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14 hours ago, Todd Allen said:

 

14 hours ago, Todd Allen said:

I’m not gonna look it up, but as Peter Attia would agree statins are effective in secondary prevention. That’s why I take them. But you are right as far as primary prevention is concerned taking statins is very iffy. I suppose it’s a mixed bag or a toss of the dice. Some folks will benefit and others won’t. Overall not making a difference. We need more understanding of who would benefit in primary prevention that is clear

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8 hours ago, Mike41 said:

I’m not gonna look it up, but as Peter Attia would agree statins are effective in secondary prevention.

Here's an excerpt:

Quote

For women, all published trials have failed to demonstrate decreased mortality when therapy with statins has been compared with a placebo. For both genders, the lack of all-cause mortality benefit is also illustrated by all published studies using atorvastatin vs. placebo, including the summary of 49 in-house studies including 14,236 individual patients.12 The secondary prevention study SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) ended with five more deaths on highdose atorvastatin than on placebo (31 in 1). To date, there are no placebo-controlled studies showing a mortality benefit when patients used lovastatin, fluvastatin, cerivastatin, or pitavastatin. This is true for rosuvastatin as well if one discounts the finding of fewer cancer deaths in the treated group in JUPITER. Moreover, no mortality benefit has ever been shown in patients older than 70 years of age (the study-group of the PROSPER study), in patients with heart failure (ie, CORONA [Controlled Rosuvastatin Multinational Study in Heart Failure] and GISSI-HF [Gruppo Italiano per lo Studio della Sopravvivenza nell Infarto Miocardico–Heart Failure]) and in patients with kidney failure (AURORA [A Study to Evaluate the Use of Rosuvastatin in Subjects on Regular Hemodialysis: An Assessment of Survival and Cardiovascular Events]).  Clearly therefore, meta-analyses that blend patient groups, ages, and gender cannot change the lack of mortality benefit findings in the individual statin studies.

 

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10 hours ago, Todd Allen said:

Here's an excerpt:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6832139/
 

the best guess based on the above which I’ve posted before is very low ldl is really bad and really high ldl is very bad. Who would have ever thought of that. Geez, did we even need science! 100-129 ldl is the sweet spot according to the above based on overall mortality. 
btw the data are for non statin users

Our novel results show that low levels of LDL-C (<70 mg/dL) were associated with increased risk of CVD mortality, cancer mortality, and even all-cause mortality especially in men who were not treated with lipid lowering therapy. The finding of increased CVD mortality in men with low levels of LDL-C (<70 mg/dL) was observed in both different cohorts even though it showed a U shape. In this study, we were able to take account of multiple confounders and the young age of the cohort helped decrease the influence of potential reverse causality between clinically relevant outcomes and low levels of plasma LDL-C concentrations. Additionally, we excluded subjects who died within 3 years of follow up to avoid the possibility of reverse causality. Furthermore, to validate these associations, we then analyzed other dataset from a large population-based cohort study with government funding, named the Korean genome and epidemiology study (KoGES) which consists of community-dwellers aged ≥40 years at baseline

Edited by Mike41

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Yet, I think I remember the latest podcast with Attia+Dayspring where Dayspring, an eminent expert on lipids,  stated that very low LDL does not cause problems (usually associated with use of lipids lowering drugs)

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5 hours ago, mccoy said:

Yet, I think I remember the latest podcast with Attia+Dayspring where Dayspring, an eminent expert on lipids,  stated that very low LDL does not cause problems (usually associated with use of lipids lowering drugs)

 

I'd like to hear his explanation of why ALS (the most common misdiagnosis for my disease SBMA) isn't a problem.

Amyotrophic Lateral Sclerosis Associated with Statin Use: A Disproportionality Analysis of the FDA's Adverse Event Reporting System

Quote

Results: RORs for ALS were elevated for all statins, with elevations possibly stronger for lipophilic statins. RORs ranged from 9.09 (6.57-12.6) and 16.2 (9.56-27.5) for rosuvastatin and pravastatin (hydrophilic) to 17.0 (14.1-20.4), 23.0 (18.3-29.1), and 107 (68.5-167) for atorvastatin, simvastatin, and lovastatin (lipophilic), respectively. For simvastatin, an ROR of 57.1 (39.5-82.7) was separately present for motor neuron disease.

Conclusion: These findings extend previous evidence showing that significantly elevated ALS reporting extends to individual statin agents, and add to concerns about potential elevated occurrence of ALS-like conditions in association with statin usage.

 

Edited by Todd Allen

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22 hours ago, mccoy said:

Yet, I think I remember the latest podcast with Attia+Dayspring where Dayspring, an eminent expert on lipids,  stated that very low LDL does not cause problems (usually associated with use of lipids lowering drugs)

Yes, but the key point is that statins reduce mortality in secondary prevention and the lower the better; however in healthy controls NOT TAKING STATINS  low levels of ldl ( below 100)  ARE associated with significant  higher mortality. That suggests an intrinsic factor is involved and that simply lowering ldl with a drug does not have the same effect.

wrt to ALS not surprising considering the lipophilic statins show even worse outcomes. When ya throw stuff into your body shit may happen.

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On 11/26/2020 at 9:56 AM, Mike41 said:

wrt to ALS not surprising considering the lipophilic statins show even worse outcomes. When ya throw stuff into your body shit may happen.

Or maybe "bad" cholesterol isn't so bad.  Here is a study suggesting it is good for people with ALS.

Dyslipidemia is a protective factor in amyotrophic lateral sclerosis

Quote

As far as ALS is concerned, increasing the lipid content of the diet offers neuroprotection and extends survival in animal models of the disease6,7 but, on the contrary, calorie restriction exacerbates the motor symptoms.8

...

Conclusions: Hyperlipidemia is a significant prognostic factor for survival of patients with amyotrophic lateral sclerosis. This finding highlights the importance of nutritional intervention strategies on disease progression and claims our attention when treating these patients with lipid lowering drugs. Neurology® 2008;70:1004–1009

 

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https://www.tandfonline.com/doi/abs/10.1080/21678421.2018.1511731?journalCode=iafd20&amp;
 

This study contradicts the statin ALS connection and claims statins LOWER RISK!

Results: ALS risk was reduced with statin use (OR = 0.87 (95% confidence interval (CI) = 0.83–0.91)). While risk was unrelated to three cholesterol-lowering medications (nitrates, bile acid sequestrants, and ezetimibe), it was associated with fibrates (OR = 0.88 (95% CI = 0.80–0.97)). Risk for lipophilic statins was slightly lower than for other statins. ALS risk was lower in all statin categories for dyslipidemic individuals, but only lipophilic statins were associated with lower risk in non-dyslipidemic individuals and demonstrated an inverse trend with duration

Edited by Mike41

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On 11/25/2020 at 11:22 AM, mccoy said:

Yet, I think I remember the latest podcast with Attia+Dayspring where Dayspring, an eminent expert on lipids,  stated that very low LDL does not cause problems (usually associated with use of lipids lowering drugs)

The systematic review of randomized controlled trials of PCSK9 antibodies challenges their “efficacy breakthrough” and “the lower, the better” theory

Quote

Conclusion

The impressive LDL-C lowering results of PCSK9 abs and a first reading of the large FOURIER trial have led many cardiologists to talk about a great innovation, a real breakthrough in the management of the CV disease and of the CV risk with these drugs. However, a closer look to the overall evidence shows a different picture. Indeed, the analysis of the relation between LDL-C lowering and the majority of the health outcomes do not support “the lower the better” theory. Moreover, the reduction in the risk of CV events is much lower than the CTTC predictions, and these predictions are not at all respected in all-cause mortality. Even the FH patients’ limited data show a tendency to harm for almost all the endpoints analyzed. Therefore, the cardiologists’ enthusiasm seems hardly justified, for now.

 

Edited by Todd Allen

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Association between hyperlipidemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score matched cohort study and a meta-analysis

Quote

Conclusions
The current findings, based on large unselected hospital-based patient-populations, provide strong evidence that after incident AMI or ADHF, a diagnosis of HLP, compared with no HLP, was associated with reduced long-term mortality, a longer median survival and modest attenuation of the magnitude of mortality risk associated with other competing CCs. Our data support a protective role for HLP against all-cause mortality following incident AMI and ADHF. Further studies are needed to understand the complex relationship between HLP and mortality, especially in the presence of other competing comorbidities and to define appropriate HLP targets to maximise the benefits.

And graphs showing the longevity benefits of hyperlipidemia and the higher the cholesterol the better the longevity after heart attacks or heart failure!

bmjopen-2019-December-9-12--F1.large.jpg.26eca15576ce10ad48e1998344464cb8.jpg

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4 hours ago, Mike41 said:

This study contradicts the statin ALS connection and claims statins LOWER RISK!

I think the explanation for why the two studies published in the same year have what look to be completely contradictory findings may be due to them actually looking at quite different things.  The study I posted was looking at the rate of filed reports of ALS as an adverse outcome of having taken statins while your study is finding the  number of people developing ALS declines with longer duration of statin use.  So it might be that people more resistant to developing ALS are more likely to continue statin use for longer time periods versus those prone to ALS developing adverse reactions quickly and terminating statin usage.  To answer the question of whether statins contribute to developing ALS I think a study that took a large cohort of people eligible for statin use and randomly selected half to forced statin usage and half to no statins and followed them until death would be more definitive.  But that would be unethical.

Edited by Todd Allen

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At this point, I prefer not to descend down the rabbit hole of the lipids controversy, where many agendas clash against each other (the paleo and lowcarbers, the vegans, the low-fat vegans and so on). I'll simply choose not to read the literature, where we can find drastically opposite conclusions on everything, and apply consolidated knowledge and common sense. Consolidated knowledge and common sense dictates that high cholesterol is usually inadvisable and potentially dangerous for the general population, that to me is a fixed point.  Whereas the very low LDL figures seems to be such a rare occurrence, it there are suspicions that it can be harmful, why not to change drugs or lower the dosages of the powerful PCSK9 medicinals for example?

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22 hours ago, Todd Allen said:

Association between hyperlipidemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score matched cohort study and a meta-analysis

And graphs showing the longevity benefits of hyperlipidemia and the higher the cholesterol the better the longevity after heart attacks or heart failure!

bmjopen-2019-December-9-12--F1.large.jpg.26eca15576ce10ad48e1998344464cb8.jpg

This is interesting indeed. I have seen numerous studies showing lower rates of cardio mortality with statin use and Psk9 inhibitors. In fact a Cochran review showed that statin users with cardiovascular disease who also took a PSK9 inhibitor were 25% less likely to die of heart disease, however overall mortality was slighter higher for heart patients taking PSK9 inhibitors. The review questioned the use of these drugs. Which brings up a very important distinction between these two drugs and why statins don’t raise overall mortality in cardiac patients. The reason may have to do with the inflammatory power of these drugs and other possible pleiotropic effects that are lacking in the inhibitors. There are so many variables and complications that it would seem to me if a person did not have any family history of early heart disease I’d be very reluctant to advise statins. Rather do all the lifestyle heart healthy habits and forget about cholesterol unless it’s sky high.

 

Edited by Mike41

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3 hours ago, Mike41 said:

This is interesting indeed.

One thing I found interesting although bordering on ridiculous:

Quote

The results of Cox model 3 are shown in figure 2. Magnitude of HRs for mortality associated with cancer, COPD, CKD, diabetes, HF and stroke were all modestly attenuated with concurrent HLP across study cohorts. By comparison, protective effect of HLP on mortality was enhanced when paired with hypertension (HTN) in both AMI (HR 0.77, 95% CI 0.72 to 0.83) and ADHF (HR 0.86, 95% CI 0.78 to 0.94).

While I have seen studies questioning how low to drive BP with meds I had yet to see a case where hypertension was considered beneficial.  I wonder if they had stratified out hypotension from normotension would the hypertension group still fare best?  My thinking being that after a heart attack or with heart failure low BP is likely a sign cardiac insufficiency.  It would have been interesting to see the change in BP with the heart diagnosis/event.  I suppose if one had a big drop in BP after a heart attack even if BP dropped into the normal range it might still be indicative of heart damage.

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On 11/15/2020 at 2:16 PM, Todd Allen said:

Their inverse correlations to my body fat % have been pretty tight and if I make it to a goal of 10% body fat I predict I'll plateau around HDL 100, LDL 350 and T 2700.

Looks like this prediction needs upward revision.  I think I've only made a little progress towards 10% body fat  and I made a lot of progress on my newest lipid panel:

Component Your Value Standard Range Flag
CHOLESTEROL 395 mg/dL 100 - 199 mg/dL H
TRIGLYCERIDE 67 mg/dL 0 - 149 mg/dL  
HDL CHOLESTEROL 100 mg/dL >39 mg/dL  
VLDL CHOLESTEROL CALC 8 mg/dL 5 - 40 mg/dL  
LDL CHOL CALC 287 mg/dL 0 - 99 mg/dL H

I should receive new sex hormone results in another day or two and I'm guessing T of 2400...

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Got additional lab results.  Unfortunately my doc previously used Quest but now orders labs through Labcorp which has different reference ranges and an upper limit of reporting on testosterone limiting the usefulness.

TESTOSTERONE    >1500 ng/dL    264 - 916 ng/dL
FREE TESTOSTERONE    31.6 pg/mL    7.2 - 24.0 pg/mL
DIHYDROTESTOSTERONE    142 ng/dL    30 - 85 ng/dL

One fate of androgens is aromatization to estrogen so I requested that too and was a bit surprised to see this
ESTROGEN    263 pg/mL    40 - 115 pg/mL

Getting leaner is likely to increase my androgens by decreasing loss to aromatization.  My cholesterol and sex hormones have been rising as I've gotten leaner and it remains to be seen how high they might go.  Through the LMHR group I recently heard of a non FH guy who has managed to get his LDL over 1000 suggesting the limits of human physiology can still surprise.  We also tested catecholamines and all were high including dopamine.  The combination of high T and dopamine might be contributing to my inordinate confidence in my health and indestructability.  My doc offered to refer me to an endocrinologist and I agreed with the caveat that I want one more interested in analyzing abnormality than treating abnormality.

The draw for this IGF-1 was done after an extended fast which ought to roughly represent a lower bound of my IGF-1.  I plan to do my next test within a couple hours of breakfast such as an 8 oz beef steak, 4 eggs, 2 oz beef liver, 8 oz whole milk kefir with 2 TBL whey protein concentrate, ie ~100 g of protein rich in leucine and methionine to get a better sense of my upper bound.

IGF-I    179 ng/mL    68 - 247 ng/mL
INSULIN GH BP-3    4,366 ug/L    2,133 - 5,711 ug/L
 

Just found this paper which suggests my hormonal profile was predictable.  I'm guessing it typically isn't seen in men with AR CAG repeat counts similar to mine because their hormones are suppressed by poor metabolic health.

Increased Estrogen Rather Than Decreased Androgen Action Is Associated with Longer Androgen Receptor CAG Repeats

Quote

Taken together, men with longer AR CAG repeats had higher T levels, which could compensate partly or totally for the weaker activity of their AR. This is a highly plausible explanation for the lack of any clear signs of androgen deficiency in the EMAS men with longer CAG repeats. A potentially more important finding was the higher E2 levels in men with longer repeats, which paralleled with phenotypic effects indicative of elevated estrogen action. Hence, our current findings suggest that the increased estrogen action and increased estrogen/androgen ratio in association with longer AR CAG repeats is paradoxically the main determinant of phenotypic effects of this polymorphism, rather than an androgen-AR effect.

 

Edited by Todd Allen

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1 hour ago, Todd Allen said:

within a couple hours of breakfast such as an 8 oz beef steak, 4 eggs, 2 oz beef liver, 8 oz whole milk kefir with 2 TBL whey protein concentrate, ie ~100 g of protein rich in leucine and methionine

Todd, congratulations, your breakfast is larger than Eddie HAll's the human gorilla (500 kg deadlift ) , LOL

image.png.fc329ea1cb212bf5c1ee9d58aadbb943.png

Edited by mccoy

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47 minutes ago, mccoy said:

Todd, congratulations, your breakfast is larger than Eddie HAll's the human gorilla (500 kg deadlift ) , LOL

But my breakfast is a fraction of Dean's.  Eddie probably eats at least 6 times a day.  I sometimes eat once a day and rarely eat more than twice a day.

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2 hours ago, Ron Put said:

What's the glucose number that goes with this?

My blood glucose was 89 although I think it was bumped up by riding my bike to the appointment.  Without exertion I expect it would have been 75-80.  With more intense exertion I'll commonly spike to 100-110.  Last year I rode to an appointment in freezing rain and between the ice and heavy traffic had several close calls and got my highest BG since going keto of 135.

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On 4/29/2021 at 7:45 PM, Todd Allen said:

But my breakfast is a fraction of Dean's.  Eddie probably eats at least 6 times a day.  I sometimes eat once a day and rarely eat more than twice a day.

I almost fainted when I read what he had at lunch for dessert before successfully attempting his monster 500 kg deadlift: 1 kg of lard  🤮🤮

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2 hours ago, mccoy said:

for dessert before successfully attempting his monster 500 kg deadlift: 1 kg of lard

Lard, flour and salt is the classic recipe for pie crust.  All three are demonized but I suspect flour does the killing and the accomplices are mostly innocent bystanders. 

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On 5/1/2021 at 1:50 PM, Todd Allen said:

All three are demonized but I suspect flour does the killing and the accomplices are mostly innocent bystanders.

While lard does have a bit less saturated fat than butter, neither is good for one's health, based on most studies I've seen.
 

 

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14 hours ago, Ron Put said:

While lard does have a bit less saturated fat than butter, neither is good for one's health, based on most studies I've seen.

The video you linked discusses evidence that saturated fat raises cholesterol but the connection to health is based on the assumption that increasing LDL cholesterol is bad for health.  On a vegan diet my LDL was acceptable but health was terrible.  As my cholesterol has been rising, both HDL and LDL have more than tripled, my health is profoundly better in how I feel, look, perform and by every other biomarker.  Things such as being able to sleep soundly for 8 hours without needing to pee are much more important to me then concern over the risk of rising "bad" LDL cholesterol for which the evidence is very mixed.

Edited by Todd Allen

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It obviously works for you at an individual level, but I believe that the preponderance of the evidence still points to high cholesterol as a broad marker for CVD.

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