One of my favourite parts of one of my favourite books (The Great Cholesterol Con) is this: “How can eating saturated fat raise LDL levels? It is not merely biologically implausible; it is biologically impossible. It always was and it always will be. (Boy does that statement make me a hostage to fortune!)” Dr Malcolm Kendrick.
I read this in 2008 and it inspired me to seek and meet with a biochemist, which I did at a local university. I asked the biochemist whether he thought it was possible that consuming saturated fat could raise LDL levels and he couldn’t see how but he said he didn’t understand the dietary process sufficiently. He suggested that we ask a dietician to join us, at which point I thought – if we’re relying on a dietician to exonerate saturated fat for anything, we’re in trouble!
I have not since found any evidence that saturated fat can raise LDL-cholesterol, let alone that it does. This brings us to a classic article for this week’s note, which was published in January 2018 (Ref 1). The study also featured on a BBC programme around that time. The article was called “Randomised trial of coconut oil, olive oil or butter on blood lipids and other cardiovascular risk factors in healthy men and women”, which makes it rare and important in our world. Not many randomised controlled trials are undertaken in the field of nutrition and this one was also conducted on healthy people and so is generalisable to healthy people.
The opening sentence of the abstract was: “High dietary saturated fat intake is associated with higher blood concentrations of low-density lipoprotein cholesterol (LDL-C), an established risk factor for coronary heart disease.” No reference for this was given. It’s one of those deeply held beliefs – rather like the calorie theory (Ref 2).
The experiment recruited volunteer adults through the BBC websites. Eligibility criteria were men and women aged 50–75 years, with no known history of cancer, cardiovascular disease, or diabetes, not on lipid lowering medication and with no contraindications to a high-fat diet. They needed to be willing to be randomly assigned to consume one of the three dietary fats for four weeks. Of 160 individuals initially expressing an interest and assessed for eligibility, 96 were randomised to one of three interventions; 2 individuals subsequently withdrew, and 94 men and women attended a baseline assessment. Their mean age was 60 years, 67% were women and 98% were European Caucasian. Of these, 91 men and women attended a follow-up assessment 4 weeks later.
The intervention was for participants to consume 50g daily of extra virgin coconut oil, extra virgin olive oil, or unsalted butter for 4 weeks “which they could incorporate into their usual diet or consume as a supplement.”
The main outcome measure was change in LDL-cholesterol (LDL-C). Secondary outcome measures were changes in total and HDL cholesterol, weight, BMI, waist circumference, per cent body fat, blood pressure, fasting plasma glucose and C reactive protein.