OT Aged Garlic for artery health

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@VeeEnn this is separate from the internet crud.

The idea refers to Aged Garlic Extract (AGE), often prepared by aging garlic in an extracted solution (like diluted alcohol) for extended periods of time, which can take up to 20 months (around 600 days) in dark storage.

[image]ZOE

Clinical research, notably studies from the Lundquist Institute at Harbor-UCLA Medical Center, indicates that taking 2,400mg of aged garlic extract daily may slow the progression of coronary artery calcification. It has also been shown to reduce “soft plaque” (non-calcified plaque) in the arteries, which helps to stabilize atherosclerosis.

[image]National Institutes of Health (.gov) +4

Key details of how this works include:

  • Plaque Regression: Rather than “stripping” away dense, hard calcium (which is generally permanent once established), aged garlic extract primarily helps stabilize and shrink the softer, more vulnerable fatty plaques that lead to heart attacks.

[image]Nutraceutical Business Review +1

  • The Aging Process: Commercial products like Kyolic Aged Garlic Extract go through a specialized, prolonged extraction and aging process in dark conditions. This converts the unstable, pungent compounds of raw garlic (like allicin) into stable, highly bioavailable antioxidants, such as S-allylcysteine (SAC).

[image]National Institutes of Health (.gov) +4

  • Cardiovascular Benefit: While it does not outright cure heart disease, consistent daily use over the course of a year has been shown in trials to reduce arterial inflammation, lower blood pressure, and slow the overall accumulation of arterial plaque by up to 80%.

[image]National Institutes of Health (.gov) +2

Anyone considering high-dose garlic supplements should consult their doctor first. Because garlic acts as a natural blood thinner, combining it with prescription blood pressure medications or anticoagulants can increase the risk of bleeding.

[image]Kahn Center for Cardiac Longevity +2

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Thanks for considering me, @Leap1 … but this supplement is something I wouldn’t bother with really. I’ve come across its purported benefits in the past on the H&N site and found the evidence flimsy at best.

What prompt did you use to generate this overview?..a serious question as opposed to JAQing off, BTW. The way it’s reproduced here is really just an amorphous mass of detritus, as opposed to fresh dog’s vomit that you can sort through with a stick or something. Meaning that the evidence to support the individual statements isn’t readily available…the citations aren’t hyperlinks to click on quickly and do a superficial check to see if AI overview has mulled over reproducible studies in high impact journals, low rent, pay to publish documents in predatory journals, reddit jibber jabber, or statin-averse internet influencers like Joel Kahn (actually, we can see he was one source)

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Try as you might, you can not shoot an AI messanger.

You can look up the National Institute of Health .gov for more information. If you want.

There is some evidence, but it is not yet determined how much of a role statins played in the results.

Discussion

In this study, 1 year of AGE therapy was associated with a regression of LAP. LAP [non-calcified plaque (NCP) <30 HU] is one of the high-risk plaque features. The results of this study are in concordance with those of previously published studies demonstrating the regression of LAP in participants with metabolic syndrome and general population in studies of AGE (10,17), as well as statin studies (18,19).

According to certain data, LAP represents an intravascular ultrasound (IVUS) equivalent of the necrotic core (19). In contrast to more stable F plaques, plaques with a lipid-rich necrotic core play a significant role in the development of acute coronary syndrome (ACS) (20). Recent advancements in cardiac imaging modalities have provided an accurate and detailed quantitative assessment of plaque composition and burden based on differences in CCTA (21). Previous studies have demonstrated an increased risk of myocardial infarction and cardiovascular death in patients with a larger volume of non-calcified and low-attenuation plaque (22,23).

Motoyama et al (24) demonstrated that patients with ACS exhibited a significantly increased frequency of low attenuation plaque (79 vs. 9%, P<0.001). Balestrieri et al (9) reported that the patients with stable chest pain with adverse plaque features, including LAP, spotty calcification and positive remodeling found an association with a 60% increased risk of future adverse cardiovascular events. Furthermore, LAP along with other vulnerable plaque features have been shown to be associated with rapidly progressive CAD (25). The SCOT-HEART trial, which consisted of mostly intermediate risk patients, demonstrated that low attenuation was associated with a 3-fold increased risk of non-fatal MI or coronary heart disease-associated mortality (26). In this study, there was a 57% increase in low attenuation plaque in the placebo group, representing the natural history of plaque progression. By contrast, a 29% reduction was observed in LAP in the AGE group over a period of 1-year follow-up, strongly suggesting the therapeutic potential of AGE in the diabetic population (Fig. 1).

The present study has several limitations. First, this relatively small sample size and short-term follow-up study did not have enough power to demonstrate the significant differences in TP volume, NCP and DC. Second, patients were under different therapies for hyperlipidemia and T2DM, and some patients used varying medications at different doses. Due to the small sample size, a separate analysis with different hyperlipidemia and T2DM medications was not performed. Further research is thus required to evaluate whether AGE has the ability to stabilize vulnerable plaque and to decrease adverse cardiovascular events.

This next study shows a reduction in inflammation.

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@VeeEnn

This result is better than I expected.

Conclusions

AGE inhibits CAC progression, lowers IL–6, glucose levels and blood pressure in patients at increased risk of cardiovascular events in a European cohort. An algorithm was made and was used to predict with 80% precision which patient will have a significantly reduced CAC progression using AGE. The algorithm could also predict with a 74% precision which patient will have a significant blood pressure lowering effect pressure using AGE.

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Really?

This recent lurch into citing AI overview chosen studies is an interesting about face. It wasn’t so long ago that every time data driven evidence was under discussion, your response was always along the lines of “All research/researchers/PhDs are rubbish”. **Strange that you should glom onto such a selective bunch as convincing evidence.

Here’s the primary document, BTW. I got round to reading it mainly because of the boast in the abstract of the development of an algorithm with 80% precision in CAC progression and I just wondered what this algorithm consisted of.

The effect of aged garlic extract on the atherosclerotic process – a randomized double-blind placebo-controlled trial - PMC The effect of aged garlic extract on the atherosclerotic process – a randomized double-blind placebo-controlled trial - PMC

After slogging through it, I still didn’t find the data any more compelling than in the past when such compounds have been touted. My “meh” comes from the relatively low impact factor of the pay-to-publish journal, smallish numbers of study subjects, short term nature of the study, and the biomarker used (CAC)…not a measurement that’s generally used to measure short term success (or otherwise) of a therapeutic intervention.

** As I’ve mentioned on many an occasion, depending upon the prompt, Google’s AI overview is a major brown noser in that it cherry picks its sources in a way that doesn’t resemble a real systematic evaluation of evidence, tending to produce the data most likely to “please”.

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“Selective” being the operative word.

I have always been drawn to garlic.

Seriously, now, what would you consider a successful treatment?

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Well, I’ll repeat my usual caveat here … that I know enough about the topic to be aware I might be wrong and, so, not due a worthwhile opinion. That being the case, I tended defer to academic medical writers in the field…

The Skeptical Cardiologist’s Guide To The Coronary Artery Calcium Scan Updated for 2023 – The Skeptical Cardiologist https://share.google/xNZPfa38Ij48zbZkX

…but more specifically my own intervention cardiologist…

John Messenger MD | Interventional Cardiology | UCHealth John Messenger MD | Interventional Cardiology | UCHealth

A bloke who, in addition to his serious credentials in the field has a knack of answering my questions in such a way that provides the answers I need in addition to what I wanted.

For instance, I asked a couple of years ago if there was an objective way to measure if/how well my lipid lowering therapy was working … or was it a just a question of trusting the process. I already knew the limitations of a CAC scan (and even the study authors note that…in the primary document but not the abstract, of course) so I was thinking more of CT angio with contrast. No that wasn’t a way either. Apparently the Gold Standard in Real World Cardiology is a measurable reduction in MACE…major adverse cardiovascular events. Oh well

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Yes

The Kyolic becomes a cardiac anti-inflammation compound. It won’t heal me much. But the arteries can heal from plaque. In the process, the rate of calcification in my arteries will hopefully slow down.

All of that means less in your circumstances. It means much more in my circumstances. Those small bits of scattered calcium are unstable bits of plaque building. The Kyolic will help stabilize and reduce that plaque.

You’ve been helpful.

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