now that the dust has settled, what unironically went wrong?

now that the dust has settled, what unironically went wrong?

  1. 4 weeks ago
    Anonymous

    If you fell for the low carb meme, you should unironically remove yourself from the gene pool.

    • 4 weeks ago
      Anonymous

      Probably ate too fatty for too long.
      Never go full retard with a diet.

      you're both unfortunately retarded

      • 4 weeks ago
        Anonymous
        • 4 weeks ago
          Anonymous

          weird propaganda

      • 4 weeks ago
        Anonymous

        Interesting opinion, however, you did not post body.
        I'm afraid I'll have to discard it. Sorry.

        • 4 weeks ago
          Anonymous

          wow very fascinating, i shall be sure to disregard your propaganda.

          • 4 weeks ago
            Anonymous

            >being male
            >liking "cute" things

            • 4 weeks ago
              Anonymous

              >being insecure
              that's rough. i've personally never lacked confidence, but i see it in people all the time. i wish you the best

    • 4 weeks ago
      Anonymous

      Post body

    • 4 weeks ago
      Anonymous

      Retard spotted

  2. 4 weeks ago
    Anonymous

    Probably ate too fatty for too long.
    Never go full retard with a diet.

  3. 4 weeks ago
    Anonymous

    You can do all the stuff he did and still have chronic vascular inflammation due to genetic or environmental factors.
    Stress, air pollution, chronic infection, poor gut health, etc.
    Cholesterol doesn't cause heart disease in and of itself, but it will make it worse if you have any of the underlying causes.
    If you're really, genuinely, unironically interested in a hypothesis that explains all aspects of heart disease and why all the myriad risk factors that have nothing to do with your diet can influence your vascular health, then read this article

    https://pubmed.ncbi.nlm.nih.gov/35938775/

    >Assessing cardiovascular disease: looking beyond cholesterol
    >Purpose of review: The low-density lipoprotein (LDL)-cholesterol level is a weak predictor of developing cardiovascular (CV) disease and can only explain a small proportion of CV risk. It is not used to determine CV risk on either the atherosclerotic cardiovascular disease (ASCVD) calculator in the United States, or the Qrisk3 in the UK.A study in JAMA in 2022 suggested that ' the absolute benefits of statins are modest and may not be strongly mediated through the degree of LDL reduction '. Perhaps it is time to look beyond cholesterol to a different causal model - the 'thrombogenic' model of ASCVD.
    >Recent findings: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) pandemic demonstrated that infectious agents damage the endothelium and the glycocalyx - the glycoprotein layer protecting underlying endothelial cells. There are numerous other conditions leading to this kind of damage, which can trigger thrombus formation, causing strokes and myocardial infarctions.
    >Summary: The cholesterol hypothesis, that a raised LDL is directly causal for ASCVD, does not adequately explain cardiovascular risk in individuals, or populations. An alternative 'thrombogenic' hypothesis is proposed as a more valid causal model.

    • 4 weeks ago
      Anonymous

      The ‘low density lipoprotein (LDL)-cholesterol hypothesis’ is widely accepted as the best model explaining how atherosclerotic cardiovascular disease (ASCVD) develops. It states that a raised LDL level causes thickenings within arterial walls which gradually develop into larger plaques.

      More vulnerable plaques may then ‘rupture’, triggering the final thrombotic event, fully occluding an artery, leading to events such as myocardial infarction (MI) and strokes.

      However, the association between a raised LDL level and the development of ASCVD is weak. Indeed, many studies have found no association or even an inverse association, particularly in the older population, where most deaths from ASCVD occur [1▪].

      The inability of LDL to accurately predict risk highlighted by the fact that the two most widely used calculators for ASCVD, in the United States and UK, do not use LDL levels to establish the risk of a future cardiovascular (CV) event [2,3].

      Whilst it is true that statins reduce the risk of ASVCD, the absolute reduction in risk is small [4▪▪]. Additionally, several agents that significantly lower LDL demonstrated no benefit on ASCVD, including cholesterol ester transfer protein inhibitors such as torcetrapib and evacetrapib. Evacetrapib reduced LDL by 37% and increased high-density lipoprotein (HDL) by 120% but had no effect on CV risk [5].

      Examining ASCVD from a process perspective, plaques have been found to contain lipoprotein remnants, assumed to originate from LDL. However, there remains the likelihood that the majority of these remnants actually originated from lipoprotein(a) (Lp(a)). This points to a different causal model, as Lp(a) plays a role in thrombus formation and lysis, not lipid transport.

      • 4 weeks ago
        Anonymous

        The different causal model was first postulated in 1852 by Karl von Rokitansky, which he called the encrustation hypothesis. It is possibly better known as the ‘thrombogenic hypothesis’ [6]. He proposed that ASCVD develops as a result of a dysfunction in a normal three-step process.

        Step one damage to the endothelium/glycocalyx. This damage leads to step two, the formation of a thrombus to cover the damaged area. The thrombus is, in turn, covered by a new layer of endothelium which effectively draws the thrombus into the artery wall.

        Step three is that the remnant thrombus is broken down or lysed by various repair mechanisms, such as macrophage action, which can break down and remove the remnants of damaged material.

        However, if damage is accelerated, plaques are bigger and/or more difficult to break down, or repair is hampered, plaques can develop and grow.

        Therefore, the thrombogenic hypothesis proposes that factors that can increase the risk of ASCVD are those that do one of three essential things:

        (1) Increase the rate of endothelial/glycocalyx damage beyond that which the repair mechanism can handle.
        (2) Drive the formation of larger and/or more difficult to lyse/remove thrombi.
        (3) Interfere with the repair processes (see Fig. 1).
        >Fig 1
        The Three processes that drive ASCVD. This figure outlines that ASCVD is driven by three interlinked processes. Endothelial/glycocalyx damage, accelerated thrombus formation and impaired repair to the resultant damage/thrombus. If all three processes are occurring ASCVD will be greatly accelerated. ASCVD, atherosclerotic cardiovascular disease.

        • 4 weeks ago
          Anonymous

          To put this another way, if the process of damage occurs faster than repair, plaques will form, and grow larger. If the repair systems are working at a rate matching the damage, plaque growth will be slowed, or prevented.

          This is a concept supported by the paper ‘Why atherothrombosis is in principle a hematologic disease’. The authors present evidence that conditions, and drugs, which affect thrombosis also affect the development of atherosclerotic plaques. They propose that plaques develop from the organisation of mural thrombi that have not been fully cleared away by the repair processes, thus creating a ‘vulnerable’ area for further thrombi to develop [7].
          RECENT EVIDENCE IN SUPPORT OF THE THROMBOGENIC HYPOTHESIS
          This review will look at the three interlinked processes involved in atherosclerotic plaque formation

          (1) Glycocalyx and endothelial damage
          (2) Formation of larger/more difficult to lyse thrombi
          (3) Interference with repair processes

          All blood vessels are lined with endothelial cells which are, in turn, covered by a ‘gel’ layer, the glycocalyx, which is where nitric oxide (NO) is synthesised, along with many other anticoagulant factors (see Fig. 2).
          >Fig 2
          The glycocalyx. This graphic shows the structure of the glycocalyx, which protrudes from endothelial cells in all blood vessels and creates a protective and anticoagulant ‘gel’ layer. It is constructed from combined molecules of glucose and various proteins.

          The glycocalyx acts as the protective layer necessary to maintain vascular endothelial cell function, and homeostasis. It is also important to protect the underlying endothelial cells from direct physical damage [8].

          It has been increasingly recognised that in many acute illnesses the glycocalyx is thinned and weakened. This, in turn, increases the risk of acute cardiovascular events [9▪▪].

          • 4 weeks ago
            Anonymous

            For example, destruction of the glycocalyx/endothelium is critical in sepsis, where it is a major contributor to the underlying pathophysiology. The destruction of the glycocalyx is primarily due to exotoxins released by bacteria in the bloodstream. This, in turn, is followed by widespread thrombus formation, known as disseminated intravascular coagulation [10].

            In Sars-Cov2 infection the glycocalyx/endothelium is also attacked and weakened, and this is the trigger for the blood clots that are commonly seen with coronavirus disease 2019 (COVID-19) infection [9▪▪].

            Unlike sepsis, where the glycocalyx broken down by an external agent, with severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the damage occurs within endothelial cells. Endothelial cells in the lungs, and the vasculature, have a high concentration of Angiotensin Converting Enzyme 2 receptors, and SARS-CoV2 hijacks this receptor to gain entry before multiplying and ‘bursting out’. So, the cells are damaged from ‘within’, rather than in sepsis, from ‘without’. The end result is similar.

            It is now also known that there is also considerable overlap between SARS-CoV2 infection and Kawasaki's disease. In both conditions there is a form of widespread vasculitis, with the glycocalyx/endothelium seriously compromised. With SARS-CoV2 the presence of virions within cells provides an additional target for ‘attack’ by the immune system, increasing the damage [11].

            It seems that the process Kawasaki's is very similar, although an infectious agent has not been identified. In Kawasaki's, ASCVD can develop rapidly, and in the years following the acute episode the risk of a CV event can be increased by >50-fold [12].

            The acute problems, seen shortly after an initial triggering event, highlight the role that the healthy glycocalyx plays in preventing thrombus formation. However, it is also hypothesised to be critical in the longer-term progression and development of ASCVD

            • 4 weeks ago
              Anonymous

              Looking at longer term conditions, one important factor known to cause chronic damage to the glycocalyx is a raised blood glucose level. Interestingly, patients with type II diabetes are at an increased risk of ASCVD, sepsis, and other infection diseases. Possibly due to a damaged glycocalyx allowing infectious agents to enter cells more easily.

              Here, we have a possible ‘positive reinforcement loop’, increasing both infection risk and thrombus formation, which may also be why patients with type II diabetes are more susceptible to severe SARS-CoV2 infections.

              Other chronic conditions known to damage the glycocalyx and increase the risk of CVD include:

              (1) Systemic lupus erythematosus (SLE)
              (2) Smoking
              (3) Hypertension
              (4) Antiphospholipid syndrome
              With antiphospholipid syndrome (APS), the immune system attacks the endothelial cell membrane itself, creating widespread vascular damage. Many patients with SLE have APS, and it is this subset of patients at greatest risk of ASCVD.

              It is not within the scope of this article to describe all conditions, or agents that can damage the endothelium/glycocalyx. However, an increasing body of evidence suggests that any factor, or disease, with this effect, increases the risk of ASCVD

              >FORMATION OF LARGER/MORE DIFFICULT TO LYSE THROMBI
              Once the endothelium has been damaged this triggers thrombus formation. One of the key mechanisms here is that an undamaged and healthy endothelium expresses tissue factor pathway inhibitor (TFPI). TPFI limits the actions of tissue factor (TF), which is perhaps the single most potent pro-coagulant factor.

              Thus, when TFPI production falls, TF is released to drive thrombus formation. In addition to this mechanism, the glycocalyx is where NO, a highly potent anticoagulant, is synthesised (indeed, there are a host of anticoagulant actions which require a healthy glycocalyx to function). This means that, when damage occurs, the endothelium shifts towards a prothrombotic state

              • 4 weeks ago
                Anonymous

                It would not be possible to review all the factors involved in thrombus formation and breakdown, as this is a highly complex process. So it may be most useful to look at three important players: von Willebrand factor (vWF), fibrinogen, and Lp(a) to review their impact on thrombi.

                These three factors operate in very different stages of coagulation. vWF has a key role in formation of the initial platelet plug, fibrinogen is the raw material of the final ‘fibrin’ clot, and Lp(a) is critical in thrombus breakdown or lysis.

                >Von Willebrand factor

                vWF is a glycoprotein required for the formation of haemostatic ‘plugs’ and arterial thrombi. It binds to platelets, factor VIII, and collagen in the underlying artery wall.

                A meta-analysis of patients admitted to hospital with major adverse CV events found that they had significantly higher vWF levels. The difference in CV risk versus those with normal levels of vWF was very nearly 50% [24].

                >Fibrinogen

                Fibrinogen has a key role in the final act of thrombus formation. After the platelet/erythrocyte plug has formed, strands of fibrinogen link to form fibrin, which wraps around the plug, binding it. This is the final step in the clotting ‘cascade’.

                A Scottish study of risk factors for coronary heart disease showed that high levels of fibrinogen were associated with a greatly increased CV risk, for both men and women [25].

                In a more recent meta-analysis, the increased risk was independent of other CVD risk factors including lipid levels, and antithrombotic and other medications, such as aspirin. It is of interest that the risk of ASCVD was much greater in patients with type II diabetes, who have higher levels of other pro-coagulant factors [26▪]”.

              • 4 weeks ago
                Anonymous

                Lipoprotein(a)
                The issue of Lp(a) is complex, but important. Lp(a) is identical to LDL, apart from the attachment of an additional protein, known as apolipoprotein(a) (apo(a)).

                This apparently small difference is highly significant, because apo(a) is virtually identical in structure to plasminogen. The key difference is that apo(a) has different folding structure (kringle) at one end. It is this ‘folding’ difference that turns apo(a) into, effectively, ‘antiplasminogen’.

                Plasminogen is incorporated into all thrombi as they form. It is inactive until it is converted to plasmin by tissue plasminogen activator (TPa), which is an enzyme synthesised by endothelial cells. Once TPa has triggered this conversion plasmin lyses strands of fibrin, essential for the breakdown of thrombi.

                However, if there is a higher concentration of Lp(a)/apo(a) within thrombi, this blocks the action of TPa on plasminogen, resulting in a thrombus that is highly resilient [27].

                Lp(a) also binds to TFPI. Thus, Lp(a) can stimulate clot formation and make it more difficult to remove the resultant thrombi. A raised Lp(a) is associated with a tripling of CVD risk [28▪▪].

                Why does Lp(a) have this function? Linus Pauling first hypothesised that, because humans cannot synthesise vitamin C, which plays a key role in the production of collagen, a lack of vitamin C will lead to a breakdown and ‘cracks’ in blood vessel walls.

                Lp(a), which is almost exclusively found in animals that cannot synthesise vitamin C, binds very strongly to the endothelium. and the underlying arterial wall, creating thrombi that are particularly ‘tough’. This reduces blood loss, allowing the animal to survive until sufficient vitamin C can be consumed [29].

                However, this protective role is a double-edged sword. As Lp(a) can also drive the formation of thrombi which are more difficult to lyse. This, in turn, results in accelerated plaque formation.

              • 4 weeks ago
                Anonymous

                Haemophilia
                To briefly examine this area from a different perspective, it is worth looking at people with haemophilia. A recent study found that the relative risk of CV events in haemophilia was around one third of predicted risk. The authors concluded that ‘haemophilia protects against CVD’ [31].

                INTERFERENCE WITH REPAIR PROCESSES
                Endothelial damage, clot formation and repair, represents a continual process. This is highlighted in people who smoke – who have a significantly higher risk of CVD. Smoking leads directly to glycocalyx damage, reduced NO production and bioavailability which, in turn, creates a pro-coagulant and inflammatory environment [32▪].

                This damage can, in turn, be measured by an increase in microparticles – the breakdown products of endothelial cells. However, smoking also stimulates the production and release of endothelial progenitor cells (EPCs), which cover over areas of endothelial damage, driving the healing process [33].

                Therefore, with smoking, increased damage and repair occurs simultaneously. This means that damage to the endothelium/glycocalyx does not necessarily lead to (accelerated) atherosclerotic plaque formation.

                However, if the repair systems are impaired, or the damage is simply too extensive, plaque formation/growth will occur. This is probably why, as people become older, and the repair systems become less robust, a risk factor such as smoking becomes more significant [34].

                The conjecture that reduced repair is as important as damage is supported by the fact that low EPC levels are an initial sign of endothelial dysfunction and represent one of the early signs of ASCVD.

                Of course, EPCs do not represent the only repair system(s). But it is clear that protection against ASCVD requires a positive balance between repair and damage. This can perhaps be most clearly seen when we look at agents, which have been designed to block endothelial cell growth and repair, simultaneously reducing NO synthesis.

              • 4 weeks ago
                Anonymous

                These are vascular endothelial growth factor (VEGF)-inhibitors. VEGF is a hormone which drives endothelial cell proliferation, survival, and migration [36]. It also stimulates the production of EPCs in the bone marrow.

                VEGF-inhibitors are used in cancer treatments to prevent endothelial growth and thus angiogenesis, as new blood vessels to deliver the blood supply required for growth in many tumours.

                It is no surprise, therefore, that the adverse effects of VEGF-inhibitors centre around vascular damage, including haemorrhage, retinal detachment, venous thrombosis, strokes, MI and heart failure [37].

                At one time, the increased cardiovascular risks associated with bevacizumab, the first widely used VEGF-inhibitor, nearly led to its withdrawal from the market. This highlights the critical importance of repair in the triad of endothelial damage, clot formation, impaired repair.

              • 4 weeks ago
                Anonymous

                >SUMMARY
                For the last seventy years the LDL-cholesterol hypothesis has been the most widely accepted causal model for the development of ASCVD. However, it cannot explain how many different factors such as smoking, SLE, or chronic kidney disease can lead to ASCVD.

                In addition, a raised LDL level is a relatively weak predictor of risk. Indeed, LDL is not used to calculate CV risk using Qrisk3, or the ACC/AHA risk calculator.

                An alternative model is one that was first proposed over one hundred and fifty years ago by Karl von Rokitansky, which is that atherosclerotic plaques represent the build-up/metamorphosis of thrombi that have been deposited onto, then incorporated into the arterial wall.

                Other researchers, for example, Elspeth Smith, promoted the thrombogenic hypothesis widely. Forty years ago, she wrote: ‘After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved. Not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development, from the initiation of atherogenesis to the expansion and growth of large plaques’ [38].

                It should be recognised that this was written before NO and EPCs had been identified, and also before the protective function of the glycocalyx and the structure of apo(a) had been established.

              • 4 weeks ago
                Anonymous

                >CONCLUSION
                We now have a greater understanding of the endothelial/glycocalyx function and how endothelial damage links to thrombus formation and lysis, and these new findings strongly suggest that Rokitansky, Duguid, Ross and Elspeth Smith, and others, may well have been correct.

                Thus, whilst this article is entitled “Assessing cardiovascular disease: looking beyond cholesterol”, it may have been more accurate to call it, ‘Assessing cardiovascular disease, looking before cholesterol’, because the thrombogenic hypothesis precedes the cholesterol hypothesis by many years. It is fascinating that recent research now provides an increasing evidence base.

                >Acknowledgements
                None.

                >Financial support and sponsorship
                None.

                >Conflicts of interest
                The author has written three books critical of the LDL-cholesterol hypothesis. The Great Cholesterol Con, A Statin Nation and The Clot Thickens.

                https://journals.lww.com/co-endocrinology/Fulltext/2022/10000/Assessing_cardiovascular_disease__looking_beyond.4.aspx

              • 4 weeks ago
                Anonymous

                ApoB clogs your arteries and causes heart disease therefore ldl which is raised by saturated fat and cholesterol cause clog your arteries, particle size of ApoB doesn't matter all sizes are equally damaging to the arteries, simple as.
                >ivor retard
                He was refuted by a MD Phd in this video

                %21

              • 4 weeks ago
                Anonymous

                >Dr. Malcom Kendrick
                appears to be obese

                Why the fuck should I listen to him or read his faggy book?

      • 4 weeks ago
        Anonymous

        >However, the association between a raised LDL level and the development of ASCVD is weak.
        lol lmao
        https://academic.oup.com/eurheartj/article/38/32/2459/3745109?login=false
        >European Heart Journal
        >Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.

        • 4 weeks ago
          Anonymous

          higher LDL makes you live longer
          > High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.
          https://pubmed.ncbi.nlm.nih.gov/27292972/

          • 4 weeks ago
            Anonymous

            That trash study was debunked here:
            https://www.cebm.ox.ac.uk/news/views/cebm-response-lack-of-an-association-or-an-inverse-association-between-low-density-lipoprotein-cholesterol-and-mortality-in-the-elderly-a-systematic-review-a-post-publication-peer-review
            >However there are serious methodological flaws with their study, not least the lack of a published protocol, searching of only one database, nonuniform application of inclusion/exclusion criteria, a lack of critical appraisal of the methods used in the included studies, no indication of the quality or uncertainty of the included data and issues with the accuracy of data extraction. A lack of controlling for confounding due to the effect of lipid-lowering treatment and HDL-C levels presents major bias and more likely underpins the majority of the observed inverse associations.
            And here too by multiple MDs
            https://www.sciencemediacentre.org/expert-reaction-to-systematic-review-reporting-lack-of-an-association-between-ldl-cholesterol-and-mortality-in-the-elderly/
            In reality the more ldl the more mortality, pic related

            • 4 weeks ago
              Anonymous

              >A lack of controlling for confounding due to the effect of lipid-lowering treatment
              if theyre on lipid lowering treatment they shouldnt have high ldl. doesnt make sense
              >HDL-C level
              why should this matter?
              >searching of only one database
              not atypical
              shit "debunking" attempt

              • 4 weeks ago
                Anonymous

                >why should this matter?
                Total cholesterol raises CHD so it matters
                >if theyre on lipid lowering treatment they shouldnt have high ldl
                Were they or not? If you who posted the trash study who you don't know nothing about

              • 4 weeks ago
                Anonymous

                >If you who posted the trash study who you don't know nothing about
                the lipid lowering treatment confounding was raised by the critique you posted. i explained why its not a valid critique and you ignored it

              • 4 weeks ago
                Anonymous

                Statins do lower mortality by reducing ldl
                https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884492/
                >Ten trials involving 79 494 subjects were included in the meta-analysis.
                >Statins reduce coronary events, strokes and all-cause mortality without increasing noncoronary mortality.
                LDL does not make you live longer. An actual graph of a real study was posted here already, more saturated fat more mortality see

                https://i.imgur.com/pdIWRxb.png

                That trash study was debunked here:
                https://www.cebm.ox.ac.uk/news/views/cebm-response-lack-of-an-association-or-an-inverse-association-between-low-density-lipoprotein-cholesterol-and-mortality-in-the-elderly-a-systematic-review-a-post-publication-peer-review
                >However there are serious methodological flaws with their study, not least the lack of a published protocol, searching of only one database, nonuniform application of inclusion/exclusion criteria, a lack of critical appraisal of the methods used in the included studies, no indication of the quality or uncertainty of the included data and issues with the accuracy of data extraction. A lack of controlling for confounding due to the effect of lipid-lowering treatment and HDL-C levels presents major bias and more likely underpins the majority of the observed inverse associations.
                And here too by multiple MDs
                https://www.sciencemediacentre.org/expert-reaction-to-systematic-review-reporting-lack-of-an-association-between-ldl-cholesterol-and-mortality-in-the-elderly/
                In reality the more ldl the more mortality, pic related

              • 4 weeks ago
                Anonymous

                the statin mortality benefit only exists if you look at RCTs conducted before the New Clinical Trial Regulations in 2005 due to pharma misconduct with Vioxx and Celebrex. not to mention the raw clinical trial data is almost entirely held under lock and key by the manufacturers and CTT and has NEVER been subject to independant analysis. its not even clear that the supposed benefit is related to LDL lowering or some other pleiotropic effect
                >The study results suggest that the absolute benefits of statins are modest, may not be strongly mediated through the degree of LDL-C reduction
                https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2790055

              • 4 weeks ago
                Anonymous

                Are the chud vegans shilling statins now as well as sugar? Lol, lmao even

              • 4 weeks ago
                Anonymous

                Nah they still lower mortality because they lower ldl
                https://www.ahajournals.org/doi/full/10.1161/CIRCOUTCOMES.121.008552
                >A total of 21 trials with 184012 patients and an average mean follow-up of 4.4 years were included
                >The benefits of LDL-C lowering do not seem to be fixed but increase steadily with longer durations of treatment. The results from short-term randomized trials are compatible with the very strong associations between LDL-C and cardiovascular events seen in Mendelian randomization studies.

              • 4 weeks ago
                Anonymous

                unclear as the raw data have never been independently analyzed

              • 4 weeks ago
                Anonymous

                Do you want it to be analyzed by the keto guru youtubers you follow

              • 4 weeks ago
                Anonymous

                any group of researchers not directly funded by industry would be just fine. the CTSU at Oxford has signed an NDA with industry and recieved millions of dollars to keep the raw data under lock and key. surely this isnt "the science" you people love to praise. if they are such wonderful drugs more transparency would pose no threat to their business model. i suspect that sooner or later the data will be released too little too late now that the drugs are coming out of patent and will be replaced by PCSK9 inhibitors

              • 4 weeks ago
                Anonymous

                Aha, here's another, statins lower ldl and morality
                > Across all 26 trials, all-cause mortality was reduced by 10% per 1·0 mmol/L LDL reduction
                https://pubmed.ncbi.nlm.nih.gov/21067804/

              • 4 weeks ago
                Anonymous

                what i said in

                the statin mortality benefit only exists if you look at RCTs conducted before the New Clinical Trial Regulations in 2005 due to pharma misconduct with Vioxx and Celebrex. not to mention the raw clinical trial data is almost entirely held under lock and key by the manufacturers and CTT and has NEVER been subject to independant analysis. its not even clear that the supposed benefit is related to LDL lowering or some other pleiotropic effect
                >The study results suggest that the absolute benefits of statins are modest, may not be strongly mediated through the degree of LDL-C reduction
                https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2790055

                still applies. a review of post 2005 data shows no effect on mortality

              • 4 weeks ago
                Anonymous

                >a review of post 2005 data
                Did it review this one

                Nah they still lower mortality because they lower ldl
                https://www.ahajournals.org/doi/full/10.1161/CIRCOUTCOMES.121.008552
                >A total of 21 trials with 184012 patients and an average mean follow-up of 4.4 years were included
                >The benefits of LDL-C lowering do not seem to be fixed but increase steadily with longer durations of treatment. The results from short-term randomized trials are compatible with the very strong associations between LDL-C and cardiovascular events seen in Mendelian randomization studies.

                ? No? Then it should be ignored

              • 4 weeks ago
                Anonymous

                >post 2005
                Data from 2002 says the same thing, statins work by reducing ldl
                >Pravastatin given for 3 years reduced the risk of coronary disease in elderly individuals.
                >Mortality from coronary disease fell by 24% (p=0.043) in the pravastatin group. Pravastatin had no significant effect on cognitive function or disability.
                https://pubmed.ncbi.nlm.nih.gov/12457784/

              • 4 weeks ago
                Anonymous

                2002 is before 2005. are your statins damaging your cognition?

              • 4 weeks ago
                Anonymous

                You are dismissing all data after 2005 while data before 2005 says the same things. Reduction in mortality

              • 4 weeks ago
                Anonymous

                no difference in all cause mortality

              • 4 weeks ago
                Anonymous

                24% less mortality idiot

              • 4 weeks ago
                Anonymous

                all cause mortality no difference

                You are dismissing all data after 2005 while data before 2005 says the same things. Reduction in mortality

                post 2005 data shows zero mortality benefit

              • 4 weeks ago
                Anonymous

                24% less mortality from heart disease therefore statins reduce mortality. Heart disease is the main cause of death everywhere

              • 4 weeks ago
                Anonymous

                if you die of cancer instead of heart disease youre still dead

              • 4 weeks ago
                Anonymous

                Cool. Still, statins decrease mortality. No one said they cure cancer lel

              • 4 weeks ago
                Anonymous

                no difference on all cause mortality. they might increase cancer rates per what you posted

              • 4 weeks ago
                Anonymous

                > they might
                Nice hypothesis, comeback with a study meanwhile statins decrease mortality whether you like it or not

              • 4 weeks ago
                Anonymous

                >New cancer diagnoses were more frequent on pravastatin than on placebo (1.25, 1.04-1.51, p=0.020)
                its an observation from what you posted...

              • 4 weeks ago
                Anonymous

                > However, incorporation of this finding in a meta-analysis of all pravastatin and all statin trials showed no overall increase in risk.
                No risk from cancer, from literally the next line after what you quoted

              • 4 weeks ago
                Anonymous

                >hey our drug caused cancer but look when we throw it together with a bunch of other low quality data the effect disappears
                amazing... really

              • 4 weeks ago
                Anonymous

                Yes, statins decrease mortality because they reduce ldl, anything else

              • 4 weeks ago
                Anonymous

                no mortality benefit despite how much misplaced faith you want to place in pharmaceutical companies

              • 4 weeks ago
                Anonymous

                I don't have faith at all, it's reality, lowering ldl reduces cvd mortality, here's another bunch RCTs about cholesterol and ldl from animal products
                https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400894/
                >Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c.

              • 4 weeks ago
                Anonymous

                more junk "science"

                https://i.imgur.com/JTKzi6f.png

                >not even remotely
                Wrong
                The lower the ldl, the lower the risk of cvd

                junk. all debunked in

                the statin mortality benefit only exists if you look at RCTs conducted before the New Clinical Trial Regulations in 2005 due to pharma misconduct with Vioxx and Celebrex. not to mention the raw clinical trial data is almost entirely held under lock and key by the manufacturers and CTT and has NEVER been subject to independant analysis. its not even clear that the supposed benefit is related to LDL lowering or some other pleiotropic effect
                >The study results suggest that the absolute benefits of statins are modest, may not be strongly mediated through the degree of LDL-C reduction
                https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2790055

              • 4 weeks ago
                Anonymous

                not an argument, statins lower mortality see this whole thread and
                https://www.ahajournals.org/doi/full/10.1161/CIRCOUTCOMES.121.008552,
                >each mmol/L LDL-C lowered was associated with a relative risk reduction in major vascular events of 12% (95% CI, 8%–16%) for year 1, 20% (95% CI, 16%–24%) for year 3, 23% (95% CI, 18%–27%) for year 5, and 29% (95% CI, 14%–42%) for year 7.

                And one last study to finish you off
                https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30135-X/fulltext
                >Low carbohydrate dietary patterns favouring animal-derived protein and fat sources, from sources such as lamb, beef, pork, and chicken, were associated with higher mortality, whereas those that favoured plant-derived protein and fat intake, from sources such as vegetables, nuts, peanut butter, and whole-grain breads, were associated with lower mortality,
                Animal protein increases mortality, whereas plant protein does the opposite
                Now you can go back to watch your bald keto youtuber

              • 4 weeks ago
                Anonymous

                oh and they might give you dementia

                pharma is smart enough not to fund any RCTs testing statins on cognition. its never mentioned by shills because its very inconvenient.
                >This pilot study found an improvement in cognition with discontinuation of statins and worsening with rechallenge.
                https://pubmed.ncbi.nlm.nih.gov/22921881/

                and they increase risk of diabetes etc etc etc

              • 4 weeks ago
                Anonymous

                hot off the presses. another cholesterol drug that kills people that the industry tried to hide
                >After readjudication, deaths of cardiac origin were numerically higher in the evolocumab group than in the placebo group in the FOURIER trial, suggesting possible cardiac harm. At the time the trial was terminated early, a non-significantly higher risk of cardiovascular mortality was observed with evolocumab, which was numerically greater in our readjudication. A complete restoration of the FOURIER trial data is required. In the meantime, clinicians should be sceptical about prescribing evolocumab for patients with established atherosclerotic cardiovascular disease.
                https://bmjopen.bmj.com/content/12/12/e060172

              • 4 weeks ago
                Anonymous

                >look at this random drug
                i don't care, has nothing to do with the statin i posted

              • 4 weeks ago
                Anonymous

                yes, they reduce chnaces to die from a heart attack. no shit holmes. the only issue is that they increase chances to die from lots of other things.
                the side effect are litteraly dementia. cholesterol is vital for the brain health. remove it and your brain goes to shit.

              • 4 weeks ago
                Anonymous

                pharma is smart enough not to fund any RCTs testing statins on cognition. its never mentioned by shills because its very inconvenient.
                >This pilot study found an improvement in cognition with discontinuation of statins and worsening with rechallenge.
                https://pubmed.ncbi.nlm.nih.gov/22921881/

            • 4 weeks ago
              Anonymous

              >this study was brought to you by the Californian Walnut Committee

    • 4 weeks ago
      Anonymous

      https://jamanetwork.com/journals/jama/fullarticle/2728487
      >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. These results should be considered in the development of dietary guidelines and updates.
      The reality is animal products which all have cholesterol increases heart disease and all cause mortality

      • 4 weeks ago
        Anonymous

        >The reality is animal products which all have cholesterol increases heart disease and all cause mortality
        there is not one single RCT demonstrating this

        • 4 weeks ago
          Anonymous

          > a systematic review and meta-analysis of randomized controlled trials
          >These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs. This suggests that rather than trying to lower PUFA consumption, a shift toward greater population PUFA consumption in place of SFA would significantly reduce rates of CHD.
          https://pubmed.ncbi.nlm.nih.gov/20351774/
          And where does saturated fat comes from? Animal products

          • 4 weeks ago
            Anonymous

            no effect on mortality and that review includes studies failing its own inclusion criteria. in the bin it goes. the vast majority of reviews conclude no effect. you post the outlier that confirms your bias

            • 4 weeks ago
              Anonymous

              Here's a systematic review about saturated fat deaths
              >Replacement of saturated fat with unsaturated fat lowers CHD events and replacement with linoleic acid lowers CHD deaths as well.
              >Replacement of saturated fat with linoleic acid lowers CHD deaths as well.
              >Replacement of saturated fat with high quality carbohydrate lowers CHD events.
              https://www.nmcd-journal.com/article/S0939-4753(17)30237-5/fulltext

              And another one
              > Nineteen studies including 1,013,273participants and 195,515deaths were identified.
              >Diets high in saturated fat were associated with higher mortality from all-causes, CVD, and cancer, whereas diets high in polyunsaturated fat were associated with lower mortality from all-causes, CVD, and cancer. Diets high in trans-fat were associated with higher mortality from all-causes and CVD. Diets high in monounsaturated fat were associated with lower all-cause mortality.
              https://pubmed.ncbi.nlm.nih.gov/32723506/

              Saturated fat and animal products are trash and unhealthy, simple as.

              • 4 weeks ago
                Anonymous

                now youre back to posting association studies. do you realize the difference? i suspect you dont care as long as they confirm your bias

              • 4 weeks ago
                Anonymous

                >association studies
                They are systamatic reviews, idc if you don't have an argument against them, consuming animal products raises mortality by clogging your arteries as well raising cancer risk, that's reality
                https://jamanetwork.com/journals/jama/fullarticle/2728487
                >Objective To determine the associations of dietary cholesterol or egg consumption with incident CVD and all-cause 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.

              • 4 weeks ago
                Anonymous

                >They are systamatic reviews
                of association studies. the vast majority of reviews on the rigorous evidence (RCTs) conclude no effect on mortality, CHD, or cancer. the associations you post are so small and confounded they are unlikely to be correct

              • 4 weeks ago
                Anonymous

                >the associations you post are so small
                > Nineteen studies including 1,013,273participants and 195,515deaths were identified.
                high in saturated fat were associated with higher mortality from all-causes, CVD
                https://pubmed.ncbi.nlm.nih.gov/32723506/
                Yeah a million participants definitely small lmao

                And I already posted a systematic review of RCTs on CHD, why are you lying, do you have an argument or just coping at this point
                > a systematic review and meta-analysis of randomized controlled trials
                >These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs
                https://pubmed.ncbi.nlm.nih.gov/20351774/

              • 4 weeks ago
                Anonymous

                strength of association not number of participants. and yes you posted the single outlier review that includes and excludes studies improperly to get that fallacious result. the Rose Corn Oil trial was excluded which would have been unfavorable. the Oslo Diet Heart Study and STARS trial both included failed the authors inclusion criteria due to multiple interventions and or improper randomization (Oslo)

              • 4 weeks ago
                Anonymous

                >. the Rose Corn Oil trial was excluded which would have been unfavorable. the Oslo Diet Heart Study and STARS trial both included failed the authors inclusion criteria due to multiple interventions and or improper randomization (Oslo)
                All small irrelevant old studies that you can't even properly find on the net, good thing they were excluded, anyway the RTCs are clear, saturated fat increases risk of CHD
                >strength of association not number of participants
                see

                >association studies
                They are systamatic reviews, idc if you don't have an argument against them, consuming animal products raises mortality by clogging your arteries as well raising cancer risk, that's reality
                https://jamanetwork.com/journals/jama/fullarticle/2728487
                >Objective To determine the associations of dietary cholesterol or egg consumption with incident CVD and all-cause 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.

                that's a dose response one, just eating half an egg everyday is about 6% increase in mortality

              • 4 weeks ago
                Anonymous

                the RCTs are clear saturated fat reduction has no effect on mortality. the vast majority of reviews conclude this. if you really want i can post all ~20 of them for you to ignore

              • 4 weeks ago
                Anonymous

                >the vast majority
                LDL is causal for atherosclerosis see, that's what large studies say

                https://i.imgur.com/AkrctV4.png

                ApoB clogs your arteries and causes heart disease therefore ldl which is raised by saturated fat and cholesterol cause clog your arteries, particle size of ApoB doesn't matter all sizes are equally damaging to the arteries, simple as.
                >ivor retard
                He was refuted by a MD Phd in this video

                %21

              • 4 weeks ago
                Anonymous

                none of those are RCTs on nutrition

              • 4 weeks ago
                Anonymous

                >nuh uh
                Yes they are, they are clinical nutrition trials

              • 4 weeks ago
                Anonymous

                post one then.

              • 4 weeks ago
                Anonymous

                see

                https://i.imgur.com/AkrctV4.png

                ApoB clogs your arteries and causes heart disease therefore ldl which is raised by saturated fat and cholesterol cause clog your arteries, particle size of ApoB doesn't matter all sizes are equally damaging to the arteries, simple as.
                >ivor retard
                He was refuted by a MD Phd in this video

                %21

                They are all large studies on nutrition

              • 4 weeks ago
                Anonymous

                do you know what RCT means? they are not.

              • 4 weeks ago
                Anonymous

                Yes they, are Randomized controlled trials see plus they large cohort studies as well

                https://i.imgur.com/AkrctV4.png

                ApoB clogs your arteries and causes heart disease therefore ldl which is raised by saturated fat and cholesterol cause clog your arteries, particle size of ApoB doesn't matter all sizes are equally damaging to the arteries, simple as.
                >ivor retard
                He was refuted by a MD Phd in this video

                %21

              • 4 weeks ago
                Anonymous

                LDL is still causal for atherosclerosis
                https://jamanetwork.com/journals/jamacardiology/article-abstract/2786334
                > The debate is over. In this issue, Marston and colleagues supply decisive evidence from a large, prospective observational study, UK Biobank, and 2 clinical trials, FOURIER (Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk) and IMPROVE-IT (Improved Reduction of Outcomes: Vytorin Efficacy International Trial), that apoB should be the primary marker to assess the cardiovascular risk due to the apoB lipoproteins.

              • 4 weeks ago
                Anonymous

                once again none of these are nutrition trials.

              • 4 weeks ago
                Anonymous

                They are clinical trials about ldl. Clinically ldl clogs your arteries. Period

              • 4 weeks ago
                Anonymous

                not nutrition. period.

              • 4 weeks ago
                Anonymous

                Is cholesterol part of nutrition? Yes therefore they are about nutrition. Period.
                For studies that look into dietary cholesterol and eggs you have this one see

                >association studies
                They are systamatic reviews, idc if you don't have an argument against them, consuming animal products raises mortality by clogging your arteries as well raising cancer risk, that's reality
                https://jamanetwork.com/journals/jama/fullarticle/2728487
                >Objective To determine the associations of dietary cholesterol or egg consumption with incident CVD and all-cause 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.

                In conclusion eggs and cholesterol foods are a superpoison and increase mortality because ldl is causal to clogged arteries

              • 4 weeks ago
                Anonymous

                for the nth time not an RCT. post a nutrition RCT if you have an argument about nutrition

              • 4 weeks ago
                Anonymous

                see

                https://i.imgur.com/AkrctV4.png

                ApoB clogs your arteries and causes heart disease therefore ldl which is raised by saturated fat and cholesterol cause clog your arteries, particle size of ApoB doesn't matter all sizes are equally damaging to the arteries, simple as.
                >ivor retard
                He was refuted by a MD Phd in this video

                %21

                It's multiple clinical trials, idc if you call them nutrition or not, ldl still causes atherosclerosis according to clinical evidence from multiple studies

              • 4 weeks ago
                Anonymous

                not even remotely
                >Some have argued that there is a linear relation between low-density lipoprotein (LDL) levels and CHD events[14]. This analysis may be inaccurate because it combines different types of CHD events from diverse studies into one endpoint even though each study defines CHD events differently. A more meaningful analysis compares total mortality rates to LDL cholesterol levels. When we performed such an analysis on these same statin trials - those analyzed in reference 14 - we found no statistically significant relationship

              • 4 weeks ago
                Anonymous

                >not even remotely
                Wrong
                The lower the ldl, the lower the risk of cvd

              • 4 weeks ago
                Anonymous

                see

                LDL is still causal for atherosclerosis
                https://jamanetwork.com/journals/jamacardiology/article-abstract/2786334
                > The debate is over. In this issue, Marston and colleagues supply decisive evidence from a large, prospective observational study, UK Biobank, and 2 clinical trials, FOURIER (Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk) and IMPROVE-IT (Improved Reduction of Outcomes: Vytorin Efficacy International Trial), that apoB should be the primary marker to assess the cardiovascular risk due to the apoB lipoproteins.

  4. 4 weeks ago
    Anonymous

    >thank the Lord for my iwatch
    Most american sentence.

    • 4 weeks ago
      Anonymous

      >pic

      Burgerpunk kino

  5. 4 weeks ago
    Anonymous

    the vax

    • 4 weeks ago
      Anonymous

      23rd post, correct post

  6. 4 weeks ago
    Anonymous

    Did he get vaxxed maxxed? If so then everything else falls into place

  7. 4 weeks ago
    Anonymous

    >cortisolmaxxing for 3 years
    >w-why did i get a blockage?
    retard deserved it

  8. 4 weeks ago
    Anonymous

    Gilbert Gottfried looking good. rip.

  9. 4 weeks ago
    Anonymous

    >ctrl+f
    >"sugar"
    >no results

    • 4 weeks ago
      Anonymous

      Sugar is not keto so it would not have contributed

  10. 4 weeks ago
    Anonymous

    Definitely not the vaccine

    • 4 weeks ago
      Anonymous

      dude why are vaxxies suddenly dying?

      • 4 weeks ago
        Anonymous

        how many billions of doses were administered again? at least the last time someone tried this retarded argument they got back to me with a source that disproved their own point kek

      • 4 weeks ago
        Anonymous

        those articles are all from 2018?? what point are you even making here? people die suddenly all the time. are you suggesting it's because of vaccinations? that's a hell of an accusation to throw out, especially when the evidence you've given could just as easily have you attribute it to like ice cream consumption or some shit

  11. 4 weeks ago
    Anonymous

    His head screams former fatty. It has the same look that Kevin Smith, Pen Jillette, Jim Norton, and a million other examples.

  12. 4 weeks ago
    Anonymous

    > what are probabilities

  13. 4 weeks ago
    Anonymous

    things associated with heart and artery disease:
    >sleeping on your left side
    >sun exposure
    >studying too hard
    >getting the flu
    >working out
    >low-carb diets

    things NOT associated with heart and artery disease:
    >____

  14. 4 weeks ago
    Anonymous

    trust the science only

  15. 4 weeks ago
    Anonymous

    The human body is literally designed to absorb sugar as the most efficient form of energy for us and eating excessive fats is unhealthy.
    Not sure why everyone is coping, but it's true.
    >hurr sugar bad hurrrrr
    well yeah dumbass if you're eating nothing, but sugar, but god damn newfags you seriously think getting more than half your energy from fat is healthy? there are only two civilizations on the planet that eat such a way and one is retarded africans and the other is slightly retarded ruskies that still eat berries and shit.

    • 4 weeks ago
      Anonymous

      >The human body is literally designed to burn sugar as fast as possible because high levels of blood sugar are toxic (diabetes)
      FTFY

      • 4 weeks ago
        Anonymous

        there are only two civlizations on the planet that eat excessive fats naturally.
        only two, both are utterly fucking retarded.

        • 4 weeks ago
          Anonymous

          >excessive fats
          drinking excessive water can kill you. does that mean water is bad?

  16. 4 weeks ago
    Anonymous

    Not seeing any vegan shill bodies posted yet

  17. 4 weeks ago
    Anonymous

    Both of these gentlemen are taking statins to reduce ApoB.

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