The definition of MCFA is a little unclear. Wikipedia lists lauric acid as a MCFA, making the range C:6-12, whereas commercial MCTs are almost completely made from C:8 and C:10, as C:6 is not available in any significant amount from coconut oil, and about 32% of lauric acid is not deposited into to the hepatic portal vein, whereas the totality of shorter chain MCFAs is. It is likely that both lauric and myristic (C:14) acids exist in a grey zone where they have partial MCFA properties. It is also relevant that triglycerides that contain longer chain fatty acids are hydrolysed more slowly and a rapid rate of hydrolysis in the gut is one of the properties desired of MCTs.
In a previous post I wrote about a case study where a ketogenic diet prevented symptomatic hypoglycaemia in a child with hyperinsulinism. I wrote at the time that this was as close as we would get to a proof that slightly elevated ketone levels due to carbohydrate restriction are protective against symptomatic hypoglycaemia in people with type 1 diabetes treated with insulin.
I was wrong - there has been a human trial of the concept, using MCT oil.[1]
In this study "A total of 11 intensively treated type 1 diabetic subjects participated in stepped hyperinsulinemic- (2 mU · kg−1 · min−1) euglycemic- (glucose ∼5.5 mmol/l) hypoglycemic (glucose ∼2.8 mmol/l) clamp studies. During two separate sessions, they randomly received either medium-chain triglycerides or placebo drinks and performed a battery of cognitive tests."
"During the medium-chain triglycerides session, a total of 40 g of medium-chain triglycerides (derived from coconut oil containing 67% octanoate, 27% decanaote, and 6% other fatty acids; Novartis) was ingested at 25-min intervals with front loading of 20 g then 10 g twice. During the control session, cherry-flavored water sweetened with sucralose was ingested at identical time intervals."
The beta-hydroxybutyrate level attained 40 minutes after the MCT drinks was about 3.4 mmol/l.
"We conclude that ingestion of medium-chain triglycerides improves cognitive function without affecting the adrenergic hormonal or symptomatic responses to acute hypoglycemia in intensively controlled type 1 diabetic patients. These findings suggest that medium-chain triglycerides could be used as prophylactic therapy for such patients with the goal of preserving brain function during hypoglycemic episodes, such as when driving or sleeping, without producing hyperglycemia."
 |
| BOHB levels for MCT vs Placebo in insulin-induced hypoglycaemia after overnight fast, down arrows = 20g, 10g, 10g MCT or placebo drinks. 100 umol/l = 0.96 mmol/l. |
"In vitro rat hippocampal slice preparations were used to assess the ability of β-hydroxybutyrate and octanoate to support neuronal activity when glucose levels are reduced."
The reason for this is, that the authors wanted to be sure whether the protective effects of MCT oil were due to the brain using ketone bodies or due to the brain's use of MCFAs. It turns out that the MCFAs used in MCTs can cross the blood-brain barrier and be used in brain metabolism. In another rat paper, "We found that oxidation of 13C-octanoate [C:8] in brain is avid and contributes approximately 20% to total brain oxidative energy production."[2]
The C:8 is mainly being oxidised by astrocytes. If this happens in a hypoglycaemic brain, it's possible that due to lack of oxaloacetate ketone bodies will be produced, which can be used by the neurons.
What I really want to know is how coconut oil compares to MCT oil as a means to elevate serum ketone bodies. I suspect that ketone elevation from coconut oil has a slower onset and is more protracted due to the slower rate of hydrolysis of MCFAs from triglycerides with some longer-chain fatty acids, and if so this "time release" effect could be beneficial during sleep.
There is only one study I can find online which shows ketone levels after feeding coconut oil, and this is Mary Newport's n=1 experiment.[powerpoint here]
I don't know what to make of this, beyond the expected drop in glucose (due to insulin response to lauric acid - this wouldn't apply in type 1 diabetes); the levels, though elevated by both interventions, are still within the reference range (and very different from those in the diabetes paper), unless I'm reading the measurements wrong, and the time scale with coconut oil stops short. I'd like to see many more comparisons like this, with higher doses, in healthy volunteers. The coconut oil industry and coconut oil aficionados have been accused of extrapolating from MCT studies in the absence of evidence about coconut oil, for example by the Heart Foundation of New Zealand here. While I don't think it's justifiable to ignore animal studies of coconut oil, which tell us that coconut oil protects the liver and pancreas from chemical injury, totally consistent with the MCT research, I don't see why the coconut oil industry can't fund proper comparative studies of ketogenesis in humans, which would not be at all expensive.
A 1982 review of medium chain triglycerides stated that "MCTs are ketogenic in the normal subject
and even more in the patient with hyperosmolar diabetic syndrome (117). Hence, MCTs should not be given to patients with diabetes. They should also not be given to patients with ketosis or acidosis."[3]
Whilst no-one would treat diabetic ketoacidosis with MCTs, the statement "MCTs should not be given to patients with diabetes" is unfounded. People with type 2 diabetes, due to hyperinsulinaemia, are not at an increased risk of diabetic ketoacidosis*, and the experiment I posted above shows that those with intensively controlled type 1 diabetes may benefit from their use. The reference (117) which is the only reference in this section is a rat experiment; the hyperosmolar diabetic syndrome described is high glucose with normal ketones, not DKA.
A 2010 review cites several reports that "suggest that MCFAs/MCTs offer the therapeutic advantage of preserving insulin sensitivity in animal models and patients with type 2 diabetes".[4]
This is consistent with the Malmö Diet and Cancer study epidemiology I posted here. Which implies that even the small amounts of MCFAs in foods such as coconut and dairy are beneficial for maintaining metabolic homeostasis at a population level.
*Edit: thanks to Carol Loffelman for reminding me of this - type 2 diabetes is a risk factor for ketoacidosis if it's being treated with a SLGT2 inhibitor. See this link, but there are many cases of ketoacidosis on SLGT2 inhibitors where a low carb diet is not involved. I have looked for case studies of ketoacidosis in diabetic patients that were triggered by carbohydrate restriction or MCTs without SLGT2 administration and have not yet found one.
This is a case study of DKA in a woman with decompensated T2D [link] where there is not enough insulin to prevent it. There's no low carb diet or SGLT2i involvement, and my expectation is that a normal calorie very low carbohydrate diet would most likely have prevented the syndrome in this patient as it did in the patients of Newburgh and Marsh back in the day.
[1] Page KA, Williamson A, Yu N et al. Medium-Chain Fatty Acids Improve Cognitive Function in Intensively Treated Type 1 Diabetic Patients and Support In Vitro Synaptic Transmission During Acute Hypoglycemia. Diabetes. 2009 May; 58(5): 1237–1244
[2] Ebert D, Haller RG, Walton ME. Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy. J Neurosci. 2003 Jul 2;23(13):5928-35.
[3] Bach AC, Babayan VK. Medium-chain triglycerides: an update. Am J Clin Nutr. 1982 Nov;36(5):950-62.
[4] Nagao K, Yanagita T. Medium-chain fatty acids: functional lipids for the prevention and treatment of the metabolic syndrome. Pharmacol Res. 2010 Mar;61(3):208-12. doi: 10.1016/j.phrs.2009.11.007. Epub 2009 Nov 30.
23 comments:
Interesting, due to lauric and higher chain length fatty acids being able to somewhat to mostly bypass the portal vein and enter circulation as chylomicrons via the thoracic duct peripheral tissue gets first dibs on the fatty acid content.
I would imagine that the diffusion rate of an MCFA-CoA into a mitochondria by which it can bypass the carnitine shuttle is lower the larger the MCFA chain length also.
I wonder if triacetin would be better than MCT's when it comes to ketone production.
Hi John, that's a good point, you need peroxisomal oxidation to get longer chain FAs into the mitochondria, anything C:8 or under has free ingress. But carnitine may not be the difference, because feeding MCTs in carnitine-acylcarnitine translocase deficiency deficiency, though expected to work, doesn't work.
"We conclude that the utilization of medium-chain triglycerides is only partial in carnitine-acylcarnitine translocase deficiency and cannot reasonably be considered an optimal source of energy for these patients."
http://www.ncbi.nlm.nih.gov/pubmed/10472533
I read somewhere recently that the brain doesn't oxidise acetate very much compared to MCFAs. It might be in that rat brain paper.
However, acetate is ketogenic, that's why cows are more prone to ketoacidosis at lactation than humans, and the mechanism of soft drink ketosis (fructose -> acetate -> acetoacetate).
http://www.ncbi.nlm.nih.gov/pubmed/20960264
Is there such a thing as a short or medium chain unsaturated FA ? I couldn't find any in a quick search. If they did exist would they travel a similar path to MCSFA, at least part of the way?
Soft drink ketosis - eeeuw. Somewhere in the world you will find populations adapted to just about any imaginable food source.
C.
In two separate experiments, I've eaten low carb, with the fat mostly coconut. Protein sources were ground beef, fish/shellfish, and some dairy. After about 6-7 days, my skin was extraordinarily smooth, like I have never seen before. I wasn't able to keep up the diet because of boredom, and low carb alone didn't do the trick. I'm not sure exactly what caused it, but maybe I'll try it again.
That's similar to my experience.
When I went full Atkins (I tried to eat only beef cooked in dripping with a few veges, to test the effect of a high SFA diet) I was still on methadone and regularly burned my hand on the oven when cooking. I'd get blisters and they'd hurt for days, and I'd easily get sore fingers from splinters and small cuts that also got worse before they got better. I was using rice bran oil and taking cod liver oil prior to the experiment.
Within a week or so of a high-SFA diet I found that if I burned my hand it no longer blistered. I just got a patch of dead skin that vanished overnight. In the 5 years since then I think I've had one blister, and very few cuts and scratches, and those have healed right away, instead of passing through an inflammatory stage. I'm also more resistant to sunburn than I was.
I don't think it's a coincidence that fire-walking was developed in places where coconuts are the main source of dietary fat.
I've had similar experiences with long term improvements in skin tone and texture. Perhaps too many variables in my case due to giving up cereal grains and seeds, beans and pufa at the same time as adding plenty of suet coconut lard and butter but it's a profound transition and unlike anything that ever happened during the long dark years of low fat eating. Dripping and coconut oil are not only good from the inside but good barrier protection from the outside.
My question about PUSCFA above was to query naturally occurring ones. I'm sure you could concoct some but there were no references to anything less than crotonic acid which is a MUSCFA. Maybe they're volatile?
C.
Yeah, I imagine there's some technical reason why it's impossible to fit two unsaturated bonds in a short chain, at least using naturally-occurring reactions. But all sorts of odd fats exist as rare sports, such as cyclised fats and fats with radicals. Never say never.
But MCFAs are intermediate stages in de novo lipogenesis, and the chain isn't usually subject to unsaturation till it's elongated further.
Hard to say what is benefit of cutting vegetable PUFA and sugar and what is benefit of increasing specific SFAs. But that there is a benefit is certain. The gut probably is similar to the skin.
you might have to eat windows to get some PUSCFA in your diet
https://en.wikipedia.org/wiki/Acrylic_acid
C.
@George Henderson:
"...Within a week or so of a high-SFA diet I found that if I burned my hand it no longer blistered. I just got a patch of dead skin that vanished overnight. In the 5 years since then I think I've had one blister, and very few cuts and scratches, and those have healed right away, instead of passing through an inflammatory stage. I'm also more resistant to sunburn than I was."
+1 on this. My wife was the first to notice she was more burn-resisant, after spilling some hot grease on her hand.
I think it's the low omega-6 factor, as much as the high-SFA aspect, as omega-6 is a well-known facilitator of both sun burn and skin cancer, as well as leading to increased perception of pain, if not actually causative to pain.
I'm fair-skinned, and used to burn severely with 40+ minutes of sun exposure. I recently went to the Alps, and spent three days at altitude in bright sun on snow without sun screen.
No burn, got a bit of a tan.
My resistance to pain and speedy recovery from injury has actually got me a bit concerned a few times, as I've noticed injuries a few days after they've happened, with no recollection of them happening! (No signs of peripheral neuropathy or leprosy, happily: peripheral circulation and feeling are both excellent.)
"I don't think it's a coincidence that fire-walking was developed in places where coconuts are the main source of dietary fat."
Interesting observation. I'll also note that the famed Kitivans, who eat a high-carb diet and show none of the ill-effects, eat most of their fat from coconuts or fish. No omega-6, and that's clearly causative in non-alcoholic fatty liver disease.
"Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease—A pilot study"
"...Following the six-month dietary intervention, hepatic steatosis resolved completely in all patients...."
http://www.sciencedirect.com/science/article/pii/S1098882315300101
Thanks Tucker,
Good comment, and great study that you linked; there's not a lot of research linking omega-6 to NAFLD in humans (compared to rodents) and that's an excellent "smoking gun" for the connection, and for the benefit of limiting PUFA in liver diseases.
There were a couple of low-fat trials for skin cancer prevention, restricting PUFA as well as SFA, back in the day - it worked well in this one,
http://www.ncbi.nlm.nih.gov/pubmed/7622291
but not in the WHI sub-group analysis
http://www.ncbi.nlm.nih.gov/pubmed/23697610
"...there's not a lot of research linking omega-6 to NAFLD in humans (compared to rodents) and that's an excellent "smoking gun" for the connection, and for the benefit of limiting PUFA in liver diseases...."
There is a lot of research, actually, although it's not where anyone would look for it. Parenteral nutrition has used soybean-oil based fats for decades, and hepatic steatosis, leading to cirrhosis and liver failure is a well-documented result, in humans. Using a fish-oil based fat instead cures it. Last I checked, it was stuck in studies, but the FDA allowed use of the fish-oil product (Omegaven) when the soy-based product (Intralipid) caused steatosis.
"Gura et al,30 from Children's Hospital Boston, published the first report of 2 children with severe end-stage IFALD who demonstrated complete IFALD reversal after a change from soy-based Intralipid (Fresenius Kabi) to Omegaven (Fresenius Kabi), a fish oil–derived ILE. The most recent detailed publication of outcomes from this group focuses on 42 infants who received Omegaven compared with 49 individuals from a historical cohort.31 Overall resolution of cholestasis while receiving PN in the Omegaven group was 19 compared with 2 in the control group. The risk of death or transplantation was also substantially lower in the Omegaven group (4 of 42 vs 17 of 49)."
"Novel Lipid-Based Approaches to Pediatric Intestinal Failure–Associated Liver Disease"
http://archpedi.jamanetwork.com/article.aspx?articleid=1151637
"Total parenteral nutrition (TPN) induces a high rate of liver disease in infants, yet the pathogenesis remains elusive."
"Total Parenteral Nutrition Induces Liver Steatosis and Apoptosis in Neonatal Piglets"
http://jn.nutrition.org/content/136/10/2547.full
I think at this point the evidence is overwhelming, here's more at Google Scholar:
https://scholar.google.com/scholar?as_ylo=2012&q=FDA+steatosis+omegaven&hl=en&as_sdt=0,7
"Omegaven – How To Obtain"
http://www.fda.gov/Drugs/DevelopmentApprovalProcess/HowDrugsareDevelopedandApproved/ApprovalApplications/InvestigationalNewDrugINDApplication/ucm368740.htm
The study I posted above is the first I've found, however, where steatosis was reversed simply by limiting ingestion of omega-6 fats.
"but not in the WHI sub-group analysis"
That study only looked at total fats, not the omega-6 subfraction. If they were being given dietary advice by a bunch of doctors, they were likely advised to eat oils. Given that fat reduction was to ~20%, they could still have gotten a lot of n-6...
This study, however, did look at the fat subfractions:
"Overall, these results indicate that an excess energy-adjusted intake of
linoleic acid and a lower consumption of soluble carbohydrates may increase
melanoma risk."
(PDF) http://journals.cambridge.org/download.php?file=%2FPHN%2FPHN8_08%2FS1368980005001576a.pdf&code=f6a474c8f3f2e9c1559d97c60a9e146d
Oh, and for non-melanoma skin cancer, which is what people mostly get:
"In the present case control study of incident SCC of the skin, alterations in the erythrocyte membrane fatty acid profile were associated with skin cancer risk. Reduction in skin cancer risk was associated with higher levels of one of the primary saturated fatty acids, palmitic acid. Levels of arachidonic acid, a polyunsaturated fatty acid, were significantly greater among SCC cases compared with controls. Consistent with findings of the differential effects of these two types of fatty acids, individuals with a first skin SCC had an increased ratio of polyunsaturated to saturated fatty acids in erythrocyte membranes compared with noncancer-affected controls."
(PDF) http://cebp.aacrjournals.org/content/14/4/906.full.pdf+html
Homer Black demonstrated that reducing total fat consumption and increasing carbohydrate consumption reduced risk of actinic keratosis (common skin cancer). I suspect this may be because the body converts excess carbs to palmitic acid, which may have been enough to alter tissue composition.
(PDF) http://www.nejm.org/doi/pdf/10.1056/NEJM199405053301804
Great references Tucker!
I'm aware of the parenteral feeding studies, but there is so little fat and so much glucose in those diets that extralopating them to free-living humans is tricky. NAFLD is of course associated with diabetes, obesity, and CVD, but epidemiology says those conditions are inversely associated with PUFA (usually). So that's why the Polish study (and a few other similar biopsy studies) is so valuable.
Your last comment seems to have disappeared but I have an email copy so will post it next.
Your missing comment Tucker:
"...there's not a lot of research linking omega-6 to NAFLD in humans (compared to rodents) and that's an excellent "smoking gun" for the connection, and for the benefit of limiting PUFA in liver diseases...."
There is a lot of research, actually, although it's not where anyone would look for it. Parenteral nutrition has used soybean-oil based fats for decades, and hepatic steatosis, leading to cirrhosis and liver failure is a well-documented result, in humans. Using a fish-oil based fat instead cures it. Last I checked, it was stuck in studies, but the FDA allowed use of the fish-oil product (Omegaven) when the soy-based product (Intralipid) caused steatosis.
"Gura et al,30 from Children's Hospital Boston, published the first report of 2 children with severe end-stage IFALD who demonstrated complete IFALD reversal after a change from soy-based Intralipid (Fresenius Kabi) to Omegaven (Fresenius Kabi), a fish oil–derived ILE. The most recent detailed publication of outcomes from this group focuses on 42 infants who received Omegaven compared with 49 individuals from a historical cohort.31 Overall resolution of cholestasis while receiving PN in the Omegaven group was 19 compared with 2 in the control group. The risk of death or transplantation was also substantially lower in the Omegaven group (4 of 42 vs 17 of 49)."
"Novel Lipid-Based Approaches to Pediatric Intestinal Failure–Associated Liver Disease"
http://archpedi.jamanetwork.com/article.aspx?articleid=1151637
"Total parenteral nutrition (TPN) induces a high rate of liver disease in infants, yet the pathogenesis remains elusive."
"Total Parenteral Nutrition Induces Liver Steatosis and Apoptosis in Neonatal Piglets"
http://jn.nutrition.org/content/136/10/2547.full
I think at this point the evidence is overwhelming, here's more at Google Scholar:
https://scholar.google.com/scholar?as_ylo=2012&q=FDA+steatosis+omegaven&hl=en&as_sdt=0,7
"Omegaven – How To Obtain"
http://www.fda.gov/Drugs/DevelopmentApprovalProcess/HowDrugsareDevelopedandApproved/ApprovalApplications/InvestigationalNewDrugINDApplication/ucm368740.htm
The study I posted above is the first I've found, however, where steatosis was reversed simply by limiting ingestion of omega-6 fats.
"but not in the WHI sub-group analysis"
That study only looked at total fats, not the omega-6 subfraction. If they were being given dietary advice by a bunch of doctors, they were likely advised to eat oils. Given that fat reduction was to ~20%, they could still have gotten a lot of n-6...
This study, however, did look at the fat subfractions:
"Overall, these results indicate that an excess energy-adjusted intake of
linoleic acid and a lower consumption of soluble carbohydrates may increase
melanoma risk."
(PDF) http://journals.cambridge.org/download.php?file=%2FPHN%2FPHN8_08%2FS1368980005001576a.pdf&code=f6a474c8f3f2e9c1559d97c60a9e146d
"Your missing comment Tucker"
Thanks, George. Blog comment software doesn't seem to like comments with too many links, in my experience.
I got a lot of the information about parenteral nutrition from a fellow who had a full intestinal transplant. Apparently the high glucose content is really good at destroying the veins and arteries into which it's injected. Read into that what you may. ;)
His story's here:
http://roarofwolverine.com/wolverine
His diet (which he emailed to me) is a low-carb, high-nutrient-density Paleo diet, and he credits this with avoiding the infections that kill most of the other transplant patients, as he mentions. Thought you'd appreciate that link between low-carb and infection...
"NAFLD is of course associated with diabetes, obesity, and CVD, but epidemiology says those conditions are inversely associated with PUFA (usually)."
So they induce metabolic syndrome in rodents by feeding them Research Diet's D12492, which has a macro-nutrient profile pretty similar to the Modern American Diet, although much higher in linoleic acid. Hibbeln's study:
"Dietary linoleic acid elevates endogenous 2-AG and anandamide and induces obesity."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458187/
Seems -to me- to be designed to demonstrate that if you replace linoleic acid with saturated fat, it doesn't induce obesity, or stimulate lipogenesis in the liver.
His lab has also done some work showing that the inverse association of CVD with linoleic acid is basically because they looked at the wrong end-points: lowered cholesterol rather than actual CVD events.
"Compared with the control group, the intervention group had an increased risk of all cause mortality (17.6% v 11.8%; hazard ratio 1.62 (95% confidence interval 1.00 to 2.64); P=0.051), cardiovascular mortality (17.2% v 11.0%; 1.70 (1.03 to 2.80); P=0.037), and mortality from coronary heart disease (16.3% v 10.1%; 1.74 (1.04 to 2.92); P=0.036)"
"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"
http://www.bmj.com/content/346/bmj.e8707
(Studies don't get cooler than that one, btw.)
I suspect that linoleic acid is effective at lowering cholesterol because it's a liver toxin (like statins), and is busy inducing fatty liver.
I kept poking around and found this:
"These observations suggest novel therapeutic strategies. In fact, because LA cannot be synthesized de novo in humans, dietary LA is the sole source of LA for the human body, therefore also being the sole source for OXLAM synthesis. Lowering LA in the diet might help to reduce OXLAMs in the blood and other tissues such as the liver, leading to an improvement of liver histology. Recently, a study was designed to evaluate the effect of low dietary LA on plasma and erythrocyte fatty acids, and it has demonstrated that a 12-week diet low in n-6 PUFAs significantly reduced the plasma levels of OXLAMs and reduced the LA content of several circulating lipid fractions that may serve as precursors of endogenous OXLAM synthesis [54]. LA reductions were more pronounced in phospholipids and TGs, indicating that these fractions may be more responsive to dietary modifications [51]. These data clearly suggest that if the same reduction of LA and OXLAMs may be achieved in the liver, it may help to reduce or even cure NASH."
"Oxidized metabolites of linoleic acid as biomarkers of liver injury in nonalcoholic steatohepatitis"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578804/
Well, we know the answer to that now! That's exactly what the Polish study did.
Thanks!
I have a few studies and ideas on NASH here that are searchable through tags to the right.
One very interesting finding is that the bulk of dietary LA is converted to cholesterol in the liver. This can be problematic if conditions favour the accumulation of free cholesterol (what would prevent this? Long chain omega 3's, taurine, glycine, magnesium, acetyk donors such as NAC and ALCAR, I'm guessing.) This free cholesterol if it starts to oxidise in situ will oxidise adjacent cardiolopin, causing mitochondrial apoptosis and liver failure.
This conversion of LA to cholesterol also over-rides the normal feedback controls on cholesterol synthesis, so that dietary cholesterol on top of a high-LA diet can result in added accumulation. Basically, this effect of LA can, in theory, make it unsafe to eat a diet high in cholesterol.
Cardiolipin. Now that's an interesting story. Excess dietary linoleic acid changes the composition of many tissues, including cardiolipin, where LA concentrates, altering it's function and causing increased mitochondrial ROS production, leading to LA oxidation and apoptosis. Oddly, it also makes mitochondria more efficient at burning glucose.
I suspect that's the root of the whole problem with oxidized LA, excluding dietary sources of oxidized LA.
But it's late. I'll try to post links tomorrow.
Links:
"The effect of dietary lipid manipulation on hepatic mitochondrial phospholipid fatty acid composition and carnitine palmitoyltransferase I activity."
http://www.ncbi.nlm.nih.gov/pubmed/7866292
Impact of this, from Wikipedia:
"CPT1 is associated with type 2 diabetes and insulin resistance. Such diseases, along with many other health problems, cause free fatty acid (FFA) levels in humans to become elevated, fat to accumulate in skeletal muscle, and decreases the ability of muscles to oxidize fatty acids. CPT1 has been implicated in contributing to these symptoms. The increased levels of malonyl-CoA caused by hyperglycemia and hyperinsulinemia inhibit CPT1, which causes a subsequent decrease in the transport of long chain fatty acids into muscle and heart mitochondria, decreasing fatty acid oxidation in such cells. The shunting of LCFAs away from mitochondria leads to the observed increase in FFA levels and the accumulation of fat in skeletal muscle."
https://en.wikipedia.org/wiki/Carnitine_palmitoyltransferase_I
And if you are on the high-LA diet:
"Moreover, [Linoleic]L4CL[Cardiolipin] is the major CL species in the mitochondria of most mammalian tissues [Not correct, depends on diet, as above] and it constitutes more than 70% of mitochondrial CLs in the heart [33]. Thus formation of 4-HNE via this novel mechanism is likely important in the context of cardiovascular diseases. Our current study clearly demonstrates that formation of 4-HNE from CL operates in vivo and has significant pathophysiological relevance with the detection of the characteristic product EAA-CL and other CL oxidation products ( Fig. 3). This mechanism is further substantiated by the observation that the presence of only one un-oxidized fatty acid (such as oleic acid) in some minor cardiolipin species significantly decreases the formation of this characteristic bioactive lipid and other oxidation products such as HODE-CL (Fig. 4)."
"Formation of electrophilic oxidation products from mitochondrial cardiolipin in vitro and in vivo in the context of apoptosis and atherosclerosis"
http://www.sciencedirect.com/science/article/pii/S2213231714000561
Moving on to cardiolipin in the brain:
"In the rat some protection of the brain against diets containing little fat or with high dietary ratios of 06:03 FA is afforded by the poor breeding performance of rats maintained on these diets (Tinoco, Williams, Hincenbergs & Lyman, 1971; Sinclair & Crawford, 1973)."
Boy, that last sentence is a dry one! As is the summary:
"In view of the important role of milk in the immediate postnatal nutrition of humans it is of interest to note that the PUFA content of six common brands of artificial milk (mg/g total FA) ranges from 27 to 352, compared with about IIO in human milk. Furthermore the ratio, 06:03 FA in these milks varies from 1.5:' up to 129:1, compared with a ratio of 2.8:1 in human milk. Therefore consideration of the foregoing observations may be relevant to human nutrition."
May be, indeed! Paper is from 1975!
"Long-chain polyunsaturated fatty acids in the mammalian brain"
(PDF) http://journals.cambridge.org/download.php?file=%2FPNS%2FPNS34_03%2FS0029665175000535a.pdf&code=5c036659715f816da467b20ce538f628
Boy, after reading those it sounds to me like we have our smoking gun for the metabolic syndrome...
And ran into this, so this is truncated.
"Your HTML cannot be accepted: Must be at most 4,096 characters" :)
Very informative. I have found a lot of information from here about MCT's. For the C6 MCT, we believe it is removed from MCT oil due to its poor taste and smell. For C12, it is not easily absorbed in the body. Thanks for sharing
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