The good doctor must not be rude or dismissive- this is absolutely given! Good specialist, for example a cardiologist, besides being respectful and listening carefully for the patients complaints, must be on top of the current research in the field and is able to apply this knowledge for the patient’s benefit, understanding that each patient is unique.
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The study above had a statistical non-significant result as far as I can tell, meaning it could be due to chance.
I haven’t seen any MR on ACM except the one linked today but I do remember seeing something relating to longevity (and familial longevity IIRC). In fact, in the study I linked today, it was statistically insignificant, so I don’t know. I think it’s likely that is the case though.
sorry, I meant CVD benefits and no harm. post corrected
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Mendelian Randomization is a great marketing term for an epidemiological technique.
I give some major weight to 108,000 people followed for a median of 9.4 years. That is 1,002,361 person-years of follow-up. Yes, it is a classic epidemiological study, not a MR epi study.
As MR studies are an epi technique, and they cannot prove benefit any more than the study I shared can prove harm from low LDL. They can be suggestive, and you can give them weight in accordance with your judgment.
MR studies cannot show the impact of actually lowering LDL by any particular technique. They can only show that certain genes, that predispose people to have high or low LDL, are associated with certain outcomes (longer or shorter lives, say). And those genes may be the targets of certain drugs, which is suggestive of a causal relationship. But this is still a proxy measure for interventions such as a statin, which may have pleiotropic effects.
On a related note, the phrase “keeping LDL low” and similar terms aren’t clear. “Low” is in the eye of the beholder. Is low less than 200 mg/dL? Less than 150? Less than 100? Less than 75? What level does it have to be above such that efforts to reduce it will extend life?
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“Low” means as low as possible. As I said, potential harms vs costs vs benefits from any LDL-modifying intervention should be taken into account before undertaking such an intervention. Dismissing MR studies as a “marketing term” is a huge mistake and a fundamental misunderstanding of the value of such studies, IMO. The specificity of a gene that encodes a protein such as PCSK9 that (in essence) only affects LDL, the fact that the gene is not under control of the person who has it, the gene doesn’t change over time, can be easily objectively measured, does not rely on the honesty of the subject (unlike food and behavioral questionnaires, etc). These factors eliminate many of the confounding variables that make standard epidemiologic studies so riddled with problems of confounders, causality and uncertainty. The specificity also virtually eliminates the possibility of pleiotropic effects that can result from drug treatments such as statins.
This is not the same thing as saying “everyone should be on a high dose statin”. Statins have potential side effects (I can’t tolerate even low doses, in fact).
Show me a study that demonstrates negative ACM as a consequence of an LDL-lowering intervention. That’s the only thing at this point that could convince me that keeping LDL as low as possible could be a bad thing.
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Don’t forget they are randomly allocated, mendelian randomization is a natural RCT.
One of the best tools for humanity.
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Indeed! I knew I was forgetting something important 
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This is actually a hilarious situation if you step back and look at it. We have the guy who takes a statin and ezetimibe arguing that it isn’t always clear that lowering LDL will improve all-cause mortality, and we have the guy who does not take a statin (albeit for good reasons) arguing that it does.
If we were Wall Street types we would both be fired for failing to ‘talk our books’ appropriately.
So at least one of us is wrong, probably me, but at least we both seem to be reasonable intellectually honest.
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Lol I was just thinking the exact same thing before you said it😆
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I think we can all agree that aggressive intervention is appropriate for those at high baseline risk of CVD and events.
Paul Ridker MD , a preventive cardiologist out of Harvard, presented some sobering findings at the American Cardiology meetings. He evaluated high risk patients already on statin therapy and found that residual inflammation was a greater prognostic indicator for future cardiac events than was LDL cholesterol. The implication being , in the high risk patient, a hsCRP should be performed to evaluate inflammation , and steps should be taken to lower arterial inflammation.
This isn’t a completely new finding since both Jupiter and Cantos trials showed the impact of reducing inflammation, independently of reducing lipids, on the incidence of CVD.
But what do we do exactly to resolve arterial inflammation? Palmitoylethanolamide offers an intriguing answer. PEA has known arterial anti inflammatory activity, and in this study was found to decrease early atherosclerosis , and offer plaque stabilization in later cases.
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[quote=“rivasp12, post:1616, topic:1434”]
Has anyone used Palmitoylethanolamide as an anti-inflammatory supplement?
Yes, I’ve taken the micronized PEA with luteolin for about 4 years on an intermittent schedule. As a neurologist you may like this recent look at PEA and neuroinflammation.
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Which brand are you using?
I use Gold Health micronized with luteolin a few times a week.
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[quote=“rivasp12, post:1618, topic:1434”]
Are you using it for a neuropathic pain or as an antiinflammatory support? I found multiple studies about treatment of different types of pain, and very few about using PEA for chronic inflammation, for example, for reducing hsCRP.
I use it to reduce chronic inflammation, the root of all evil.
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Have you reviewed the use of LDN as a reduced of inflammation?
The LDN 2023 Medical Conference is
June 23rd to June 25TH 2023 in
Carbondale, PA
Yes. About 5 years ago I read The LDN Book by Linda Elsegood and also spoke to her . Read some of the studies and tried it on about a hundred patients at 3mg dose .It works in some people to reduce food cravings and help with joint and muscle pains.
It seems to work via toll like receptors in the brain to calm microglial overactivation and reduce inflammation. I spoke to a neurologist at Hershey Medical Center and he said that it works well in his MS patients.
The biggest obstacle is that you need to get it from a compounding pharmacy which can be a difficult process.
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“The biggest obstacle is that you need to get it from a compounding pharmacy which can be a difficult process.”
Naltrexone in 50mg tablet form is fairly inexpensive. Splitting it into 16s would yield ~3.13mg which is in the LDN range. Would going this route be less effective than getting LDN from a compounding pharmacy? Why? Please explain. Thanks!!
There are many compound ing pharmacy’s that provide LDN.
4.5mg a day for 90 day cost an average of $100.00 delivered, yes you would need a prescription.
LDN Pharmacists
Find an LDN compounding pharmacy in your area see the link below;