For those who received a recent high Lp(a) test result: My recent Lp(a) is 355 ml/L, but I Iearned I had a 17 mg/L (high) Lp(a) 11 years ago, as a follow up to a very high (96th percentile) heart scan. I was very fit, exercised regularly, ate a decent diet and had no symptoms, so both results were very surprising. I was already taking a statin and my cholesterol levels were very good, and remain so. I’ve seen very good doctors, I tried niacin and full aspirin for a few years, and all these years improved my diet, kept a good exercise routine, stayed fit and played sports. I currently take a low dose statin, 81 mg aspirin, eat well and exercise 5-6 times a week. I’m fit and I feel fine. It’ll be nice when we have a safe and effective therapy for this, but in the meantime, life goes on.
4
@E I meant Nmol/L not Mg/L
i was cure of coronary artery disease (CAD) with the use of natural herbs.My name is Wilson from Zurich i was diagnosed with CAD (coronary artery disease in June of 2017.I was told i have only six months to live,i only believe the doctor for some time,then i took a bold step and I embarked on a journey when i saw a post by Charles and how he was cured by herbs by Dr Okpoko,so I contacted him and that was where i receive my healing.dr.Okpoko herbalist herbs cause a turning point in my life.since I have been on these African herbs drugs, i have been doing perfectly,no more heart disease all thanks to Dr Okpoko the great herbalist.if you are out there with the same disease or similar disease why not give him a try now on his email [email protected] or call +2348151731392
1
WOW...I just spent a lot of time reading everyone's posts. I'm a heterozygote, I have a Lp(a) of 506 nmol/l! Crazy, I know. My recent calcification score was zero and I'm 53. Needless to say, I'm having several cardiac tests done next week to determine if there's any plaque build up thus far. I have no symptoms.
My doctor recently placed me on 500mg of Niacin, 2,000 mg of L-Carnitine and 2,000mg of Aronia. If there's any buildup present then I will be given the injections. There is HD I my family, the only good news is that no one has died before the age of 70! Wish me luck!
6
The article states that "Studies show that diet and exercise have almost no impact on lp(a).” However, to what kind of diet does the article refer?
Recent research indicates that diet might in fact decrease Lp(a) levels — but it must be a plant based diet.
A recent research trial (2017) stated "A plant-based diet has not been previously used in an attempt to influence the concentration of Lp(a).” (https://clinicaltrials.gov/ct2/show/NCT03172611)
And initial results concluded:
— A defined, plant-based diet has a favorable impact on Lp(a) and other atherogenic lipoproteins and particles. Lp(a) concentration was previously thought to be only minimally altered by interventions. In this protocol however, a defined plant-based diet was shown to have a significant impact on this biomarker. Further investigations are required to elucidate the specific mechanisms that contribute to the reductions in Lp(a) concentrations, which may include alterations in gene expression. —
(from an abstract of a presentation of research results at a conference in Nov 2017: Abstract 15119: Consumption of a Defined Plant Based Diet Reduces Lp(a) and Other Atherogenic Lipoproteins and Particles in Four Weeks; http://circ.ahajournals.org/content/136/Suppl_1/A15119)
2
@Dr. J:
Any diet that reduces sugars, refined starches, and other highly processed foods will improve lipid profiles and CVD risk factors.
Veganism is a religious ideology.
9
Citizens of Ethanolia drink 3 shots of whisky with every meal starting at age 13. They do "everything in moderation" balancing out the alcohol out with other foods. They also work out a lot.
Despite Ethanolians' balanced diet and exercise culture, the nation still spends a huge chunk of its national budget on treating liver cirrhosis and liver cancer. Ethanolian scientists are still trying to figure out why some Ethanolians get cirrhosis and liver cancer, while others don't. They have identified some genes that seem to explain the difference and a race is on to be the first to develop a treatment that targets those genes. Billions of dollars and the nation’s health is at stake!
An Ethanolian friend of mine is concerned because tests from his doctor showed that he has high levels of factors that predispose him to cirrhosis, unsurprising as both his parents, and a sibling already have cirrhosis. I guess he lost the genetic lotto.
I really hope those scientists come through for my friend.
4
Really? "Ethanolia"?
Why waste everyone's time if you have nothing of value to contribute?
5
Bravo, Chu!
Please please read the work Matthias Rath and two times Nobel Price winner Linus Pauling have done about cardiovascular disease and the rol of ascorbic acid (vitamin C).
They have scientificaly demostrated that Lp(a) is a repair molecule compensating for the structural deterioration of the vascular wall due to chronic deficiency of vitamin C.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447075/
https://www.youtube.com/watch?v=O0lEmXJD7p4&index=40&list=FLBx7L...
I cannot emphasise enough the value of their work.
11
@Tom Thanks so much Tom. This is not a rare condition. I have very high levels of Lpa. It is present in 20% of the population as you are aware.
The drug companies are less than honest about heart disease. They are making a huge fortune from Statins.
https://www.pharmaceutical-journal.com/opinion/insight/the-cholesterol-a...
Keep with Pauling. He won two Nobel prizes. That is rare.
He remains the only person to have won two unshared Nobel Prizes, the first for Chemistry (1954) and the second for peace (1962). In addition to being one of the greatest scientists ever, he was a renowned humanitarian.
https://www.medicalnewstoday.com/releases/12154.php
1
Very important to include emphasizing the following fundamental point:
Individuals who develop coronary heart disease in the setting of elevated Lp(a) levels benefit greatly from the pillars of prevention of recurrent events:
1. consistent moderate cardiovascular and strength exercise
2. a diet very low in sugars and starches while high in fresh fruits and vegetables and healthy fat and protein sources like fish, lentils, nuts, olive oil, etc., and restricting carbohydrates to limited amounts of whole grains
3. statin therapy. I have patients who have been mislead on this: If you have CAD, while we search for a better risk-reducing directed therapy at high Lp(a), statins significantly reduce risk.
3
Carbs, carbs, carbs. Just too many carbs.
7
Bob Harper also works and lives in a high stress part of society.
There are "good carbs"- (whole plant, minimally processed foods - like beans, whole grains, brown rice, lentils) - which are high in fiber, absorbed slowly by body, and do not cause abnormal metabolic syndrome.
Versus - "bad carbs" (processed foods - like sugar, high fructose corn syrup, sweetened sodas, white flour, many processed and bakery goods) -
which are low in fiber, absorbed quickly, cause spikes in blood sugar, and are associated with abnormal metabolic syndrome
1
@Carol:
Try a glucose meter, you might be surprised at the glucose spikes from those supposedly healthful whole grains.
4
I also have a high level of lp(a) (112mg/dl), as well as a high LDL particle number (without a statin it was 1700). Both are risk factors that increase risk of CVD events. I am 64, run and walk for exercise, have a healthy weight and a diet that is plant based, not vegetarian, and partly Mediterranean (heavy on olive oil and nuts for fat), and am on the lowest level of Pravastatin. . 8 year ago I had a heart CAT scan and had a calcium score of zero. None of the levels of lipids have been rechecked, except for LDL and once LDL particle number, and my doctor will only order the regular LDL /HDL / TG lipid panel, because of the new recommendations for screening for CVD. Should I insist on retesting lp(a) and LDL particle number even if I have to pay out of pocket? Thanks!!!
Absolutely get retested. Demand it, or pay for it out of pocket because you want to know. Don't let insurances dictate your wellness. Guidelines are designed for the masses, not individuals, and to have excellent care sometimes takes being outside the box. Lp(a) is not part of standard of care, yet it affects up to 30% of the population. Why wouldn't we treat it when present? Why do we wait in this country until something happens before even looking for it?
You might also wish to repeat your calcium scoring heart scan, and if it again is zero, look at your neck arteries. Any plaque anywhere means you have risk, as any plaque is dangerous. Also remember, it doesn't take much to affect the little tiny arterioles which feed the brain, eyes, kidneys, etc, and lead to other vascular based diseases such as dementia, chronic kidney disease, erectile dysfunction, etc. As you may know, we can do everything very well, yet genetics has a funny way of sneaking up on us if we are not on the lookout. Best wishes.
8
A diet high in any oil, including everyone's favorite olive oil, destroys the endothelium, which is the gateway (leads) to atherosclerotic heart disease. This is true despite improving lipid profiles.
In the words of Caldwell Esselstyn, "NO OIL!"
2
"...coronary heart disease..."
Is there such a thing as non-coronary heart disease?
Yes. Coronary refers to the blood vessels supplying the heart. You could have (e.g.) cardiomyopathy (a problem with the heart muscle itself), or valvular disease of some sort (e.g., aortic stenosis, narrowing of the aortic valve), conduction disorders (e.g., atrial fibrillation), and so on.
8
Lowered my Lp(a) from 31 to 18 by increasing my Vitamin C intake. When I had a couple of months off the Vit C it went back to 30 plus before dropping again when readministering the Vit C. I would therefore suggest full flush Niacin and daily Vit C. You can take a supp but also increase via the diet, for example I eat a daily Grapefruit for breakfast along with Kiwi on my porridge. Remember heart disease is a food born illness in most cases.
10
Not all doctors are ignorant or acting like they know it all. Being humble and knowing when to admit that we do not have all the answers is essential to a good practice of medicine. After all, just as Hippocrates advised, "it is more important to know which patient has a disease then to know which disease a patient has". Lp(a) is one of many markers that points to interaction of genetics with the environment, and probably has an epigenetic link as well. I found in my integrative cardiac practice that patients who follow an elimination diet with increased proportion of healthy fats and receive anti-oxidant supplementation are able to reduce Lp(a) and other markers such as hsCRP substantially. Will be trying high doses of vitamin C next to see if the reduction can be improved further.
5
Lp(a) can be SIGNIFICANTLY lowered with the right brand of niacin...a supplement which is very inexpensive but not regulated of course, so you never know what you're getting. The brand that does the job is Rugby, available only from Amazon as far as I know. My savvy and brilliant cardiologist closely recorded his patients' results with various brands to discover this.
My lp(a) level was 1st checked in 2001, after my brother died of a sudden heart attack at 46. The measure was 125 and my former cardiologist immediately started me on niacin (and Lipitor) with very minimal improvement on the lp(a).
Seventeen years later my new cardiologist put me on 1,000mg of Rugby and my lp(a) was reduced to 40. And it costs me app $7/month.
13
@Hungrybrain
can you share the name of your cardiologist, please?
2
But up to one in five Americans, including Mr. Harper, have perilously high levels of it in their blood. One in five HAS
5
The number of Americans referred to, "one in five," is millions of people, hence the use of "have" instead of "has." On the other hand, if you were talking about one person out of five people tested, then "has" would be correct.
9
I think I see what you're saying, which I assume is that the word "millions" is implied, but I believe Rick Mieller is correct.
"One has." You never say "One have." The "five" from "in five" does not determine the noun-verb agreement; the "one" does.
If it read "one million in five million" (or "one thousand in five thousand") then sure, you would say "one million in five million have. . ." But what is meant is: take five people, and odds are that one has high Lp(a).
3
How sad to read that the doctors know little about the lipoprotein (a). But more sorrow I suffer from seeing that a outstanding newspaper, like NYTimes. ignores that ATP Constitution-Dependent, Inherite Real Risk of CAD is the conditio sine qua non of heart disease: Sergio Stagnaro and Simone Caramel (2013). The Inherited Real Risk of Coronary Artery Disease, Nature PG., EJCN, European Journal Clinical Nutrition, Nature PG., [MEDLINE]
3
Careful of the wording in this article. Statins, excercise and diet don’t strongly affect lpa levels, but they still decrease your risk of having a heart attack or stroke, while increasing your chances of a good outcome if you do have one. Keep your arteries clear of the other junk that clogs them up and plaques caused by lp(a) alone will grow much slower. Stay healthy and fit, because it will make it easier to survive and compensate for the damage.
Nobody outruns the reaper forever. But if you were dealt a bad hand by genetics you might be able to run a little longer if you make the right choices.
15
lp (a) isn't a risk factor. It's the bodies method to do temporary repair of damaged arteries. Those temporary patches are supposed to be replaced when enough vitamin C is available to make collagen. Certain primates developed the ability to produce lp (a) in order to facilitate these repairs. How did it come about? As we move further from regular sources of vitamin C those that survived had to adapt until vitamin C was available. That's how lp (a) was so to speak born. This factor does not exist in any creature that produces it's own vitamin C. It only exists in those that do not. There is a theory that these artery buildups occur from what amounts to subclinical scurvy. Our ancestor especially in colder climates didn't have access to fresh fruits and vegetables during cold winters or out in the Savannah. This adaptation allow us to survive. Unfortunately in today's fast food world many aren't getting enough vitamin C, E, D, and A to keep us healthy.
12
Sufficient vitamin C would certainly be an easy fix. Do you have literature to support your premise?
1
The use of ascorbic acid to bowel tolerance, often tens of grams, and 3-6 grams of l-lysine and 1-2 grams of l-proline are the recommendation of Matthias Rath, Linus Pauling, and collaborators to reduce cardiovascular disease. Pauling's hypothesis for the mechanism was the removal of lp(a) from the arterial wall (Rath and Pauling, Proc Natl Acad Sci U S A. 1990 Aug; 87(16): 6204–6207). There seem to be no corroborating studies of these specific amounts, though a quick search of PubMed produces some weakly supporting literature. Two examples are an anecdotal report (Dalessandri, Arch Intern Med. 2001 Mar 12;161(5):772-3) and a murine model showing an increase in lp(a) with vitamin C deficiency (J. Cha, et al., Am J Cardiovasc Dis. 2015; 5(1): 53–62). Several articles reference a modest reduction in lp(a) from the use of ascorbic acid and l-lysine but give no details.
2
There are recent research that suggest cholesterol is not the primary factor in arterial plaque, but rather inflammation caused by blood sugar and correlated insulin spikes. In light of this assumption, if true, LDL levels are probably less a risk factor than blood sugar levels, and therefore dietary intake of sugars and other simple carbohydrates. As overlooked as it has been, lipoprotein(a) may just be just one more "actual culprit" to the heart disease and treatment puzzle. These findings triangulate to some rather scandalous implications on the medical, pharmacological and health science community.
16
Two of my grandparents, one from each side of the family, died by age 42 of heart attacks, but that was 78 and 100 years ago, so I'm not sure what it means for me today at age 70, with high LDL, high HDL and no sign of heart disease.
I always questioned whether the methods of "The Biggest Loser" made sense in the long run, since they were extreme. Yes, people lost weight, but did they keep it off?
I'm glad Mr. Harper survived his heart attack and wish him and the people he worked with on tv long and happy lives.
5
Don't kid yourself. Over half the time, the first symptom of heart disease is death. That includes people who have passed stress tests with flying colors.
1
I agree with Kristin about the effects of diet on different LDL levels and cholesterol levels in general. Why was this not mentioned in the article? I posted a link to one reference about the effects of eggs in response; there are more references listed here: https://nutritionfacts.org/?fwp_search=ldl&fwp_content_type=video Nutrition facts is a non-profit the reviews scientific articles published in peer reviewed journals and presents the information in easily understood videos. (There are also transcripts of the videos, and links to the articles cited.)
I eat a whole foods plant based diet (whole foods = unprocessed, and plant based = no animal products). The food is good, and it's effects on my health and the health of the planet are also good. (Not to mention the effects on the animals raised by the meat industry, antibiotic resistance, etc)
6
Thanks for your comments, Kristin and Dr. J! So true! When I read the article's headline I was impressed that a big American newspaper would finally write about the truth of heart diseases and health considering a whole foods plant based diet. I also realized after educating myself through scientific books and documentaries that animal protein and processed food have been bringing more harm to our health and our planet than anything else. Wake up, guys! Parents and grandparents have been dying through heart attacks because they 'educated' their kids the same wrong and unhealthy diet. Makes sense. Lp(a) might be genetic, but I guess that is definitely not the true reason for family disease patterns. Instead of getting to know more about lp(a) get out their and eat the right diet!!
1
The website you mentioned, nutrititionfacts.org, is a very biased website promoted by a vegan doctor with an agenda, named Michael Greger. Perhaps you missed the part of the article that says very clearly that (unlike with LDL) diet has a very MINIMAL impact on lp(a) levels. In fact the research is very clear that low-fat diets such as a low-fat vegan diet actually make lp(a) levels slightly WORSE, and high fat diets with animal and vegetable fats actually make lp(a) levels slightly BETTER. You can go to the Lipoprotein(a) Foundation website and see for yourself. Please don't spread misinformation.
Reference: http://www.lipoproteinafoundation.org/page/DietExerciseandLpa
13
JJ,
You might be biased as well if you were a doctor that was able to prevent and reverse heart disease with minimal medications by recommending and advocating for a certain diet like Dr. Greger has a proven record of doing.
Bias isn't inherently bad, we just need to think about why there is a bias and who benefits. In this case, the "why" is to prevent/cure chronic health conditions and the "who" is the people who follow the diet. There is no "big veggie" like there is a "big pharma" (unless I'm mistaken).
As to your data from the Lipoprotein(a) foundation, correct me if I'm wrong but is there data from actual outcomes (i.e. rate of heart attack or heart disease) from people following a low-fat and whole foods plant based diet with those who have elevated lp(a) because that would seem to be the only thing that might be relevant to the discussion.
Cheers!
Philip
Nobody is talking about his diet, also the whole article also doesn't mention it. He always had a "balanced diet" but what does that mean? You can see here that he had 2-3 eggs per day plus 4 egg whites... not to mention lots of animal protein. 19284_bob_harper_24_hour_diet
And now he is promoting a diet book and a new drug is mentioned? I strongly recommend to watch one of the many documentaries like "What the Health" or "Forks over Knives" on Netflix. It is all about eating healthy.
10
Thank you, Kristin! "eggs increase LDL, but it’s large LDL, this concept that large fluffy LDL are not as bad as small dense LDL. And indeed large LDL only raises heart disease risk 44%, instead of 63% for the small LDL. Light large buoyant LDL still significantly increases our risk of dying from our #1 killer. This was for women, the same was found for men. Large LDL only increases risk of heart attack or death 31% instead of 44%." And "Consumption of eggs increases the susceptibility of LDL cholesterol to oxidation. They found that not only does eating eggs raise LDL levels, but also increases LDL oxidizability, in addition to the oxidizability of your entire bloodstream." https://nutritionfacts.org/video/does-cholesterol-size-matter/
2
This is the correct link where Bob Harper describes his pre-attack diet. https://www.rachaelrayshow.com/lifestyle/health/19284_bob_harper_24_hour...
1
The website you mentioned, nutrititionfacts.org, is a very biased website promoted by a vegan doctor with an agenda, named Michael Greger. Perhaps you missed the part of the article that says very clearly that (unlike with LDL) diet has a very MINIMAL impact on lp(a) levels. In fact the research is very clear that low-fat diets such as a low-fat vegan diet actually make lp(a) levels slightly WORSE, and high fat diets with animal and vegetable fats actually make lp(a) levels slightly BETTER (that includes eggs). You can go to the Lipoprotein(a) Foundation website and see for yourself. Please don't spread misinformation.
Reference: http://www.lipoproteinafoundation.org/page/DietExerciseandLpa
The documentary movie What the Health has been debunked because it contains a lot of misinformation. As a very thorough article in Vox concluded, What the Health "mischaracterizes what we know about food and disease." Read the Vox article for yourself right here:
https://www.vox.com/science-and-health/2017/7/25/16018658/what-the-healt...
10
I'm confused. Is lp(a) the real risk factor...not "bad" cholesterol or is lp(a) a separate independent risk factor?
separate risk factor, though some people can have both elevated bad colesterol (LDL) and Lp(a), and some it's just Lp(a).
2
The cause was lipoprotein a? Oh, c'mon there is a cause for high levels of lipoprotein a,and eli genetics should have taught us by now that we cannot hide behind the excuse that ythe cause is just genetic! The oxygen biochemistry switches genes on and off. This guy was doing intensive work outs which generate a lot of free radical stress, and apparently did not have the antioxidant network to quench that stress properly. We knowfrommuch research that oxidation is the culprit at the molecular level. It is almost a mathematical equation. Tip the balance on oxygen homeostasis in various ways, and cardiovascular disease will result. The big picture is more instructive, than the focus on lipoprotein a and more expensive drugs. Nobody can develop a drug that will keep the body in oxygen homeostasis, that requires, as Dr. Majid Ali says,"Thinking like a gardener,not like mechanic."
11
This is nonsense unless you can prove that Lp(a) can be altered by taking antioxidants. Can you?
4
Heart to Heart: care for your heart naturally (book/eBook) helps prevent/treat heart disease and guides patients and caregivers who are rarely prepared for the stress, pain, guilt and frustrations involved with heart disease. The two authors, a heart patient and a natural health expert, wrote the book based on years of research, and loving care. Stress is a major issue. Michael got an "A" on his heart tests in February and had a major heart attack in May after losing money in the stock market. Be prepared for stress and avoid drug side-effects, including a 46% risk of diabetes with statin drugs. (https://www.amazon.com/Heart-heart-naturally-Karma-Unlimited/dp/19735273...
3
This is a great article, and I appreciate all the comments. One treatment that I think should be considered in individual cases for this condition is high dose statin therapy, to the maximum tolerable level. Although most people think of statins as a treatment to lower cholesterol, this class of drugs also has another very important property - they dramatically decrease inflammation in arteries. This effect is in addition to their lipid lowering properties, and can be monitored by testing the C-reactive protein blood test. The precipitating event in an acute heart attack is the rupture of an inflamed atheromatous coronary artery plaque. Statin drugs are great at helping to prevent this outcome.
My own family situation is illustrative. On my fathers side of the family, multiple family members had early heart attacks, and my father himself underwent coronary artery bypass surgery on two occasions. I have always had normal lipid panel studies, but when I serendipitously discovered over 50% stenosis of my left main coronary artery, my Lp(a) level was tested and found to be 10 times normal. There are no large clinical trials that support this approach, but I am doing a lot better than previous generations of my family, by using this approach.
37
Aren't you worried about the side effects of statin therapy? They can be brutal. Glad it works for you though.
1
Is this protein a cause of anything or simply a marker of people at risk? Is this possibly true with LDL also and the cholesterol lowering drugs also have other effects that are improving longevity while also lowering cholesterol?
2
My Lp(a) is 390 mg/dl, a number higher than the highest mentioned in this article. I have two copies of a mutant allele that raises Lp(a) - a variant of rs10455872 found in less than 10% of the population (less than 1 in 400 people have two copies). At 42, I was diagnosed with calcific aortic valve stenosis. It was an uphill battle to get a coronary CT scan, which two docs told me was "unnecessary" at my age and which revealed an Agatston score of 156 -- in the worst 1% for a man my age. And THEN it was an uphill battle to get my Lp(a) checked, which two docs told me "would not change my treatment". Well I figured out that it was the root of my problems, and that ALL of my kids have high Lp(a) because they can only inherit the bad allele from me because I have two copies of it.
I am INCENSED at the docs who assert that we are better off not knowing about this. Would they hide the fact that a diabetic patient is diabetic? If I had known I was born with this defect, I would have made some very different life choices. How DARE they decide for us to keep us in ignorance! This is criminal negligence!
79
Your story is THE pertinent one here. My husband will now follow up with his cardiology team. He had a large coronary blockage event at age 69, 4 months after his 6th Boston Marathon in 2013, while training for his Sacramento Marathon, and thought he had “the flu” 2 weeks before the race. He had never before had any signs of heart disease. Normal cardiology treadmill testing. Normal lipids. Ideal diet over a very long period. Lean and fit. Weight about 145 lb.
He went to bed for 5 days and recovered, going for his yearly check up 2 weeks later. 100% major vessel blockage found. Cardiac cath lab tried, but could not unblock the vessel. But he had created collateral circulation by then, enough to give his ejection fraction level an adequate function.
That was 11/2013. His lipid levels remained “fine”. On a statin, aspirin, etc. plus “new lifestyle” of no races, less running limited to 1 hr. daily. But, 6/2017, he had a stroke of 4cm affecting speech. No TPA was warranted. Now on more-significant meds.
Now, should he consult for lipoprotein(a) level? He will follow up on this. We have been runners for 45 years. My “story”, colon cancer.
have been
2
They will keep us in ignorance until they have a money-making drug to sell us. That is how this whole thing works.
3
I have used Niacin in my practice for over a decade. It lowers lipoprotein(a) by as much as 30% depending on phenotype. It works synergistically with statins, improving LDL reduction by 30%. It's metabolic effects are temporary. The flushing effects are controlled by increasing dosage from a low level.
Lowering of lipoprotein(a) level under niacin treatment is dependent on apolipoprotein(a) phenotype; Slim Study; HATS trial and followup; Dr. Katz correspondence.
20
Thank you Dr Katz. My cardiologist anecdotally discovered that the best results for lowering lp(a) came from Rugby brand niacin, and my personal testing bore this out...1,000mg/day lowered mine from 125 to 40. Just FYI.
"When he woke up, he was as baffled by it as his doctors..."
Glad that Bob Harper was saved by someone nearby --we all need to be trained in CPR/defibrillator use-- and the responding paramedics! Modern medicine is miraculous, though obviously in this case, does not have all the answers. Mr.Harper was always the one on "The Biggest Loser" show who used kindness and rapport to motivate his team members rather than the bullying and screaming tactics the other coach employed.
Information is power, not just about lipoprotein(a) but about quality of life. There are no guarantees, even if you 'follow all the rules'. Take good care of the inner you, too.
Yesterday is history, tomorrow's a mystery, today is a gift- that's why they call it the present.
7
Actually there IS something that can be done to treat high Lp(a) - apheresis treatments. In a process similar to donating blood platelets, the excess Lp(a) is "spun out" of the bloodstream every couple of weeks. Studies coming out of Germany, where apheresis is given to people with high Lp(a), show a lowering of the rate of heart events by 85% in people with high Lp(a) who undergo apheresis treatments to bring it down. But here in the USA, we don't even talk about apheresis, because it would cost the insurance companies too much to pay for. Here, we believe in the Power of Prayer.
53
No, the medical community believes in the power of the pharmaceutical industry. Still have heart trouble? More statins! It's like fixing a leak in a swimming pool by lowering the water below the leak. Why does the cholesterol stick to certain spot? Why isn't there plaque in the veins? The bottom line is inflammation. It has to be controlled. It is a factor in nearly every disease. We eat sugar by the barrel and it is probably the worst pro-inflammatory item entering our bodies. Then there is the garbage called margarine. Trans-fat, oxidized fat garbage. Why do doctors think that leaving our natural fats like butter and lard for the oxidized junk sold in stores and promoted by the huge soy and corn lobbies is better for us? Vegetable oils are always oxidized and become more so with even slight heat. They are damaging the arteries. Don't eat them! Statins lower co-enzyme Q10 which is a very important antioxidant. Heart trouble was rare until Ancel Keys came along.
11
I'm glad you mentioned apheresis! I am a LDL apheresis nurse who treats patients with elevated Lp(a) as well as LDL. All the patients we treat with elevated Lp(a) came to us after having a cardiac event and/or surgery, and were not aware they had it before that! I hope with more articles like this awareness grows. It is genetic, our patients are all different ages, weights and activity levels. We treat many with French-Canadian decent. Since there is no med to effectively lower Lp(a), this treatment gives them hope until then.
12
Nailed it!
1
So how exactly is this test supposed to improve my life? According to an online cardiac risk calculator (based on a well-studied model), I have a 2.4% risk of heart attack or stroke within the next 10 years. If I were tested for Lp(a) and it turned out to be really high, then it might re-estimate my risk a bit higher, let's say 3% or 4%. My motivation for healthy eating and exercise is medium, and changing the 10 year risk from 2.4% to 4% just wouldn't be enough to make any difference in my behavior. (50% or 60% risk might, but Lp(a) just isn't that strong a risk factor). Likewise, it's not going to make the difference between my doctor recommending I take a statin or not. All in all, this article suffers from the same technology hype as way too much medical science journalism. The reporter should have spoken with someone with expertise in overdiagnosis (yes, this is a subject of serious academic inquiry) before undertaking this story.
4
I did a cardiac risk calculator because both my parents had heart disease. My cholesterol levels were great, and I was in very good health. According to the calculator, my risk was very low. I then had a heart attack and bypass surgery at age 55 (I am a woman). I would have preferred to have all the information I could get about my risk - I would have taken statins and low dose aspirin and perhaps would have avoided this life-changing event.
6
It is bizarrely negligent that your doctors never placed you on a low dose aspirin! I am the middle of seven children, and 72 years old. my father died (like his father % HIS father's brother) for sudden cardiac arrest. My father was 42, his father & uncle were 43 & 45 respectively. My mother (also IGNORED by her doctors) had a 95% blockage in her main coronary artery (discovered AFTER I insisted the cardiologist do an angiogram.) She also simultaneously had a profusely leaking aortic valve, which her FAKE doctor ignored for decades. Her open heart surgery at age 86 was grueling for her, but she survived & lived to be 100. Heart disease is the #1 killer of women. Yet, women take maintain this ridiculous attitude that "wee, my doctor never mentioned it." Bet you last dollar that your doctor takes the aspirin, however. Women are passive in the doctors office; they are simply docile.
And, then they die.
3
By the way, I was placed on atone regular aspirin per night by my VERY smart family doctor. It turns out aspirin is a major help in preventing colon cancer (nine cases on maternal side.) All of them, except one cousin perished from colon cancer. As of six years ago, my annual colonoscopy found more than a few "newborn"flat, sessile BRAF type polyps hiding in the lining of my colon. BRAF of a VERY aggressive type of colon cancer. As it turns out, one 325.mg regular aspirin (not the low dose) helps to prevent BRAF polyps in the colon, and certainly reduces the number of newborn polyps. Aspirin is a major anti-inflammatory & a safe blood thinner. I sadly note that four of my siblings developed it, and also had either quadruple or triple bypass surgery in their 40's. All had refused to take the aspirin. BRAF kills, but it has to be at least 2.5cm to be malignant. Two years ago, I read that Vitamin D at 5000mg and up is now used to prevent the return of colon cancer in patients who survive it. I figured out that I should start the 5000mg to see what happens at the next colonoscopy. One year later, my doctor found ZERO polyps during the (2016) colonoscopy. He asked if I had changed anything? Yes, I was faithfully and daily taking Vitamin D at 5000mg per day.
Now, he is taking it.
4
It's odd that the doctors commenting on this article suggest that since we can't do anything about it, recommend that we stay ignorant about this condition. Speaking of ignorant, hey docs, this is a really bad idea. People have a right to know the risks that came with the body they were issued.
35
They are not saying we should be ignorant. If a test won't change how you live your life or your treatment options, then there is no point of doing the test.
3
Exactly! The primary conclusion is to eat a healthy diet , exercise and don't smoke. That advice never changes.
Way, way too much testing in this country. If you can't fix it why test for it?
I appreciated the article very much, thank Anahad for taking time to pursue it.
Briefly, I had quadruple bypass surgery at the age of 40, in 2011. Not completely unexpected based on the signs - high blood pressure, cholesterol and angina. I adopted a plant based diet post-surgery (Esselstyn, Campbell approach to reversing) and generally feel pretty good.
I also learned about Lp(a) after - 55mgs. Its a little frustrating, considering the effort that goes into maintaining a healthy heart lifestyle to be told there is nothing you can do about it. I agree the Niacin solution is a non-starter. The evidence is not there and there is a pile of studies showing a-fib risk, beyond the flushing they tell you about.
The silver lining - since it is accelerated and generally affects people earlier in life - your stroke, surgery, will likely be survivable.
I plan on taking more time on the Lipoprotein site.
As an aside, I feel blood tests should also include C-reactive protein. CRP measures inflammation and a baseline should be established. Mine was quite high, in the 3's - now under 1.
Feel free to contact me anytime if you are in the Lp(a) club. [email protected]
Ian
12
Ian, do you know if the plant-based diet has reduced your Lp(a) or just reduced other factors that can add to heart attack risk?
I find it troubling that so few doctors talk about the many things that patients CAN do to reduce the risk of heart attack, stroke, diabetes, cancer.
4
I suppose ya just gotta die of something. Maybe an ultra fitness neurosis isn't so stress free, huh Mr. Harper?
4
Seems like anyone with a family history of early death should get tested.
3
Please expand on this comment " But niacin, a B vitamin, has many side effects," The only known side effect of plan Niacin that I know of is flushing which is completely harmless but uncomfortable for a few minutes. This side effect almost never occurs if you take a baby aspirin prior to the Niacin. I take it and it raised my HDL's from the low 20's to 55 ! It also lowers VLDL's, LDL and Triglycerides. The drug companies try to discredit Niacin because they can't patent it and it costs pennies. Endur.com sells Plain Niacin. I hope this helps others but I would like to a response to the "many side effects" sytated in this article. Anyone?
17
Niacin can raise blood glucose and give you diabetes.
3
And crystals in your urine.
2
Yes, my blood sugar was starting to get into the pre-diabetic range, so I stopped niacin, and it went down.
I tried niacin, man that's nasty stuff. The straight stuff caused "flushing" like nothing I've ever experienced. The designer niacin caused digestive issues, even at fractional doses.
So beyond a statin, a healthy diet, a current will and living each day like it could be your last what's to do?
The good news is I don't need to pay attention during retirement commercials.
5
"“I would say that somewhere between 15 to 20 percent of the population would clearly benefit from knowing that this is their problem.”
How? If there's nothing that can be done about it?
7
At this point the science is in a darkness. As the doctors. Read my comments below and see how you can check if you are at risk. Meantime I am going to try propionyl-L-carnitine. What is interesting, not just from my point of view, is that my elevated cholesterol numbers, LP(a) and bilirubin move in tandem. All elevated, but if it go down or up a bit, all numbers go in the same direction. LP(a) is cleared in a kidney. Not sure if anyone is looking at the kidney direction.
If you are a male, you get better chances of doctor's attention. Check your PLAC number-that would give you some peace (depends on numbers). You can do it yourself in a lab, but not if you are in NY state. Women have to fight. 60% of women have coronary microvascular disease, not CAD. More women die than men, because their complaints are ignored by doctors, or not taking seriously including ambulance. I am 106 lb, look 35 , therefore don't look ill, despite LP(a) 131, TH 300 etc and severe, long lasting episodes of chest pain with shortness of breath and postural tachycardia.
4
Yikes! I just looked at my latest lab and my Lp(a) is 321. Even though the number is bolded in the "high risk" column of the lab report, my cardiologist never mentioned it. And, the number from the prior year's lab was 298 and he didn't mention it then, either. Fortunately I have an appointment to see him in two weeks; but, I think I'll call and try to get in sooner. I'm going to read through all the comments below; very glad I happened upon this article which I will print and bring with me. Thank you NYT.
42
Good luck. Ask for a PLAC® Test that Identifies Atherosclerotic Plaques Ready to Rupture and educate yourself about coronary microvascular disease. Those tiny blood vessels that doctors pay no attention to, only on an autopsy.
10
For something like this two weeks is not going to make a difference.
6
If you last that long.
4
Wasn't almond consumption shown to significantly reduce lp(a)?
3
Almond, as long as you are not allergic to nuts, is a good clean protein and fat. Other useful proteins are mushrooms and nori seaweed. High sodium can be a factor in heart failure for overweight people and a small serving of seaweed, like a pinch of dulse or tablespoon of kelp furnishes sea minerals and helps satisfy a salt craving without the side-effects of table salt which is a processed denatured food. Eliminating sodium all together makes the body retain water so sea vegetables are actually balancing. www.asianhealthsecrets.com
1
the lurking lp(a) condition brings to my mind a recent 'expose' i heard on public radio, in which a sample of general public was polled and asked if how many would say Yes, to having certain common heath intervention 'procedures' used used on them. then a sample of credentialed pracising doctors was asked the same question.
one question was "would you be ok with having CPR?' to which the public answered 80 percent with yes. same question to the docs, they answered over 80 percent no, to the question of allowing or wanting CPR.
well, the doctors know the stats on what the mortality, and the survival rates, over either some hours, days, or years.
They know that the results of health restored to those who have had CPR is about 9%, the rest die, or have some unhealthful results traced to the CPR.
i paraphrased this, but it startled me.
now i ask, of the guy 'lucky' enough to have CPR in this case,
is he still alive?
probably. but i'm interested to hear the report in a year from now, and in five years.
trust me; i'm a public radio kibitzer.
4
"Enjoying life because it could end at any moment" -- finally, a health prescription I feel I can unequivocally embrace!
25
We fool ourselves into thinking we know all of the things that are good for us and all of the things that are bad for us, and that knowing them, we are at no risk of the "unknowns" as we think those aren't really important in our modern age.
As this article and countless others show, we are still learning how fragile our understanding is about our world, and how much more we need to learn. We have just touched the tip of the tail of the elephant in the room.
16
As a cardiologist I found this intriguing. But looking for a problem when you have nothing you can do about it is a flawed strategy. We already know that lifestyle factors should be attended to and medications where appropriate. There isn’t any good evidence yet to support treatment in people specifically with high levels of lipoprotein a.
9
Acknowledging is the first step that you can do. As for "nothing you can do about it", you haven't tried anything yet.
Angina. Research suggests that carnitine can be used along with conventional treatment for stable angina. Several clinical trials show that L-carnitine and propionyl-L-carnitine can help reduce symptoms of angina and improve the ability of people with angina to exercise without chest pain. DO NOT self treat chest pain with carnitine, however. See your health care provider for diagnosis and conventional treatment, and take carnitine only under your provider's supervision.
Heart attack. A few studies suggest that carnitine may help when used with conventional medicines after a heart attack, but not all studies agree. Some small studies suggest that people who take L-carnitine supplements soon after a heart attack may be less likely to have another heart attack, die of heart disease, have chest pain and abnormal heart rhythms, or develop heart failure. However, other studies show no benefit. Treatment with oral carnitine may also improve muscle weakness. Carnitine should be used along with conventional medication under your provider's supervision.
Heart failure. A few small studies have suggested that carnitine (usually propionyl-L-carnitine) can help reduce symptoms of heart failure and improve exercise capacity in people with heart failure. However, more research is needed.
(from the University of Maryland School of Medicine)
1
How dare you. There is plenty you can do about it, and giving people a "heads up" that all of this good health stuff is doubly or triply important to them can change behaviors. My Lp(a) is 390 (you read that right), and if I had just been warned as a child how much danger I was in, I would have made some very different life choices and maybe avoided or pushed by my calcific aortic valve stenosis and premature CAD by a decade or more (I was diagnosed in my early 40s). How dare you blithely espouse the practice of keeping highly at-risk patients in ignorance about the danger they are in! Would you advocate keeping diabetic patients in ignorance too, if the only treatments available were diet and exercise? I hope you and those who share your mindset get slapped with a major malpractice lawsuit soon!
14
Are you a carnitine sales rep?
2
It is cavalier for the non-physicians in this article to proclaim that doctors don't know about lp(a). We were all taught about it years ago, and primary care physicians hear about it, along with other ongoing research, at every cardiology-topic CME course and in many of the journals we read. Everyone knows about it unless they've been living under a rock. But we also know that there is no direct intervention for this, so at present it only serves as a risk-stratification factor, so that if someone has an elevated lp(a), they need to get all the more aggressive with the other risk factors that they can control. So until a specific intervention becomes available that directly targets lp(a), widespread testing for this is really of no great value. Instead, why don't we all live "as if" ours were high, and do a better job with our diets, weight control and exercise? We can do that without the test.
41
You have missed the main point Doctor. LP(a) doesn't respond to diets and exercise. And many live with severe chest pain the cause of which in undeterminable according to your kind. Check coronary microvascular disease and Postural orthostatic tachycardia disease. ..the chest pains experienced in POTS are almost never thought to be due to
coronary artery obstruction, but may be associated with electrocardiographic (EKG) changes in the
inferior leads, particularly when upright. They suggest the left sided heart pain common among POTS
sufferers is due to differences in heart chamber pressures, abnormal heart wall motions, and/or nerve
damage. However, based on the Qi Fu's study the chest pain may be associated with reduced blood
supply to the heart, hence ischemia, which will result in the angina like chest pain.
I am sure doctors never heard about it either
5
Sam, I know all about Postural Orthostasis Tachycardia Syndrome and other autonomic phenomena in cardiology. It is you who miss the point, so let me state it again. Yes, lp(a) does not respond to diet and exercise, that is known and has been clearly stated, so I don't know why you feel the need to make that point. But there is also no direct intervention at present for it, so it is only a risk stratifier. And POTS can be related to Ehrler Danlos Syndrome, which has other vascular abnormalities even in the GI tract. But please know this...since you are making generalizations referring to physicians as "our kind," most of the patients I've had with POTS were also a bit "off," similar to "fibromyalgia" patients and those with "chronic fatigue." Just sayin'.
4
How dare you. There is plenty you can do about it, and giving people a "heads up" that all of this good health stuff is doubly or triply important to them can change behaviors. My Lp(a) is 390 (you read that right), and if I had just been warned as a child how much danger I was in, I would have made some very different life choices and maybe avoided or pushed back my calcific aortic valve stenosis and premature CAD by a decade or more (I was diagnosed in my early 40s). How dare you blithely espouse the practice of keeping highly at-risk patients in ignorance about the danger they are in! Would you advocate keeping diabetic patients in ignorance too, if the only treatments available were diet and exercise? I hope you and those who share your mindset get slapped with a major malpractice lawsuit soon!
4
More doctors know about Lp(a) than you might think. That they are not testing for it and "treating" it does not mean they don't know about it. The problem with Lp(a) testing in 2018 is that there is no treatment for elevated Lp(a) per se. If a patient has coronary artery disease (especially at a young age) they should receive aggressive non-HDL cholesterol-lowering therapy no matter what their Lp(a) level is. Until there is a specific treatment for elevated Lp(a), the benefit of testing is unclear and the harm of testing to patient bank accounts and to national health care costs is real. This landscape might be changed by the exciting new Lp(a)-lowering agents under development, but this change will NOT occur during 2018. Even more exciting is the possibility that lowering Lp(a) would prevent aortic stenosis (for which there is currently no medical therapy). The connection between Lp(a) genetics and human aortic stenosis is solid. Exciting area!
29
The strongest possible risk factor for heart attack is a history of early heart attacks in the family -- been known since the very first Framingham data came in in the 1970s. This risk factor is regularly ignored because there's nothing you can do about it, and all the attention goes to life style. As a consequence, people who are "doing everything right" have a false sense of security. And heart attacks.
It would make sense if people with a parent-dead-of-a-heart-attack-at-50 (remember Jim Fixx?) were counseled to be tested for everything, and not just told to go out there and exercise.
26
Sadly it sounds as if presently there's not to much you can do if you have elevated levels. Present precautions seem to have little effect.
Great. So there is no treatment? So the advice is still exercise, eat right, keep your weight, blood pressure, and cholesterol down? Thanks, NYT, for giving me yet another thing to worry about.
8
LDL apheresis treatments every 2 weeks lowers levels significantly. See my response to Ron, RI.
".......Doctors Know Nothing......"
I suggest the abbreviated title for this article (and most others about medicine).
First, let's first understand who we refer to as "doctor".
If it's the typical primary care physician - they really know nothing beyond the very rudimentary medicine. Second they have no control over how much time they can spend with a patient or look into "esoteric" risk factors (like Apo a).
If it's the specialist (cardiologist in this case) and specifically interventional cardiologist who might be the first specialist a symptomatic patient might see, the first response would be to try and put in a stent (perform a procedure). This is how they get compensated - the doctor, the hospital.......
No one will take the time or incentive to look deeper and diagnose. Takes too much time and does not pay.
This unfortunately is the state of medicine........
Meanwhile we rant at the exorbitant cost or insurance and health care.
A classic misdirection - the real issue is the pathetic state of medical practice.
3
Nope. Cardiologists, at least in my case, want nothing to do with it either. (Fort Myers Lee memorial cardiologists)
1
Primary care doctors know a lot beyond "very rudimentary medicine", and are as capable of anyone else as checking a box on a computer screen or lab order form to check Apo a, lp(a), or any other expensive, highly-promoted and not very useful test.
2
PLAC® Test Identifies Atherosclerotic Plaques Ready to Rupture
The PLAC® test measures blood levels of an enzyme called lipoprotein phospholipase A2 (Lp-PLA2). The Lp-PLA2 enzyme unleashes a chain of harmful events culminating in endothelial dysfunction, which is a pathological abnormality in the blood vessel wall that sets the stage for atherosclerosis, plaque accumulation, and rupture.
An elevated level of Lp-PLA2 may signal that an arterial plaque is susceptible to rupture, which could cause a clot to break loose, precipitating a heart attack or stroke.
6
Being Indian, I had this tested for many years back but my insurance wouldn't pay for it. I had to pay for it my self. The South Asian Heart Center in San Jose is very active to get Indians tested for this.
6
It is CHEAP! No excuses for not doing it yourself. 23andme genetic test is under $200
1
Be on the lookout for Amgen's new AMG-890, about to start clinical trials. RNAi treatment will be possible for high Lp(a).
6
how does it cause a myocardio? is it a myocadio (generally of the left ventricle is what kills first time around). if he had AFIB he'd probably know it (being a fitness guru). so WHAT does it cause? people should have their arteries scanned (ultrasound) every 5 years or so beginning at 40 for plaque being present. because for sure something was wacked with this guy's. if something shows up there, then look for something underlying. SAM below says could be "coronary microvascular disease". never heard of it. however she mentioned pain and shortness of breath. reading about it states that people with diabetes could have it. I have diabetes AND I have shortness of breath. but like her no heart related disease known and total is in the toilet... sometimes even too low (shb >= 120). however unlike her I've never had chest pain (male 75yo) so go figure. cardio guy does not know why the shortness of breath thus cause is undiagnosed at this juncture. EKG, stress test. rate, pressure. normal. a very perplexing issue to say the least. could be pulmonary related. never smoked & do not consume ANY alcohol (think Trump!) though. could be I'm just getting old as things going wacko then we need no "excuse"!
Don't forget about microvascular disease. Consider this scenario: You are a woman, admitted to a hospital with chest pain, and you undergo an X-ray imaging test called an angiogram to see if you have blockages in the arteries that supply blood to your heart. The test comes back clear, but you have been experiencing chest pain (angina), and another test - called a stress test - finds that portions of your heart are not receiving enough oxygen-rich blood. Both you and your physician know that something is wrong. Now what?
Scenarios such as this are common in women who might have what is called coronary microvascular disease. As the name implies, this is disease of the smaller (micro) blood vessels (vascular) that supply the heart with blood.
7
It’s about time. We’ve been testing for this at the University of Wisconsin since 1985. It’s very important that people from India or Pakistan, African Americans, Latinos get tested as it is even more common in these populations.
54
For decades, it was a mystery why there was such a high rate of early MIs in Indians & Pakistanis. "Lipo-little-a," as many call it, is common in South Asian populations. At first, cardiologists blamed diet, especially those high in sat fats like ghee (butter) and coconut oil combined with high simple carb intake. Even vegetarian & vegan South Asians seemed to be susceptible.
Then studies of blood drawn from the umbilical cords of random S. Asian-ethnic newborns revealed high levels of lipo-little-a, far more often than in other populations--so lifestyle was eliminated as a factor. (My husband--a cardiologist with many S. Asian colleagues--and I attended a dinner of the Indian-American Medical Assn. about 15 years ago at which this was revealed, to the shock of many doctors in attendance).
However, this is the first I've heard of its prevalence among Latinos as well. Are there any other ethnic groups at risk? I would imagine those with traditionally low rates of intermarriage could carry a gene for it (much as Ashkenazi Jews are more likely than other ethnic groups to carry the BRCA 1 & 2 gene mutations that dramatically raise breast and ovarian cancer risk).
8
and French-Canadian
1
md,
Can you say more about the French-Canadian population? Thanks
I had this test done several years ago with results of 13 mg/dl. At that time, this was considered out of range. Now "studies suggest that the threshold for high lp(a) begins around 30 milligrams per deciliter of blood". The discrepancy in the threshold in just a few years should make one cautious in latching on to new drugs and genetic tests. I am 75 and do not have heart disease.
19
This is not really news, and the story is not so simple. Niacin, for example, may well reduce lp(a), but it does not seem to do any good - one of the largest studies of it ("AIM-HIGH") was halted prematurely by its sponsors, the NHLBI with the conclusion that "high-dose, extended-release niacin offered no benefits beyond statin therapy alone in reducing cardiovascular-related complications in this trial. The rate of clinical events was the same in both treatment groups, and there was no evidence that this would change by continuing the trial." There was also a slight increase in strokes in the group of patients who took niacin. The most recent comprehensive review of niacin (2017) concluded that "Moderate- to high-quality evidence suggests that niacin does not reduce mortality, cardiovascular mortality, non-cardiovascular mortality, the number of fatal or non-fatal myocardial infarctions, nor the number of fatal or non-fatal strokes but is associated with side effects. Benefits from niacin therapy in the prevention of cardiovascular disease events are unlikely.“ There may well be a role for testing for it, but then what? Reducing lp(a) does not seem to do much good.
15
There's no way to know if what you say is true.
1
You can Google AIM-HIGH or Cochrane 2018 review of niacin
1
Beware of all trials that are halted prematurely. The AIM-HIGH trial had many defects. The Coronary Drug Project (1975) still shows more benefit than any statin.
2
It is important to get the mesage out about this independent-of-LDL risk factor for cardiovascular disease. In addition to the drug from Ionis Pharmaceuticals (mentioned in the article), other drugs are in development targeting LP(a), including one from Amgen (AMG890)-hopefully a number of effective therapies can be available for treating this condition.
5
If you had 23andme test done, look for rs3798220, the #1 gene responsible for elevated LP(a). There are 16 SNPs that are significantly associated with LP(a) level. 23andme tests 14 or so. All 13 in my case have one
or both copies of the genes mutations, but #1 is normal. The meta‐analysis showed a significant reduction of Lp(a) levels following L‐carnitine supplementation.
46
Ignore previous request for information re: finding 23andme data; I found it. Thanks.
1
I have had the 23andme testing but am unable to locate the "list" where I might find re3798220. Is it in the "Reports" section? Thanks.
to those who need to know how to navigate 23andme data:
click on Tools than browse Raw Date, enter rs3798220. By the way T/T genotype is normal. And if you then click on LPA, the first column, it would give you the list of all LPA genes tested. Also google "Genetic Variants Associated with Lp(a)
Lipoprotein Level and Coronary Disease"
1
I truly believe there will be a day when statins will disappear from our formularies. We still do not know for certain what causes plaque formation to begin. We know the risk factors, and how to mitigate most of them. There will be an aha moment, the day will come when vascular health will be assured. But for now I’d rather succumb to a massive MI rather than die from cancer or dementia.
68
one has to bite the bullet at times, and choose, or decide in theory, if one wants certain 'interventions' applied, supposedly to help, cure, or revive one who has suffered some dreadful attack.
well:
the lurking lp(a) condition brings to my mind a recent 'expose' i heard on public radio, in which a sample of general public was polled and asked if how many would say Yes, to having certain common heath intervention 'procedures' used used on them. then a sample of credentialed pracising doctors was asked the same question.
one question was "would you be ok with having CPR?' to which the public answered 80 percent with yes. same question to the docs, they answered over 80 percent no, to the question of allowing or wanting CPR.
well, the doctors know the stats on what the mortality, and the survival rates, over either some hours, days, or years.
They know that the results of health restored to those who have had CPR is about 9%, the rest die, or have some unhealthful results traced to the CPR.
i paraphrased this, but it startled me.
now i ask, of the guy 'lucky' enough to have CPR in this case,
is he still alive?
probably. but i'm interested to hear the report in a year from now, and in five years.
trust me; i'm a public radio kibitzer.
1
Whether statins "will disappear from our formularies" entirely remains to be seen. Their role is to inhibit cholesterol synthesis even though overproduction of cholesterol by our bodies is not a significant cause of atherogenesis and heart attacks. Since cholesterol is essential for life, statins can have unwanted side effects. A paper published in 2005, "Atherin, a newly identified, lesion-specific, LDL-binding protein in human atherosclerosis" gets much closer to what initiates pathologic LDL binding, but as far as I know, the findings have been ignored. (Atherin is now known as SAMD1.) If one were to discover an agent that blocked binding between LDL and atherin in the artery wall, it could be a valuable way to reduce the incidence of atherosclerosis -- non-toxic because it would not inhibit a normal process, like cholesterol synthesis.
https://www.ncbi.nlm.nih.gov/pubmed/16159594
3
From what I know there is no direct relationship between stains, dementia, cancer... as you imply. And there seems to be ample evidence that statins do work...(PS some people like my 102 yr. old aunt will simply die of old age.)
There's lots we don't know isn't that great?? room for new research... but I find disturbing that people actually agree with you -- unless... they cannot tolerate statins, which does happen...Statins, metformin for diabetes all of these meds would have meant that beloved members of my family prob. would have died about 10 years later than they did... and as dementia doesn't seem to appear in this family until people are well into their 90s --- the pleasure of having them around would definitely have been ours..
4
Will Medicare or private insurance cover this part of a blood test?
10
Yes, it covers it. But you can do it yourself. It is not expensive. Privatemdlab or any Directlab offers it, no script needed. Use 15% off coupons.
14
My insurance, Blue Cross Blue Shield, does not cover it.
I am not a doctor and I know about it since forever. Mine is 131. And I am a female 106lb. I don't have coronary artery disease. What I probably have is coronary microvascular disease. And doctors don't know about it either. My severe chest pain and shortness of breath in the last few months is ignored.
42
Find another doctor, please.
8
Niacin ("nicotinic acid" only), in my personal experience, has no side effects after a day or two. Only a hot flash (flush) that leaves after an hour or so. To prevent it - take an aspirin 30 minutes before taking niacin the first few times.
The "No-Flush Niacin" products are completely worthless. They do prevent pellegra (deficiency disease) but do absolutely nothing else. Ah - they do increase profits at companies selling them. 500 mg tables are no better than 30 mg tabs for treating/preventing pellagra; just more expensive.
No flush "niacins" include nicotinamide, niacinamide and inositol hexanicotinate. Worthless.
No flush - true but also no benefit.
22
Nicotinamide helps reduce incidence of squamous cell carcinoma. This treatment was developed in Australia where skin cancer is most prevalent.
3