There are actually 3 different forms of folate—folate, folinic acid, and folic acid. Which one should you take? We will describe them in this podcast.

Which type of arterial plaque is better—calcified or soft plaque? According to the Honda study, calcified/hard plaque is safer and more stable than soft plaque. Here are the crucial points:

(a) In ultrasound, "echogenic" appears as a solid, white mass. "Echolucent" would be transparent.

(b) Soft plaques are echolucent. 29 CV events happened in 112 patients with echolucent plaque (25.9%).

(c) Hard/calcified plaques are echogenic. Only 4 events happened in 103 patients without echolucent plaque (3.9%).

What is the carotid IMT (CIMT) scan? Why is it such an excellent plaque screening test? This video is an excerpt from our recent Louisville conference. I'll discuss the basics of CIMT, the CAFES-CAVE study, and the certain limitations surrounding the CIMT test.

Statins are primarily known as LDL cholesterol-lowering medication. But statins (even in low doses) can decrease cardiovascular inflammation. Some statins also help regulate insulin resistance. All these combined effects make a low-dose statin a good component of a patient's regimen for reducing CV plaque.

This is part 3 of our series on David Sinclair's new book, "Lifespan: Why We Age and Why We Don't Have To." We'll talk about 3 concepts—rapamycin, mTOR, autophagy. Rapamycin (an antibiotic) inhibits mTOR (a protein). mTOR inhibits autophagy. Autophagy is a natural process by which the body eliminates unnecessary components (like dead mitochondria). So, does rapamycin have an effect on aging and longevity? That's what we'll discuss in the podcast.

This podcast covers the sulfur-containing anti-oxidants N Acetyl Cysteine and Glutathione. Glutathione supplementation doesn't make it past the stomach acid. Acetyl Cysteine is better for supplementation. But cruciate sulfur-containing vegetables are best - asparagus, brussels sprouts, broccoli, etc. We also geek out on a little metabolic pathway discussion, showing relationships between the anti-oxidant vitamins A, C, E, Glutathione, and the Methylation pathways involving the B complex vitamins and homocysteine.

Autophagy is the key link between CV inflammation and plaque reversal. And Fasting stimulates autophagy. If the plaque reversal process is uncontrolled, and the LDL continues to get deposited in the arterial wall, the mast cells and polymorphs over-gorge and die, releasing the lysosomal contents into the bloodstream, creating a risk for heart attack and stroke.

What causes LDL to be continually deposited in artery walls? Injury to the intima/endothelium. LDL then goes through the cracks & holes in the endothelium. Mast cells & leukocytes (polymorphs) then attack the plaque.

Remember the Inflammation panel?

MPO is released by the polymorphs. Lp-PLA2 is released by the mast cells. And the MACR (Micro Albumin Creatinine Ratio) is the measure of the number of holes & cracks in the intima/endothelium.) What causes cracks & holes in the intima/endothelium? High glucose & insulin.

Fasting & low carb diets result in prolonged periods of lower blood glucose and lower insulin levels. That's why they help.

The coronary artery calcium scan (CACS) detects and measures calcium in arterial plaque. Thus, it can only check for calcified plaque. In this video, know the basics of the coronary calcium scan and how to interpret your calcium score.

The PULS test (stands for Protein Unstable Lesion Signature) is a new test for heart attack and stroke risk assessment from Cleveland Heart Labs and GD BioSciences. It's probably a better test than the stress test. Why do I say that? There are two reasons. 1. The stress test only tells us that you currently have flow. It's a flow study. It doesn't tell us whether we have the bad actor - an inflamed, unstable plaque. 2. Unfortunately, it is not that clear what the predictive value of the PULS test will be.

They basically took a lot of indicators and risks - like HDL and HgA1c, and indicators of plaque inflammation - like HGF ( human Growth Factor), IL( INterleukins), etc. Again, there is insufficient data now for any single indicator. Putting them all together will help in some ways, and complicate things for others. There are some critical inflammatory markers missing - like MPO, LP-PLA2, and MACR. I would have included these in an overall evaluation of cardiovascular inflammation ( not so much everyone's favorite - hsCRP). In fact, that's what I do for my patients. I get an inflammation panel. It does include Lp-PLA2, MPO, hsCRP, and MACR. I look forward to future predictive results from the PULS test. I don't use it at this point.

LDL gets most of the flak for heart disease risks, but there's another type of cholesterol we should also be watching—remnant cholesterol. It's made up of VLDL (very low-density lipoprotein) and IDL (intermediate-density lipoprotein).