Lipoprotein (a) is interesting enough that I might put up some more thoughts about it, but this post is based on the Bantu cross sectional study cited, as all the best cardiac studies are, by Dr Davis of Track Your Plaque.
The initial link is to this paper which explains quite a lot about Lp(a) and its genetics.
I wanted to compare values of the Bantu with an intervention trial in some Swedes, and to think about eating fish and taking fish oil, to reduce that "risk factor" for heart disease. And yes, Lp(a) is a "risk factor" for all forms of vascular disease; ischaemic heart disease, peripheral vascular disease, cerebrovascular disease and abdominal aortic aneurism.
First the Bantu. That first paper covered the Bantu genetics, apoprotein (a) sizes and Lp(a) blood levels. Basically, if you match individual gene types, the fish eating Bantu always have lower Lp(a) than their matched apo(a) size vegetarian Bantu equivalents. You get nothing about diet in this initial paper, for that you need to go to a previous publication from the same group.
Fish eaters and vegetarians were pretty well matched for calorie intake at around 2100kcal/d. The fish eaters ate 18% of calories from protein, 12% from fat and 70% from complex carbohydrate. The values for the vegetarians were 11% from protein, 7% from fat and 82% from complex carbohydrate. Dean "Mcdonalds" Ornish would be proud of the vegetarians. BTW, both groups ate 4g/day of salt, worth remembering that.
On a fully vegetarian, completely home grown, ultra low fat, low salt, complex carbohydrate diet these Bantu natives show exactly the same rise in blood pressure with age as Westeners do. Their systolic pressure approximates quite closely to that "age plus 100" rule of thumb which used to be considered normal in the UK and diastolic pressure followed systolic as you would expect. Fish eaters stuck with a systolic around 120-130mmHg and a diastolic around 70mmHg, life long. Remember both groups only ate 4g/d of salt. Now what does that tell you about salt and hypertension? Anyway, the politically correctest Bantu had significant markers of CV deterioration with age, not so the fish eaters.
BTW, as an aside, HDL figures were abysmal with both groups at under 1.0mmol/l, exactly as you'd expect on a low fat diet. They were slightly higher in the vegetarian group, presumable because they drank more alcohol. Triglycerides were higher in the veggie group, again pretty much as you'd expect from their carb intake.
The theory was/is that it was the omega three fats which were saving the fish eaters from hypertension and Lp(a) elevation. They undoubtedly did eat more omega three fats, and less omega six fats, and we know from the Lyon Heart Study that this is probably a Good Thing.
The Bantu fishermen were getting roughly 5% of calories from fish derived fat, that's 105kcal, equivalent of about 12ml of fish oil per day, as fish. This intake of fish oil is associated with a Lp(a) concentration of 201mg/dl as opposed to 321mg/dl in the vegetarians.
So what happens if we take a group of Swedes and give them more than twice that dose of fish derived lipid, as 30ml of fish oil per day, then track their Lp(a) level? Initially the subjects were on a typical Swedish diet (no information given) and were advised not to change it throughout the study. The fish oil was added at 30ml plus some vitamin E per day for three weeks, then there were two weeks off of fish oil, then three more weeks on fish oil, but without the vitamin E (for Bruce; yes, lipid peroxides rocketed on the later protocol).
Lp(a) before fish oil plus vit E: 128mg/dl, after three weeks supplemented: 125mg/dl. Back on Swedish diet for 2 weeks: 124mg/dl, after fish oil without E for three weeks: 128mg/dl.
All of these figures are essentially identical. Fish oil at 30ml per day does nothing to Lp(a) levels on a Swedish diet. It's also worth noting that, although we don't know the Swedish geneotypes for apoprotein (a) size, these values are all much lower than either of the Bantu groups. Maybe 35% of calories from fat in Sweden?
So is it really the fish oil which is saving the carnivorous Bantu from the hypertension and elevated Lp(a) which are prevalent in their vegetarian cousins?
Somehow I doubt it, based on the Swedish data and the behaviour of Lp(a).
Intervention studies show us that low fat diets increase Lp(a) and high fat diets decrease it, I put the studies here.
The fish eating Bantu got through more than half a kilo of fish on a good day. If your average calorie in take stays unchanged, that's an awful lot of complex carbohydrate you didn't eat. If I assume causality, not eating complex carbohydrate appears to be extremely good for your cardiovascular system. And your Lp(a) levels.
You don't need any "magic" fats to drop Lp(a), unless those magic fats are saturated fats, which seem to do the job best (just turn the DELTA study on its head).
BTW: No, I don't believe our liver manufactures Lp(a) to kill us. Again, more thoughts on Lp(a) to come. I might even talk hedgehogs if I can get my head around what they were doing with their lipids!
Another BTW, the Kitava studies showed these islanders ran at 70% calories from carbs but with Swedish levels of Lp(a). Kitava was lowish in fat at 20% of calories, but their dietary fats were almost all saturated (from coconut), with just a little omega 3s from fish. So it looks to be arguable whether you need to consume saturated fats to keep you Lp(a) levels down or keep carbs below the vegetarian Bantu levels. Ignoring genetics. Open to discussion on that one.
EDIT 28th Feb: Just been back to the Kitava papers for something else and noticed Lipoprotein(a) was around 300mg/dl, ie Bantu levels, bad Bantu levels. No heart disease. Bear in mind Lp(a) is notoriously variable from lab to lab. But still needs slotting in to Lp(a) and heart disease.