In this, my final post on coconut oil, I’ll discuss some purported benefits of consuming the oil. This will include its effects on bacteria, viruses, cancer, the liver, and oxidation. Alright!
Antibacterial and antiviral properties:
The idea that coconut oil has antibacterial and antiviral properties is a pretty common opinion, but most of the evidence for this is based on in vitro studies. Unfortunately, putting coconut oil in an agar dish with rabbit cells and some bacteria and observing the growth is not quite the most convincing evidence of how coconut oil consumption is protective against pathogens. Still, let’s look at some studies that have been performed:
In vitro, components and metabolites of coconut oil (including glycerol monolaurate, lauric acid, and capric acid), inhibit the growth of:
- H.pylori, the primary cause of ulcers (33,102)
- S.auerus (33,34,102)
- B.anthracis stern (33), though not always (102)
- Vesicular stomatitis virus(46)
- Cytomegalovirus (65)
- Candida albicans (66)
- Listeria (100)
- Herpes simplex virus type 1 (67,112)
- Haemophilus influenzae (67)
- Group B streptococcus (67)
- Respiratory syncytal virus (68)
- Human parainfluenza virus type 2 (68)
- M.terrae (102)
- Visna virus (108)
Some of these same compounds may also decrease of prevent resistance to beta lactams (like penicillin) in Staphylococcus aureus (36,40) and resistance to vancomycin in E. faecalis (41).
Furthermore, these coconut oil compounds may also prevent toxicity of:
- Staphylococcal a-hemolysin and b-hemolysin (34,36,37)
- Endotoxin (37,38)
- Anthrax toxin (37)
- Toxic shock syndrome toxin-1 from S. aureus (34,36,39)
However, studies have shown that not only do compounds in coconut oil not inhibit E.coli (33,34,112), glycerol monolaurate may even increase E.coli hemolysin release (34).
Of course, none those studies examined effects inside the body, so their application is limited. We have no idea how metabolism of coconut oil, pH (111), or other conditions in the body might have an affect. As far as reducing infection, the only study measuring this is I could find is from 1948, in which rats fed coconut oil survived tuberculosis at a higher rate than rats fed olive oil and flaxseed oil (43).
In several other studies, coconut oil consumption in animals greatly reduced various negative responses to endotoxin (104,105,106). However, these studies also noted a direct relationship between increased dietary linoleic acid and increased negative effects from endotoxins. This is likely due to linoleic acid inducing greater permeability of the intestines to endotoxin (107). Thus, such studies could be reflective of this and not the unique effect of coconut oil on decreased toxicity to endotoxins.
So there you go. I definitely think the effects of coconut oil derived compounds on bacterial infections (especially Staphylococcus aureus) and viruses (109) deserve more attention, but as of right now I don’t think we have enough data with practical application to suggest anything definitive.
Verdict: Coconut oil definitely may have antibacterial and antiviral properties, but the proof is in the pudding. And we need some more pudding.
It can be hard to study the effect of diet on cancer clinically. One way of attempting to do it has been to feed rats different diets, give them all a carcinogen, and see who gets the most cancer. Not really the most fun study to be a part of if you’re a rat.
The first study we’ll look at fed rats about 20% of calories as corn oil, fish oil, or coconut oil. Then the rats got a nice dose of DMBA, a carcinogen. Ultimately, the corn oil group experienced a much higher rate of mammary tumors than the other two groups, which were essentially even (1). Another study used azoxymethane to induce colon tumors in rats fed a number of different diets. Corn oil and safflower oil did promote tumor growth, while olive oil and coconut oil didn’t (all at 23.35% of calories) (2). Another study found coconut oil was better than soybean oil at preventing cancer (3). Finally, this study (4) found that coconut oil was protective against DNA damage in the liver.
In a study by Cohen et al. various oils were fed to rats and cancer was initiated using N-nitrosomethylurea. In the first study, consistent with the other studies we looked at, there was a correlation between linoleic acid content of the diet and cancer prevalence (5) and coconut and olive oil produced the least number of tumors while corn and safflower produced the most. A follow up study produced the same results, with coconut oil resulting in the least tumors (6). The authors speculated that linoleic acid’s role as a prostaglandin precursor may explain its effects on cancer, though other’s have suggested each fat’s effect on blood cholesterol is the important element (7).
Personally, I think linoleic acid is likely playing the biggest role in these studies and thus, coconut oil is only cancer preventative via its low content of LA. There are human interventions that support this idea (8), but it would be presumptuous to say we know linoleic acid causes cancer.
Verdict: Coconut oil may be better for cancer development than oils with more linoleic acid, but such evidence is in its infancy.
There is some evidence that coconut oil is beneficial to liver health. Rats fed coconut oil don’t develop fatty liver disease (9), but there is a large amount of evidence suggesting that rats fed corn oil develop fatty liver disease readily (10,11,12). In methionine and choline deficient diets, coconut oil protects against the development of fatty liver and corn oil does not (13).
In this study (14), rats fed 15% of their diet as coconut oil had significantly less lipid peroxides in their livers than rats fed the same amount of fish oil. In this and another study I looked at during part 2 (15) rats fed fish oil develop lower blood lipids (cholesterol and triglycerides) than coconut oil, but at the expense of their livers. Another study examined lipid peroxidation in the livers of rats fed different oils (with vitamin E levels constant); olive oil and coconut oil produced the least.
However, it appears that saturated and possibly monounsaturated fats in general (like beef fat, palm oil, and coconut oil) are protective against fatty liver disease under varied conditions and polyunsaturated oils (like corn oil and fish oil) are not (16,17,18).
Verdict: Coconut may be good for your liver, but I’m waiting for studies done on humans. Mostly, it looks more like polyunsaturated fats (like linoleic acid) are just bad for the liver. I’m noticing a trend here.
Some Final Benefits:
The following discuss studies done on rats:
Coconut oil, especially virgin, produces lower levels on lipid peroxides in rats than high polyunsaturated oils(19,20,21,23).
Virgin coconut oil increases antioxidant levels (20,21,22).
Virgin coconut oil increases vitamin A levels compared to fish oil and sunflower oil (20,23).
Coconut oil increases vitamin E levels compares to corn oil and fish oil (22,23).
Virgin coconut oil may be good for the testicles (24,21).
Verdict:Virgin coconut oil seems to be good at reducing oxidation in the body. This will likely translate to numerable benefits, but not enough studies have been done to elucidate the extent of this.
Coconut oil may have antibacterial and antiviral properties (I would bet on it), but much remains to be studied to before we can discuss this as a benefit. Coconut oil is clearly good for the liver, but more likely this is due to low quantities of linoleic acid. It also appears to be one of the least cancer promoting oils, again likely due to low linoleic content. Finally, virgin coconut oil seems to be good at preventing oxidation in the body. This is certainly a good thing.
I think the take away message from this series is that coconut oil may not be the magical, super powered, god-like oil its sometimes hyped as (its effects on bacteria and viruses not withstanding), but it’s probably fairly healthy. This is likely due to its decent antioxidant content and its low levels of linoleic acid, an omega-6 fatty acid I believe is worth limiting in most diets.
So go out and enjoy coconut oil! Unless you don’t want to. That’s cool too, I’m not forcing you to do anything!
10. Deng QG, She H, Cheng JH, et al. Steatohepatitis induced by intragastric overfeeding in mice. Hepatology. Oct 2005;42(4):905-914
11. Baumgardner JN, Shankar K, Hennings L, Badger TM, Ronis MJ. A new model for
nonalcoholic steatohepatitis in the rat utilizing total enteral nutrition to overfeed a high polyunsaturated fat diet. Am J Physiol Gastrointest Liver Physiol. Jan 2008;294(1):G27-38.
12. Lieber CS, Leo MA, Mak KM, et al. Model of nonalcoholic steatohepatitis. Am J Clin Nutr. Mar 2004;79(3):502-509.