I strongly feel tirzepatide and berberine play a big role in my results. I also take citrus bergamot every night. Additionally I’ve been taking D-limonene which I’ve heard is really good for cardiovascular health.
Hard to say which thing is causing this.
Funny how the blood test says my APOB is low. Maybe I need to go on an APOB boosting regimen haha (joking)
For d-limonene, I simply consume citrus peel daily at breakfast (mandarin, orange, or both). I’ve been doing this for a few years now. FWIW, I have not detected any effect on blood lipids that I could tell.
I picked up d-limonene from some TRT guy who claimed it helps with cardiovascular health while on TRT. It’s a very cheap supplement so I will continue.
A new video by Gil Carvalho of Nutrition Made Simple! about the benefits of aged garlic extract for reducing plaque:
(I’m sure the topic has been mentioned again and again on this forum, so there likely isn’t anything new.)
Thx for posting because using aged garlic is new to me. I didn’t watch the video… do you know if this has to be a supplement (which I’m not keen on adding), or can it be in food form?
…and it’s orally bioavailable
And a pharma company has jumped on it:
https://www.diapin.com/dt-109
Aged Garlic Extract (AGE) is garlic that has been aged for many months. One could make it oneself, probably, but would have to wait for 2 years for it to age.
It’s chemically different from just ordinary garlic or garlic powder. As I understand it, AGE has very little allicin; but contains metabolites of allicin that have health benefits. Allicin is what makes garlic burn when you eat it, and also gives it its smell. AGE doesn’t have that characteristic smell. In fact, it’s odorless.
You can buy it online or even in Vitamin Shoppe in pill form.
I have seen some videos on the web about some interesting other properties of raw garlic (and probably also garlic powder) that might not hold for AGE. e.g. I saw a video a year or two ago about how you can put your feet in crushed garlic, and then eventually you’ll smell and taste garlic in your nose and mouth. The allicin can make its way through your bloodstream all the way from your feet, which must mean that allicin has good skin permeability (and may serve as a permeabilty-enhancer similar to DMSO).
…
Now about that video: it’s made by Gil Carvalho, as I said. He’s considered well-respected and skeptical, and is one of the few people that Brad Stanfield really looks up to for health information. Matt Kaeberlein is maybe another hero of his.
The video has some incredible findings, though Carvalho takes a cautious stance and says the expected things about “checking with your doctor” and that it shouldn’t be seen as a replacement for medicines or doctors – it could be considered an “add-on”, though more studies are needed to confirm its effects.
One of the studies Carvalho mentions showed that diabetics (control group) saw an increase in “low attenuation plaque” by 57% in one year, while diabetics who took a sufficient amount of AGE saw a 29% decrease in low attenuation plaque. That’s a MASSIVE difference!
History teaches us that science creates dogma which can thereafter impede objective research until it is broken down. Such, I believe, goes to portions of the case against saturated fats where I find that the most relied upon studies have confounded their designs with unanalyzed contributions of refined carbohydrates and sugars.
If you ask a good LLM the following question as I did with the advanced versions of GPT and Gemini (assuming you have an embedded meta prompt to be rigorously scientific, separate findings according to confidence, etc.) You will get a much different answer, than its response to the circumscribed prompt above, I won’t paste the detail in here but will summarize with my own bullets.
General Nature of a Broader Prompt
Since the consumption of sugars is both ubiquitous and high in the US and most other advanced nations, it could be argued that this consumption has the potential to confound research on the role of saturated fats in ASCVD. What controlled research do we have demonstrating the impact of saturated fats in a diet free of refined sugars? List the full argument then summarize in bullets, noting the study from which the bullet was derived.
Brief Summary
The analyses I got back were very long and carefully argued. Below is my summary, selecting only a few key points:
Of course, this is only the tip of the evidentiary iceberg pertaining to a complicated question that runs in several direction. It appears that saturated fats from some cheeses, as one example, effect different outcomes than those from meats. And genes play into this: we know that a few people can eat a high saturated fat diet for life yet have no CAC or plaque (not me, sadly). Diets that produce an intestinal biome having adequate amounts of certain forms of Lactobacillus reuteri (requires fats) reduce factors associated with ASCVD.
Is a diet high in saturated fats the best thing you can do for your heart? Current evidence doesn’t suggest that. Are saturated fats causal to ASCVD and therefore to be avoided? Current evidence doesn’t suggest that either.
“unanalyzed contributions of refined carbohydrates and sugars.”
My personal point of view is: For the majority of people with no genetic problems, maintaining a BMI between 18 and 22 will give good results from cholesterol tests whatever the diet, vegan or carnivore.
The American Heart Association says:
“18.5 to 24.9: Healthy weight, associated with the lowest risk of most chronic diseases.” I think 24.9 is still too high.
It’s possible to have mostly body fat and no muscle mass at a BMI of 24.9. Waist size or body fat percentage is important as well, and as a result strength and muscle mass of course.
“For the majority of people with no genetic problems, maintaining a BMI between 18 and 22 will give good results from cholesterol tests whatever the diet, vegan or carnivore.”
That has been my general (but not universal) observation as well but I wonder if it points to another unanalyzed relationship. Would we see the same broad relationship among those whose BMI or body fat and muscle metrics naturally tend to fall in the optimal range that we would see in those who fall in the same range but only with great effort and diligence to stay there. If I had to guess, I would think not.
The gap in this position lies not with Apo(b) for which there is substantial evidence that it accounts for more variance in ASCVD than other commonly used metrics, but in making the leap from saturated fats, over the top of the empirical question, landing on Apo(b).
A small but important separate point. A meta-analysis is a statistical tool that combines and synthesizes data from multiple studies to estimate an overall effect size or relationship. The notion of causality is not a transitive property that can be automatically inherited from evidence of causality in the individual studies included in a meta-analysis.
Another thought @desertshores. Men lose about one inch between the ages of 30 and 70, and another inch between 70 and 80. My “original height” BMI is 22 but is now over 23 due not to a change in muscle, fat, waist size, etc. but to vertebral compression. Sucks!
I’m sorry @A_User but this still misses the entire point of discussion. Instead of taking up more public space, PM me and I’ll try to unpack it.
You can post here. I agree a large RCT is better if it’s not methodologically flawed, and I agree that a meta analysis of RCT’s doesn’t automatically inherent causality of its constituent studies. There are junk meta-analytic reviews based on junk data.
The studies included in the meta was determined to have a low risk of bias.
https://iris.who.int/handle/10665/246104
Of note, it is not EPA or DHA PUFA that lowers apoB as that was not the studies included (linolenic and alpha-linolenic acid only).
The discussion topic was not on whether saturated fats are associated with ASCVD in aggregate population data; neither was it about the well established fact that Apo(b) is a robust marker in this regard. If you read my initial prompt, you will see that the discussion was focused exclusively on whether the research on saturated fats and ASCVD, including the few you drew upon, is confounded with respect to variables having to do with the consumption of sugar, fructose in particular, and refined carbohydrates. Very few studies have isolated these variables even though there is strong reason to suspect that they might be robust. Those studies that have attempted to do so, have mostly done this retrospectively with varying degrees of isolation of the variables of interest. To the extent that these variables have been parsed, unconfounded if you will, they show what I summarized above in the first posting on this topic.
Neither did they research the effects of SFA replacement in the context of no sugar/fructose/ refined carb intake.
