What comes to mind when you read these two words:
Pure poison? The Word’s Greatest Superfood? Somewhere in-between? You might be wondering why ‘they’ (the collective group of health professionals, blog authors, scientists, professors, agencies issuing nutrition guidance) cannot just get on the same darn page!
I hear ya.
As an integrative nutritionist, I often feel like I’m living in the ‘grey zone’- Weighing out available evidence and experience and saying these two little words a LOT: it depends.
Unfortunately, news snippets and even public health guidelines are often not designed to communicate nuance. Instead, complex nutrition issues are often reduced down to simple talking points. My view? Coconut oil has been the victim of over-simplifcation all around that darn saturated fat content. I want to let you in on some lesser-known details about alll that. Because I work primarily with women, that’s what I’ll focus on below! The basic premises, as I see it:
- Premise #1: High total and LDL-C cholesterol levels always raise your risk for cardiovascular disease
- Premise #2: All Saturated fat is the same
Premise #1: High cholesterol levels always raise your risk for cardiovascular disease
My thoughts: Heart disease risk is definitely much more complicated than your cholesterol level. The Population Attributable Risk (PAR) for dyslipidemia in women was recently estimated at 47.1%. What does that mean? Population attributable risk is the ‘proportion of the incidence of a disease in the population (exposed and unexposed) that is due to exposure’. (source). That means that over 50% of cardiovascular disease cases in women are NOT attributed to elevated cholesterol levels. Check out the image below for more info on emerging, nontraditional ASCVD risk factors-you’ll see that just one has to do with cholesterol levels (source).
When ‘classic’ lipid profiles ARE being considered, we know that high LDL numbers do not seem to simply and predictably = high cardiovascular risk. Instead, lipid particles (LDL/HDL-think of these as cholesterol carriers) come in different sizes and densities where small, dense LDL-P particles (driven by excess energy consumption) are more strongly associated with increased coronary heart disease risk (Source).
Thinking about the ‘measurements that matter’, Houston (source) states that we could be doing a much better job with cardiovascular risk assessment using lipid profiles; he recommends in his paper ‘The role of noninvasive cardiovascular testing, applied clinical nutrition and nutritional supplements in the prevention and treatment of coronary heart disease” more extensive risk profiling, including with the following labs :
- Total LDL-C
- LDL-P (LDL particle number) which drives CHD risk
- LDL size (the dense type B LDL is more atherogenic versus large type A LDL)
- Modified LDL (oxidized, glycated, glyco-oxidized and acetylated)
- Apolipoprotein (APO) B and APO A; Lipoprotein a [Lp(a)]
- Total high-density lipoprotein (HDL); HDL particle number (HDL-P)
- HDL size and HDL mapping (large 2bversus small type 3) or five types of HDL
- Dysfunctional HDL
Moreover, women are LESS likely to develop coronary atherosclerosis (the ‘traditional’ model of heart disease), and instead are more likely to present with endothelial dysfunction and microvascular disease (source). What impacts endothelial function and vascular disease? High blood sugar levels, high triglycerides (often goes right along with those high blood sugar levels), inflammation, oxidative stress & vascular immune dysfunction. What causes THOSE things? A dietary pattern high in sodium chloride (salt) intake, refined carbohydrates, sugars, starches, AND certain Saturated Fatty Acids.
From Nettleton et al. (source): “Compared with studies on CHD risk, fewer data link SAFA intakes to the risk of ischemic stroke. Moreover, the results of meta-analyses are inconsistent. When replacement nutrients were not considered, dietary SAFA were not significantly associated with the risk of ischemic stroke or mixed types of stroke. In a recent meta-analysis, higher SAFA intakes appeared associated with lower risks of both stroke types. However, significant effects were limited to males, East Asians, participants with lower body mass index, and studies of high quality and long follow-up. A meta-analysis of 7 intervention studies concluded that SAFA reduction had no clear effect on any type of stroke. Although partial replacement of SAFA by PUFA reduced stroke risk in this study by 32%, with only 4 studies and 41 stroke cases, this effect was not significant.”
When thinking about the health profile which will result from any given behavior, I always think that a great place to start is with population studies of people who are doing a lot of that ‘thing’-in this case, consuming coconut! “The Pukapuka and Tokelau Island study by Prior et al. found a low incidence of CVD in the populations of these two islands, despite a large portion of energy intake (34% among Pukapukans and 63% among Tokelauans) and dietary fat intake being from coconut flesh. It has been reported that the diets of these two populations were low in sugar and high in fiber-rich foods, resulting in low cholesterol levels (4.5 mmol/L and 4.6 mmol/L in Pukapukans and Tokelauans, respectively)”
Which brings us to Premise #2: All Saturated Fat is the Same
Saturated fat is often talked about as ‘one single compound’-‘limit your saturated fat’ ‘saturated fat as 10% of your calories’, foods ‘high in saturated fats’. Instead, there are different types of saturated fatty acids which impact cholesterol levels differently:
- Palmitic (C16)
- Stearic (C18)
- Lauric (C12)
- Myristic (C14)
Briggs et al. (source) put it this way: the most common saturated LCFA in the American diet are myristic acid (14:0), palmitic acid (16:0) and stearic acid (18:0). There is a great deal of overlap in their typical food sources. For example, dietary sources of myristic acid include palm kernel oil, coconut oil and butter, while dietary sources of palmitic acid include palm kernel oil, dairy fat, meats, cocoa butter, soybean and sunflower oils. Myristic and palmitic acids have comparable effects on both LDL and HDL cholesterol, but overall have little effect on the total cholesterol: HDL cholesterol ratio. Stearic acid, compared with other SFA, has been shown to lower plasma LDL cholesterol levels, and have no effect on HDL cholesterol. Therefore, even though stearic acid is a SFA, it does not appear to adversely affect CVD risk, possibly because it is desaturated in part to oleate (18:1 n–9) during metabolism. So, how does the fatty acid composition compare between some different common fat sources?
Coconut oil: 94% saturated fatty acids, composed of lauric acid C12:0 (48%), myristic acid C14:0 (19%) and palmitic acid C16:0 (9%)
Butter: 66% saturated fatty acids, of which the main components were palmitic acid C16:0 (28%), stearic acid C18:0 (12%) and myristic acid C14:0 (11%).
Olive oil: 19% saturated fatty acids, mainly palmitic acid C16 (15%) with stearic acid C18:0 (3%) and 68% monounsaturates with the main component being oleic acid C18:1n9 (64%). (source)
Let’s take a look at each component:
The main fatty acid in coconut oil is lauric acid (C12:0). Lauric acid can be classified as either a medium-chain or a long-chain fatty acid. In terms of digestion and metabolism, however, it behaves more as a long-chain fatty acid because the majority of it (70%–75%) is absorbed with chylomicrons.11 In comparison, 95% of medium-chain fatty acids are absorbed directly into the portal vein. While Lauric acid is associated with higher cholesterol, it has a more substantial impact on High Density Lipoprotein (HDL) than Low-Density Lipoprotein (LDL) (source) In a study of Filipino women dietary coconut oil intake was positively associated with high density lipoprotein cholesterol especially among pre-menopausal women, suggesting that coconut oil intake is associated with beneficial lipid profiles (source).
When it comes to other considerations about coconut oil consumption, the anti fungal and anti microbial elements of Lauric Acid are often considered: Lauric acid has been shown to have antimicrobial activity against Propionibacetrium acnes, implicated in inflammatory acne (source). Lauric Acid, the predominant fatty acid in coconut oil, is fungistatic and fungicidal for C. albicans, an opportunistic bacteria that can ‘take over’ in the gastrointestinal tract. In a mouse model, it was shown that GI colonization with C. Albicans is lower in coconut-oil fed mice versus beef tallow and soybean oil (source).
A couple of other considerations: the (PREDIMED) study reported approximately 30% lower cardiovascular events in both Mediterranean diet arms (supplemented with olive oil or nuts) after 4.8 years (which is not limited to impact on cholesterol!). I’ve not seen research around coconut oil lowering cardiovascular risk to a significant extent, which is an important consideration. However, coconut meat (think unsweetened coconut flakes) and coconut flour have their own unique properties-in the case of coconut flour, composition has been able to lower serum cholesterol and a decrease in blood glucose (likely due to all of that fabulous prebiotic fiber) (source) (source)
My take, overall? When it comes to fat intake, Prioritize meeting essential fatty acids needs (Omega 3 and Omega 6, in appropriate balance), use unheated extra-virgin, cold pressed olive oil whenever possible for dressings & drizzles, integrate coconut meat (unsweetened flakes, coconut flour) into your diet, and use coconut oil for fun, flavor, when seeking an HDL boost or the anti-fungal benefits it seems to hold. Substitute coconut oil for butter when desired, and focus just as much on the OTHER risk factors for cardiovascular disease, remembering that health is so much more than your cholesterol levels.