I enjoy coconut. This article disturbs me.

http://fanaticcook.blogspot.com/201...flammation.html
http://www.acc.org/media/releases/h...igh_sat_fat.pdf

Carrot cake + milkshake=meal?

The same blog has an article on corrupted research.
http://fanaticcook.blogspot.com/200...d-research.html

It sounds like the coconut oil tested was the refined, industrial grade crap that is in most processed foods. I wonder if the coconut oil hadn't been surrounded by sugar and carbs if the results would have differed.

Why is it mostly the only research anybody will do that involves saturated fat, HAS to be utterly buried in SUGAR? Like the research that has "bacon and twinkies" in in one group like they're the same thing. Or this which has to combine saturated fat with cake with icing and dairy milkshake? Like they just can't help vastly compounding the variables to do ANYTHING to make saturated fat look bad. (And as Kathy noted, I'd like to know whether they used an industrialized version of coconut oil, first.)

An ambulance and tow truck also contribute to traffic jams but are they the primary cause of the accidents that ensue? Of course not, the ambulance and tow truck are there to repair the damage done. So what's the cause of the accidents? Probably some moron who doesn't drive properly.

So, does coconut oil (i.e. palmitic acid) cause the damage or is it there to fix the damage that some other moron (i.e. glucose + insulin) did?

What's the hypothesis anyway? If it's "saturated fat causes heart disease", that's been refuted.

The aim of the study was:

"... to define the effect of consuming a single high-fat meal, differing in fatty acid composition, on the ability of high-density lipoproteins (HDLs) to inhibit the expression of proinflammatory adhesion molecules by endothelial cells and on large and small vessel function."

It still doesn't answer the question "what's the hypothesis". And it still looks like the hypothesis is "saturated fat causes heart disease and this is the mechanism by which it does so".

Chris Masterjohn replied to that research pointing out that it is possible the differences reported were not due to the saturated/unsaturated nature of the oil but the amount of Vitamin E it contained.
see here

However I suspect that a single meal is never a good trial.

If you've never eaten coconut oil your GI system will not be used to dealing with it. Try eating it every day for 3 months and then repeat the trial and it's possible you will have developed a gut flora that knows what it's dealing with and is well able to cope.

FTR, Chris Masterjohn was writing a letter to the editor to comment on this:

http://www.ncbi.nlm.nih.gov/pubmed/16904539

Objectives are mentioned in the study; hypothesis is not. Nothing is proved. But there are conclusions.

The conclusion of the above mentioned article was:
'Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.'

What Masterjohn said in his letter was that, since the oils were unrefined, vitamin E should be considered. 'The respective vitamin E concentrations of the oils may therefore have contributed to their observed differential effects on ICAM-1 and VCAM-1 expression. Future research should investigate the relative contribution of fatty acid composition and micronutrient composition to this effect.'

'Why is it mostly the only research anybody will do that involves saturated fat, HAS to be utterly buried in SUGAR? '

The research shouldn't be buried in sugar. However, few people (relatively speaking) add coconut oil to their coffee when they drink it, or eat coconut oil directly from a spoon. Or fry with it. I've done all of the above, and it affects the taste of the food it is paired with. Not in a good way, for me, but that is me.

So if someone is going to put coconut oil in food, they put it with sugar, most likely because that is where it often appears and is palatable. And is in the dishes most people ingest.

Until Thai cuisine hit the restaurants and tables here, I don't think I had ever had coconut milk. Even in that case, the number of people in the U.S. eating coconut milk is relatively small. I cook Chinese food at home sometimes, Indian food and Thai food, too - but even then, it's a small part of our overall diet in my household.

If I go to the supermarket, what prepared food is likely to have coconut oil as an ingredient that I am likely to buy and take home and eat? I'm guessing next to none, actually, but coconut does appear on and in baked sweet goods.

You can take coconut away from sugar but it is likely to be eaten with sugar - now, anyway. Maybe in the future, that could change.

The purpose of those adhesion molecules is not to cause atherosclerosis, they're integral to the healing process.





So the effect of HDL from subjects fed safflower oil or coconut oil on inflammatory markers in isolated umbilical cells was tested. What are the chances that these cells were somewhat traumatized in the process of isolation? I find it very hard to imagine that they weren't traumatized. HDL from safflower-oil fed subjects may have quenched inflammation in these cells, but as far as I'm concerned, those cells had every right to be traumatized.

Inflammation doesn't cause heart disease, misplaced, improperly co-ordinated, and unresolved inflammation is a more likely cause.

I don't know the cause of atherosclerosis. But isn't it possible for a process to have more than one effect?

http://www.neurology.org/cgi/conten...ract/60/12/1890

This article discounts the role of adhesion molecules (cellular adhesion molecules) in patients with advanced carotid artery disease.

What's interesting is that the testing used human subjects but they already had advanced carotid artery disease!

Here's an article about the background of the adhesion molecule/athersclerois relationship:

http://www.ncbi.nlm.nih.gov/pmc/art...l00087-0138.pdf

Yes, a process can have more than one effect.

You can't have a mis-healing without many of the factors that go into proper healing being involved. You can't just point at an increase in one of these factors and declare that you have caused heart disease in isolated umbilical endothelial cells. This may or may not be a pathological response.

Every compound, hormone, enzyme etc. in the body has a legitimate purpose. That purpose is not to encourage cancer to grow, atherosclerosis to develop, etc.

I'm still reading the second article you posted, MathManiac. So far I'm at this part;




Tumour necrosis factor induces ICAM-1 and VCAM-1?

I found this a while back on tumour necrosis factor and healing in mice;





Without tumour necrosis factor, stuff doesn't heal right.

'You can't just point at an increase in one of these factors and declare that you have caused heart disease in isolated umbilical endothelial cells. This may or may not be a pathological response.'

One thing that impresses me when reading these articles is that no one is declaring that heart disease is caused by anything.

If they say anything at all, it is that *this* suggests *that* and then the grand finale (conclusion), that *something* MAY lead to *something*.

While healing may be an interesting topic in itself, its relationship to atherosclerosis is what? They may share factors.

I included the second article (all I'm doing is googling this stuff) because it seemed to explain the background of the role of adhesion molecules. It is just a starting point. What about tumor necrosis factor? (Specifically, ' a healing mouse cutaneous wound.')

For a clear answer, I'd e-mail the author. (Tumor necrosis factor is not mentioned at all in the article about fats...)

Not according to Doctors Oz and Ornish!