People on a med. diet followed till death and this is the pertinent graph:
Lustgarten spends a bunch of time on this in his amazing book on microbial burden and longevity. K1 helps get rid of the LPS to detoxify, makes more of the proteins that seal the gut barrier, and increases the IAP (intestinal alkaline Phosphatase). The study also talks about osteocalcin activity and all the wonderful things that does for you and how K1 increases it.
Green leafys or take the pill. You need 1400 or more K1 daily.
@Bicep thank you, that is great info! And I guess it explains why my supplement has so much k1.
I do try to eat a lot of greens, and Google just told me too much K1 can help blood clot. It makes me wonder if clotting is less than ideal for someone with heart disease… so much to learn!
I guess it’s time for a deep dive to learn more about this topic and to find out how much is too much k1.
@Paul This is the first I’m hearing of this, so thanks for sharing. I just did a quick google and it appears it might help a lot!!! And because there is no free lunch, it appears too much could cause heart attacks :). I’ll ask my docs about this asap!
Participants in the upper quartile of energy-adjusted dietary phylloquinone intake consumed nearly twice as many vegetables (especially leafy green vegetables and fruits) as those in the lower quartile. Increased menaquinone intake was associated with higher consumption of dairy products and meat (Supplemental Table 1).
The decision to discontinue the Repatha® Pushtronex® system was made to uphold the high standards Amgen holds for patient experience , focusing on delivering optimal care for patients with cardiovascular disease and hyperlipidemia (high bad cholesterol).
Dr Attia takes PCSK9 Inhibitors:, are probably needed to get lower. Very expensive 43 is excellent. Crestor 5 mg gives you appx. 85% of benefit. 10 mg 100% You can buy a combo pill of Crestor/Ezetimibe 10/10 for 1/2 cost. Good Luck on Lp(a) EZ is good, but BA?
Pharmacodynamic effect of bempedoic acid and statin combinations: predictions from a dose–response model
"Dose–response models predicted that combining bempedoic acid with the lowest statin dose of commonly used statins would achieve a similar degree of LDL-C lowering as quadrupling that statin dose; for example, the predicted LDL-C lowering was 54% with atorvastatin 80 mg compared with 54% with atorvastatin 20 mg + bempedoic acid 180 mg, and 42% with simvastatin 40 mg compared with 46% with simvastatin 10 mg + bempedoic acid 180 mg.
Conclusion
These findings suggest bempedoic acid combined with lower statin doses offers similar LDL-C lowering compared with statin monotherapy at higher doses, potentially sparing patients requiring additional lipid-lowering therapies from the adverse events associated with higher statin doses."
My wife said the same thing. Duh. But Lustgarten in his book pretty much takes it as a result of the vitamin k1. He goes on and on about it. Hard to prove it without testing with the vitamin instead of the vegetables. I agree this study is not proof.
They say they have adjusted for confounders, but we would need to see the detailed calculations to assess as to whether the adjustment is reasonable.
what effects on mortality of human beings does vitamin K1 have
ChatGPT said:
Vitamin K1 (phylloquinone), primarily known for its role in blood clotting, has also been studied for potential effects on mortality, especially cardiovascular-related. Here’s what is known based on current research:
1. Cardiovascular Mortality
Some studies suggest that higher dietary intake of vitamin K1 may be associated with a reduced risk of cardiovascular disease (CVD) and mortality. This is likely due to its role in activating matrix Gla-protein (MGP), which helps prevent vascular calcification.
However, evidence is mixed, and the associations are generally stronger for vitamin K2 (menaquinones), which has a more direct effect on vascular health.
2. All-Cause Mortality
Observational studies (like the EPIC and Rotterdam studies) have shown a possible inverse association between vitamin K1 intake and all-cause mortality, but the data is not consistent or conclusive.
Most of these findings are associative, not causal, and may reflect generally healthier diets rather than a specific effect of vitamin K1.
3. Cancer-Related Mortality
Some preliminary research has looked at vitamin K1’s role in reducing cancer progression, but evidence is weak and limited compared to vitamin K2.
Summary:
Vitamin K1 may have modest beneficial effects on mortality, particularly cardiovascular mortality, but the evidence is not strong or definitive.
The more pronounced effects on health and mortality have been observed with vitamin K2, not K1.
More randomized controlled trials (RCTs) are needed to establish any direct impact.
Thank you for the clip! (I have to learn how to do that!)
I’m pro statin, but I don’t feel well on them. Him sharing that you get 85% of the benefit from low dose statins is incredibly helpful and I’ve shared that with my family whose docs just keep raising it without suggesting EZ etc.
I was on repatha when it first came out a few years ago, and then I went on EZ last summer, and then started BA over the winter in an effort try to get my apob even lower.
Many years ago, I was told that I shouldn’t bother with EZ because, due to my diet, I’m not really consuming anything for it to work on…. IDIOTS
My apob 30 goal was advice from Attia (I messaged him and he kindly responded)
Long-term cardiovascular risk and mortality associated with uric acid to HDL-C ratio: a 20-year cohort study in adults over 40
Cardiovascular diseases (CVD) and mortality remain significant public health challenges, especially among middle-aged and older adults. However, their relationship with Uric Acid to High-Density Lipoprotein Cholesterol Ratio (UHR) has not been extensively studied in the US population. This study aimed to examine these associations in adults aged ≥ 40 based on the National Health and Nutrition Examination Survey (NHANES) 1999–2018. 29,742 participants’ data in NHANES between 1999 and 2018 were retrospectively analyzed. Multivariable logistic regression, Cox proportional hazards models, restricted cubic spline (RCS) analyses, and subgroup analyses were used to assess the associations between UHR and various CVD outcomes. Among the participants, 4,505 (15.15%) reported a history of CVD. A positive association was observed between UHR and the risk of total CVD, including coronary heart disease, heart attack, heart failure, angina pectoris, and stroke (P all < 0.05). UHR was associated with increased risks of all-cause mortality (HR = 1.02, 95% CI: 1.02–1.03) and CVD-specific mortality (HR = 1.03, 95% CI: 1.02–1.05). UHR had a linear dose-response relationship with CVD and a nonlinear relationship with all-cause mortality by RCS analyses. Subgroup analyses confirmed that these associations remained stable across different groups. The findings highlight UHR as a significant predictor of CVD risk and mortality in middle- and older-age adults. Given its strong association with adverse health outcomes, UHR can be a valuable indicator in facilitating the early identification of individuals at elevated cardiovascular risk.
Again a case where I wish I had a before and after measurement. On my recent blood test I decided to measure my uric acid, because I went on 12.5mg/day empagliflozin for several months. It came back as 3 mg/dL which LabCorp flagged as “Low” (reference interval 3.8 - 8.4). Unfortunately the only other uric acid level I had measured was like 15 years ago, so that’s useless as comparison (fwiw, it was 4.6 mg/dL back then). Now I’m worried what’s next, because I’ve upped my empagliflozin dose to 25mg/day, because the lower dose has not moved my A1c, still at prediabetic 5.8.
According to Mike Lustgarten, for men, lowest ACM is at 5mg, and it starts getting notably bad at 2.9 and below. I guess I’m right at the danger zone.
But I can’t help wondering, if these numbers apply to people who have very low systemic inflammatory levels. Remember, these “optimal” reference numbers are derived from the general population. If you are a significant outlier in important respects, these reference numbers may not apply. You need some uric acid for antioxidant purposes among others, but perhaps if you have unusually low levels of inflammation, your body doesn’t make/need as much, so a number below reference might be appropriate for your situation. So low uric acid levels due to low need might be different from low levels caused by disease or poor physiological functioning. Obviously I’m totally speculating, but perhaps it’s not time to panic quite yet. YMMV.
Just to be clear, it’s one version of the plastic injection device thingy which is being discontinued, not the drug itself. The regular “SureClick” pen (that I assume 99% of people (including myself) are using) will continue to be made and sold as normal. For me, the 140mg pen is mega effective, and reduced by ApoB by ~50%.
Independent and joint associations of sedentary behaviour and physical activity with risk of recurrent cardiovascular events in 40,156 Australian adults with coronary heart disease
As always with such associations, reverse causality is a consideration. Perhaps those who had fatal or MACE outcomes were just sicker and less capable of physical activity.
I say this as I just skipped a heavy exercise session, because my knee was bothering me, and I didn’t want to risk an injury. I’m off rapa for another couple of weeks. As soon as I feel better, I will resume my exercise program. Meanwhile an observer could say, “gee, he’s exercising less intensively, and we see that his knee is bothering him, he should’ve been exercising intensively”.
All of this on a much bigger scale, of course. The runner who developed terminally bad knees, quits running, while the one who because of lucky genetics has good knees, continues running.
Now, if you get intervention studies, we can try to chicken and egg this association.
