of safflower oil include of 6% palmitic, 12% oleic, 74% linoleic acids18, and omega-6 linoleic acid, with two double bonds67. Derivatives of safflower oil cake include N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]ferulamide, N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]-p-coumaramide, N,N'-[2,2'-(5,5'-dihydroxy-4,4'-bi-1H-indol-3,3'-yl)diethyl]- di-p-coumaramide, N-[2-[3'-[2-(p-coumaramido)ethyl]-5,5'-dihydroxy- 4,4'-bi-1H-indol-3-yl]ethyl]ferulamide, and N,N'-[2,2'-(5,5'-dihydroxy-4,4'-bi-1H-indol-3,3'-yl)diethyl]- diferulamide, N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]- p-coumaramide, and N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]ferulamide.68
  • Anti-carcinogenic effects: Data from a retrospective case-control study show an inverse relationship of breast cancer risk with intake of seed oils, including safflower oil.69
  • In an in vitro study, the compound (Zhu-xiang) from herbal extracts containing ginseng and Carthamus tinctorius showed a significant dose dependent inhibition in cell proliferation in MDA-MB-231 breast cancer cell and normal human mammary gland cell lines and had significantly greater inhibitory effect than commonly used cytotoxic drugs2
  • According to an animal study, the effect of a high fat diet rich in n-6 polyunsaturated fatty acids (safflower oil) depends upon the time at which the oil is ingested: if before tumor cell inoculation such a diet promotes tumor growth, whereas if after tumor growth is initiated, it does not.31 This suggests that n-6 polyunsaturated fatty acids promote the initiation of colon tumor growth, but do not exert growth-promoting effects on colon tumors once they are established.
  • In an in vitro study, safflower oils inhibited the HT-29 malignant human colon cell line.70 In another in vitro study, safflower oils, which contain large amounts of linoleate in triglyceride form, selectively inhibited malignant melanoma growth over normal melanocytes.71
  • Anti-inflammatory effects: According to in vitro study, N-(p-coumaroyl) serotonin and its derivatives in safflower seeds have a suppressive effect on pro-inflammatory cytokine production from monocytes.65,66 Other in vitro study indicates that N-(p-coumaroyl) serotonin and its derivatives inhibit the production of pro-inflammatory cytokines through multiple mechanisms.66 Furthermore, a serotonin derivative, N-(p-coumaroyl) serotonin, augments the proliferation of normal human and mouse fibroblasts in synergy with basic fibroblast growth factor (bFGF) or epidermal growth factor (EGF).72 In addition, various in vitro and animal studies showed that safflower yellow produces a decline in both nonspecific and specific immune functions.64 Dietary supplementation in dyslipidemic patients with safflower oil did not affect significantly C-reactive protein, serum amyloid A and IL-6 concentrations, but decreased cholesterol levels.73
  • Antioxidant effects: Seven antioxidative serotonin derivatives were isolated from safflower (Carthamus tinctorius L.) oil cake.68 Their structures were established as N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]ferulamide, N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]-p-coumaramide, N,N'-[2,2'-(5,5'-dihydroxy-4,4'-bi-1H-indol-3,3'-yl)diethyl]- di-p-coumaramide, N-[2-[3'-[2-(p-coumaramido)ethyl]-5,5'-dihydroxy- 4,4'-bi-1H-indol-3-yl]ethyl]ferulamide, and N,N'-[2,2'-(5,5'-dihydroxy-4,4'-bi-1H-indol-3,3'-yl)diethyl]- diferulamide, N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]- p-coumaramide, and N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]ferulamide. Antioxidative activities of the compounds were measured by the ferric thiocyanate method and the alpha,alpha-diphenyl-beta-picrylhydrazyl (DPPH) method, and only N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]- p-coumaramide, and N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]ferulamide were found not to have relatively strong antioxidative activity.
  • In a clinical trial, safflower oil supplementation attenuated age-related differences in membrane phospholipid total n-6 and total n-3 fatty acids.74 In blood samples from humans ingesting safflower oil, there was increased 16:0, 18:0, 18:1n-9, and 22:5n-6 in ghosts of young cells only, and safflower oil ingestion increased the susceptibility of both young and old erythrocytes to oxidative damage by free radical generation (p< 0.001).75
  • According to an animal study, n-3 fatty acid supplementation did not affect lipid peroxidation and protein aggregation in circulating erythrocytes, but did increase peroxidation, but not protein aggregation in isolated erythrocytes under aerobic conditions.76 In a laboratory study, the total free radical scavenger capacity of safflower oil was significant due to the presence of phenolic compounds.77
  • Body fat composition effects: Feeding lambs high-oleate or high-linoleate safflower seeds with mono- and polyunsaturated fatty acids increased tissue 18:1(trans-11) and conjugated linoleic acids (CLA), which is a favorable change in regard to current human dietary guidelines.78
  • Blood pressure effects: In a clinical study, normotensive adults ingesting safflower oil did not show any significant changes in systolic blood pressure or diastolic blood pressure, but resting mean arterial pressure significantly decreased to 79 +/- 2 (p<0.05).20
  • In a clinical trial, whole blood and plasma viscosity, and red blood cell Li/Na countertransport, Na/K cotransport, and Na pump systems (V max ) were unchanged by ingestion of dietary linoleic acid.24
  • In a clinical study, 50mL of safflower oil (39g of n-6 fatty acids) did not significantly affect blood pressure in eight white men with essential hypertension.38
  • Carcinogenic effects: In rats, diets rich in n-6 polyunsaturated fatty acid enhanced the development of pre-neoplastic lesions and tumors in the liver.26 A high-fat diet containing safflower oil also showed a striking induction of hepatic IGFBP-1, a protein that has been implicated in liver cancer development.
  • Animal studies suggest that dietary polyunsaturated fatty acids (PUFAs) of the n-6 class, found in corn and safflower oils, may be precursors of intermediates involved in the development of mammary tumors, whereas long-chain (LC) n-3 PUFAs, found in fish oil, may inhibit these effects.28,29 According to a clinical trial, the total n-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that LC n-3 PUFAs, derived from fish oils, may have a protective effect.28 In another animal study, micrometastases were observed most frequently in the 5% corn oil and 2% linoleic acid dietary groups, but none of the differences were statistically significant.30
  • According to an animal study, the effect of a high fat diet rich in n-6 polyunsaturated fatty acids (safflower oil) depends upon the time at which it is ingested: if before tumor cell inoculation such a diet promotes tumor growth, whereas if after tumor growth is initiated, it does not.31 This suggests that n-6 polyunsaturated fatty acids promote the initiation of colon tumor growth, but do not exert growth-promoting effects on colon tumors once they are established.
  • Cardiovascular effects: In a clinical trial in adult patients following cardiopulmonary bypass procedures, 30-minute intravenous administration of Liposyn® 10% and Intralipid® 10% did not exert significant changes in left ventricular stroke work, left ventricular filling pressure, cardiac output, systemic vascular resistance, mean systemic arterial blood pressure, central venous pressure, or mean pulmonary artery pressure.4
  • Cellular effects: In a clinical trial of normotensive volunteers, ingesting 4g daily of safflower oil significantly decreased leukocyte-ionized calcium at the end of active treatment compared with the end of placebo period.22 The authors concluded that cell membrane fatty acids play a role in the regulation of intracellular calcium in the leukocyte, and perhaps therefore in other tissues. Similar results were observed in an earlier clinical trial by the same authors.23
  • According to a clinical trial, at physiological concentrations, membrane linoleic acid content influences transmembrane sodium fluxes, but not through modulation of sodium pump activity.79
  • Coagulation effects: In a clinical trial, different concentrations of dietary alpha-linolenic acid did not affect the thrombotic risk factors in vegetarian men.37 According to another clinical trial, infusion of 10% emulsion of safflower oil (Liposyn® 10%) decreased Lee-White clotting time.9 In an in vivo titration of the effects of dietary linoleate on human platelet function, platelet aggregation time significantly increased within 48 hours in response to an increase in dietary linoleate of 4% of calories, while disaggregation time decreased significantly in 96 hours.11 A change as small as 0.5% of calories was associated with significant alterations within four days.
  • According to a clinical trial, ingestion of 60mL of safflower oil a day increased platelet linoleic acid (C18:2 omega 6) content from 5.53 +/- 0.52μg to 10.1 +/- 0.92μg/100μg total fatty acids (p<0.001), and decreased platelet aggregation to ADP; fibrinolysis and bleeding times were unaltered.10
  • According to a randomized study on the effects of fish oil on hypertension, 50mL of safflower oil (39g of n-6 fatty acids) did not significantly change serum thromboxane levels in eight white men with essential hypertension.38
  • Cognition/memory effects: Energy intake from safflower oil improved delayed paragraph recall (p<0.001) and improved or tended to improve immediate paragraph recall (p<0.04) 15 minutes after ingestion and independently of elevations in blood glucose.80 Additionally, fat tended to improve attention at 60 minutes (p<0.05).
  • Dermatological effects: In a laboratory study, kinobeon A, produced from cell cultures of safflower, demonstrated potent inhibition of human tyrosinase activity.34
  • Endocrine effects: High-fat feeding of rats with a safflower oil (18:2) diet produced insulin resistance and increased total long-chain acyl-CoAs (LCACoA) content (p<0.0001) by specifically increasing 18:2-CoA.8 However, in a clinical study, young sedentary individuals (age, 21.5 +/- 0.4 year (mean +/- SEM); body mass, 77.6 +/- 3.4kg) receiving 4g safflower oil placebo for eight weeks had no change in insulin sensitivity index 55.
  • In a clinical trial, fasting blood glucose increased 11% during safflower oil supplementation compared with baseline (p<0.05), whereas body weight, fasting serum insulin levels, and insulin sensitivity were unchanged.7 The absolute increase in fasting blood glucose correlated with the baseline fasting blood glucose (safflower oil, r=0.75, p=0.012).
  • Hepatic effects: In an animal study, rats fed a diet containing 10% safflower oil had only 25% the level of hepatic mRNA for Delta-5 and Delta-6 desaturase of that found in the liver of rats fed a fat-free diet or a diet containing triolein.32 In another rat study, a high-fat diet containing safflower oil showed a striking induction of hepatic IGFBP-1, a protein that has been implicated in liver cancer development.26
  • In a clinical trial in four undernourished adults (15%-37% below ideal body weight) on fat-free total parenteral nutrition, supplementation with oral linoleic acid (as safflower oil) reversed the elevation of serum liver enzymes.81
  • Hyperlipidemia effects: The substitution of safflower oil led an increase of cholesteryl linoleate, one of the main cholesterol ester fatty acids.45 According to a clinical trial, ingestion of 60mL of safflower oil a day decreased serum cholesterol.10 The mechanism of the hypolipidemic action of the n-6 rich vegetable oils containing linoleic acid such as safflower oil still remains obscure.82,83 Clinical data suggests that cholesterol synthesis is lower during diets rich in coconut fat and safflower oil compared with diets rich in butter and might be associated with lower production rates of apoB-containing lipoproteins.39 Hepatic accumulation of cholesterol, possibly resulting from the combination of the enhanced cholesteryl ester transfer to apolipoprotein B-containing lipoproteins and increased hepatic uptake of cholesterol, may contribute to the cholesterol-lowering effect of high-oleic acid safflower oil (monounsaturated fatty acids; MUFA) and safflower oil (polyunsaturated fatty acids; PUFA in cholesteryl ester transfer protein (CETP) transgenic mice.40 In several clinical trials conducted in hyperlipidemic populations, safflower oil was used as a placebo and did not significantly change any of the lipid/lipoprotein values.48,49,50,51,52,53 According to a clinical trial, safflower oil as compared to butter has no appreciable effect on plasma cholesterol concentrations, but is associated with a modest rise in triacylglycerols.32 Clinical evidence shows that oleic acid is as effective as linoleic acid in lowering LDL-C levels in normo-triglyceridemic patients, and oleic acid seemingly reduces HDL-C levels less frequently than does linoleic acid.44 Neither type of unsaturated fat had striking effects on lipoprotein levels of hypertriglyceridemic patients. In addition, the content of linoleic acid and alpha-linolenic acid in intravenous fat emulsions resulted in statistically significant changes in the fatty acid profile of total plasma lipids in infants receiving total parenteral nutrition.84 Replacement of linoleic acid with alpha-linolenic acid does not alter blood lipids in normolipidemic men.54 In another clinical trial, the addition of safflower oil to very low fat (VLF) vegetarian diet resulted in significant increases in 18:2 and 20:4 omega 6 and significant decreases in 18:1, 20:5 omega 3 and 22:5 omega 3.46 These results indicate that the reduction of saturated fat content of the diet (< 6% dietary energy), either by reducing the total fat content of the diet or by exchanging saturated fat with unsaturated fat, reduced the total plasma cholesterol levels by approximately 12% in normocholesterolemic subjects. In a clinical trial by Schnell, et al. the polyunsaturated fat diet, in which the major fat source was safflower oil, increased the mean HDL(2) lag time from 45.8 +/- 12.5 to 83.3 +/- 11.6 minutes with no change in oxidation rate.85 Addition of vitamin E further increased the HDL(2) lag time to 115.6 +/- 4.4 minutes and decreased the HDL(2) oxidation rate 10-fold. Therefore, under conditions of controlled dietary fat intake, a high polyunsaturated fat intake does not increase the oxidation susceptibility of HDL subfractions, and in this setting, vitamin E supplementation reduces the oxidation susceptibility of HDL(2). In a clinical study, apolipoprotein B in LDL was significantly decreased by polyenylphosphatidylcholine and safloroil.41 The effects of both substances are comparable in the decrease of apolipoprotein B and probably cholesterol. According to one randomized, blinded trial of 16 healthy men, the ingestion of 38-40% of energy as safflower oil reduced serum total cholesterol 15% (p<0.001), LDL-cholesterol 20% (p,).001), and apo B-100 21% (p<0.001).42 Overall, 88% (N=14) of the subjects had a >10% reduction in serum total cholesterol from baseline diet values.
  • In a clinical trial of obese subjects, two- and four-week treatment with a liquid diet supplemented by maize and safflower oils decreased the dihomo-gamma-linolenic acid (C20:3n-6) concentration by 44% and increased arachidonic acid (C20:4n-6) by 26%, but the serum phospholipid linoleic acid (C18:2n-6) concentration remained constant.6
  • In a clinical trial in vascular disease patients, consumption of a meal enriched with polyunsaturated fatty acids caused a reduction in antibodies to malondialdehyde-modified low density cholesterol (MDA-LDL).43 This decrease was statistically significant from baseline at one hour (p<0.05), two hours (p<0.004), and three hours (p<0.02), with the nadir occurring at two hours.
  • Immunological effects: Safflower oil, rich in n-6 polyunsaturated fatty acid (n-6 PUFA), may affect the survival rate of septic animals and decrease the immune function.13 In a clinical trial in infants maintained on safflower oil emulsion parenteral nutrition, infused safflower oil emulsion did not adversely alter cellular immune function.56 In an animal study, ingestion of safflower oil in a mouse hemorrhage model resulted in a significant increase in PGE2 release by peritoneal macrophages, a marked suppression of peritoneal macrophage antigen presentation capacity, interleukin 1 release, splenocyte proliferation, and interleukin 2 secretion compared with shams.14 In an in vitro study, administration of safflower oil as a polyunsaturated fatty acid control devoid of gammalinolenic acid did not change cytokine secretion.57 In an animal study, safflower polysaccharides activated the transcription factor NF-kappa B via Toll-like receptor 4 and induced cytokine production by macrophages.15 In a clinical trial, ingestion of a low-fat diet supplemented with safflower oil was calculated to increase natural killer cell activity at an E/T ratio of 100:1 (about 0.79% increase for each absolute percent of calories as fat, p=0.04).16 Oral administration of safflower oil enriched in linoleic acid, the parent n-6 fatty acid, did not influence lymphocyte proliferation during a 24-hour period in a clinical trial.58
  • In a randomized, prospective, double-blind study examining the immuno-modulatory effect of fish oil in patients with HIV, safflower oil was used as a control and showed no significant activity.59
  • In a prospective clinical study, administration of a new diet for burn patients (20% of energy from whey protein, 2% from arginine, 0.5% from cysteine, and 0.5% from histidine; lipids 15% of nonprotein calories with 50% fish oil and 50% safflower oil) reduced wound infection (p<0.03), shortened hospital stay (p<0.02), and reduced death (p<0.06) when compared to other standard enteral formulations.17
  • Inflammatory effects: According to a randomized study on the effects of fish oil on hypertension, 50mL of safflower oil (39g of n-6 fatty acids) nonsignificantly increased the formation of prostaglandin (PG) E2 in eight white men with essential hypertension.38 In an animal study, ingestion of safflower oil in a mouse hemorrhage model resulted in a significant increase in PGE2 release by peritoneal macrophages, a marked suppression of peritoneal macrophage antigen presentation capacity, interleukin 1 release, splenocyte proliferation, and interleukin 2 secretion compared with shams.14
  • Metabolic effects: In an animal study, infusion of safflower oil into the duodenum of rats had no effect on the metabolic rate.86
  • In a clinical trial in obese nondiabetic subjects, rates of glycogenolysis were suppressed by safflower oil but not by palm oil following lipid infusion, indicating a differential effect of saturated fatty acids and PUFA on hepatic glucose metabolism.18 Acute changes in plasma non-esterified fatty acid concentration do not change hepatic glucose production in people with type 2 diabetes.87
  • According to clinical trials, oral fat exposure (safflower oil) increased the first phase triacylglycerol concentration due to release of stored lipid in humans.62,63 It is proposed that the sensory-enhanced release of lipid from the residual pool initiates an early triacylglycerol rise, which augments the peak attributable to absorption of meal lipid; this in turn supplements a later peak associated with release of endogenously synthesized triacylglycerol because lipid from all three sources competed for a common clearance mechanism. In addition, a mere taste of fat elevates postprandial triacylglycerol.63 Other data suggest that there is a chemosensory or tactile mechanism in the oronasal region of humans for detecting some aspect of the chemical composition of dietary fat, or a component derived from or carried in fat, that elicits a change in postprandial lipid metabolism.88
  • Mutagenic effects: Mutagenic studies using Salmonella typhimurium strains TA97a, TA98, TA100, and TA102 showed that Carthamus tinctorius has no base pair substitution mutagenic activity.27 However, several animal studies show a striking induction by dietary n-6 PUFAs of hepatic insulin-like growth factor binding protein-1 (IGFBP-1), a protein that has been implicated in liver cancer development.26
  • Platelet aggregation effects: In an in vivo study, platelet aggregation time significantly increased within 48 hours in response to an increase in dietary linoleate of 4% of calories, while disaggregation time decreased significantly in 96 hours.11 In a clinical trial, unsaturated-fatty-acid (safflower oil) diet reduced platelet aggregation at three weeks of oil-based diet feeding (p<0.01).12 In another clinical trial, safflower played a role in prohibiting platelets aggregation, anticoagulation and promoting microcirculation.1
  • Prostaglandin (PG) effects: In a clinical trial, an 8-hour infusion of Liposyn® 10% induced a profound increase in immunoassayable 6-oxo-PGF1 alpha excretion.89 Simultaneously, immunoassayable PGE excretion increased modestly. In another clinical study in pediatric subjects, a 20% safflower oil emulsion increased the concentrations of linoleic and arachidonic acids found in adipose tissue within a short interval.65 According to a clinical study, 50mL of safflower oil (39g of n-6 fatty acids) nonsignificantly increased the formation of prostaglandin E2 in patients with essential hypertension.38 In an animal study, ingestion of safflower oil in a mouse hemorrhage model resulted in a significant increase in PGE2 release by peritoneal macrophages, a marked suppression of peritoneal macrophage antigen presentation capacity, interleukin 1 release, splenocyte proliferation, and interleukin 2 secretion compared with shams.14
  • Respiratory effects: In an animal study, newborn rats born to mothers fed a high n-6 polyunsaturated fatty acid (PUFA) (safflower oil) diet demonstrated increased n-6 PUFA in lung lipids and superior tolerance to high oxygen exposure.90 Offspring of both high n-6 and high n-3 diet dams demonstrated essentially the same superior hyperoxic tolerance compared to regular diet offspring [7-day (>95% O 2 ) survival rates of 110/115 and 99/109, respectively, vs. 70/91, p<0.01].
  • Satiety effects: The satiety response to dietary fat provided in oil or whole food form is influenced by sex and is dependent on the availability of fat to stimulate cholecystokinin-release in women but not in men, according to a clinical trial.91
  • Serum lipid effects: In a clinical trial, safflower oil consumption did not increase plasma conjugated linoleic acid concentrations.61 In a phase I trial, safflower oil ingestion significantly elevated linoleic acids in both phospholipid and triglyceride fractions and significantly elevated arachidonic acid in the phospholipids fraction; oleic acid fell significantly in the phospholipid fraction and palmitic acid in the triglyceride fraction.92
  • In two clinical studies, safflower oil ingestion did not attenuate the favorable modification of certain risk factors for cardiovascular disease (membrane fatty acid composition, blood lipids, and thrombotic profile) by n-3 PUFA (fish oil).60
  • According to a clinical study, 50mL of safflower oil (39g of n-6 fatty acids) slightly increased linoleic acid in phospholipids in eight white men with essential hypertension.38
  • In a clinical trial, ingestion of safflower oil did not increase postprandial chylomicron remnants as much as olive oil ingestion.19
  • According to a clinical trial of neonates using total parenteral nutrition with alpha-linolenic acid as 0.1% or 3.0 +/- 1.5% (SD) of the fatty acids, alpha-linolenic acid and eicosapentaenoic acid were increased in the high alpha-linolenic acid group; however, another metabolite of linolenic acid, docosahexaenoic acid, decreased during intravenous fat therapy in both study groups.25 Both study groups had significantly decreased arachidonic acid levels and increased linoleic to arachidonic acid ratios.
  • According to a clinical study, the incorporation of plasma fatty acids into erythrocyte membranes may occur at a different rate for patients with essential fatty acid deficiency (EFAD) compared to those without EFAD due to an increased red blood cell turnover associated with EFAD.93
  • In a clinical trial in four undernourished adults (15%-37% below ideal body weight) on fat-free total parenteral nutrition, supplementation with oral linoleic acid (as safflower oil) reversed the essential fatty acid deficiency.81
  • In a clinical trial, the proportion of linoleic acid was increased in the plasma of subjects fed the safflower oil diet.21
  • In a clinical trial in men with mild to moderate hypercholesterolemia, cell cholesterol in plasma increased significantly (11%, p<0.004) above values for fasted plasma, the content of cell cholesterol increased significantly (70%, p<0.001) in triglyceride-rich lipoproteins and decreased significantly (p=0.006) in the LDL fraction, and there was a small (5%), significant (p<0.001) increase in plasma cholesterol esterification in postprandial plasma.47
  • In a clinical trial in hypertriglyceridemic, non-insulin-dependent diabetic subjects, the switch from a safflower oil diet to a fish oil diet significantly decreased total plasma triglyercides (p=0.01) and VLDL-apoB (p=0.04), but not LDL or total plasma apoB.94
  • Uterine stimulation effects: According to laboratory study, Carthamus tinctorius has stimulating action on the uterus of mouse in vitro , which may be related to stimulating H1-receptor and alpha-adrenergic receptor of uterus.35

Pharmacodynamics/Kinetics:
  • Absorption in cystic fibrosis patients: In a clinical trial with pediatric cystic fibrosis subjects, safflower oil (triglyceride) consumed in the absence of pancreatic enzymes did not raise in mean plasma linoleic acid levels over the next four hours.33 When linoleic acid monoglyceride (LAM) was consumed, the increase in plasma linoleic acid levels was significantly greater than for safflower oil at two (p<0.02), three (p<0.01), and four hours (p<0.01). When free fatty acid (hydrolyzed safflower oil) was ingested, there was almost no increase in plasma linoleic acid levels in cystic fibrosis or control children. The absorption of linoleic acid from triglyceride, but not from linoleic acid monoglyceride, was greater when the cystic fibrosis children also took pancreatic enzymes. Three children with cystic fibrosis had greater increases in plasma linoleic acid levels following ingestion of safflower oil when they took antacid and cimetidine with their pancreatic capsules, compared to when they only took the pancreatic capsules. In a clinical trial, plasma samples obtained 0, 2, 4, 6 and eight hours after a meal with a high safflower oil content showed that the cystic fibrosis patients absorbed all safflower preparations when administered with their regular dose of pancreatic enzyme supplement.95 Many calculated parameters useful as indices of essential fatty acid status indicated that essential fatty acid deficiency exists in cystic fibrosis.96 Treatment of 11 cystic fibrosis patients with safflower oil (1g/kg daily) failed to correct the aberrations in fatty acid pattern. The biochemical data suggest that there may be impairment in the conversion of linoleate to arachidonate as well as an impairment of absorption. However, malabsorption alone cannot account for the inadequate or marginal essential fatty acid status of cystic fibrosis patients.97 One absorption study with safflower oil demonstrated normal enteral absorption of essential fatty acids and the ability to cross the blood-cerebrospinal fluid barrier.98 Restricted linoleic acid availability in cystic fibrosis patients causes a change in red blood cell shape either directly by decreasing the linoleoylphosphatidylcholine content of the membrane or indirectly by affecting enzyme activity.99
  • Clearance: In a clinical study, administration 0.1g of fat per kilogram body weight as 10% or 20% safflower oil emulsion (Liposyn®) to healthy volunteers did not show a significant difference in the clearance rate between the two emulsions.3 It was concluded that 20% fat emulsion is a safe as 10% fat emulsion for use in intravenous nutritional support. In a study of neonates, Burckart et al. found that small neonates may have a relative deficit in clearance of free fatty acids.5
  • Metabolism: Safflower yellow B is metabolized by human intestinal bacteria.100
  • According to a clinical trial, there is a rapid transfer of dietary fatty acids from plasma chylomicrons, specifically linoleic acid, into human milk.36 Maximum increase occurred 10 hours after safflower oil ingestion and remained significantly elevated in milk for 10-24 hours (p<0.05).
  • Plasma concentrations of 18:2 n-6 fatty acids increased for two hours when 609 +/- 37μmol/L was ingested during a continuous low-dose heparin infusion in eighty healthy volunteers.101
  • Metabolism in theonin 54 (T54) carriers: Postprandial lipemia in obese and T54 carriers is significant for the areas under the chylomicron cholesterol and chylomicron triacylglycerol curves [higher values for safflower (0.635 +/- 0.053 and 2.48 +/- 0.30mmol. hour/L, respectively) than olive oil (0.592 +/- 0.052 and 2.48 +/- 0.32mmol. hour/L, respectively) or (0.425 +/- 0.043 and 1.69 +/- 0.20mmol. hour/L, respectively); p<0.05].102
  • Stability: The stability of 1:1-soybean/safflower intravenous lipid emulsions in three different all-in-one admixtures intended for neonatal and infant patients was investigated.103 The stability of soybean/safflower-based admixtures significantly and rapidly deteriorated in one of the three all-in-one compositions studied. This significant and rapid deterioration of stability was likewise observed in an earlier study.104

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