The other part comes from the persistent feeling that we ‘now’ have a good understanding of our environment. Feelings that are very strong in the lay community and are arrogantly persisted by some of the scientific community in order to maintain/re establish status.
So lets start from the basis that labels and groupings are often over-simplifications and always require a judgment call by someone. Just think that when we say that animal fat is saturated fat we are ignoring that pork for example has almost equal amounts of mono-unsaturated fats (43%) as it does saturated fats (44%), with the rest being poly-unsaturated fats.
Then lets also consider that much of what we know at cellular and molecular level is still in refinement mode and far from fully understood especially with regards to entire organisms (let alone an organism interacting with its environment). Just think of the case of cholesterol. It was found in arterial plaques and therefore was (understandably) immediately demonized. Any molecule that was carrying it ‘in’ was considered bad (LDL) any molecule carrying it ‘out’ was considered good (HDL). And from there it was a short step to demonizing all foods with cholesterol as well. It took a long time to give the right attention to the fact that the body produces most of its own cholesterol (75%) and dietary cholesterol only contributes about 25% of the total. And took even longer to accept that the body would auto-regulate production according to dietary intake. Now we know that LDL is not actually all bad and that only vLDL is the problem. We know that it is mostly grains that will raise vLDL and not saturated fats but many of the heart foundations (esp American) are still weary to change the original advice… and this is probably partly because it could lead people to loose faith in the advice and thus follow it even less… partly probably due to financial reasons ( I am sure the American heart foundation logo doesn t appear on certain cereals without some kind of ‘donation’ from the food industry –and this is even though it ends up supporting a food known to increase vLDL) and partly because it is difficult to teach an old dog new tricks… and we live in a culture where dinosaurs (and money) set the rules (and its always possible to find or fund a study that will support your view).
So on to the actual articles…
The first point they both mention is the saturated fats argument. This is now starting to become old news but it takes time for research to trickle to clinical practice and as I said above it may never trickle to ‘the old dogs’. A large metanalysis in 2010 has finally confirmed a few earlier studies on sat fats showing how they are at worst neutral and definitely not linked to heart disease or stroke (http://www.ncbi.nlm.nih.gov/pubmed/20071648). And for this we only really had to consider that human breast milk contains more than 50% of saturated fats!!
Then the second part is about MCTs
As I said above, it’s not unusual to box something in a category according to the main component and somewhat disregard the rest. Both beef and pork have marginally higher amounts of saturated fats compared to mono-unsaturated, similarly coconut oil has just over 70% MCTs. To be more accurate, it has about 55% borderline MCTs and 19% true MCTs. In fact depending on where the line is drawn (10 carbon atoms or 12 carbon atoms) the most abundant fatty acid in coconut oil –Lauric acid- can be seen as a medium or a long chain. In a way, judging from the effect that it has on the body it might make more sense to class it as a long chain, because it DOES have an impact on cholesterol like other long chain fatty acids. Does this matter? Very little, as even though some studies show that it increases LDL others show that both LDL and HDL go up (contrary to what trans fats do which increase LDL and reduce HDL). Furthermore it should also be noted that lauric acid is quite scarce in our diet and the other main source of it is… breast milk, which contains between 2-20% of this antimicrobial oil. In any case looking at just one fraction of a product and at one parameter can be interesting but it does not create a full picture of risks to health i.e the food in the way that it is consumed in relation to an entire organism with feedback mechanisms, environmental interactions etc.
Looking at research for coconut oil it is difficult to draw a clear conclusion about cholesterol; as for every negative study there is a positive one. I have no agenda on this and therefore no interest in creating an argument for one side or the other and looking at it objectively it seems to me that if research is inconclusive on the cholesterol front chances are there are other variables we are not taking into account. However which ever that specific argument swings it still is about cholesterol, which really is not a worry in the way the pharma industry goes about it. Of interest are studies looking at other parameters such as animal model studies where coconut oil was found to reduce the chances of thrombosis (implicated in heart attacks and strokes) as well as increase the amount of antioxidants vitamins and also reduces the oxidation of LDL and in particular of vLDL (http://www.sciencedirect.com/science/article/pii/S0009912004001201 ). Or studies where they found comparable amounts of coconut oil use in groups of coronary heart disease patients and healthy subjects (http://www.ncbi.nlm.nih.gov/pubmed/9316363). Or ones where 1 week of coconut oil supplementation was found to reduce waist circumference (http://link.springer.com/article/10.1007/s11745-009-3306-6#page-1). Now as the articles you provided also suggest this is unlikely to be due to the MCTs as it may be debatable if lauric acid is an MCT or not. However animal model studies have shown how coconut oil was effective at stimulating UCP1 a protein involved in thermogenesis in brown fat (a very exciting area of research with respect to energy production and weight loss) (http://europepmc.org/abstract/MED/9806312).
All this is to say that yes I totally agree there is no magic bullet food or drug and most definitely no foods we should base our entire diet on. In fact I can hardly think of a food that doesn’t have a down side… from broccoli to kale to nuts to goji. Some foods should hardly be referred to as foods all together (grains come to mind) but coconut oil, in the face of my understanding of our current research, is far from being in this category and it is still the best vegetable oil to cook with and a good addition to smoothies. However it’s probably best not to make coconut oil soup… as there is an argument for not using more extracted oils than you would eat of the food it is sourced from (the same is also valid for juices).
Breast milk between 2-20% lauric acid
If omega 3 are low in breast milk the body will increase levels of laurc acid in order to still support the immune system
here is an animal model study showing the benefits of cocont oil on LDL oxidation
same team as above study also proved its beneficial impact on blood coagulation factors (thus no likelihood of inducing thrombosis). The profile on this parameter was comparable with sunflower oil, which is composed of unsaturated fats (in particular omega 6 and a small amount of omega 3)
plus animals fed VCO presented higher levels of antioxidant vitamin (remember fats will help absorption of many nutrients) and therefore not surprisingly the LDL cholesterol from these animals was also more resistant to oxidation.
And daily administration was found to reduce cholesterol and triglycerides
again same team confirming the increased antioxidant levels after coconut oil use (albeit in rats) and also found that an oil rich in polyunsaturated fatty acids actually reduced levels of antioxidant enzymes and increased peroxidation
VCO reduced total cholesterol, tryglicerides, LDL and more importantly vLDL (which is the only porton of cholesterol which is actually dangerous) increase HDL and reduced LDL oxidation
Prolonged consumption of CO was reported for two groups of native Polynesians who consumed 63% and 34% respectively of their food energy from CO (17). The respective average serum cholesterol values (males plus females ages 15-64 years) were 209 mg/dl and 172 mg/dl. The authors observed, however, that “Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having harmful effects in these populations”
Coconut oil consistently elevated plasma cholesterol compared to beef and sunflower oil
Also proves how beef fat has a very different impact on lipid profile that the one most heart foundatons will support….
in obese women 1 week of coconut oil supplementation increased levels of HDL and reduced the ration of LDL;HDL as well as a reduction in weight circumference
Animal model study: a diet high in fat and in particular coconut oil was effective at stimulating UCP1 (a protein in brown fat which stimulates thermogenesis and thus higher caloric consumption and metabolism)
Human population: no differences found in coconut oil consumptions between coronary heart disease patients and healthy patients
Human population: Coconat fat in the form of coconut cream fond to have no detrimental impact on lipid profile and it may even lower LDL and increase HDL
human population: no pronounced changes in lipid profile and oxidative stress when using coconut oil or sunflower oil in both healthy and type 2 diabetic patients most of the recent investigations conducted in animals as well as human beings contradict claims that coconut oil increases the risk of atherosclerosis and heart disease
Lipoeto NI, Agus Z, Oenzil F, Masrul M, Wattanapenpaiboon N, Wahlqvist ML. Contemporary Minangkabau food culture in West Sumatra, Indonesia. Asia Pac J Clin Nutr 2001; 10: 10-6.
8. Nevin KG, Rajamohan T. Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem 2004; 37: 830-35
The results obtained are not uniform and are highly conflicting. There are studies that indicated that coconut oil consumption might result in undesirable lipid profile changes compared to safflower oil (21) and soya bean fat (22). Yet, there are other studies that have failed to find any association of coconut oil with adverse lipid profile changes (23) and some that showed that coconut oil consumption has beneficial effects compared to other dietary fats (24).
Results from Table 1 fail to provide any indications that coconut oil consumers have undesirable lipid profile pattern and increased risk for CAD compared to sunflower oil consumers.
Coronary artery disease is now considered as an inflammatory disease and accumulating evidence is now available to suggest that oxidative stress may contribute or aggravate the process of atherosclerosis (29,30)
The effect of various dietary fats on antioxidant enzymes and indicators for oxidative stress has been investigated in animals. The formation of the promutagenic, exocyclic DNA adducts in the liver of rats, which are markers for DNA damage by lipid peroxidation, was found to be highest in sunflower oil fed rats when compared to coconut oil, olive oil or rapeseed oil (42). It was found that rats fed with coconut oil have low susceptibility to lipid
peroxidation compared to olive or sunflower oil diets (43)
Since there was no noticeable variation for the anti oxidant enzymes of the subjects consuming either of the oils, it may be concluded that the type of dietary fat consumed may not be amajor contributory factor to oxidative stress in this population. It may be concluded that the consumption of coconut oil in moderation, as a part of routine diet, may not contribute to the risk for CAD, directly by affecting the lipid profile or indirectly by aggravating oxidative stress. It may not be the type of cooking oil, rather its quantity that may be contributing to the risk of CAD.