Steven Kaplan

@MattCarl91 @chamath Every F-T owner but one on my block relocated from the Bay Area.

@ROIdude @chamath Another bonus: the locals there will love when you tell them you relocated from California. Specifically if you say the Bay Area.

California politicians think taxes are like boiling a frog. You can keep it up as long as you only increase it by a little each time…but at some point the frog is cooked…or moved to Nevada, Texas or Florida.

@Tellit007 @Tellit007 Thanks for liking my response! DMs closed—could you email roiguy@gmail.com or suggest another way to connect? Keen to hear your thoughts on BP having multiple drivers. Thanks!

@Tellit007 @BenBikmanPhD Just one anecdote—but I’ve been insulin sensitive for 12+ years, and my BP still runs high without meds. Feels like there’s more going on than a single primary driver.

@BenBikmanPhD co-founded HLTH Code supplements and runs the Insulin IQ coaching platform. The business model requires insulin to be the primary driver of everything. This post fits the model perfectly. That is the product. Let's check it out shall we? Insulin resistance contributes to hypertension through real mechanisms. That part is true and worth knowing. What is not true is "very likely the primary driver" as a generalization applicable to everyone with elevated BP. Hypertension is multi-factorial: arterial stiffness, ApoB-driven endothelial dysfunction, renin-angiotensin activation, obstructive sleep apnea, genetic predisposition, age-related vascular remodeling. Angie Stegen, one of the most-liked replies in this thread: 15 years of strict low-carb, insulin presumably controlled, BP still elevated at 73. Milton R: fasting insulin down to 4.2 from 28, still needs BP medication. These are not outliers. These are his own followers. SPRINT: 9,361 patients, intensive BP control with medication cut cardiovascular death by 43%. The medication works. Telling 11,200 people it is "very likely" fixable by resolving insulin resistance, without that caveat, is clinical overreach dressed as metabolic science. @drpablocorral publishes on the full cardiovascular risk picture. @BenBikmanPhD sells the insulin chapter. When your own followers report the protocol did not fix their BP, the post needs a correction. Not a coaching upsell.

@yuripridemd TY & understood. But this seems like the classic discordance issue: LDL can look fine while ApoB shows higher particle burden. That’s what I’m seeing personally—low LDL but rising ApoB. Makes me wonder whether residual risk can be understated when LDL-C is the primary target.

@ROIdude The association between lowering LDL via drugs with varying mechanisms and improved outcomes is strong. ApoB predicts residual risk, but the relationship between targeting ApoB and outcomes is not yet as well established. So I target LDL <55. ApoB often follows, but not always.

CAC testing has become a big part of my prevention practice. I don't use it to decide whether to look for ischemia - a history can do that for most pts. I use it to decide intensity of therapy. I believe pretty firmly that most pts with CAC >0 should be driven to LDL <55.

@ifixhearts Personal anecdote: I've been insulin sensitive for at least the past 12 years, but LDL-C & ApoB ran on the higher side. CAC - 742

Insulin resistance is a much bigger risk factor for heart disease than LDL cholesterol.

@cremieuxrecueil What are the therapies for lowering Lp(a)?

The evidence that LDL causes heart disease is totally unequivocal, and minimizing LDL is essentially a free lunch for cardiovascular health. Similar situation with lp(a), so thank god new therapeutics are here that make both things trivial.

Lowering LDL will extend lifespans. The trials, the genetic studies, and even the prospective cohort studies all agree that the more you lower LDL, the greater the reduction in your risk of heart disease. This is one of the clearest chronic disease prevention findings there is.

@ScottAppliedSci Antagonistic pleiotropy: **LPA, PCSK9, APOE, CETP, IL6, TNF, ACE, etc.

Why is comparison of adult disease rates between modern societies and hunter gatherer societies invalid? The answer is pretty dsmning for the ‘magic ancestral diet’ crowd and the paleo-fantasists. 👇🏻

@cremieuxrecueil nails the cynicism here. @RoKhanna and @BernieSanders must know wealth taxes mean capital flight, valuation games, legal fights, & enforcement headaches—yet they push them anyway. Why? Signaling for higher office > honesty. Politicians gonna politician.

@ScottAppliedSci I find that LPP advocates can be even fiercer than carnivores though they have even less understanding of the difference between anecdote and science.

@ROIdude Yep. Sad what a mixed legacy he left.

Why pick one hill to die on when there are so many? • LDL is causal in CVD • humans are omnovires • willpower is a real thing • keto = CICO in disguise • insulin is not the enemy • Eskimos get heart disease • saturated fat is not-essential • energy balance >> hormones • statins are safe and save lives • diet gurus are in business, too • Ancel Keys was not a monster • you are responsible, not to blame • your doctor does not want you sick • seed oils are fine, maybe even good • carbs don't make you fat or diabetic • we don't understand gut microbiota • dietary guidelines did not make us fat • there are honest mainstream scientists • what worked for you might be useless for me • ancestral diets don't tell us about optimal diets These are all true. What did I miss??

@ScottAppliedSci Large fluffy LDL particles are just as harmful as small dense LDL particles.

@nullbotto @robertlufkinmd Also, ezetimibe (which has none of statins’ so-called pleiotropic effects) reduced CV events in the IMPROVE-IT randomized trial when added to statins—another strong argument that ApoB lowering itself drives benefit. Link: nejm.org/doi/full/10.10…

@nullbotto @robertlufkinmd Not true. PCSK9 inhibitors like Repatha also lower ApoB & have shown clear outcome benefits in large RCTs—FOURIER demonstrated significant reductions in heart attack & stroke beyond statins alone.

1 minute of wisdom from the great Dr Robert Lustig that could save your life. It's about cholesterol, heart disease, and sugar.

@nullbotto @robertlufkinmd The RCT evidence here is massive. Dozens of trials show statins reduce both heart attacks & cardiovascular death. Ex: The landmark 4S randomized trial (4,444 patients) demonstrated ~ 30% reduction in all-cause mortality with statin therapy.

@ROIdude @robertlufkinmd There were also trials that combined statins with other LDL lowering drugs, and didn't see any improvement relative to just statins, despite the LDL lowering working as advertised.

@peto682 @robertlufkinmd Latest: .3 / 68.

@ROIdude @robertlufkinmd What’s your hs-CRP and your HDL-C?

@nullbotto @robertlufkinmd My bad. ncbi.nlm.nih.gov/pmc/articles/P… "Across multiple randomized clinical trials, the degree of cardiovascular risk reduction was most strongly associated with the reduction in apolipoprotein B–containing particles.”

@ROIdude @robertlufkinmd That link has nothing to do with your claim.

@peto682 @robertlufkinmd Not at all true. In my case, for example, my triglycerides have been in the 50s since at least 2012. I’m also insulin sensitive, yet I was diagnosed with severe atherosclerosis two years ago. ApoB was on the higher side.

@ROIdude @robertlufkinmd ApoB is irrelevant when triglycerides are low

I read both that book along with Kendrick's other novel, "The Great Cholesterol Con". Both are quite entertaining , but unfortunately not grounded at all in science.