Disclaimer

This information HAS errors and is made available WITHOUT ANY WARRANTY OF ANY KIND and without even the implied warranty of MERCHANTABILITY or FITNESS FOR A PARTICULAR PURPOSE. It is not permissible to be read by anyone who has ever met a lawyer or attorney. Use is confined to Engineers with more than 370 course hours of engineering.

Health effects of different fatty acids

Related pages

• Tests
• Interventions
• Lp(a) Lipoprotein(a) - apo[a] - Reducing levels, isoforms

1. Health effects of different fatty acids
   1. Related pages
   2. Fatty acids
   3. Simplified Table of Fat groups and their effects
   5. Other Fats
   6. LA
      1. 1. LA Thyroid connection?
         2. Dietary Sources
   7. Conventional oils
      1. 1. Olive oil
   8. Fat contents of food
   9. Consumption of ω-6 and seed oil over time
      1. 1. Refs
   10. o-3 vs o-6 Ratios
   11. Warning About Junk Science
   12. Related pages

Fatty acids

• Look up contents here
• Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation Low carb seems to induce low inflammation.
• Types of Dietary Fat and Risk of Coronary Heart Disease: A Critical Review
• Effect of Dietary Fatty Acids on Inflammatory Gene Expression in Healthy Humans
• A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

Humans mostly make Sat-Fats from high carb diets. Mammalian fatty acyl desaturases can introduce double bonds at the Δ5, Δ6 and Δ9 positions This means that we cannot introduce double bonds at the ω3 or ω6 positions.

Simplified Table of Fat groups and their effects

It appears that PUFA's and perhaps MUFA's can induce inappropriate insulin sensitivity - the end result would be weight gain.

• The insulinotropic potency of fatty acids is influenced profoundly by their chain length and degree of saturation.

Insulin Sensitivity = opposite of insulin Resistance ( Best to think in positive/Sensitivity terms - positive means Fat going into tissue. )

• * MUFA modify SFA insulin resistance when both SFA and glucose are present and abort the apoptotic signal(s) generated when hyperglycaemia and SFA are present concurrently and insulin resistance is not wanted (ie post prandially). MUFA generation is controlled by insulin through SCD1.

• Adipocytes with enough fat become insulin resistant - SFA to MUFA ratio will go to pot as adequate MUFA will not be generated in hyperglycaemia because the adipocytes are not listening to insulin. The problem can be delayed for years by increasing PUFA (and maybe MUFA) dietary intake to re establish insulin sensitivity, especially in distended adipocytes, so metabolism appears to improve while ever the ability to get fatter also restored, until this is finally used up.

• When fat gain increases, fat is stored, insulin sensitivity is excellent UNTIL adipocytes develop distension induced insulin resistance. Then hyperinsulinaemia and hyperglycaemia follow on when glucose is fed...

• Insulin inhibits lipolysis (break down of lipids ) and suppresses glucose release from the liver. The liver extracts between 50% and 80% of all of the insulin produced by the pancreas. Relatively little ever gets to the systemic circulation (The liver receives about 75% of its blood through the hepatic portal vein, a blood vessel that conducts blood from the gastrointestinal tract and spleen to the liver.) The residue of insulin is what should be controlls adipocyte function.

• SFA generate superoxide and switch off glucose metabolism (ie cause insulin resistance) so maintain fasting glucose for brain use.

• Fasting induces adipocyte insulin resistance as well as hypoinsulinaemia and hence fat mobilisation... All physiological as apposed to autonomic nervous system control.

• We need insulin resistance to lose weight and can be a good thing if glucose is not elevated.

• FADH2:NADH ratios - FromPetro Dobromylskyj, via http://high-fat-nutrition.blogspot.com/2012/08/protons-fadh2nadh-ratios-and-mufa.html

Each cycle of beta oxidation (assuming an even numbered carbon chain fully saturated fatty acid) produces one FADH2, one NADH and one acetyl-CoA. This gives a total of 2FADH2 inputs and 4 NADHs per cycle of beta oxidation. But the very last pair of carbon atoms in a saturated fat do not need to go through beta oxidation as they already comprise acetate attached to CoA, so they can simply enter the TCA as acetyl-CoA. This last step only produces 1 FADH2 and 3 NADHs, with no extras.

So the shorter the fatty acid, the less FADH2 per unit NADH it produces. Short chain fatty acids like C4 butyric acid have an F:N ratio of 0.43 while very long chain fatty acids, up at 26 carbons, have an F:N ratio of about 0.49.

As Dr Speijer points out, differing length fatty acids are dealt with differently. Very short chain fatty acids head straight for the liver and get metabolised by hepatic mitochondria immediately. Any excess acetyl-CoA gets off-loaded as ketones.

Very long chain fatty acids end up in peroxisomes for shortening, usually to C8, which is then shunted to mitochondria for routine beta oxidation. Of course peroxisomal beta oxidation generates zero FADH2, except that from acetyl-CoA, because peroxisomal FADH2 is reacted directly with oxygen to give H2O2. And heat, of course.

Bear in mind that the ratio of F:N generated by a metabolic fuel sets the ability to generate reverse electron flow through complex I and subsequent superoxide production, macroscopically described as insulin resistance.

So fatty acids up to C8 are cool, dump them to the liver and make a few ketones. Very long chain fatty acids over C18, shorten to C8 in peroxisomes, shift them to mitochondria and make some ketones if needs must. The F:N ratio of C8 is about 0.47, a value chosen by metabolism as the end product of peroxisomal shortening. The number is important. Actually the number is even lower as peroxisomal beta oxidation generates the NADHs of beta oxidation, just not the FADH2s, but why allow facts like this to spoil a great argument. C8 from breast milk and/or coconuts seems fine and has that F:N ratio of 0.47.

Now the area of interest is, of course, C16, palmitic acid. This has an F:N ratio of about 0.48, almost as superoxide generating as a C26 fatty acid up at 0.49. And palmitic acid does, without any shadow of a doubt, produce macroscopic insulin resistance. That's 15 FADH2s and 31 NADHs.

So an F:N of 0.47 is not a serious generator of superoxide and an F:N of 0.48 is.

What happens when we drop a double bond in to palmitic acid? Mitochondrial beta oxidation generates FADH2 as it drops a double bond in to the saturated fat chain. If the double bond is already there, hey, no FADH2!

Palmitoleate has one double bond. This of course gives 14 FADH2s and 31 NADHs, an F:N ratio of 0.45.

Palmitate 0.48

C8 caprylic 0.47, chosen by peroxisomes to hand to mitochondria

Palmitoleic 0.45

Adding a single double bond to palmitic acid drops its F:N ratio from significantly superoxide generating to minimally superoxide generating. It looks like a switch to me.

List of Saturated Fatty Acids

• Saturated fat raises LDL.

• 3:0 Propionic acid -21°C (Propanoic acid)
• 4:0 Butyric acid (Butanoic acid)-7.9°C(short chain) F:N ratio 0.43
• 5:0 Valeric acid (Pentanoic acid) −34.5°C
• 6:0 Caproic acid (Hexanoic acid)−3.4°C (short chain)
• 7:0 Heptanoic(Enanthic, Oenanthic) acid (Heptanoic acid) −7.5 °C
• 8:0 Caprylic acid (Octanoic acid)16.7°C (medium chain)F:N ratio about 0.47 chosen by peroxisomes to hand to mitochondria
• 9:0 Pelargonic acid (Nonanoic acid)
• 10:0 Decanoic(Capric ) acid 31.6°C (medium chain)
• 11:0 Undecylic acid (Undecanoic acid)
• 12:0 Lauric(dodecanoic)acid 43.8°C (medium chain) - main acid in coconut oil
• 13:0 Tridecylic acid (Tridecanoic acid)
• 14:0 Myristic acid, (tetradecanoic acid) 54.4°C - found in palm oil, coconut oil, butter fat,
• 15:0 Pentadecylic acid (Pentadecanoic acid)
• 16:0 palmitic acid (Hexadecanoic acid) 62.9°C F:N ratio of about 0.48 That's 15 FADH2s and 31 NADHs - oxidizing . (palm oil - Butter, cheese, milk and meat also have some)
• 17:0 Margaric acid (Heptadecanoic acid) - in Milk
• 18:0 Stearic acid (Octadecanoic acid) 69.3°C Found in Cocoa
  • Stearic acid is the only long chain saturated fatty acid that does not raise LDL cholesterol(reference?).
  • Also - stearic acid has been shown associated with increases in Lp(a)
• 19:0 Nonadecylic acid (Nonadecanoic acid) 69°C
• 20:0 Arachidic acid (Eicosanoic acid)75.5°C
• 21:0 Heneicosylic acid (Heneicosanoic acid)
• 22:0 Behenic acid (Docosanoic acid) found in Ben oil, rapeseed (canola) and peanut oil
• 23:0 Tricosylic acid (Tricosanoic acid)
• 24:0 Lignoceric acid (Tetracosanoic acid)
• 25:0 Pentacosylic acid (Pentacosanoic acid)
• 26:0 Cerotic acid (Hexacosanoic acid) F:N ratio of about 0.49
• 27:0 Heptacosylic acid (Heptacosanoic acid)
• 28:0 Montanic acid (Octacosanoic acid)
• 29:0 Nonacosylic acid (Nonacosanoic acid)
• 30:0 Melissic acid Triacontanoic acid)
• 31:0 Henatriacontylic acid (Henatriacontanoic acid)
• 32:0 Lacceroic acid (Dotriacontanoic acid)
• 33:0 Psyllic acid (Tritriacontanoic acid)
• 34:0 Geddic acid (Tetratriacontanoic acid)
• 35:0 Ceroplastic acid (Pentatriacontanoic acid)
• 36:0 Hexatriacontylic acid (Hexatriacontanoic acid)

Other Fats

• 16:1
• 16:1ω-7 Palmitoleic Acid AKA POA F:N ratio of 0.45 - biosynthesized from palmitic acid via SCD1 - Increases insulin sensitivity by suppressing inflammation via FAS, as well as inhibit the destruction of insulin-secreting pancreatic beta cells. Short term this looks like a good effect - but long term causes weight gain.
• 18:1
  • 18:1 ω-9 Oleic acid (heart healthy) - Reduces oxLDL Olive oil - or is it the polyphenols?
  • LDL Isolated From Greek Subjects on a Typical Diet or From American Subjects on an Oleate-Supplemented Diet Induces Less Monocyte Chemotaxis and Adhesion When Exposed to Oxidative Stress
  • Increased production of apolipoprotein B and its lipoproteins by oleic acid in Caco-2 cells
• 18:1 trans-9 Elaidic acid very bad. This is the major trans fat found in hydrogenated vegetable oils and occurs in small amounts in caprine and bovine milk (very roughly 0.1% of the fatty acids) [1] and some meats. Elaidic acid (C18:1) (2-5% of the fatty acid in beef), which can raise LDL in serum (Abbey and Nestel, 1994; Muller et al., 1999, Judd et al., 2002). These different numbers may reflect different feeds that beef get.
  • Plasma lipoprotein lipid and Lp(a) changes with substitution of elaidic acid for oleic acid in the diet
  • Plasmacholesterylestertransferproteinactivity is increased when trans-elaidicacid is substituted for cis-oleicacid in the diet The association of this increased activity has not been shown to be the cause - the cause may be an immunal response to this health destroying FA.

LA

LA speculation

• 18:2 ω-6 linoleic acid -5°C increases LDL oxidation - One really does not want to eat much of this - varnish, linoleum, industrial waste.
  • A high linoleic acid diet increases oxidative stress in vivo and affects nitric oxide metabolism in humans
  • Linoleic Acid Increases Lectin-Like Oxidized LDL Receptor-1 (LOX-1) Expression in Human Aortic Endothelial Cells
  • Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet.
  • Osteoarthritis and Omega-6 Fats (Linoleic Acid)
  • Measuring Blood Fatty Acids as a Surrogate Indicator for Coronary Heart Disease Risk in Population Studies
  • The Lipid Peroxidation By-Product 4-Hydroxy-2-Nonenal (4-HNE) Induces Insulin Resistance in Skeletal Muscle through Both Carbonyl and Oxidative Stress
  • Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity
  • Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and inflammation in mice
  • Measurement of HNE-protein adducts in human plasma and serum by ELISA—Comparison of two primary antibodies
  • Biomarkers of Oxidative Damage in Human Disease 4-HNE from LA
  • Lowering dietary linoleic acid reduces bioactive oxidized linoleic acid metabolites in humans
  • Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance HNE again
  • Dietary fats: a new look at old data challenges established wisdom Once hidden by Keys - how many dead?
  • Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) Where the BS started
  • 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
  • Fat accumulation in Caenorhabditis elegans triggeredby the electrophilic lipid peroxidation product 4-Hydroxynonenal (4-HNE)
  • Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders
  • Carbonylation of Adipose Proteins in Obesity and Insulin Resistance
  • FALDH Reverses the Deleterious Action of Oxidative Stress Induced by Lipid Peroxidation Product 4-Hydroxynonenal on Insulin Signaling in 3T3-L1 Adipocytes
  • Cytotoxicity of linoleic acid peroxide, malondialdehyde and 4-hydroxynonenal towards human fibroblasts

LA Thyroid connection?

• The influence of diet on the lipogenic response to thyroxine in rat liver.
• Inhibition of triiodothyronine's induction of rat liver lipogenic enzymes by dietary fat.
• Triiodothyronine-dietary interrelationships in the modulation of brown adipose tissue and liver lipogenesis in the rat.
• Effects of diet composition on serum levels of insulin, thyroxine, triiodothyronine, growth hormone, and corticosterone in rats.

Dietary Sources

• 18:3 ω-3 alpha linolenic acid or ALA
  • Long-Term Effects of Dietary .ALPHA.-Linolenic Acid from Perilla Oil on Serum Fatty Acids Composition and on the Risk Factors of Coronary Heart Disease in Japanese Elderly Subjects.

• 18:3 ω-6 gamma-linolenic acid or GLA
  • Endothelial cell monolayer dysfunction caused by oxidized low density lipoprotein: attenuation by oleic acid.
  • Effects of gamma linolenic acid on atherosclerosis induced by cholesterol-rich diet in rats
  • Linoleic acid peroxidation—the dominant lipid peroxidation process in low density lipoprotein—and its relationship to chronic diseases
• 18:3 ω-6 Calendic acid - a trans form of Linoleic

• 18:4 ω-3 Stearidonic acid (STD)
• 20:1
• 20:2 ω-6 Eicosadienoic acid
• 20:3 ω-3 Eicosatrienoic acid (ETE) anti-inflammatory - goes up on low LA diet Dietary (n-9) eicosatrienoic acid from a cultured fungus inhibits leukotriene B4 synthesis in rats and the effect is modified by dietary linoleic acid.
• 20:3 ω-6 Dihomo-gamma-linolenic acid (DGLA)inflammatory neutral -from dietary GLA (18:3 ω-6) found in, e.g. borage oil
• 20:4 ω-6 arachidonic acid or AA Inflammatory Most AA in the human body derives from dietary linoleic acid (another essential fatty acid, 18:2 ω-6)
• 20:4 ω-3 eicosatetraenoic acid (ETA)
• 20:5 ω-3 eicosapentaenoic acid (EPA) Anti-inflammatory - from oily fish or derived from dietary alpha-linolenic acid found in, for instance, hemp oil and flax oil
• 22:1 ω-9 Erucic acid - adversely affect heart tissue in Rats
• 22:2 ω-6 Docosadienoic acid
• 22:4 ω-6 Adrenic acid.
• 22:5 ω-3 Docosapentaenoic acid (DPA, Clupanodonic acid)
• 22:5 ω-6 Docosapentaenoic acid (Osbond acid)
• 22:6 ω-3 docosahexaenoic acid or DHA
• 24:1 ω-9 Nervonic acid
• 24:5 ω-3 Tetracosapentaenoic acid
• 24:6 ω-3 Tetracosahexaenoic acid (Nisinic acid)

• stearic and myristic acid-rich saturated fats increase large LDL cholesterol; palmitic acid somewhat. (reference?)

Conventional oils

Olive oil

Heart healthy - seems to reduce oxLDL - does contain some palmitic and linoleic acid

• LDL isolated from Greek subjects on a typical diet or from American subjects on an oleate-supplemented diet induces less monocyte chemotaxis and adhesion when exposed to oxidative stress

• Postprandial LDL phenolic content and LDL oxidation are modulated by olive oil phenolic compounds in humans
• Effect of virgin olive oil phenolic compounds on in vitro oxidation of human low density lipoproteins.
• Elevated Circulating LDL Phenol Levels in Men Who Consumed Virgin Rather Than Refined Olive Oil Are Associated with Less Oxidation of Plasma LDL
• Extra Virgin Olive Oil Biophenols Inhibit Cell-Mediated Oxidation of LDL by Increasing the mRNA Transcription of Glutathione-Related Enzymes
• Effects of dietary virgin olive oil phenols on low density lipoprotein oxidation in hyperlipidemic patients

Fat contents of food

These values may vary - year to year - LA in particular has increased with livestock eating ever more corn. Some measures vary +/- 2:1

• Corn oil C16:0 10.9%; C18:0 2.0%; C20:0 0.4%; C16:1 0.2%; C18:1 25.4%; C18:2 59.6%; C18:3 1.2% Source: Richard O'Brien "Fats and Oils: Formulating and Processing for Applications"
• Grass-fed beef

Consumption of ω-6 and seed oil over time

While correlation does not show causation - it seems it would be prudent to figure out if LA is what is driving the obesity pandemic. There is a problem in such studies as according to one paper there is a 600day half-life to contend with. This half-life could be separating cause and effect so that people don't pick up on what is doing them harm. It would be fairly easy to find a correlation with LA in adipose tissue with obesity.

Omega-6-consumption-from-seed-oils

• From Stephan vegetable-oil-and-weight-gain

"The linoleic acid content of body fat has increased tremendously in the US over the last 50 years, as shown in the following graph, based on a number of different studies, each of which is represented by an orange dot

Refs

• [1]
• [2]
• [3]
• [4]
• [5]
• [6]
• [7]
• chimpanzee fatpaper doesn't specify if the chimp was captive or wild
• Linoleic acid in human breast milk has also increased quite a bit over the same time period

• Increase in adipose tissue linoleic acid of US adults in the last half century. *[8]

LA in Human Fat

Omega-3 vs heart risk

US-weight-1960-2010

o-3 vs o-6 Ratios

There are many people promoting fish oil to balance this ratio - no one questions if that is the right way. All PUFA's mess with insulin sensitivity - so fish-oil has the potential to cause obesity. Also - the amount of PUFA in the diet effects the permeability of cell membranes - effecting even our immune system.

• Polyunsaturated fatty acids, membrane organization, T cells, and antigen presentation

Warning About Junk Science

• Diets are not even tested... actually full of linoleic acid

Related pages

• Interventions
• Lp(a) Lipoprotein(a) - apo[a] - Reducing levels, isoforms

Email lrak@lrak.net

(C) Copyright 1994-2019 reserved
All trademarks are the property of their respective owners.