Tag: Lpa

  • Eating to Lower Lp(a) 

    Eating to Lower Lp(a) 

    What should we eat—and not eat—to lower the cardiovascular disease risk factor lipoprotein(a)?

    Lipoprotein A, also known as Lp(a), is an independent, genetic, and causal factor for cardiovascular disease and heart attacks. At any level of LDL cholesterol, our risk of heart attack and stroke is two- to three-fold higher when our Lp(a) is elevated. With a high enough Lp(a) level, atherosclerosis continues to progress even if we get our LDL cholesterol way down, which may help explain why so many people continue to have heart attacks and strokes even under treatment for high cholesterol. It’s been suggested that “it would be worthwhile to check Lp(a) levels in a patient who has suffered an event but has no traditional risk factors to explain it.” What’s the point of checking it, though, if there isn’t much we can do about it? “To date, no drug to reduce circulating Lp(a) levels has been approved for clinical use.”

    Some researchers blame our lack of knowledge on the fact that Lp(a) is not found in typical lab animals, like rats and mice. It’s only found in two places in nature: primates and hedgehogs. Hedgehogs? How strange is that? No wonder Lp(a) is “an enigmatic protein that has mystified medical scientists ever since” it was first discovered more than half a century ago. But who needs mice when you have men? The level in our bloodstream is “primarily determined” by genetics. For the longest time, Lp(a) was not thought to be significantly influenced by factors such as diet. Given its similarity to LDL, though, one might assume lifestyle changes, “such as increased physical activity or the adoption of a healthy diet,” would help. “However, the effects of these interventions on Lp(a) concentrations are so far either only marginal or lacking in evidence,” but might that be because they have not tried a plant-based diet yet?

    As I discuss in my video How to Lower Lp(a) with Diet, when it comes to raising LDL cholesterol, we’ve known for years that the trans fats found in meat and dairy are just as bad as the industrially produced trans fats found in partially hydrogenated oil and junk food. But, when it comes to Lp(a), as you can see below and at 2:05 in my video, trans fats from meat and dairy appear to be even worse. 

    Just cutting out meat and following a lacto-ovo vegetarian diet did not appear to help, but, as you can see below and at 2:19 in my video, when study participants were put on a whole food, plant-based diet packed with a dozen servings of fruits and vegetables a day, their Lp(a) levels dropped by 16 percent within four weeks. 

    Of course, in those 30 days, the study subjects also lost about 15 pounds, as you can see below and at 2:28, but weight loss does not appear to affect Lp(a) levels, so you figure that it must have been due to the diet. 

    If you’re already eating a healthy plant-based diet and your Lp(a) levels are still too high, are there any particular foods that can help? As with cholesterol, even if the average total cholesterol of those eating strictly plant-based may be right on target at less than 150, with an LDL under 70, there’s a bell curve with plus or minus 30 points that fall on either side, as you can see below and at 2:45 in my video

    Enter the “Portfolio Diet,” which is not only plant-based, but also adds specific cholesterol-lowing foods—so, think nuts, beans, oatmeal, and berries to drag cholesterol down even further. The infographic is below and at 3:11 in my video.  

    What about Lp(a)? Nuts have been put to the test. Two and a half ounces of almonds every day dropped levels, but only by about 8 percent. That is better than another nut study, though, that found no effect at all, as you can see below and at 3:29 in my video. An additional study found “no significant changes,” and researchers reported that subjects in their study “did not experience a change in Lp(a).” Ah, nuts.  

    There is one plant that appears to drop Lp(a) levels by 20 percent, which is enough to take people exceeding the U.S. cut-off down to a more optimum level. And that plant is a fruit: Emblica officinalis, otherwise known as amla or Indian gooseberry. A randomized, double-blind, placebo-controlled study asked smokers before and after the trial about their “mouth hygiene, cough with expectoration, shortness of breath on exertion, loss of appetite, feelings of impending doom, palpitation, sleep deprivation, irritability, heartburn and tiredness,” as well as such objective measurements as their blood count, cholesterol, DNA damage, antioxidant status, and lung function. The amla extract used “showed a significant improvement compared to the placebo group in all the subjective and objective parameters tested with no reports of adverse events.” No side effects at all. That’s unbelievable! No, that’s unbelievable. And indeed, it’s completely not true.  

    Yes, subjective complaints got better in the amla group, but they got better in the placebo group, too, with arbitrary scoring systems and no statistical analysis whatsoever. And, of the two dozen objective measures, only half could be said to reach any kind of before-and-after statistical significance and only three were significant enough to account for the fact that if you measure two dozen things, a few might pop up as positive if only by chance. Any time you see this kind of spin in the abstract, which is sometimes the only part of a study people read, you should suspect some kind of conflict of interest. However, no conflicts of interest were declared by the researchers, but that’s bullsh*t, as the study was funded by the very company selling those amla supplements! Sigh.

    Anyway, one of those three significant findings was the Lp(a), so it might be worth a try in the context of a plant-based diet, which, in addition to helping with weight loss, can dramatically improve blood pressure (even after cutting down on blood pressure medications) and contribute to a 25-point drop in LDL cholesterol. Also, it may contribute to a 30 percent drop in C-reactive protein and significant reductions in other inflammatory markers for “a systemic, cardio-protective effect”—all thanks to this single dietary approach.

    You may be interested in my video on Trans Fat in Meat and Dairy. Did you know that animal products are exempted from the ban? See Banning Trans Fat in Processed Foods but Not Animal Fat.

    For more on amla and what else it can do, check out the related posts below.

    If you missed my previous video on Lp(a), watch Treating High Lp(a)—A Risk Factor for Atherosclerosis



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  • How to Treat High Lp(a), an Atherosclerosis Risk Factor 

    How to Treat High Lp(a), an Atherosclerosis Risk Factor 

    What could help explain severe coronary disease in someone with a healthy lifestyle who is considered to be at low cardiovascular disease risk? A young man ended up in the ER after a heart attack and was ultimately found to have severe coronary artery disease. Given his age, blood pressure, and cholesterol, his ten-year risk of a heart attack should have only been about 2 percent, but he had a high lipoprotein(a), also known as Lp(a). In fact, it was markedly high at 80 mg/dL, which may help explain it. You can see the same in women: a 27-year-old with a heart attack with a high Lp(a). What is Lp(a), and what can we do about it? 

    As I discuss in my video Treating High Lp(a): A Risk Factor for Atherosclerosis, Lp(a) is an “underestimated cardiovascular risk factor.” It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur in people who don’t even have high cholesterol—because Lp(a) is cholesterol, as you can see below and at 1:15 in my video. It’s an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But “this increased risk caused by Lp(a) has not yet gained recognition by practicing physicians.” 

    “The main reason for the limited clinical use of Lp(a) is the lack of effective and specific therapies to lower Lp(a) plasma levels.” Because “Lp(a) concentrations are approximately 90% genetically determined,” the conventional thinking has been you’re just kind of born with higher or lower levels and there isn’t much you can do about it. Even if that were the case, though, you might still want to know about it. If it were high, for instance, that would be all the more reason to make sure all the other risk factors that you do have more control over are as good as possible. It may help you quit smoking, for example, and motivate you to do everything you can to lower your LDL cholesterol as much as possible.  

    Lp(a) levels in the blood can vary a thousand-fold between individuals, “from less than 0.1 mg/dL to as high as 387 mg/dL.” You can see a graph of the odds of heart disease at different levels in the graph below and at 2:20 in my video. Less than 20 mg/dL is probably optimal, with greater than 30 to 50 mg/dL considered to be elevated. Even when the more conservative threshold of greater than 50 mg/dL is used, that describes about 10 to 30 percent of the global population, an estimated 1.4 billion people. So, if we’re in the one in five people with elevated levels, what can we do about it? 

    The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There is something called apheresis, which is essentially like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and give your blood back to you. And when you do that, you can reverse the progression of the disease. As you can see in the graph below and at 3:06 in my video, atherosclerosis continues to get worse in the control group, but it gets better in the apheresis group. This is great for proving the role of Lp(a), but it has limited clinical application, given the “cost, limited access to centers, and the time commitment required for biweekly sessions of 2 to 4 h each.” 

    It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, as you can see in the graph below and at 3:26 in my video, costing more than $50,000 a year. 

    There has to be a better way. We’ll explore the role diet can play, next.  

    I’ve been wanting to do videos about Lp(a), but there just wasn’t much we could do about it until now. So, how do we lower Lp(a) with diet? Stay tuned for the exciting conclusion in my next video.

    What can we do to minimize heart disease risk? My video How Not to Die from Heart Disease is a good starting point. 



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