Cholesterol and dietary fats, the truth.

Genetic Freak

Moderator: SIED
Staff member
Joined
Mar 18, 2012
Messages
2,759
Some interesting notes regarding Trans fats and Cholesterol:

1. Vegetable oils are more toxic when heated. One study reported that polyunsaturates turn to varnish in the intestines. A study by a plastic surgeon found that women who consumed mostly vegetable oils had far more wrinkles than those who used traditional animal fats. A 1994 study appearing in the Lancet showed that almost three quarters of the fat in artery clogs is unsaturated. The "artery clogging" fats are not animal fats but vegetable oils.

2. Trans fats, produced in vegetable oils when they are partially hydrogenated, The research group at the University of Maryland found that trans fatty acids not only alter enzymes that neutralize carcinogens, and increase enzymes that potentiate carcinogens..

3. Trans fats contribute to osteoporosis. Hanis, a Czechoslovakian researcher, found that trans consumption decreased testosterone, caused the production of abnormal sperm and altered gestation.
Trans consumption interferes with the body?s use of omega-3 fatty acids found in fish oils, grains and green vegetables, leading to impaired prostaglandin production. Some deep fried foods have been tested at almost 50% trans.


4. The scientific literature delineates a number of vital roles for dietary saturated fats, they enhance the immune system, are necessary for healthy bones, provide energy and structural integrity to the cells, protect the liver and enhance the body?s use of essential fatty acids.

5. Stearic acid, found in beef tallow and butter, has cholesterol lowering properties and is a preferred food for the heart. As saturated fats are stable, they do not become rancid easily, do not call upon the body?s reserves of antioxidants, do not initiate cancer, do not irritate the artery walls.

6. Your body makes saturated fats, and your body makes cholesterol about 2000 mg per day. In general, cholesterol that the average American absorbs from food amounts to about 100 mg per day. So, in theory, even reducing animal foods to zero will result in only a 5% decrease in the total amount of cholesterol available to the blood and tissues.

7. In practice, such a diet is likely to deprive the body of the substrates it needs to manufacture enough of this vital substance; for cholesterol, like saturated fats, stands unfairly accused.

8. It acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone; it is a precursor to vitamin D, a very important fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function;

9. It is the precursor to bile salts, which are vital for digestion and assimilation of fats in the diet. Recent research shows that cholesterol acts as an antioxidant. This is the likely explanation for the fact that cholesterol levels go up with age.

10. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer. Cholesterol is the body?s repair substance, manufactured in large amounts when the arteries are irritated or weak.

11. Cholesterol is needed for proper function of serotonin receptors in the brain. Serotonin is the body's natural "feel-good" chemical. This explains why low cholesterol levels have been linked to aggressive and violent behaviour, depression and suicidal tendencies..

12. Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system. Dietary cholesterol plays an important role in maintaining the health of the intestinal wall, which is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.

13. Animal foods containing saturated fat and cholesterol provide vital nutrients necessary for growth, energy and protection from degenerative disease. Like sex, animal fats are necessary for reproduction. Humans are drawn to both by powerful instincts. Suppression of natural appetites leads to weird nocturnal habits, fantasies, fetishes, bingeing and splurging.


B B Teter, et al, "Milk Fat Depression in C57B1/6J Mice Consuming Partially Hydrogenated Fat," Journal of Nutrition, 1990, 120:818-824; Barnard, et al, "Dietary Trans Fatty Acids Modulate Erythrocyte Membrane Fatty Acid

Composition and Insulin Binding in Monkeys," Journal of Nutritional Biochemistry, 1990, 1:190-195

T Hanis, et al, "Effects of Dietary Trans Fatty Acids on Reproductive Perforamnce of Wistar Rats," British Journal of Nutrition, 1989, 61:519-529

B Koletzko and J Muller, "Cis- and Trans-Isomeric Fatty Acids in Polasma Lipids of Newborn Infants and Their Mothers," Biology of the Neonate, 1990, 57:172-178

D Horrobin, "The Regulation of Prostaglandin Biosynthesis by Manipultion of Essential Fatty Acid Metabolism," Reviews in Pure and Applied Pharmacological Sciences, 1983, 4:339-383

G V Mann, "Metabolic Consequences of Dietary Trans Fatty Acids," The Lancet, 1994, 343:1268-1271

L Kohlmeier, et al, "Stores of Trans Fatty Acids and Breast Cancer Risk, "Am J Clin Nutr, 1995, 61:896;A25

R P Mensink and M Katan, "Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects," N Eng J Med, 1990, 323:439-445

M G Enig, et al, "Isomeric Trans Fatty Acids in the U.S. Diet," J Am Coll Nutr, 1990, 9:471-486

W C Willett, et al, "Consumption of Trans-Fatty Acids in Relation to Risk of Coronary Heart Disease Among Women," Society for Epidemiology Research, June 1992, Annual Meeting, Abstract 249

W C Willett, et al, "Intake of Trans Fatty Acids and Risk of Coronary Heart Disease Among Women," Lancet, 1993, 341:581-585

J J Kabara, The Pharmacological Effects of Lipids, J J Kabara, ed, The American Oil Chemists? Society, Champaign, IL, 1978, 1-14; L A Cohen, et al, J Natl Cancer Inst, 1986, 77:43

B A Watkins, et al, "Importance of Vitamin E in Bone Formation and in Chrondrocyte Function" Purdue University, Lafayette, IN, AOCS Proceedings, 1996;

B A Watkins, and M F Seifert, "Food Lipids and Bone Health," Food Lipids and Health, R E McDonald and D B Min, eds, Marcel Dekker, Inc. New York, NY, p 101

J F Mead, et al, Lipids: Chemistry, Biochemistry and Nutrition, Plenum Press, 1986, New York

A A Nanji, et al, Gastroenterology, Aug 1995, 109(2):547-54; Y S Cha, and D S Sachan, J Am Coll Nutr, Aug 1994, 13(4):338-43

M L Garg, et al, The FASEB Journal, 1988, 2:(4):A852; R M Oliart Ros, et al, Meeting Abstracts, AOCS Proceedings, May 1998, p 7, Chicago, IL

L D Lawson and F Kummerow, "B-Oxidation of the Coenzyme A Esters of Vaccenic, Elaidic and Petroselaidic Acids by Rat Heart Mitochondria," Lipids, 1979, 14:501-503

E M Cranton and J P Frackelton, "Free Radical Pathology in Age-Associated Diseases: Treatment with EDTA Chelation, Nutrition and Antioxidants," Journal of Holistic Medicine, Spring/Summer 1984, pp 6-37

H Engelberg, "Low Serum Cholesterol and Suicide," Lancet, March 21, 1992, 339:727-728

R B Alfin-Slater, and L Aftergood, "Lipids," Modern Nutrition in Health and Disease, 6th ed, 1980, R S Goodhart and M E Shils, eds, Lea and Febiger, Philadelphia, p 134

M Gurr, "A FFresh Look at Dietary Recommendations," Inform, April 1996, 7:4:432-435
 
Some Notes on Cholesterol:

Lipoproteins carry cholesterol; there are various sizes of lipoproteins, HDL, VLDL, LDL, IDL, ULDL... VLDL is very small compact (dense), large LDL is fluffy and buoyant, both having different metabolic and pathologic properties.

People of greater risk have small particle LDL (which surprisingly has less cholesterol in particles), greater potential to bind arterial wall, oxidise easier.
Cholesterol is vital for every aspect of human biology, all cells capable of creating cholesterol; LDL originates in liver of lipids and proteins complexed together creating cholesterol, being triglyceride rich.

There are different forms, VLDL, and LDL origin from different precursors in the liver. Lipase breaks down lipid via donating triglycerides to cells into smaller and smaller dense particles as part of metabolic processes LDL is a bi-product of metabolic conversion. These smaller particles seem to be the greater risk factor for atherosclorotic plaque formation. Humans don?t have efficient ways of removing LDL from blood.

HDL is a particle associated with lower heart disease risk, as opposed to LDL. HDL scavenges cholesterol from blood.

Inflammation increases VLDL, inflammation increases the release of endotoxins which is a lipo polysaccharide from bacterial cell wall in the gut and binds to lipoproteins, which is an adaptive response to prevent infection. Endotoxins bind lipoprotein VLDL. Inflammation is a measure factor in converting cholesterol into a dangerous form.
Lipoproteins play a vital part in defence mechanisms, the liver makes apo-B which gives integrity to lipoprotein particles, they are synthesised in the liver and degrade constantly, VLDL is a huge molecule which contains components that help promote inflammation in circulatory systems. VLDL are pro-inflammatory proteins which fight infection stimulated by cytokines released in response to plaque or bacterial rapid response.

LPS is produced through infectious inflammatory process. The role of LDL receptors in liver is crucial to regulating LDL in blood, which in turn lowers LPS levels. The binding of LPS to lipid proteins stimulate more LDL receptors, they are cell surface receptors that mediate endocytosis of cholesterol in inflammatory response rich LDL by recognising apo-B which is imbedded in the outer phospholipid layer of LDL particles, the receptor is found in almost all cells. LDL receptors are most abundant in the liver, where about 70% recycling occurs. LPS binds LDL, LDL receptors in liver decrease LDL and LPS levels. HDL does to some extent.

. The smaller the particle the less affinity for the LDL receptor, less capable of being removed by liver.
. Smaller particles have greater binding affinity to arterial wall.
. Saturated fat increases large LDL NOT small LDL, there is no evidence saturated fats increase plaques.
. Processed meats confound heart disease risk.
. Large LDL on low fat diets increases small LDL.
. High carbohydrates increase small particle LDL.
. Simple sugars (fructose) have a high potential to increase small particle LDL, and increase obesity. That is refined fructose, not in the context of fruit, as the dose is low as opposed to coke, which is concentrated with a high absorption potential. Fruit with its fibre content buffer response, and slow breakdown. Fructose in the liver = fat.

Statins increase LDL receptor activity, and receptor mediated uptake. Small particle LDL is not cleared as much by statins, unquestionably statins lower risk by as much as 30-40%, but not without some notable side effects, such as muscle damage/breakdown, changes in metabolism, changes in function, reduced strength. Increased risk of type 2 diabetes 11-12%, in women this is can be as much as 30-40%..

gJThM9e.png


VwmuyQP.png



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3494250/
 
Here's the basics of research I've been reading recently condensed into about 10 lines:

The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated...

Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped.

Inflammation is not complicated ? it is quite simply your body?s natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process, a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial...

What are the biggest culprits of chronic inflammation? Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, flour and all the products made from them) and the excess consumption of omega-6 vegetable oils like soybean, corn and sunflower that are found in many processed foods.

Take a moment to visualize rubbing a stiff brush repeatedly over soft skin until it becomes quite red and nearly bleeding. you kept this up several times a day, every day for five years. If you could tolerate this painful brushing, you would have a bleeding, swollen infected area that became worse with each repeated injury. This is a good way to visualize the inflammatory process that could be going on in your body right now...
 
I know it's good info if I have to re-read it twice, even 2 years into going to college for nutrition.

Very interesting as this somewhat goes against the consensus that meat will hurt cardiovascular health. Though hydrogenated trans fats are bad, that much has always been clear.

Maybe I'm misintepreting but does this mostly apply to processed vegetable oils? Soy, corn, etc? As a vegetarian I try to keep track of how my unique diet might fuck me over and I don't notice (maybe erroneously) many of these "bad" fats in my diet.
 
I know it's good info if I have to re-read it twice, even 2 years into going to college for nutrition.

Very interesting as this somewhat goes against the consensus that meat will hurt cardiovascular health. Though hydrogenated trans fats are bad, that much has always been clear.

Maybe I'm misinterpreting but does this mostly apply to processed vegetable oils? Soy, corn, etc? As a vegetarian I try to keep track of how my unique diet might fuck me over and I don't notice (maybe erroneously) many of these "bad" fats in my diet.

As you may have read, it's quite a complex process, basically refined sugars combined with hydrogenated vegetable oils (trans fats) can produce chronic inflammation, this inflammatory process can lead to atherosclorotic plaque build up..

Of note, trans fatty acids not only alter enzymes that neutralize carcinogens, and increase enzymes that potentiate carcinogens..
 
Up until now I had neglected thyroid status, a brief perusal opened up a whole new can of worms.. :eek:

. Thyroid function significantly affects lipoprotein metabolism as well as some cardiovascular disease (CVD) risk factors, thus influencing overall CDV risk..

. Within the normal range of thyroid-stimulating hormone (TSH) values, a linear increase in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides (TGs) and a linear decrease in high-density lipoprotein cholesterol (HDL-C) levels has been observed with increasing TSH

. Triiodothyronine (T3) upregulates LDL receptors by controlling the LDL receptor gene activation.

. T3 has also been associated with protecting LDL from oxidation

. Thyroid hormones can influence HDL metabolism by increasing cholesteryl ester transfer protein (CETP) activity, which exchanges cholesteryl esters from HDL2 to the very low density lipoproteins (VLDL) and TGs to the opposite direction

. Thyroid hormones stimulate the lipoprotein lipase (LPL), which catabolizes the TG-rich lipoproteins, and the hepatic lipase (HL), which hydrolyzes HDL2 to HDL3 and contributes to the conversion of intermediate-density lipoproteins (IDL) to LDL and in turn LDL to small dense LDL (sdLDL)

. Another effect of T3 is the up-regulation of apolipoprotein AV (ApoAV), which plays a major role in TG regulation. Increased levels of ApoAV have been associated with decreased levels of TGs

. A greater clearance of lipoprotein core remnants, caused by increased hepatic uptake due to an enhanced affinity for the LDL receptor, has also been ascribed to ApoAV

. TSH is positively associated with fasting and postprandial insulin concentration and negatively with insulin sensitivity

. Endothelial and cardiac function as well as atherosclerosis have been positively associated with thyroid hormone levels.

. Oxidative stress is also affected by thyroid function

pqBNOjt.jpg



Bakker O, Hudig F, Meijssen S, Wiersinga WM. Effects of triiodothyronine and amiodarone on the promoter of the human LDL receptor gene. Biochem Biophys Res Commun. 1998;249:517?21.

Shin DJ, Osborne TF. Thyroid hormone regulation and cholesterol metabolism are connected through Sterol Regulatory Element-Binding Protein-2 (SREBP-2) J Biol Chem. 2003;278:34114?8.

Faure P, Oziol L, Artur Y, Chomard P. Thyroid hormone (T3) and its acetic derivative (TA3) protect low-density lipoproteins from oxidation by different mechanisms. Biochimie. 2004;86:411?8.

Lagrost L. Regulation of cholesteryl ester transfer protein (CETP) activity: review of in vitro and in vivo studies. Biochim Biophys Acta. 1994;1215:209?36.

Kuusi T, Saarinen P, Nikkila EA. Evidence for the role of hepatic endothelial lipase in the metabolism of plasma high density lipoprotein2 in man. Atherosclerosis. 1980;36:589?93.

Santamarina-Fojo S, Gonzalez-Navarro H, Freeman L, Wagner E, Nong Z. Hepatic lipase, lipoprotein metabolism, and atherogenesis. Arterioscler Thromb Vasc Biol. 2004;24:1750?4.

Prieur X, Huby T, Coste H, Schaap FG, Chapman MJ, Rodriguez JC. Thyroid hormone regulates the hypotriglyceridemic gene APOA5. J Biol Chem. 2005;280:27533?43.

Rensen PC, van Dijk KW, Havekes LM. Apolipoprotein AV: low concentration, high impact. Arterioscler Thromb Vasc Biol. 2005;25:2445?7.
 
Abdominal Obesity

Something I've been working on which is of similar theme:

Abdominal Obesity:
Noting some of the problems occurring with abdominal obesity: There is growing recognition abdominal obesity is driving a new World wide epidemic of cardiovascular disease.
What we are beginning to understand why this is occurring, one of the major factors that contribute are abnormalities of blood fats: cholesterol and triglycerides.
There is a condition that accompanies abdominal adiposity that has been called atherogenic dyslipidaemia, that term signifies a collection of lipid traits that include high triglycerides and low HDL, that are the mainstays of dyslipidaemia.

U3dPGzV.png


Understanding plaque formation as a consequence of atherogenic dyslipidemia:

There are also abnormalities in LDL which is the main particle in blood that ends up in arteries and causes atherosclerosis. So these conditions tend to come together, and the form of LDL that appears to be the most dangerous to this condition is small particles, that are not commonly measured but tend to go along with high triglyceride low HDL. So measuring triglycerides and LDL which are standard measurements one can get a picture of the severe atherogenic dyslipidaemia which is the basis for cardiovascular disease risk in patients with abdominal obesity.

Most people with abdominal obesity will have this problem with small dense LDL particles. LDL particles end up in the artery wall they cause damage through a number of factors in the artery wall including the ability to stick to the artery and get oxidized. Smaller particles have greater propensity to stick to the artery wall and get oxidized. This is often under the surface and not recognised when we measure for cholesterol which is the more common way we assess for cholesterol in blood because blood levels are often normal, despite the fact there is an increase number of LDL particles. These particles are more dangerous than other forms of LDL and actually contain less cholesterol.

Its important to recognise in patients that have normal LDL particles, there is underlying pathology of LDL particles that create a high risk that should really be part of the goal of improving abdominal adiposity should be to normalise this profile.
We can be confident that if someone has this abdominal profile and small dense atherogenic LDL particles if they can lose that abdominal fat they can correct the problem.

Its very important to recognise this is reversible. There is a strong genetic component to this condition, but it is really susceptible to wrong kind of behaviour that includes in the case of small LDL increased amounts of carbohydrates, particularly the sugars that tend to drive a lot of the features of abdominal adiposity, that are detrimental to health, including dyslipidaemia. Carbs meaning white starches found in potatoes, breads, white rice, and especially fructose which is the chief culprit such as found in coca cola, and other high sugar soft drinks.

7gjtMR4.png


The physiology of lipoproteins:

Low Level of HDL:
This is the fraction that does not cause atherosclerosis and may actually protect against atherosclerosis. HDL particles are smaller and less likely to protect, we know that normal HDL has ability to remove cholesterol out of the artery wall, and promote regression of atherosclerosis, HDL has the ability to inhibit inflammation in the artery, its an antioxidant, its an antithrombotic, and even promotes the repair of artery wall that have been damaged.

There is some controversy regards HDL particle content what we really need is to understand HDL function, there is evidence people with abdominal obesity have HDL that doesn’t function as effectively as normal.
Reduce abdominal fat, and there is evidence HDL becomes functional again and increases in concentration.

What we have is a combination of LDL particles that are more likely to cause atherosclerosis, especially the small dense particle, and HDL that is decreased in concentration and not as functional as it ought to be.
One important aspect is these abnormalities travel together and one can achieve immense benefit simply by adopting healthy lifestyle practices, increase physical exercise, maintain healthy balanced diet, specifically trying to reduce refined carbohydrates, and sugary drinks.

Evaluating the risk associated with dyslipidemia and improvements we hope to achieve, one can adopt some fairly simple measurements, beyond LDL particles which doesn’t necessarily capture the risk associated with LDL particles, without necessarily measuring the individual fractions, such as measuring ApoB, which is often available as a standard test which measures a number of LDL particles which is a very good marker for risk. Another test is non HDL cholesterol which is calculated as a difference between total and HDL cholesterol, without having to complete many sophisticated tests. Recognizing LDL itself may not be the most important measurement in patients.

One complication is the question people frequently ask is the low HDL that is the problem, is it the high triglycerides, this unnecessarily confuses and complicates matters. Its people that have high triglycerides, small dense LDL fraction and low HDL concentration, all of which associate with abdominal obesity, that creates the total picture. We know if we can get rid of abdominal fat all of these abnormalities correct themselves.

With that the target should be to get rid of the abdominal fat! That takes away the whole lipid package plus many other risk factors for heart disease and diabetes. That way we can reverse an alarming increase in an epidemic of cardiovascular disease that is driven by abdominal obesity.

Taken from papers and interviews with Dr Ronald Krauss..

Images based on works from Armando..
 
Some interesting notes regarding Trans fats and Cholesterol:

1. Vegetable oils are more toxic when heated. One study reported that polyunsaturates turn to varnish in the intestines. A study by a plastic surgeon found that women who consumed mostly vegetable oils had far more wrinkles than those who used traditional animal fats. A 1994 study appearing in the Lancet showed that almost three quarters of the fat in artery clogs is unsaturated. The "artery clogging" fats are not animal fats but vegetable oils.

2. Trans fats, produced in vegetable oils when they are partially hydrogenated, The research group at the University of Maryland found that trans fatty acids not only alter enzymes that neutralize carcinogens, and increase enzymes that potentiate carcinogens..

3. Trans fats contribute to osteoporosis. Hanis, a Czechoslovakian researcher, found that trans consumption decreased testosterone, caused the production of abnormal sperm and altered gestation.
Trans consumption interferes with the body?s use of omega-3 fatty acids found in fish oils, grains and green vegetables, leading to impaired prostaglandin production. Some deep fried foods have been tested at almost 50% trans.


4. The scientific literature delineates a number of vital roles for dietary saturated fats, they enhance the immune system, are necessary for healthy bones, provide energy and structural integrity to the cells, protect the liver and enhance the body?s use of essential fatty acids.

5. Stearic acid, found in beef tallow and butter, has cholesterol lowering properties and is a preferred food for the heart. As saturated fats are stable, they do not become rancid easily, do not call upon the body?s reserves of antioxidants, do not initiate cancer, do not irritate the artery walls.

6. Your body makes saturated fats, and your body makes cholesterol about 2000 mg per day. In general, cholesterol that the average American absorbs from food amounts to about 100 mg per day. So, in theory, even reducing animal foods to zero will result in only a 5% decrease in the total amount of cholesterol available to the blood and tissues.

7. In practice, such a diet is likely to deprive the body of the substrates it needs to manufacture enough of this vital substance; for cholesterol, like saturated fats, stands unfairly accused.

8. It acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone; it is a precursor to vitamin D, a very important fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function;

9. It is the precursor to bile salts, which are vital for digestion and assimilation of fats in the diet. Recent research shows that cholesterol acts as an antioxidant. This is the likely explanation for the fact that cholesterol levels go up with age.

10. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer. Cholesterol is the body?s repair substance, manufactured in large amounts when the arteries are irritated or weak.

11. Cholesterol is needed for proper function of serotonin receptors in the brain. Serotonin is the body's natural "feel-good" chemical. This explains why low cholesterol levels have been linked to aggressive and violent behaviour, depression and suicidal tendencies..

12. Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system. Dietary cholesterol plays an important role in maintaining the health of the intestinal wall, which is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.

13. Animal foods containing saturated fat and cholesterol provide vital nutrients necessary for growth, energy and protection from degenerative disease. Like sex, animal fats are necessary for reproduction. Humans are drawn to both by powerful instincts. Suppression of natural appetites leads to weird nocturnal habits, fantasies, fetishes, bingeing and splurging.


B B Teter, et al, "Milk Fat Depression in C57B1/6J Mice Consuming Partially Hydrogenated Fat," Journal of Nutrition, 1990, 120:818-824; Barnard, et al, "Dietary Trans Fatty Acids Modulate Erythrocyte Membrane Fatty Acid

Composition and Insulin Binding in Monkeys," Journal of Nutritional Biochemistry, 1990, 1:190-195

T Hanis, et al, "Effects of Dietary Trans Fatty Acids on Reproductive Perforamnce of Wistar Rats," British Journal of Nutrition, 1989, 61:519-529

B Koletzko and J Muller, "Cis- and Trans-Isomeric Fatty Acids in Polasma Lipids of Newborn Infants and Their Mothers," Biology of the Neonate, 1990, 57:172-178

D Horrobin, "The Regulation of Prostaglandin Biosynthesis by Manipultion of Essential Fatty Acid Metabolism," Reviews in Pure and Applied Pharmacological Sciences, 1983, 4:339-383

G V Mann, "Metabolic Consequences of Dietary Trans Fatty Acids," The Lancet, 1994, 343:1268-1271

L Kohlmeier, et al, "Stores of Trans Fatty Acids and Breast Cancer Risk, "Am J Clin Nutr, 1995, 61:896;A25

R P Mensink and M Katan, "Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects," N Eng J Med, 1990, 323:439-445

M G Enig, et al, "Isomeric Trans Fatty Acids in the U.S. Diet," J Am Coll Nutr, 1990, 9:471-486

W C Willett, et al, "Consumption of Trans-Fatty Acids in Relation to Risk of Coronary Heart Disease Among Women," Society for Epidemiology Research, June 1992, Annual Meeting, Abstract 249

W C Willett, et al, "Intake of Trans Fatty Acids and Risk of Coronary Heart Disease Among Women," Lancet, 1993, 341:581-585

J J Kabara, The Pharmacological Effects of Lipids, J J Kabara, ed, The American Oil Chemists? Society, Champaign, IL, 1978, 1-14; L A Cohen, et al, J Natl Cancer Inst, 1986, 77:43

B A Watkins, et al, "Importance of Vitamin E in Bone Formation and in Chrondrocyte Function" Purdue University, Lafayette, IN, AOCS Proceedings, 1996;

B A Watkins, and M F Seifert, "Food Lipids and Bone Health," Food Lipids and Health, R E McDonald and D B Min, eds, Marcel Dekker, Inc. New York, NY, p 101

J F Mead, et al, Lipids: Chemistry, Biochemistry and Nutrition, Plenum Press, 1986, New York

A A Nanji, et al, Gastroenterology, Aug 1995, 109(2):547-54; Y S Cha, and D S Sachan, J Am Coll Nutr, Aug 1994, 13(4):338-43

M L Garg, et al, The FASEB Journal, 1988, 2:(4):A852; R M Oliart Ros, et al, Meeting Abstracts, AOCS Proceedings, May 1998, p 7, Chicago, IL

L D Lawson and F Kummerow, "B-Oxidation of the Coenzyme A Esters of Vaccenic, Elaidic and Petroselaidic Acids by Rat Heart Mitochondria," Lipids, 1979, 14:501-503

E M Cranton and J P Frackelton, "Free Radical Pathology in Age-Associated Diseases: Treatment with EDTA Chelation, Nutrition and Antioxidants," Journal of Holistic Medicine, Spring/Summer 1984, pp 6-37

H Engelberg, "Low Serum Cholesterol and Suicide," Lancet, March 21, 1992, 339:727-728

R B Alfin-Slater, and L Aftergood, "Lipids," Modern Nutrition in Health and Disease, 6th ed, 1980, R S Goodhart and M E Shils, eds, Lea and Febiger, Philadelphia, p 134

M Gurr, "A FFresh Look at Dietary Recommendations," Inform, April 1996, 7:4:432-435

Bump..
 
Men can you please fill in the gaps I stumble upon. How bad is heating a vegetable oil. I am guessing fats of palms aren't considered oils in this context.

I am concentrating on the differences between the oils through their mono and poly contents, and their use in baking. But also have question about the extra virgin variety's, which should be called cold pressed if I am correct.

So there is a cold pressed olive oil, rich in mono unsaturated fats. Which is said to contain aromatics that burn when heated. Is this indeed through?

Currently I am baking in cold pressed Rapeseed oil, rich mono-unsaturates ment for baking. They have a other variety for lesser heat and cold use, also low on mono's, which has an obvious hue, brownish instead of the yellow I have. Just like the extra virgin olive oil has a greenish one. Can I conclude from this the olive extra-virgin is unfit. And is the rapeseed baking variety, although probably better also a bad choice?

The reason I chose it was not because I am scared for the saturated fats in palms, or because the sustainability. Where I live proper palm oil production is not a option.

It's my wallet. Both butter, which I could turn into ghee, and rapeseed oil are just affordable. The butter being the expensive one. Palm and coco oils are way more expensive. Not talking about non biological as I trying as hard as I can to get these out of the house. For the monkey's sake ;)
 
Last edited:
Top