Also see:
Israeli Paradox: High Omega -6 Diet Promotes Disease
Unsaturated Fats, Oxidative Stress, and Atherosclerosis
Thyroid Status and Cardiovascular Disease
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
A Cure for Heart Disease
Hypothyroidism and A Shift in Death Patterns
Arachidonic Acid’s Role in Stress and Shock
Dietary Fats, Temperature, and Your Body
The Questionable Link Between Saturated Fat and Heart Disease
Quotes by Ray Peat, PhD:
“Heart damage is easily produced in animals by feeding them linoleic acid; this “essential” fatty acid turned out to be the heart toxin in rape-seed oil. The addition of saturated fat to the experimental heart-toxic oil-rich diet protects against the damage to heart cells.”
“Selye’s demonstration of corn oil’s toxicity to the heart is an important link in the general picture of stress injury and adrenalin toxicity. The protective effects of saturated fats are not surprising when seen against the background of the toxic effects of adrenalin, causing the mobilization of fatty acids and the resulting lipid peroxidation.”
“The reason for this increase seems to be that the saturated fatty acids are preferentially oxidized by many types of cell, (fat cells can slowly oxidize fat for their own energy maintenance). Albumin preferentially delivers saturated fatty acids into actively metabolizing cells such at the heart (Paris, 1978) for use as fuel. This preferential oxidation would explain Hans Selye’s results, in which canola oil in the diet caused the death of heart cells, but when the animals received stearic acid in addition to the canola oil, their hearts showed no sign of damage.”
The American Journal of Cardiology (May 1969), 23 (5), pg. 719-722
Sensitization by corn oil for the production of cardiac necroses by various steroids and sodium salts
Hans Selye; Árpád Somogyi; Gaston Côté
In the rat, the production of extensive and usually fatal myocardial necroses by fluorocortisol or desoxycorticosterone in combination with Na2HPO4 is greatly accelerated and aggravated by the oral administration of corn oil. Cortisol, progesterone and methyltestosterone do not produce myocardial necroses under these conditions even if, in addition to Na2HPO4, corn oil is given.
Not all sodium salts are equally potent in producing myocardial necroses when administered in combination with fluorocortisol and fat supplements. In this respect, NaH2PO4, Na2HPO4, NaClO4 and NaHSO4 are most effective, NaHCO3 is somewhat less active, whereas NaCl is inactive under otherwise comparable conditions.
Lipids. 1982 May;17(5):372-82.
Reduction of myocardial necrosis in male albino rats by manipulation of dietary fatty acid levels.
Kramer JK, Farnworth ER, Thompson BK, Corner AH, Trenholm HL.
A comprehensive statistical analysis had shown a significant correlation between the incidence of myocardial lesions in male albino rats and the concentration of certain dietary fatty acids. To test this result under controlled conditions, male rats were fed for 16 weeks diets containing 20% by weight soybean oil or a low erucic acid rapeseed (LEAR) oil. Both dietary oils contained substantial amounts of linolenic acid, and both groups developed a high incidence of myocardial necrosis. The addition of dietary saturated fatty acids to the oil in the form of cocoa butter significantly lowered the incidence of heart lesions in both groups. The addition of cocoa butter resulted in increased absorption of saturates and increased growth. Replacement of the cocoa butter by at least an equal amount of synthetic triolein resulted in no significant changes in the cardiopathogenic response compared to the original oils, thus ensuring that the reduction in heart lesions associated with the addition of cocoa butter was not due to dilution of cardiopathogenic compounds in the original vegetable oils. These results support the hypothesis that myocardial lesions in male rats are related to the balance of dietary fatty acids and not to cardiotoxic contaminants in the oils. Changes in the dietary fatty acids did not appear to influence the proportion of the cardiac phospholipids, but their fatty acid composition was markedly influenced. Dietary linolenic acid affected the C22 polyunsaturated fatty acids (PUFA) and dietary saturates increased the level of saturates in cardiac phospholipids. The level of arachidonic acid and total C22 PUFA did not appear to be affected by diet.
J Nutr. 1982 Feb;112(2):231-40.
Role of dietary saturated fatty acids on lowering the incidence of heart lesions in male rats.
Farnworth ER, Kramer JK, Thompson BK, Corner AH.
Male weanling rats were fed soybean or low erucic acid rapeseed oils alone or in combination with cocoa butter (a source high in saturates) or triolein for 16 weeks. All diets contained 20% by weight of the test oils. The apparent digestibility of all diets and test oils increased with the age of the rat. The apparent digestibility of saturated fatty acids was lower in rats fed the diets containing cocoa butter. The relative organ weights, however, were not affected by diet, but growth was improved by supplementing the vegetable oils with cocoa butter. This growth difference was significant for the addition of cocoa butter to low erucic acid rapeseed oil. After 16 weeks all groups of rats developed myocardial necrosis. A dramatic lowering of myocardial lesion incidence was observed in rats fed diets enriched with saturated fatty acids. The results of the present experiment suggest that enriching a vegetable oil with saturated fatty acids affects both nutritional and cardiopathological properties of the oil.
Lipids. 1980 Sep;15(9):651-60.
Comparative studies on composition of cardiac phospholipids in rats fed different vegetable oils.
Kramer JK.
Male Sprague-Dawley rats were fed diets for 1 or 16 weeks, containing 20% by weight vegetable oils differing widely in their oleic, linoleic and linolenic acid content. No significant changes were observed in the level of the cardiac lipid classes. The fatty acid composition of the 2 major phospholipids, phosphatidylcholine and phosphatidylethanolamine, showed a remarkable similarity between diets in the concentration of total saturated, C22 polyunsaturated and arachidonic acids. Monounsaturated acids were incorporated depending on their dietary concentration, but the increases were moderate. Dietary linolenic acid rapidly substituted C22 polyunsaturated fatty acids of the linoleic acid family (n-6) with those from the linolenic acid family (n-3). The results suggest that dietary linolenic acid of less than 15% does not inhibit the conversion of linoleic to arachidonic acid but the subsequent conversion of arachidonic acid to the C22 polyunsaturates was greatly reduced. Significant amounts of dietary monounsaturated fatty acids were incorporated into cardiac cardiolipin accompanied by increases in polyunsaturated fatty acids, apparently to maintain an average of 2 double bonds/molecule. The cardiac sphingomyelins also accumulated monounsaturated fatty acids depending on the dietary concentration. It is quite evident from the results of this study that the incorporation of oleic acid and the substitution of linolenic for linoleic acid-derived C22 polyunsaturated fatty acids into cardiac phospholipids was related to the dietary concentration of these fatty acids and was not peculiar to any specific oil. Even though it is impossible to estimate the effect of such changes in cardiac phospholipids on membrane structure and function, results are discussed which suggest that the resultant membrane in the Spragu-Dawley male rat is more fragile, leading to greater cellular breakdown and focal necrosis.
Biull Eksp Biol Med. 1983 Apr;95(4):46-8.
[Calcium and lipid peroxidation in the heart mitochondrial and microsomal membranes].
[Article in Russian]
Kagan VE, Savov VM, Didenko VV, Arkhipenko IuV, Meerson FZ.
Effect of the lipid peroxidation (LP) on the Ca2+-transport and the effect of different Ca2+-concentrations on the LP activation were studied in microsomes and mitochondria of the heart. A slight accumulation of LP-products in the microsomal fraction results in a complete inhibition of the membrane calcium-transport activity. Preliminary administration of antioxidants (4-methyl 2,6-ditretbutylphenol and alpha-tocopherol) prevents both the accumulation of LP-products and damage of the Ca2+-transport system. Calcium at 10(-6) M to 5 X 10(-5) M concentrations stimulates LP and while being increased to 2 X 10(-3) M it inhibits LP. The data obtained evidence an interrelation between alterations of the Ca2+-concentrations and LP activation in cardiomyocytes.
Cardiovasc Res (2011) doi: 10.1093/cvr/cvr258
High Intake of Saturated Fat, But Not Polyunsaturated Fat, Improves Survival in Heart Failure Despite Persistent Mitochondrial Defects
Tatiana F. Galvao, Bethany H. Brown, Peter A. Hecker, Kelly A. O’Connell, Karen M. O’Shea, Hani N. Sabbah, Sharad Rastogi, Caroline Daneault, Christine Des Rosiers and William C. Stanley
Aims The impact of a high fat diet on the failing heart is unclear, and the differences between polyunsaturated fatty acids (PUFA) and saturated fat have not been assessed. Here we compared a standard low fat diet to high fat diets enriched with either saturated fat (palmitate and stearate), or PUFA (linoleic and α-linolenic acids) in hamsters with genetic cardiomyopathy.
Methods and Results Male δ-sarcoglycan null Bio TO2 hamsters were fed a standard low fat diet (12% energy from fat), or high fat diets (45% fat) comprised of either saturated fat or PUFA. Median survival was increased by the high saturated fat diet (P<0.01; 278 days with standard diet and 361 days with high saturated fat)), but not with high PUFA (260 days) (n=30-35/group). Body mass was modestly elevated (~10%) in both high fat groups. Subgroups evaluated after 24 weeks had similar LV chamber size, function and mass. Mitochondrial oxidative enzyme activity and the yield of interfibrillar mitochondria were decreased to a similar extent in all TO2 groups compared to normal F1B hamsters. Ca2+-induced mitochondrial permeability transition pore opening was enhanced in interfibrillar mitochondria in all TO2 groups compared to F1B hamsters, but to a significantly greater extent in those fed the high PUFA diet compared to the standard or high saturated fat diet.
Conclusions These results show that a high intake of saturated fat improves survival in heart failure compared to a high PUFA diet or low fat diet despite persistent mitochondrial defects.
Nutrition. 2004 Feb;20(2):230-4.
Diets rich in saturated and polyunsaturated fatty acids: metabolic shifting and cardiac health.
Diniz YS, Cicogna AC, Padovani CR, Santana LS, Faine LA, Novelli EL.
OBJECTIVE:
The aim of this study was to determine the effects of diets rich in saturated and polyunsaturated fatty acids on metabolic pathways and the relation of metabolic shifting to oxidative stress in cardiac tissue.
METHODS:
Male Wistar rats (age, 60 d; n = 10) were fed with a control low-fat diet, a diet rich in saturated fatty acids (SFAs), or a diet rich in polyunsaturated fatty acids (PUFAs). After 5 wk of treatment, sera were used for protein and lipid determinations. Protein, glycogen, triacylglycerol, lactate dehydrogenase, citrate synthase, beta-hydroxyacyl coenzyme-A dehydrogenase, catalase, glutathione peroxidase, superoxide dismutase, lipoperoxide, and lipid hydroperoxide were measured in cardiac tissue.
RESULTS:
The SFA group had higher triacylglycerol, cholesterol, low-density lipoprotein cholesterol, and atherogenic index (ratio of cholesterol to high-density lipoprotein) than did the PUFA and control groups. The PUFA group had low serum cholesterol, triacylglycerol, and low-density lipoprotein cholesterol as compared with the SFA group. SFA increased myocardial lipid hydroperoxide and diminished glutathione peroxidase. Despite the beneficial effects on serum lipids, the PUFA diet led to the highest levels of myocardial lipoperoxide and lipid hydroperoxide and diminished superoxide dismutase and catalase activities. The PUFA effects were related to increased feed efficiency, increased susceptibility to lipoperoxidation, and metabolic shifting in cardiac tissue. PUFA elevated triacylglycerol levels and decreased myocardial glycogen concentrations. The ratios of lactate dehydrogenase to citrate synthase and beta-hydroxyacyl coenzyme-A dehydrogenase to citrate synthase were increased, indicating myocardial reduction of tricarboxylic acid cycle.
CONCLUSIONS:
PUFAs have been recommended as a therapeutic measure in preventive medicine to lower serum cholesterol, but PUFAs increased oxidative stress in the heart by providing cardiac susceptibility to lipoperoxidation and shifting the metabolic pathway for energy production. The control diet, which was much lower in calories and fat, produced better overall clinical outcomes, better fat profiles, and less oxidative stress than did the diets rich in fatty acids.
Lancet. 1994 Oct 29;344(8931):1195-6.
Dietary polyunsaturated fatty acids and composition of human aortic plaques.
Felton CV, Crook D, Davies MJ, Oliver MF.
How long-term dietary intake of essential fatty acids affects the fatty-acid content of aortic plaques is not clear. We compared the fatty-acid composition of aortic plaques with that of post-mortem serum and adipose tissue, in which essential fatty-acid content reflects dietary intake. Positive associations were found between serum and plaque omega 6 (r = 0.75) and omega 3 (r = 0.93) polyunsaturated fatty acids, and monounsaturates (r = 0.70), and also between adipose tissue and plaque omega 6 polyunsaturated fatty acids (r = 0.89). No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered.
Cardiovasc Res. 2012 Jan 1;93(1):24-32. Epub 2011 Sep 29.
High intake of saturated fat, but not polyunsaturated fat, improves survival in heart failure despite persistent mitochondrial defects.
Galvao TF, Brown BH, Hecker PA, O’Connell KA, O’Shea KM, Sabbah HN, Rastogi S, Daneault C, Des Rosiers C, Stanley WC.
The impact of a high-fat diet on the failing heart is unclear, and the differences between polyunsaturated fatty acids (PUFA) and saturated fat have not been assessed. Here, we compared a standard low-fat diet to high-fat diets enriched with either saturated fat (palmitate and stearate) or PUFA (linoleic and α-linolenic acids) in hamsters with genetic cardiomyopathy.
METHODS AND RESULTS:
Male δ-sarcoglycan null Bio TO2 hamsters were fed a standard low-fat diet (12% energy from fat), or high-fat diets (45% fat) comprised of either saturated fat or PUFA. The median survival was increased by the high saturated fat diet (P< 0.01; 278 days with standard diet and 361 days with high saturated fat)), but not with high PUFA (260 days) (n = 30-35/group). Body mass was modestly elevated (∼10%) in both high fat groups. Subgroups evaluated after 24 weeks had similar left ventricular chamber size, function, and mass. Mitochondrial oxidative enzyme activity and the yield of interfibrillar mitochondria (IFM) were decreased to a similar extent in all TO2 groups compared with normal F1B hamsters. Ca(2+)-induced mitochondrial permeability transition pore opening was enhanced in IFM in all TO2 groups compared with F1B hamsters, but to a significantly greater extent in those fed the high PUFA diet compared with the standard or high saturated fat diet.
CONCLUSION:
These results show that a high intake of saturated fat improves survival in heart failure compared with a high PUFA diet or low-fat diet, despite persistent mitochondrial defects.
J Environ Pathol Toxicol Oncol. 1986 Mar-Apr;6(3-4):115-21.
Medium chain triglycerides (MCT) in aging and arteriosclerosis.
Kaunitz H.
Some of the nutritional work with triglycerides consisting mainly of C8 and C10 fatty acids (MCT) lends itself to speculations about their influence on arteriosclerosis. Arteriosclerosis is thought to be part of the normal aging process which is due to age associated molecular biological changes. The lipid theory of arteriosclerosis is rejected. Pertinent studies with MCT include these observations. Feeding of MCT to rats resulted in animals of low body weight, small fat deposits and excellent survival rate. This deserves emphasis because of the beneficial influence of low body weight on aging and arteriosclerosis. MCT feeding was associated with low linoleate and low tocopherol requirements in rats. This may lead to reduced formation of those linoleate derived prostaglandins which favor thrombosis formation. Lower linoleate requirements may also lead to the presence of fewer uncontrolled free radicals in the cells. MCT feeding is associated with low levels of serum and liver cholesterol involving speculations that tissue conditions are such that an adaptive increase of cholesterol is unnecessary. The Demographic Yearbook of the United Nations (1978) reported that Sri Lanka has the lowest death rate from ischemic heart disease. Sri Lanka is the only of the countries giving reliable data where coconut oil (containing over 50% medium chain fatty acids) is the main dietary fat.
BMJ. 2013 Feb 4;346:e8707. doi: 10.1136/bmj.e8707.
Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.
Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR.
Objective To evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death.
Design Evaluation of recovered data from the Sydney Diet Heart Study, a single blinded, parallel group, randomized controlled trial conducted in 1966-73; and an updated meta-analysis including these previously missing data.
Setting Ambulatory, coronary care clinic in Sydney, Australia.
Participants 458 men aged 30-59 years with a recent coronary event.
Interventions Replacement of dietary saturated fats (from animal fats, common margarines, and shortenings) with omega 6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine). Controls received no specific dietary instruction or study foods. All non-dietary aspects were designed to be equivalent in both groups.
Outcome measures All cause mortality (primary outcome), cardiovascular mortality, and mortality from coronary heart disease (secondary outcomes). We used an intention to treat, survival analysis approach to compare mortality outcomes by group.
Results The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6% v 11.8%, hazard ratio 1.62 (95% confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2% v 11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3% v 10.1%, 1.74 (1.04 to 2.92), P=0.04). Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).
Conclusions Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.
Lipids. 1993 Jul;28(7):651-5.
Rat vitamin E status and heart lipid peroxidation: effect of dietary alpha-linolenic acid and marine n-3 fatty acids.
Javouhey-Donzel A, Guenot L, Maupoil V, Rochette L, Rocquelin G.
Three groups of sixteen male rats each were fed semi-purified diets containing 15% by weight of lipid for a period of 4 wk. The diets contained the same amount of polyunsaturated fatty acids (PUFA) (20% of total fatty acids) and saturated fatty acids (19% of total fatty acids). Dietary PUFA were represented exclusively by linoleic acid (18:2 diet), or 10% linoleic acid and 10% linolenic acid (18:3 diet), or 10% linoleic acid and 10% long-chain n-3 fatty acids (LCn-3 diet). The overall amount of vitamin E was similar in the three diets, i.e., 140, 133 and 129 mg/kg diet, respectively. Following appropriate extraction, tocopherol levels in heart, liver, brain, adipose tissue (AT) and plasma were measured by high-performance liquid chromatography. The level of vitamin E in the heart decreased with n-3 PUFA diets, most markedly with LCn-3 PUFA. Liver and AT vitamin E contents also decreased with n-3 PUFA diets when expressed as micrograms/mg total lipids and micrograms/mg phospholipids, respectively. Total plasma vitamin E was lower in rats fed the LCn-3 diet, but there was no significant difference when expressed as microgram/mg total lipids. Brain vitamin E was not affected by the various diets. In vitro cardiac lipid peroxidation was quantified by the thiobarbituric acid reactive substances (TBARS) test. Heart homogenates were incubated at 37 degrees C for 15 and 30 min in both the absence (uninduced) or presence (induced) of a free radical generating system (1 mM xanthine, 0.1 IU per mL xanthine oxidase, 0.2 mM/0.4 mM Fe/ethylenediaminetetraacetic acid). TBARS release was time-independent but significantly higher when LCn-3 fatty acids were fed to rats in either the uninduced or induced system. The study demonstrated that n-3 PUFA diets can influence vitamin E status of rats even in short-term experiments and can change the susceptibility of the heart to in vitro lipid peroxidation.
Mitochondrion. 2011 Jan;11(1):97-103. doi: 10.1016/j.mito.2010.07.014. Epub 2010 Aug 5.
Dietary fatty acids and oxidative stress in the heart mitochondria.
Lemieux H, Bulteau AL, Friguet B, Tardif JC, Blier PU.
Our study compared the effects of different oils on oxidative stress in rat heart mitochondria, as well as on plasma parameters used as risk factors for cardiovascular disease. The rats were fed for 16 weeks with coconut, olive, or fish oil diet (saturated, monounsaturated, or polyunsaturated fatty acids, respectively). The cardiac mitochondria from rats fed with coconut oil showed the lowest concentration of oxidized proteins and peroxidized lipids. The fish oil diet leads to the highest oxidative stress in cardiac mitochondria, an effect that could be partly prevented by the antioxidant probucol. Total and LDL cholesterols decreased in plasma of rats fed fish oil, compared to olive and coconut oils fed rats. A diet enriched in saturated fatty acids offers strong advantages for the protection against oxidative stress in heart mitochondria.
Am J Cardiovasc Dis. 2013;3(1):17-26. Epub 2013 Feb 17.
Interaction between sphingomyelin and oxysterols contributes to atherosclerosis and sudden death.
Kummerow FA.
Despite major public health efforts, coronary heart disease continues to be the leading cause of death in the United States. Oxidized lipids contribute to heart disease both by increasing deposition of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a major contributor to heart attack and sudden death. Oxidized cholesterol (oxysterols) enhances the production of sphingomyelin, a phospholipid found in the cellular membranes of the coronary artery. This increases the sphingomyelin content in the cell membrane, which in turn enhances the interaction between the membrane and ionic calcium (Ca(2+)), thereby increasing the risk of arterial calcification. Patients undergoing bypass surgery had greater concentrations of oxysterols in their plasma than cardiac catheterized controls with no stenosis, and had five times more sphingomyelin in their arteries than in the artery of the placenta of a newborn. The oxysterols found in the plasma of these patients were also found in the plasma of rabbits that had been fed oxidized cholesterol and in frying fats and powdered egg yolk intended for human consumption. Together these findings suggest that oxysterols found in the diet are absorbed and contribute to arterial calcification. Oxidized low-density lipoprotein (OxLDL) further contributes to heart disease by increasing the synthesis of thromboxane in platelets, which increases blood clotting. Cigarette smoke and trans fatty acids, found in partially hydrogenated soybean oil, both inhibit the synthesis of prostacyclin, which inhibits blood clotting. By increasing the ratio of thromboxane to prostacyclin, these factors interact to interrupt blood flow, thereby contributing to heart attack and sudden death. Levels of oxysterols and OxLDL increase primarily as a result of three diet or lifestyle factors: the consumption of oxysterols from commercially fried foods such as fried chicken, fish, and french fries; oxidation of cholesterol in vivo driven by consumption of excess polyunsaturated fatty acids from vegetable oils; and cigarette smoking. Along with the consumption of trans fatty acids from partially hydrogenated vegetable oil, these diet and lifestyle factors likely underlie the persistent national burden of heart disease.
Br Med J. 1965 Jun 12;1(5449):1531-3.
CORN OIL IN TREATMENT OF ISCHAEMIC HEART DISEASE.
ROSE GA, THOMSON WB, WILLIAMS RT.
Am J Clin Nutr ajcn122671 January 20, 2016, doi: 10.3945/ajcn.115.122671
The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the European Prospective Investigation into Cancer and Nutrition–Netherlands cohort
Jaike Praagman, Joline WJ Beulens, Marjan Alssema, Peter L Zock, Anne J Wanders, Ivonne Sluijs, and Yvonne T van der Schouw
Background: The association between saturated fatty acid (SFA) intake and ischemic heart disease (IHD) risk is debated.
Objective: We sought to investigate whether dietary SFAs were associated with IHD risk and whether associations depended on 1) the substituting macronutrient, 2) the carbon chain length of SFAs, and 3) the SFA food source.
Design: Baseline (1993–1997) SFA intake was measured with a food-frequency questionnaire among 35,597 participants from the European Prospective Investigation into Cancer and Nutrition–Netherlands cohort. IHD risks were estimated with multivariable Cox regression for the substitution of SFAs with other macronutrients and for higher intakes of total SFAs, individual SFAs, and SFAs from different food sources.
Results: During 12 y of follow-up, 1807 IHD events occurred. Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93). Substituting SFAs with animal protein, cis monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), or carbohydrates was significantly associated with higher IHD risks (HR per 5% of energy: 1.27–1.37). Slightly lower IHD risks were observed for higher intakes of the sum of butyric (4:0) through capric (10:0) acid (HRSD: 0.93; 95% CI: 0.89, 0.99), myristic acid (14:0) (HRSD: 0.90; 95% CI: 0.83, 0.97), the sum of pentadecylic (15:0) and margaric (17:0) acid (HRSD: 0.91: 95% CI: 0.83, 0.99), and for SFAs from dairy sources, including butter (HRSD: 0.94; 95% CI: 0.90, 0.99), cheese (HRSD: 0.91; 95% CI: 0.86, 0.97), and milk and milk products (HRSD: 0.92; 95% CI: 0.86, 0.97).
Conclusions: In this Dutch population, higher SFA intake was not associated with higher IHD risks. The lower IHD risk observed did not depend on the substituting macronutrient but appeared to be driven mainly by the sums of butyric through capric acid, the sum of pentadecylic and margaric acid, myristic acid, and SFAs from dairy sources. Residual confounding by cholesterol-lowering therapy and trans fat or limited variation in SFA and PUFA intake may explain our findings. Analyses need to be repeated in populations with larger differences in SFA intake and different SFA food sources.
Pharmacology. 2016 Jun 2;98(3-4):134-170. [Epub ahead of print]
Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes.
Okuyama H1, Langsjoen PH, Ohara N, Hashimoto Y, Hamazaki T, Yoshida S, Kobayashi T, Langsjoen AM.
BACKGROUND:
Positive associations have been observed between cardiovascular disease (CVD) and type 2 diabetes mellitus (DM), but their causal relationship has not been clarified. Nevertheless, guidelines from relevant medical societies recommend using cholesterol lowering medication (statin) for both types of patients. Medicines with several different action mechanisms have been developed, and the effectiveness of different lifestyle modifications has been studied extensively for the prevention of DM, which was successful in improving clinical marker status in relatively short-term treatments, but none have been shown to be effective in improving long-term outcomes (mortality from CVD and all causes).
SUMMARY:
Statin-induced suppression of prenyl intermediates in the cholesterol biosynthetic pathway has been linked to stimulated atherosclerosis and heart failure. On the other hand, certain types of vegetable oil and hydrogenated oil shortened the survival of stroke-prone spontaneously hypertensive rats by decreasing platelet number, increasing hemorrhagic tendency and damaging kidney functions, which could not be accounted for by their fatty acid and phytosterol compositions. These vegetable oils and medicines such as statin and warfarin share, in part, a common mechanism to inhibit vitamin K2-dependent processes, which was interpreted to lead to increased onset of CVD, DM, chronic kidney disease, bone fracture and even mental disorder. Impaired vitamin K2-dependent processes by some types of vegetable oils and medicines, but not plasma high low density lipoprotein cholesterol, were proposed as the cause of CVD, DM and other lifestyle-related diseases. High n-6/n-3 fatty acid ratio of ingested foods, but not animal fats, was emphasized to be another risk factor for many of the diseases described above.
KEY MESSAGES:
To date, no randomized controlled trials (RCTs) have been performed to prove the above interpretation. However, the opposite types of RCT trials have been performed by increasing the intake of high-linoleic vegetable oils and reducing that of animal fats, which resulted in increased CVD and all-cause mortality. The amounts of these vegetable oils to exhibit adverse effects in animal studies are not huge (<6 energy %), which should not be overlooked nor disregarded.
International Science and Investigation journal, [S.l.], v. 5, n. 5, p. 157-168, Nov. 2016
Vegetable Oils Consumption as One of the Leading Cause of Cancer and Heart Disease.
NIKNAMIAN, Soroush; KALAMIAN, Miriam.
This review takes a deep look at increases in the incidence of cancer and heart disease after the introduction of industrial vegetable oils in the world. Most vegetable oils are highly processed and refined products, which completely lack the essential nutrients. Omega-6 Linoleic acid from vegetable oils increases oxidative stress in the body of humans, contributing to endothelial dysfunction and heart disease. The consumption of these harmful oils which are high in mega-6 polyunsaturated fats results in changing the structure of cell membrane which contribute to increasing inflammation and the incidence of cancer.
Thank you for the articles!