Jump to content

Ron Put

Member
  • Posts

    1,791
  • Joined

  • Last visited

Posts posted by Ron Put

  1. For what it's worth, I went through the snips identified as most significant for LDL-C, including the ones Dayspring mentions, and my genetic profile put me at a somewhat elevated risk.

    It may explain why my total cholesterol hovers around 150-160 despite a pretty low fat diet, that averages about 47 g of total fat, including 7g Omega-3, 13g Omega-6, 8.5g saturated fat and 0.1g transfats.

    But TC was about 180 or so before I cut out EVOO at home, and supplementation with Omega-3 increases my TC and LDL-C as well.

    But my Pulse Wave Velocity is about 6.5 m/s which is not bad for my age.

    So, IMO diet and lifestyle do make significant difference, and in my book they beat the pharmaceutical interventions pushed by Attia and Dayspring any day.

  2. On 5/14/2023 at 1:24 AM, mccoy said:

    This is a pretty concise summary, does dietary cholesterol influence plasma cholesterol? Surprisingly, the answer is little, yes and no. Little in individual who express the average amount of specific receptors in enterocytes, yes in the hyperabsorbers, no in the hypoabsorbers. Genetics govern here and with unlucky combinations of the above receptors some people may be big hyperabsobers and suck up all the dietary cholesterol they eat. Basic concept is that individual variability governs, and this is a main aspect in human biology, which is too often neglected.

    There is a kernel of truth at the core of this, but Dayspring, just like Attia, spins it to make unsupported claims that make little sense, but are aimed at giving comfort to those who like their bacon and eggs too much, and to industry.

    Of course genetics matter, but so do epigenetics and behavior that affects them. And no, most of the genetically endowed cannot eat 20 eggs a day without adverse consequences, as Dayspring claims in almost every interview. Sure, they will have lowER cholesterol compared to the genetically unlucky, but dietary cholesterol and saturated fat still matter.

    Associations of Dietary Cholesterol or Egg Consumption With Incident Cardiovascular Disease and Mortality
     

    Conclusions and Relevance  Among US adults, higher consumption of dietary cholesterol or eggs was significantly associated with higher risk of incident CVD and all-cause mortality in a dose-response manner.

  3. I would also highly recommend the Withings Body Cardio scale.

    In my experience, it provides Body Fat, Lean Mass and Bone Density results that are consistent with my DEXA scans (well, body fat is about 1.5% lower than DEXA according to Withings, but it has been consistently lower by by the same number 4 measurements, so now I can estimate the true number).

    Its unique feature is that it estimates Pulse Wave Velocity and according to what I've seen, it's reasonably accurate.

    (PDF) Withings Body Cardio Versus Gold Standards of Pulse-Wave Velocity and Body Composition (researchgate.net)

  4. On 6/30/2023 at 12:52 PM, mccoy said:

    I received the polar H10 chest

    I have it, but frankly have not used it for quite a while. I use the Venu 2 Plus nowadays and it generally tracks really well with the H10 results, so I eventually abandoned the chest strap, since it's kind of a pain compared to the watch.

    Also, the Venu 2 Plus provides other health information, and its Sleep tracking is definitely improved over past Garmins (it sucked at the very beginning, but then it suddenly improved noticeably).

  5.  

    6 hours ago, IgorF said:

    Just got my fresh report from omegaquant. From the last year I had almost the whole time taken 2 large caps from nowfoods, 1200mg with 500epa/250dha per caps. I would say not a small amount. I had maybe 3 weeks during the year when my bottle with 1200s run out and I dropped to 3-4times smaller amounts daily until my older vegan caps emptied and switched back to these 1200 ones. I also take one caps (1000mg) per 10 days of DGLA.

    I have o6/o3 the same 4,8:1 in the diapason of desirable 3:1-5:1 (close to the less desirable higher part of the range). aa/epa 2.6:1 in desirable 2.5:1-11:1 (lower side mostly due to low AA) and completely not interesting individual acids values.

    Interesting comparison, thanks.

    I got mine recently too, and with no Omega-3 supplementation at all, my Omega-3 Index is 5.33 (less than their "desirable 8%-12%).

    n6:n3 = 5.4:1
    AA:EPA = 7.8:1
    Trans = 0.55%

    Until I see something compelling to make me try EPA/DHA supplementation again, I am done with this experiment. It makes no sense on some many levels, other than as marketing tests and supplements.

    None of the Blue Zone populations traditionally consumed much fish. The Sardinian Blue Zone population was made up of hill-dwellers, who did not consume fish and consumed less dairy products and olive oil that the rest of the Sardinians. Even the Okinawans had very minimal fish intake before the 1960s, far less than that on mainland Japan. Ditto for the Seventh Day Adventists in Loma Linda.

    Fish oil increases LDL-C and the preponderance of the evidence tells us that this is harmful in the long term. Most studies that extol the virtues of fish oil are industry-related and usually done with unhealthy subjects, unhealthy alternatives, or have other issues that make me question them.

    For me, fish oil studies are kind of like olive oil, and even saturated fat/dietary cholesterol studies. They use methodology that often does not apply to healthy populations (for example, those with already high LDL-C saturation often show minimal or no further increases), comparisons to clearly more harmful alternatives, and are often structured to align with industry interests and generate headlines.

    BTW, I used to like Rhonda at the beginning, but she has gone to pill and services pushing nowadays, so I listen far less to her shows. Getting there with Attia too...

  6. On 6/28/2023 at 1:02 PM, Mike Lustgarten said:

     

    Thanks for making the video, Mike.Of course, the correlation may be (and it more likely is) due to other factors, such as various mostly terminal diseases that in advanced stages result in lower cholesterol.

    Or, it may be that many of those on the lower end are on high statin regimens, and side effects like increased blood sugar disregulation and possibly onset of diabetes contribute to their demise (Attia's followers who disregard diet in favor of farmaceuticals to keep Apo B low should be a bit weary of stuff like this).

  7. 1 hour ago, kpfleger said:

    As we've covered in this thread already, vitamin D is a controversial topic with many experts who are strong enthusiasts who think that levels above 30ng/ml are important for a variety of health related areas (not just skeletal health) and other experts who think that it's only relevant for skeletal health or that supplements don't work or that government serum targets that the enthusiasts claim are too low should be lowered, so your ability to find experts who wrote the parts you quoted in your last message is not surprising, but those quotes are a lame thing to bring up in this thread at this point for 2 reasons: (1) The first quote at least seems to be from an April 2020 piece, and that's quite old. And (2) you quoted those experts overall skeptical summary opinions without noting what good data they are based on so those quotes aren't very useful in moving the discussion forward.

    Dude, no, repeating the same claims based on poor studies, most industry sponsored, without addressing the specific problems with your claims, does not make them more convincing.

    There are specific reputable studies that dispute your miracle D claims about specific conditions, not simply "experts who think that it's only relevant for skeletal health or that supplements don't work."

    And the Harvard article is relevant because these are the same people who wrote the guidelines, based on extensive research. Read it again:

    ""... several of the leading epidemiologists and endocrinologists who were on the original IOM committee argue for a lowering of the currently accepted cutoff level of 20, stating that the level they estimated as acceptable was never intended to be used to define vitamin D deficiency. They feel that we are over-screening for vitamin D deficiency, and unnecessarily treating individuals who are perfectly fine."

    Knock yourself out and take all the D you want. But either address the specific objections (and not by reposting endless tweets of the same), or stop calling those who see your exuberance as unfounded "obtuse," and demand acceptance of your aparently fervent beliefs.

  8. 57 minutes ago, Guest said:

    I'm sorry - but did you, Ron and Todd, even read that article past the abstract?

    Guest, you are correct, I did not read beyond the abstract. But my point is not the safety of statins.

    My point is that while people who have abnormal lipids may benefit, some perhaps greatly, healthy people should rely on diet and lifestyle to maintain or optimize their health, not get on statins as Attia suggests.

    For healthy subjects, unneeded pharmaceutical lipid lowering interventions, including statins, may cause unintended deleterious consequences. At least based on what I know of the currently available options.

  9. On 3/17/2023 at 5:52 AM, mccoy said:

    Insulin: once I measured fasting insulin together with glucose, and it was a very small value, close to zero. HOMA-IR suggesting high insulin-sensitivity. I only did that once though.

    IMO fasting glucose without insulin is not all that telling, as it can be affected by many factors, such as what you ate during the last day or exercise, among others.

    My own latest numbers are sadly not great, with FG at 100 and insulin at 7.2. A1C is 5.3. I attribute this to an increase in fructose intake that I see in Cronometer, mainly because I have fallen in love with ripe papaya had it virtually every day in Asia) and carob powder. I din't realize carob has so much sugar, and I've been eating about 30-60g of the stuff a day...

  10. So, I just got my latest tests and since dropping EPA/DHA supplementation, my lipids and other markers have improved, somewhat. My total cholesterol has dropped to 161, while LDL is at 93, with TG at 66. My Apo-B is 75.

    All are still higher than what I'd like, but all are also better than when I was taking the larger dose of EPA/DHA supplementation, and this pattern seems to repeat reliably for a third round so far.

    I didn't get around to testing after the first three months when I was stricter about my fat intake, so these number are likely affected by a higher than usual for me series of restaurant meals, some with gobs of EVOO, but all undoubtedly much fattier than what I eat at home.

    I also got an Omega test in the works, will see what it shows, although I am not convinced that it means as much as they claim.

  11. 17 hours ago, Todd Allen said:

    A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

    While data I've seen generally seems to indicate that statins are beneficial to the average Joe who can't accept the idea of a dinner without a steak, Todd's link helps explain why IMO, the reasoned answer to mccoy's original question about healthy people using statins to manipulate their lipids should probably be "No."

    From Todd's link: "recent pharmacological/biochemical studies, as summarized in this review and elsewhere, have revealed that atherosclerosis is caused by statins taken to lower LDL-C, as well as by warfarin and some types of vegetable fats and oils, in the absence of significantly elevated LDL-C levels. Thus, the promotion of statin treatment by the Statement is rather risky and we do not feel that the conclusions are justified for the prevention of ASCVD." 

    Again, Attia already has had CVD issues, as has Dayspring. So, in their case there may be some confirmation bias in their dismissal of diet and in arguing for pharmaceuticals for healthy people, in addition to other factors (at least some of which are commercial).

    Also, I may have mentioned it before, but in the third part of The Proof interview mccoy posted, Dayspring appears to attribute more importance to diet than I've ever heard him do before. Nevertheless, in part two he still repeats the bombastic nonsense that if you are genetically lucky, you can eat 20 eggs a day without any absorption. 

  12. On 4/6/2023 at 11:16 PM, InquilineKea said:

    What about more involved metabolomics or proteomics? Or blood tests for oxidative stress biomarkers like MDH?

    There is real stuff in this video, but it's basically a vehicle to sell tests... There is still little consensus about markers and methods from the little I know, and the real value of these is unclear.

     

  13. On 6/6/2023 at 4:28 AM, drewab said:

    I haven't had it that I am aware of. I do sometimes question if the testing was accurate though (at the least the rapid tests)

    PCR tests, especially at the 40+ cycles that were used for the first year because of the FDAs absurd politicized recommendations, have positive results if any traces are found, dead or alive, without symptoms. It's why we have these absurd Covid death stats. The rapid tests also generally will give predominantly false positives, I've seen it as high as 60%, depending on the manufacturer. Chances are that you did not have Covid if the test was negative, but some other bug.

    I was immunized very early on with Novavax and have had a total of three doses, including a booster about a year and a half ago. I have never tested positive (and have not really felt sick) even though I generally did not wear a mask and travelled extensively, including in Africa at the start of Omicron early 2022. I am sure it's luck, or I simply did not have symptoms, although the latter is unlikely as I was forced to take numerous PCR tests in order to be able to fly.

    I hope I never witness this collective madness again, but as all involved are busy sweeping their abuse of power under the rug, and most of the media is complicit, I am not holding my breath.

  14. Interesting about turmeric and it makes sense. I've been taking 2 capsules of Curcuwin daily for 5-6 years, and my HS-CRP has been generally low. I also consume turmeric powder as part of my spice mix (together with ashwaganda, chili powder, cumin, nigella, and a few others).

    Depending on the lab, it has been 0.02, which may or may not mean anything, but last week it was a little higher than usual at 0.27 (LabCorp CRP cardio, which is the same as hsCRP). Not sure if the 0.1 increments are valuable information, or fall within lab error.

  15. On 6/8/2023 at 1:44 PM, mccoy said:

    I heard many experts in the field and they all agree that, as a rule, diet and lifestyle cannot solve serious cases of hypercholesterolemia. Also, as a rule, diet and lifestyle cannot bring cholesterol values down to neonatal values. That seems reasonable. Nobody said that diet and lifestyle have no use

    Diet and lifestyle cannot solve serious genetic issues, but they may mitigate many of them, sometimes dramatically (like type 1 diabetes, which for some may be entirely controlled by low fat vegan diet). Todd obviously knows far more about hypercholesterolemia than I do, but my guess is that even there, a balanced whole-food plant-based diet that is very low fat should be expected to help a bit, and also keep other aspects of one's health in better shape. If I remember, Todd has tried that, although the devil may be in the details. Anyway, Todd seems to be an outlier and I am happy that his high-fat diet works for him, of course. But based on my knowledge, I would go low fat balanced HF vegan instead 🙂

    I have certainly heard Attia repeatedly dismiss diet, other than his large protein recommendations. He used to do it more vehemently in the past, especially when he was essentially promoting keto, but still does it, particularly with regards to the issues with cholesterol and microbiota. Attia has personally had CV issues and may personally be justified in using pharmaceuticals, but I think he sprinkles some potentially damaging to some conclusions within his otherwise generally valuable videos.


    mcccoy, thanks for posting The Proof interview in another thread here. Dayspring still uses his "eat 20 eggs a day" quip for those who are genetically lucky, which is clearly a fallacy, even based on his own statements elsewhere, such as the actual amounts of absorption and how they are influenced by diet. Interestingly, he may have retired, as in Part 3 of the interview he is far more open to diet influences than I've ever heard him to date.
     

  16. On 6/9/2023 at 5:09 PM, kpfleger said:

    published an excellent paper in 2021 that claimed that low vitamin D levels caused by higher levels of melanin in skin were absolutely a causal reason for a significant portion of the health disparities in dark-skinned minorities (black & hispanic) in the US: https://pubmed.ncbi.nlm.nih.gov/33546262/ This is not a paper driven by some supplement industry company.

    You should check a bit more carefully before making such a claim... Grant is clearly listed as being funded by Bio-Tech Pharmacal, which claims to sell "The best Vitamin-D and all-natural supplements." (https://www.biotechpharmacal.com/)

    We have to agree to disagree. I only object to the absolute certainty you speak of on a an issue that is far from clear.

    There are a lot of really poor studies on the topic, likely most of them. They often ignore confounders: For instance, your certainty that D supplementation prevents Covid runs into the problem that the vast majority of those hospitalized with Covid were also obese (about 80%, if I recall correctly), regardless of age. Obesity causes a plethora of metabolic issues, including the reduced ability to absorb vitamin D. So, one would expect that there there would be a correlation between D levels and poor outcomes, but it doesn't mean that there is a causation.

    Similarly, with the "Non-industry" study you cited: Obesity is significantly higher in black Americans than in most other groups, and darker pigmentation combined with likely lower outdoor activities and Northern latitudes would correlate with poorer outcomes, but it is unlikely to be a significant cause, based on other evidence.

    Speaking of Harvard, you may have missed the link to their publication's take on D, that I posted earlier in this thread:

    "For the vast majority of healthy individuals, levels much lower, 15, maybe 10, are probably perfectly fine, ..." 

    And: 

    "... several of the leading epidemiologists and endocrinologists who were on the original IOM committee argue for a lowering of the currently accepted cutoff level of 20, stating that the level they estimated as acceptable was never intended to be used to define vitamin D deficiency. They feel that we are over-screening for vitamin D deficiency, and unnecessarily treating individuals who are perfectly fine.

    Based on their analysis, a more appropriate cutoff for vitamin D deficiency would be much lower, 12.5 ng/mL. They examined a massive amount of data from the National Health and Nutrition Examination Survey (NHANES) for 2007 through 2010 and found that less than 6% of Americans had vitamin D levels less than 12.5. A cutoff of 12.5 ng/mL would most certainly eliminate the "pandemic" of vitamin D deficiency."

    Cheers.

  17. 4 hours ago, kpfleger said:

    it absolutely clear that for almost every condition for which vitamin D deficiency correlates with higher incidence or worse outcomes (which includes too many conditions to list, including most of the biggest health burden conditions society faces) the good evidence suggesting that vitamin D status <20ng/ml (deficiency) is more likely to provide good health outcomes than levels above this threshhold is essentially zero.

    I am leery of "absolute" statements in most health discussions, but can't argue with avoiding deficiency.

    The question is, what is deficiency? From what I read, there are no adverse effect in healthy people who test as low as 10. Population data also doe not support the wild claims by the fast growing $2+ billion industry of a "deficiency epidemic" and one can argue that D is about the easiest way for an endocrinologist to point to a "deficiency" and justify  the tests. Many may truly believe it, of course, as they are taught this, and hear it repeated at every seminar. But it doesn't make it true.

    Nobody is arguing that special cases may need supplementation. But personally, my levels are in the 20s and sometimes 30s without supplementation, they were in the 40s with supplementation. I am supposedly genetically predisposed to lower D levels, and while I regularly consume mushrooms, I am vegan to boot.

    I personally do not find it wise to so easily dismiss evidence that this is a largely made up "epidemic.". Vitamin D regulation is pretty efficiently and well done by most healthy bodies. Rare genetic conditions play a role, and also lifestyle choices, such as being fat and never going out certainly have effects on absorption, but these effects are more likely due to a combination of factors, rather than primarily D deficiency.

    Also, one has to wonder about the long-term effects of supplementation, especially the sometimes very large doses prescribed to achieve D status that is not well supported by the evidence, Needless supplementation may interfere with otherwise healthy processes and it may indeed be harmful, or have unintended consequences.

    I don't feel particularly strongly about this, but based on my reading, I have decided to supplement only very occasionally to maintain my natural levels.

  18. On 4/22/2023 at 2:19 PM, mccoy said:

    Would you guys with an already optimal lipids panel (by conventional definitions) contemplate the adoption of Peter's Attia strategy to decrease the atherosclerotic risk to zero, by taking cholesterol lowering drugs?

    I most certainly would not.

    Attia has an agenda, as well as biases, that I disagree with, even though I regularly listen to him. Same for Dayspring.

    Both dismiss nutrition by erecting straw men arguments, without adequately addressing the evidence supporting nutrition. Instead, they focus on pharmaceuticals to remedy what is more often than not caused by poor nutrition (including high-fat and high-protein diets). Dayspring claims that you could eat 20 eggs a day without any adverse effects in many of his appearances, yet has never addresses the fundamental contradiction that saturated fat is very likely to cause long-term detrimental effects, and that some dietary cholesterol is absorbed by virtually anyone, even the genetically lucky ones.

    Dietary cholesterol and (primarily) animal fat will increase your LDL-C, and yes, will also increase your chance of an adverse event. Even the genetically luckiest have a reduced absorption of up to 40%, but first they are a small minority, and also even they can have increased cholesterol if eating 20 eggs a day. For most of us, the less dietary cholesterol and to a large extent, fat intake, the better.

    mccoy, I checked a few of my genetic markers for LDL and no, I am not lucky at all. In my case, I attribute my relatively low lipids on diets, and to a lesser extent to exercise. Diet has by far the largest effect, for example eliminating olive oil dropped my cholesterol by about 30 points, based on my tests. Adding fats increases my numbers.

  19. I take a minute amount daily, because of research I had seen before and because I had not seen anything scary at lower doses. I bought a large bag, so it should last for years.

    I combine it with L-citrulline, NAC, glycine, lutein, B-12, hyaluronic acid and magnesium gluconate.

    Edited to add all supplements I take, including my recent NAC addition.

  20. On 6/6/2023 at 1:40 PM, kpfleger said:

    Very weak observational study to put against the huge body of work (hundreds to thousands of papers) showing causality via RCTs

    Karl, these are strong and categorical statements, but I have to respectfully disagree that the issue is so cut and dry. 🙂

    While industry has been pushing tests and supplementation, most professional bodies do not appear to subscribe to the thesis that a vast number of the population is deficient to the point where it is detrimental.

    Population data does not support your claim, or is contradictory. at best Most people live perfectly healthy lives at the low end of the established minimum values (15 µg in Europe and about 15 in the US).

    Hundreds or thousand of shoddy papers are not proof, at least in my opinion, but also according to plenty of experts in the field. We saw this with Covid and masking.

    Here is something from Harvard (I believe it was posted before):

    "Dr. Finkelstein and his colleagues published a study of over 2,000 perimenopausal women who had been followed for almost 10 years, and they found that vitamin D levels less than 20 were associated with a slightly increased risk of nontraumatic fractures. They concluded that because few foods contain vitamin D, vitamin D supplementation is warranted in women at midlife with levels less than 20 ng/mL. "For perimenopausal women or other groups of people with higher fracture risk, certainly a level of 20 or above is ideal," and he adds: "For the vast majority of healthy individuals, levels much lower, 15, maybe 10, are probably perfectly fine, and so I would say I agree with what the authors of the New England Journal perspective article are saying."

    All that said, most experts, including Dr. Finkelstein, agree we should be checking vitamin D levels in high-risk people — those most at risk for a true deficiency. These include people with anorexia nervosa, people who have had gastric bypass surgeries, who suffer from other malabsorption syndromes like celiac sprue, or who have dark skin, or wear total skin covering (and thus absorb less sunlight). In addition, certain populations will require that vitamin D level of 20 ng/ml or higher. This can include perimenopausal women, people diagnosed with osteopenia (reduced bone density, but not osteoporosis) and osteoporosis or other skeletal disorders, as well as pregnant and lactating women. All of these groups should be screened and treated as appropriate."

    And here is what AMA-ASSN has to say:

    "Caution is warranted given the surprising lack of effects, or sometimes even harmful effects, found in large, long-term trials of other previously promising nutrients and hormones, such as antioxidants and hormone replacement therapy. It is likely that greater vitamin D exposure will benefit at least some in the population, but more research is needed. Conclusions: While the associations between vitamin D and various disease outcomes appear promising, clinical trials have yet to prove that vitamin D is causally related to most of these outcomes. More long-term, well-designed studies, including large intervention trials, are needed across all life stage and racial and ethnic groups to better understand vitamin D’s role in disease prevention, to determine the optimal doses and serum 25(OH)D levels, and to fully elucidate the potential for adverse outcomes at various intakes. Nevertheless, physicians should consider measuring the serum concentration of 25(OH)D in patients at risk of vitamin D deficiency and counsel those with deficient or insufficient levels on ways to improve their vitamin D status."

  21. I recall that this may have been posted before somewhere, but it's worth noting to keep things in perspective:

    Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study

    Abstract

    Background: Low levels of 25(OH) vitamin D are associated with various age-related diseases and mortality, but causality has not been determined. We investigated vitamin D levels in the offspring of nonagenarians who had at least one nonagenarian sibling; these offspring have a lower prevalence of age-related diseases and a higher propensity to reach old age compared with their partners.

    Methods: We assessed anthropometric characteristics, 25(OH) vitamin D levels, parathyroid hormone levels, dietary vitamin D intake and single nucleotide polymorphisms (SNPs) associated with vitamin D levels. We included offspring (n = 1038) of nonagenarians who had at least one nonagenarian sibling, and the offsprings' partners (n = 461; controls) from the Leiden Longevity Study. We included age, sex, body mass index, month during which blood sampling was performed, dietary and supplemental vitamin D intake, and creatinine levels as possible confounding factors.

    Results: The offspring had significantly lower levels of vitamin D (64.3 nmol/L) compared with controls (68.4 nmol/L; p = 0.002), independent of possible confounding factors. There was no difference in the levels of parathyroid hormone between groups. Compared with controls, the offspring had a lower frequency of a genetic variant in the CYP2R1 gene (rs2060793) (p = 0.04). The difference in vitamin D levels between offspring and controls persisted over the 2 most prevalent genotypes of this SNP.

    Interpretation: Compared with controls, the offspring of nonagenarians who had at least one nonagenarian sibling had a reduced frequency of a common variant in the CYP2R1 gene, which predisposes people to high vitamin D levels; they also had lower levels of vitamin D that persisted over the 2 most prevalent genotypes. These results cast doubt on the causal nature of previously reported associations between low levels of vitamin D and age-related diseases and mortality.

  22. 19 hours ago, IgorF said:

    after some thinking about ldl-c and ldl-p I could say the logic on focusing on p is like this:

    - particles number is considered a primary thing that forms the risk

    Not necessarily true per se. As the video above mentions regarding APO-B, it becomes primary only if there is a discordance. Otherwise, the studies are inconclusive, which is why it is not routinely tested in the US. My own physician, who indulges my sometimes excessive testing, told me exactly this when I first requested APO-B -- that I am metabolically healthy and total and non-HDL cholesterol are more important in my case, as there is no likelihood that there will be a discordancy. And he was right, of course, as studies show discordancy within a few years to a decade or so after one becomes metabolically diseased.

    But Attia, Dayspring and a bunch of others are by far the most prolific and vocal on social media, because LDL-C is often a problem for those on high-fat diets who are often metabolically compromised, so they keep pushing the focus on APO-B. Pharma pushes this as well, as Attia's message drives sales.

    Statins have their benefits in diseased people, but IMO it's idiotic to suggest that healthy people take them so that they can indulge in a bad diet.

  23. 13 hours ago, BrianA said:

    Article discussing evidence for hypothesis that covid could raise Parkinson's risk by 50% (taking absolute risk level in general population from 2% up to 3%).

    The fact that infectious diseases of all sorts may have longer term effects in some people is well documented and it has been discussed numerous times here as well. It's a balance, if you are never exposed, you may die, and if you are exposed, you may develop certain long-term effects. But Covid has been a unique source of so many click-bait articles (and shoddy studies) touting it as something completely new and scary.

    A quick search brings up the same for the flu...


    The Flu Factor: Is There a Link to Parkinson’s? | Parkinson's Foundation

×
×
  • Create New...