Kaneka Medical America (KMA) was established in 1997 and is a wholly owned subsidiary of Kaneka Americas Holdings, Inc. KMA, with main office located in New York, NY, is the exclusive distributor in the U.S. and Canada for the extracorporeal Lipoprotein Apheresis system, LIPOSORBER®, manufactured by Kaneka Corporation.
LIPOSORBER LA-15 is an extracorporeal apheresis therapy that enables Familial Hypercholesterolemia (FH) and Focal Segmental Glomerulosclerosis (FSGS) patients to attain the recommended therapeutic targets when diet and maximum drug therapies have failed. It is shown to acutely reduce harmful cholesterol agents: Low Density Lipoprotein Cholesterol (LDL C), Lipoprotein(a) [Lp(a)].
Testosterone with its natural conversion to 17b estradiol lowers the Lp(a) in our youth and with weekly optimal doses. * Look up 17b estradiol and lower Lp(a). (NOT estrogen which is pregnant mare urine estrogen Premarin) *17b estradiol elevating HDL cholesterol *17b estradiol lowering fibrinogen THIS is nothing new to those of us in the Bioidentical hormone specialty!! Big Pharma does NOT want you to know this because they can’t patent testosterone or oral 17b estradiol!!
I’m pretty shocked at the treatment decisions these two doctors are choosing - they treat LDLs and try to get results below 70 and they say that statin treatment can elevate LPa which causes increased risk of ASCD BUT they don’t check after initiating statin therapy because they don’t want to make their patients nervous because their therapy is elevating the LPa - to me it is recipe for malpractice - except it probably is the standard of care. How disturbing!
No no no. They're being cautious about eliminating LDL therapy in favor of minimal interventions available for LP(a). Once the LP(a) therapies are available in ~2026, we might see less focus on LDL. That said, you would need to have head-to-headbstudies for LP(a) therapy with and without LDL drugs, once the LP(a) drugs are available.
I don’t understand the rationale of waiting until a person has shown dangerous signs of the development of CVD to start looking for a major risk factor in the development of CVD. I guess the European position of testing lp(a) on everyone makes more sense to me. Especially if you consider that lp(a) represents a risk factor that is cumulative from childhood.
I’ve known about my high Lp(a) for about a year and a half. Age 49, I have never had an event and was referred for PVCs. Because I’m youngish, fit, and had a zero CAC, my cardiologist is just having me wait… wanted to see me in 3 years. With the push to get this out there now, the reality of how serious this is is setting in. It looks like the current state is to just get as healthy as possible and wait for the first heart attack if insurance is to cover anything. Very depressing.
Best treatment for atherosclerosis: Vitamin C Why do only coronary arteries clog with cholesterol and not veins or small capillaries? Scurvy = No vitamin C in your diet. Symptom: Your blood vessels break and you bleed to death. Think of the sailor of the past. Scurvy of the heart = Just enough vitamin C from food. Symptom: Arteries around the heart are not strong enough to resist high blood pressure. Damage is repaired with cholesterol LP(a) to prevent worse. After years of repair, your arteries become clogged. Enough vitamin C supplement of at least 3000 mg. per day gives strong and flexible arteries. Cholesterol is not needed as a repair agent. Cholesterol in your coronary arteries is broken down and burned in your liver. Source RU-vid: Cardiovascular disease and vitamin C (Dr. Rath Foundation) or Breakthrough Towards The Natural Control Of Cardiovascular Disease - Dr. Rath's 2018 Cyprus Lecture
Interesting - but pls start with the bottom line up front. A complex case study with no clear direction of where we are going puts a huge burden on the audience to synthesize all of this, somewhat aimlessly.
LPa is 31 nmol. I eat all animal products, minimal nuts, vegetables. IT'S THE CARBS AND SUGAR. I'm a 63-year old female. No meds. I do take Hormone replacement therapy.
Low carb is the only answer. Zero added sugar-zero problems. I'm 63, no meds. LPa 31 NMOL. VLDL 16 mg, triglycerides 93, HDL 71, LDL 179. 266 total cholesterol. Ratios excellent. CAC is Zero. CIMT all clear. Heart MRI excellent. No plaque, no inflammation. It's not an enigma! It's added sugars/refined carbs.
Lp(a) is NOT a cause of athersclerosis. It is best a mediator, s it prevents clots from being dissolved. point i, one has to avoid injuries of endothelium in the first place. Prevent high glucose, prevent inflammation, eat low carb to elevate HDL = preventing the breakdown through triglycerides, keep hmocystein in check via folate B12 and betaine.... Secondly, ordinary vit C is strongly inversely correlated with Lp(a). you are wasting 1h+ of time
You nailed it, monnoo! There is ABSOLUTELY ZERO PROOF in any study, any research, any literature that Lp(a) particles actually CAUSE atherosclerosis. The only thing that the Lp(a) zealots have to keep pushing their bogus theory on Lp(a) is a bunch of ASSOCIATIONAL data that proves nothing. As the well respected cardiologist, Dr. Nadir Ali says, "Lp(a), just like LDL, is a 'firefighter' and has nothing to do with CAUSING atherosclerosis/plaque". Dr. Nadir Ali reports that he has performed coronary angiograms on some elderly people with lifelong elevated Lp(a) levels and these senior citizens have perfectly clean coronary arteries!
What a contradiction she speaks of. Nelson has a 21% reduction in lipoprotein a and the other PCSK9 inhibitor reduces leopard protein by 20 to 30%. So they both do the same thing practically this is clearly and undoubtedly pharm bias.
I’ve been watching other channels, and there is a dietary modification with the use of high doses of vitamin C, amino acids proline, and lysine called the Pauling protocol. Looked that up. I’m also interested in that.
Lp(a) is in your genetics to live a long healthy life. "Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio. Low levels of Lipoprotein(a) are not good. 2012 article title: Low Lipoprotein(a) Concentration Is Associated with Cancer and All-Cause Deaths: A Population-Based Cohort Study (The JMS Cohort Study) The Lp(a) levels were inversely correlated with the CIMT in this population, suggesting that subjects with a low Lp(a) level may have a predisposition to carotid atherosclerosis. This finding was preliminary and should be investigated further in larger studies and in additional settings. 2012 article title, CIMT thickness in asymptomatic subjects with low Lipoprotein(a) levels.
I am 79 and no event but LPa 217 and never knew about it until 2 years ago but have been put on 5mgs Crestor and 10 mgs Zetia plus a 81 mgs aspirin daily. I feel fine and fast 18 hours a day and eat low carb/ Mediterranean. I am 5’5” and 128. All blood tests are great except LDL was 152 but now 80. APOB 80 and HDL 116 and Triglycerides 63 all prior to starting meds.
Hello - i read study paper from 10 plus yrs ago indicating significant reduction of lpa with oral l-carnitine supplementation. And slight reduction with 40mg daily flax seed. Any more can add to this with maybe newer studies or newer thinking on exactly why these of true benefit?
Let’s see if I have this right. Statins didn’t do a thing for this patient ( because they actually don’t work since LDL-C is just a marker for metabolic disfunction), and LP(a) is the better predictor but don’t give niacin to reduce LP(a) even though you showed that a lower level of LP(a) worked and instead go ever lower with LDL lowering by adding PCSk9 inhibitors? Hmmm
My Lp(a) was 246 nmol/L in June of last year, by September it was 293 nmol/L, and got it checked again in April because it was part of a package I bought and it came back at 380 nmol/L. So, in one year my Lp(a) went from 246 to 380 🙃 it was lower when I was eating lots of meat and butter and higher now that I am plantbased…on the other hand my particle count has come DOWN exponentially as well as my LDL-small particles. My LDL is actually higher now though and I don’t know why 😢 it was 117 last June and now it’s 132.
