I might have to put updates up as I continue to gather information (emails out to vetting sources) but I thought I’d put this up as a starter, maybe generate some conversation.
I’ve posted a lot about cholesterol and how and why I don’t generally see it as a problem for most people on a good (paleo-like) diet. In other words, the diet is the problem causing the inflammation markers, small dense LDL, low HDL and high triglycerides (fat in the blood, caused by sugar, not dietary fat). So fix the diet. The problem, of course, is that the standard from-on-high dietary advice is precisely what’s behind those aforementioned problems. A Paleo diet doesn’t seem to work for everyone to get the sort of lipid numbers I enjoy, so that leaves the question open as to whether "bad" lipids are generally only a concern with a bad diet of processed foods, high sugar and omega-6 polly unsaturated fats. That’s where I’ve placed my bet.
But what about familial hypercholesterolemia? Does that not substantiate if not prove the lipid hypothesis? After all, even children and infants afflicted with this genetic disorder get heart disease. But is it the high LDL itself, or what it’s able to act upon? For an amazing education in all things cholesterol, take a listen to Jimmy Moore’s recent interview of Chris Masterjohn who specifically addressed this disorder and argues that it’s rather like having a ton more cars on the road (LDL) and the real problem is that because they’re on the road so much longer that it makes them far more susceptible to oxidative stress; and combined with chronic inflammation caused by a nutritionally deficient, low fat, high sugar, high omega-6 diet, that’s the real underlying cause of the plaque buildup. Give it a listen.
Added later: Think of the causal chain mixup like this when it’s claimed that LDL is causal. It’s like having a gunman shoot you through the heart and you die, and cause of death is that your heart can’t stop bullets. So, when the underlying cause is inflammation and oxidized small-LDL, the "cause" is claimed to be that your heart can’t withstand small-LDL, inflammation and oxidation.
Now comes the added complication. Via reader Dexter I got a link to an article about this very recent study today. Be warned: it’s not a light read, at least not for me.
Strongest evidence yet that Lp(a) causes heart disease
Oxford, UK – New genetic research has identified two relatively rare single nucleotide polymorphisms (SNPs) that explain just over a third of the variance in lipoprotein(a) (Lp[a]) levels in individuals of European descent. The work confirms unequivocally that Lp(a) is a causal factor for coronary disease, say Dr Robert Clarke (University of Oxford, UK) and colleagues in their paper in the December 24, 2009 issue of the New England Journal of Medicine.
"This is the most convincing evidence so far that this protein [Lp(a)] is directly part of the pathway that causes heart disease rather than a bystander. If we can target it through treatment, we might expect to lower the risk of disease," coauthor Dr Hugh Watkins (University of Oxford) told heartwire.
Well I’ve known for sometime that high Lipoprotein(a) — Lp(a) — is a strong risk factor for CHD (mine is 4 mg/dl with "standard range" <30, so presumably low risk on that score), but that’s based on association, not causation. But now they’re saying it’s unequivocally causal. OK, good, and I’ll get to how you can naturally lower your Lp(a) in a bit. But first, here’s what really struck out at me, making my head spin around and around a bit. From the article.
In a press release issued by the British Heart Foundation , which describes Lp(a) as a "third type of cholesterol," senior author of the new paper, Dr Martin Farrell (University of Oxford), tries to put the findings into perspective: "The increase in risk to people from high Lp(a) is significantly less than the risk from high LDL-cholesterol levels. So Lp(a) doesn’t trump LDL, which has a larger impact. The hope now is that by targeting both we could get an even better risk reduction."
Say what? Here’s what I’ll state unequivocally: high LDL is only associated with CHD and even that’s tenuous because I have many times (check the cholesterol links above) demonstrated that very low LDL is also associated with CHD (as well as increased all-cause mortality, particularly in the elderly and slam dunk in women). So let me get this straight: the risk from high Lp(a) that they are calling "unequivocally causal" is a significantly less risk than a mere association?
What say you, experts? I’m confused.
At any rate, and again not a light read by any means, but one blogger and good friend, Dr. BG really stands out in blogging about Lp(a) and other risk factors.
Cardio Controversies: Lp(a) Dangerous at ANY Value (link removed)
Can Lp(a) create more damage than we previously thought?
Dr. Hecht has apparently showed it with his examination of lipoprotein, cardiac and metabolic parameter comparisons with the real measure of heart disease risk: EBCT-determined plaque burden. Lp(a) was 3rd after HDL and LDL particle diameter in being highly associated with coronary calcifications. See below. Free PDF HERE. Normally at TrackYourPlaque we consider Lp(a) greater than 20 mg/dl as a high contributor toward accelerated plaque burden. When I look at Dr. Hecht’s graphs, what I notice is that indeed this may not be true.
It appears to my observations that at ANY Lp(a) value, plaque burden is quite high reaching even 97th, 98th or 99th calcium percentile for CAD risk (of population norms) at severely low Lp(a) levels of 5 mg/dl or 10 mg/dl.
OK…what the heck?
I can make the same observations for my CAD (heart), PVD (peripheral), or CVD (stroke) patients and individuals with extensive diabetic complications. At any Lp(a), the extent of disease can still be quite pronounced.
What other factors are correlated to vascular damage?
1. Low HDL2b
2. High small dense LDL.
These THREE factors determine almost entirely the extent of disease. Both visionaries Dr. Davis and Dr. Hecht focus on these predominantly to control and halt the progression of calcifications.
How are these 3 metabolic parameters created in the first place?
–low fat SAD AHA low cholesterol low saturated fat diet
–saturated fat deficiency
–excessive carbs (>10 g/d, >20 g/d, >50 g/d, >100 g/d — depending on a person’s insulin and insulin sensitivity and pancreas/adipose/hormone status)
–inflammation (excessive omega-6 oils)
But she has a lot of stuff on Lp(a), so here’s a search link (link removed) for those wanting to dig super deep. For those of us wanting to cut to the chase, how best to lower Lp(a) and keep it low? You know what I’m gonna say, dontcha? You guessed it: high saturated fat from natural sources, i.e., animals, butter, coconut oil. The Doctor again, from another post (link removed):
Lp(a) Reduced By Saturated Fatty Acids and Raised by Low-Sat-Fat Diets
Benefits of Krauss high-saturated fat diet cannot be overstated. Saturated fats control CETP and thus control the amount of Lp(a) individuals produce. In fact, when an experiment group was put on a low fat, high veggie diet, Lp(a) increased significantly by as much as 9% (Silaste ML et al Arterioscler Thromb Vasc Biol. 2004 Mar;24(3):498-503. Free Full Text)
Additionally, the low fat diet produced HIGHER oxidized LDL (OxLDL) by 27%. Recall the small dense LDL are less resistant to oxidation than buoyant large LDL and transform to OxLDL rapidly.
For. Plaque. Burden.
OxLDL causes fatty/calcified organs: arteries (atherosclerosis); endothelium (hypertension); liver (NASH); pancreas (diabetes, MetSyn); thyroid (Hashimoto’s), visceral fat (obesity); etc.
Saturated fat lowers and controls Lp(a) and coconut oil is one great example (Muller H et al . J Nutr. 2003 Nov;133(11):3422-7. Free PDF HERE). In this study by Muller et al women with elevated Lp(a) in the 30s mg/dl were provided a coconut oil-rich diet (22.7% sat fat; 3.9% PUFA) was compared with a high PUFA-diet (15.6% PUFA !!yikes). Lp(a) was reduced 5.1% compared to baseline habitual diets with the high saturated fat diet whereas in the high PUFA diet, Lp(a) increased a whooping 7.5%. The difference between Lp(a) on the high sat fat compared to the high PUFA diet was 13.3%.
Here are the conclusions from those two study links above, respectively.
The question remains as to why the Lp(a) levels increased in response to the dietary changes. The basal levels of Lp(a) are primarily genetically determined, but some data suggest that Lp(a) may act as an acute-phase reactant under some situations.40 In a previous study, a diet high in SAFA was found to produce approximately 10% lower plasma Lp(a) concentration than diets high in oleic acid or trans-fatty acids.41 This observation is consistent with our study in that both diets led to lower SAFA and consequently increased Lp(a).
In conclusion, we found that a diet traditionally considered to be anti-atherogenic (low in saturated fat and high in polyunsaturated fat and naturally occurring antioxidants) increased plasma levels of circulating oxidized LDL and Lp(a). The question of whether the changes observed in the present study are, in fact, pro-atherogenic or anti-atherogenic remains to be solved.
The connection between Lp(a) and atherosclerosis is not entirely understood. Different studies have provided strong evidence that Lp(a) level is an independent risk factor for developing coronary artery disease in men (47,48), but the question of causality continues to be debated. Recent data suggest that Lp(a) might be atherogenic (49), in particular when combined with other risk factors. High levels of Lp(a) combined with other risk factors such as the ratio of plasma total/HDL cholesterol have been shown to increase the risk for coronary heart diseases (50). It has also been reported that when substantial LDL cholesterol reductions were obtained in men with coronary heart disease, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening (51).
In conclusion, the present results show that the HSAFA- diet lowered postprandial t-PA antigen and thus potentially improved fibrinolysis compared with the HUFA-diet. Diets with either high or low levels of saturated fatty acids from coconut oil beneficially decrease Lp(a) compared with a HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy may be of importance if the goal is to decrease Lp(a).
Alright, so for us KISS folks, it all just comes down once again to a natural, Paleo-like diet plenty high in delicious and healthful saturated fats.