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Mike Lustgarten

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Everything posted by Mike Lustgarten

  1. LDL is arguably the most debated biomarker in terms of what's optimal for health. In the video, I present data showing that 100 - 140, not 50 - 70 mg/dL may be optimal in terms of minimizing disease risk and maximizing longevity.
  2. Mike Lustgarten

    Boron/Jarrow Ultra Bone-up for osteoporosis?

    5 minutes/d of strength training is better than 0 minutes/day. It's a small commitment with huge benefits
  3. Mike Lustgarten

    Boron/Jarrow Ultra Bone-up for osteoporosis?

    What about more weight-bearing exercise? Walking, weight lifting, etc.
  4. Thanks mccoy. The microbiome analyses were done before I started eating yogurt, which indicated zero Lactobacillus in my gut. It's possible that including yogurt corrected that deficiency, but I haven't had a microbiome analysis in the past 15 months to confirm that. It's also possible that the magnitude of the whey intake (at most, 75g/d) isn't enough to negatively impact my RBCs, whereas I'm eating ~250g of yogurt/d. It's now low-fat yogurt, and was full-fat to start with at 450g/d. Whereas yogurt is correlated with higher RBCs, it's also correlated with higher creatinine and glucose in my data, and switching to low-fat for my last blood test measurement was associated with lower glucose and creatinine.
  5. The maximal reduction for biological age when using the biological age calculator, Phenotypic Age, is ~20 years. In other words, if I'm 80 years old and my biomarkers are all reflective of youth, the lowest possible biological age will be ~60 years old. One reason for that is the inclusion of chronological age in the prediction of biological age, which adds strength to the correlation while simultaneously limiting the maximal biological age reduction. To account for the possibility that youthful biomarkers at an older chronological age can yield a biological age that is more than 20 years younger, it's important to quantify biological age using a tool that doesn't include chronological age in its calculation. Aging.ai fits that criterion, and in the video I present biological age data with use of aging.ai for 24 blood tests since 2009.
  6. Young.ai is based on aging.ai, which are the creation of In Silico Medicine, which as you mentioned, was recently purchased by a HK company.
  7. LPS increases during aging, which may explain the age-related increase for CD38 and decreased NAD+. LPS is decreased on a calorie restricted diet, but what else can reduce it? In this video, I present evidence for intestinal alkaline phosphatase's (IAP) role on LPS, and posit that interventions that increase IAP may be an important approach for increasing NAD+.
  8. Similarly, serum ALP-mortality risk data in 1.9 million subjects in this paper: https://www.semanticscholar.org/paper/Using-liver-enzymes-as-screening-tests-to-predict-Fulks-Stout/3a81cb1750d9de03f022ad975dfd87d0b3627882. However, measuring IAP in stool is related to optimizing gut microbiome composition and other aspects of gut health. As far as I know, there aren''t any large epi studies for the association with stool levels of IAP with mortality risk.
  9. Right, ALP is found on the standard chem panel, not the CBC. Lef combines the chem panel with the CBC for its $35 test (https://www.lifeextension.com/lab-testing/itemlc381822/chemistry-panel-complete-blood-count-cbc-blood-test), and because that's what I usually get done, I shortened the name to CBC.
  10. I don't think that you realize that medical textbooks are written based on the published literature. I've supported my claims with an abundance of published literature, whereas you've offered opinions. "You didn't even know that intestinal alkaline phosphatase is present in serum tests of alkaline phosphatase." -This is a preposterous statement. Above, I said, "It looks like there are 2 different CPT codes for serum AP: AP by itself (84075), and the sum of all AP isoforms (84080). I'm not sure which is commonly measured on a CBC." -You're going to tell me that you know which AP test is measured on the CBC? You're assuming that it's the sum of all isoforms, which would include IAP as a small component in the serum measure, but it could easily only be serum AP by itself (not IAP, bone AP, etc).
  11. "I'm trying to help you see the Levine biological age formula is disconnected from reality and should not be used the way you are using it." -This is your opinion, and it is not based in any facts, only speculation. "Another example, ALP is highest in our youth it does not linearly increase with age." I've yet to see evidence that ALP is highest in youth. For example, ALP levels are higher in those older than 50, when compared with younger ages: https://www-tandfonline-com.ezproxy.library.tufts.edu/doi/pdf/10.1080/00365510410002742?needAccess=true. ALP increased during aging in NHANES III (Table 1, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260794/) one of the datasets that Levine used to derive the Phenotypic age test.
  12. That's not a direct, published reference. Alternatively, alcohol consumption didn't affect alkaline phosphatase in this study (https://pubmed.ncbi.nlm.nih.gov/2884551/). If you think it's so easy to "hack" biological age, whether it's alkaline phosphatase or other variables, do the experiment, see for yourself. Otherwise it's mere speculation.
  13. Do you have published evidence that someone with an alkaline phosphatase of 25 can double it by drinking? Ha, because again, it looks like the opposite is true: alcohol consumers have significantly lower ALP (https://pubmed.ncbi.nlm.nih.gov/27334005/). So she's have to give up the alcohol, which would potentially raise her ALP, and I'd bet that lots of other variables would improve, too. Levine's Phenotypic age calculator was derived on ~10,000 subjects in NHANES III, this isn't an arbitrary measure based on nothing.
  14. "Yes and this good thing increasing IAP in the intestines will increase slightly serum alkaline phosphatase". -If you have published evidence for this, I'd like to see it. In fact, the opposite is true. For ex., less IAP in the intestine-->more circulating LPS (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213802/). LPS causes increases for serum alkaline phosphatase (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3622013/). I never said that an alkaline phosphatase of 40 is better than 45. Values ~50 are optimal based on all-cause mortality data in > 9 million subjects: https://michaellustgarten.com/2019/10/07/alkaline-phosphatase/. Serum alkaline phosphatase levels also increase during aging, which is why I said that generally lower is better (with 50 as a cutoff).
  15. Mike Lustgarten

    LDL: What's Optimal For Health And Longevity?

    Haha Sibiriak, and thanks!
  16. Mike Lustgarten

    LDL: What's Optimal For Health And Longevity?

    The big question is, even on CR, with optimal values for most biomarkers, will the corresponding low TC and LDL be bad for longevity? At least 2 studies that I know of attempted to account for reverse causation and there was still an increased mortality risk for relatively low circulating levels of cholesterol. To me, that doesn't mean eat more pizza, candy or other junk. Within CR, is there an optimal diet composition that increases LDL, TC to further minimize mortality risk? Alternatively, making sure that the higher cholesterol levels wouldn't promote atherosclerosis or Alzheimer's disease would be a top priority.
  17. Mike Lustgarten

    LDL: What's Optimal For Health And Longevity?

    No, Alex, I said that within my data, coconut butter has the best correlation (close to significance, p=0.07) for lower CRP (see 14:14 in the video). Whether that's causative is unknown.
  18. I think you're misunderstanding me, Todd. High levels of IAP are good for longevity, do you dispute that? Also, relatively lower levels (~50) of serum AP are associated with a reduced all-cause mortality risk. There are papers that support each of these ideas. Do you dispute that? If you have data for age-related changes or all-cause mortality data for the various blood AP isoforms, I'd like to see that.
  19. High fat meals-->increased LPS in the blood (https://academic.oup.com/ajcn/article/86/5/1286/4651083). They're not unrelated, and higher AP, whether it's from serum, intestine, bone, or their sum in the blood is not a good thing, unless you have evidence that contradicts that statement. My initial statement was that high levels of IAP in the intestine (measured in stool samples, for ex., see https://www.thelancet.com/article/S2352-3964(15)30211-5/fulltext) is good, and relatively lower AP in the blood is optimal.
  20. It looks like there are 2 different CPT codes for serum AP: AP by itself (84075), and the sum of all AP isoforms (84080). I'm not sure which is commonly measured on a CBC. Also, if IAP is elevated in the blood, that further suggests gut barrier dysfunction (i.e. it leaks from the lumen to the blood).
  21. "But alk phos is a composite of multiple isoenzymes including IAP which as you point out here might be better to have higher in advanced age while one or more of the other flavors such as from bone or liver might be indicative of trouble when high." -That's not accurate. Intestinal alkaline phosphatase (IAP) is only found in the gut, whereas serum alkaline phosphatase is found in the blood. Yes, they're isozymes, but they're found in different locations. Levine's biological age test measures serum levels, which are correlated with IAP-lower IAP in the gut is correlated with higher serum AP. Ideally, as I mentioned in the video, having higher IAP in the gut, and correspondingly, lower serum AP is ideal. In terms of LDL, yes, that's true, and when considering that gut barrier function declines during aging, whereas LPS and LDL both increase, it makes sense that having higher cholesterol likely aids the immune system (and AP) in LPS detoxification.
  22. In the video: Data for changes in kidney function during aging, kidney function values that are associated with an increased risk of death for all causes What's my data for kidney function, 2006 - 2020? Can diet impact kidney function? Within my data, which foods are correlated with good kidney function? How are the individual components of these foods (fiber, protein, omega-3 fatty acids) correlated with kidney function?