Cardiovascular Health 2025

#1088

I actually disagree. I think the fat jabs show that people aren’t as resistant as you think. Repatha and Praluent are both simple “click pens” which you can do at home.

I think the problem is simply the cost. Antibodies generally cost a lot more to manufacture, since they need to be made by living cells, then purified etc. It’s a big industrial process. By comparison, small molecules can be made by mixing ingredients in the lab.

Still, the overall biggest factor is that price gouging in the US healthcare system, because a Repatha injection might cost $150 in other parts of the world. Not “cheap” but nowhere near as pricey as in the US.

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#1089

Cronos, I just learned from you that CVD is a particularly bad problem. Do you know what this is attributed to? They don’t eat much cow, but of course they are consuming dairy and other animals. This fact only just leads me to guess their issue is not due to consuming more sat fat, but?

And ARGH on US health insurance. @relaxedmeatball I qualify for repatha and got the pre authorization blah blah blah…. But alas, it’s still subject to my 8k deductible, so I pay for it. Fortunately, repatha offers coupons. For years, it only cost $5 a month, but a couple years ago they started to cap it to a 3k coupon benefit max per year. Still nice, but it doesn’t make me any less bitter :slight_smile:

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#1090

As popular as the injections are now, I think you’ll see how many people have been holding out for a pill once orforglipron (small molecule GLP-1 agonist, no food/water restrictions for absorption) hits the market next year. Eli Lilly already has manufactured literally billions of tablets in preparation for its release, and they pretty much know what they’re doing.

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#1091

There was a great Attia podcast about India and CVD/insulin resistance (with a doctor of Indian origin). #69 - Ronesh Sinha, M.D.: Insights into the manifestation of metabolic disease in a patient population predisposed to metabolic syndrome, and what it teaches us more broadly - Peter Attia

From what I remember (years since I listened), the guest stated that Indian origin people tend to accumulate a lot of visceral fat, tend to not have much muscle mass, and aren’t particularly “athletic” in general. (Side note: consider Indian athletes, Olympic Games performance etc). He posits that they simply don’t handle high calorie diets very well, and they store lots of fat around organs, lots of fat inside muscle tissue etc. So basically they get insulin resistant and get lots of inflammation very easily.

Attia starts the podcast by talking about a patient of his (South Asian) who had insulin resistance that the usual approaches weren’t fixing.

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#1092

@relaxedmeatball has it. There is a genetic component in the South Asians that predisposes to the TOFI phenotype (Thin Ouside Fat Inside), so already at a BMI of 21 you can have metabolic derangements leading to diabetes and CVD. The diet is problematic, because it’s pretty far from traditional these days, calories are much higher and a ton of regional cuisines have unhealthy components like high levels of SFA, and in the urban setting fried food, fast food and processed foods and sodas. And many urban Indians don’t exercise much or do anything near enough to burn all those excess calories.

The result is a diabetes and CVD epidemic. And while incidence matters, it’s the absolute numbers that are the problem - India has recently overtaken China as the most populous country on earth. There are now tens of millions who are at risk of CVD or already suffering from it. And it’s getting worse, with childhood obesity rising rapidly, setting up a huge challenge for generations to come. Education and lifestyle changes are always going to be a hard path. You’re going to have to add a pharmaceutical component to tackle this, and it has to be affordable for the population. So they’ll follow their playbook when it comes to CVD and diabetes drugs, and scour the world for the most effective drugs that can be easily replicated and either strike a deal with the original manufacturer/marketer, or make a knockoff for the domestic market. That if course is greatly facilitated by a giant pharma industry where generics are made and where a huge amount is also produced as subcontractors for Western pharma companies. That’s where we come in, placing our orders. CVD is not an exotic collection of pathologies, so odds that a drug that’s proven to be safe and effective will eventually appear in India is high, and it should be relatively affordable. We’ll see.

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#1093

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#1094

I don’t know. I use repatha every two weeks with the Sureclick pen and it hurts like a MF. I am no stranger to all sorts of injections, and that one I always dread. Its a pretty big volume and a fast flow, so that doesn’t help.

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#1095

Any idea if Dayspring also has high Lp(a)?

#1096

@Rapasailor my doc just switched me to a regular ‘manual’ syringe for repatha. LIFE CHANGING!!!

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#1097

That’s a great idea! I’m going to request that next time as well. That stupid pen hurts every time.

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#1098

Yessss, I can’t believe I’ve been using that godforsaken click pen for years!!

It didn’t hurt me very often, but O.M.G… when it did, it was torture!! It takes soooo long and you just want to pull it out, but it’s so expensive you have to just sit there and take it!!!

This still hurts a touch, but because you can control it, you can simply give yourself a break before finishing.

#1099

As promised I’m posting results of the n=1 experiment wrt. lipid medication. No changes in diet or exercise or other lifestyle factors, sleep, level of stress insofar as I can tell (low), supplements. The only med change has been the addition of 80mg/day of telmisartan for two weeks (first 20mg/day for 4 weeks, followed by 4 weeks of 40mg/day, before the final 2 weeks of 80mg/day that I have continued on with to this day). This test (4) keeps pitavastatin 4mg/day but adds a combined pill Brillo EZ of 180mg/day + 10mg/day ezetimibe.

So the tests are as follows - each intervention roughly 6 weeks with no washout period:

(1)pitavastatin 4mg/day alone (switched from atorvastatin 10mg/day)

(2)pitavastatin 4mg/day + bempedoic acid 180mg/day

(3)pitavastatin 4mg/day + ezetimibe 10mg/day

(4)pitavastatin 4mg/day + bempedoic acid 180mg/day + ezetimibe 10mg/day - CURRENT TEST ON 10/28/25.

This test (4) has been of a drug regimen that has been ongoing since the initiation on 08/09/25.

Pitavastatin 4mg/day alone vs pitavastatin 4mg/day + bempedoic acid 180mg/day vs pitavastatin 4mg/day + ezetimibe 10mg/day vs pitavastatin 4mg/day + bempedoic acid 180mg/day + ezetimibe 10mg/day

Pita alone - 5 months; Pita + BA - 39 days.

Legend: Pita alone - PA; Pita + BA - P+BA; Pita + ezetimibe P+EZ

Total Cholesterol: PA - 228 mg/dL; P+BA - 208 mg/dL; P+EZ - 195 mg/dL; P+BA+EZ - 178 mg/dL
LDL-C Calc: PA - 123 mg/dL ; P+BA - 110 mg/dL; P+EZ - 99 mg/dL; P+BA+EZ - 91 mg/dL
Trig: PA - 93 mg/dL ; P+BA - 62 mg/dL; P+EZ - 82 mg/dL; P+BA+EZ - 62 mg/dL
HDL: PA - 89 mg/dL ; P+BA - 87 mg/dL; P+EZ - 81 mg/dL; P+BA+EZ - 75 mg/dL

Not exactly thrilling results. It brings me (just) under the cutoff values for hyperlipidemia as specified by the UCLA lab range. Each additional drug brings down the values by just a few points (if any - see trigs!). To say the results are underwhelming given the arsenal of drugs deployed is a depressing understatement. I’m not impressed.

Unfortunately it also represents the end of the road for me for easily available LLT drugs I have on hand. I am aware that the next currently available drug class I might add in order to crush LDL/ApoB further would be PCSK9i. However, call me excessively paranoid, but I continue to be worried by the MR AD signal for PCSK9i. That said, I’m not absolutely excluding that I might use a PCSK9i in the future. Meanwhile I am eagerly awaiting the whole slew of LLT drugs that should be coming online in the not too distant future, fingers crossed.

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#1100

91 LDL is better than what your previous numbers were. Take it as a win and look for other ways to lower your cholesterol.

#1101

This is the sort of situation where ApoB and Lp(a) would be useful measurements.

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#1102

I agree. Your apoB matters more @CronosTempi. What is it?

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#1103

Wish I could tell you. This wasn’t a test I ordered from a lab. This was a test I got as a routine yearly physical at UCLA, and for some reason they decided this year to just do the bare bones old style blood test where the lipid panel is just the TC/LDL-C/HDL/TRG, and so on for the rest of the biomarkers. Not even fasting insulin. I was shocked when I got the results. Assholes. Again I’ll have to go get my own labs much sooner than planned just to get my data (originally was going to get my next labs Feb. 2026). Standard medical care is continuing to be useless despite my paying for insurance at UCLA for decades. Back to doing my own labs, getting my own tests and drugs and ignoring the useless establishment.

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#1104

Ah, that’s too bad. My apoB is about 2/3 of my LDL, so if you’re like me, your apoB might already be below mg/dL.

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#1105

My ApoB usually runs about 8-10 mg/dL higher than my LDL so this is interesting to hear.

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#1106

ApoB is like $12 at Goodlabs… Its easy to get a test anytime: [REFERENCE] Master list of all places to get blood tests - #24 by RapAdmin

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#1107

When assessing ASCVD risk, I’d start by measuring the full lipid panel plus ApoB and ApoA1, later on, you can often track risk using good proxies (especially ApoB). It’s essentially about how your body prefers to transport cholesterol: more via ApoA1 (HDL) usually means lower risk, more via ApoB (LDL, VLDL, etc.) means higher risk. In my case, ApoA1 is much higher than HDL-C, and ApoB is about just shy of 2/3 of LDL-C, which suggests relatively fewer ApoB particles for a given LDL-C. But the key is still the absolute ApoB level and overall clinical context.

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