Another Weapon in the Fight Against Heart Disease

It's simple, cheap, and potentially oh-so effective.

“It’s the big one! I’m coming to join you, Elizabeth.”

Chances are, if you’re not the victim of a mass shooting, manage to avoid the Big C, don’t catch a mutant strain of virus (one that doesn’t turn you into a zombie), don’t hit the gas instead of the brake and drive your Subaru into a lake, and don’t succumb to the Devil or the whisky, you’ll die of a heart attack, perhaps too quickly to announce your imminent arrival to an already-dead loved one.

Of course, the odds of you or I dying from cardiovascular disease are much greater (or, in the case of cancer, a little greater) than dying from any of the other potential causes I listed. So, like a professional gambler, I’m playing the odds and focusing a good deal of my biohacking efforts on how to thwart, or at least delay, clutching my chest and collapsing, never to get up, in a Walmart parking lot somewhere.

That’s why my pulse quickened at the findings of a couple of studies that found that supplemental manganese, at least in mice, not only reduces blood fats but also takes a roto-rooter to any existing atherosclerotic plaques. This is notable because the current drugs in the cardiologist’s tool chest (statins and PCSK9 inhibitors), while also reducing blood fats, only stabilize plaques (at best) instead of hacking away at them. Not only that, those drugs often come with a host of undesirable side effects.

That’s what makes taking supplemental manganese every day so beguiling. It’s cheap, presumably effective, and comes with no discernable side effects, at least when taken in conservative doses.

What the Scientists Did and What They Found

A group of Chinese scientists, led by a Dr. Xiao-Wei Chen, separated mice into different groups, all of which were subjected to a Western diet for several weeks so that their blood fats and degree of atherosclerosis would approximate the blood chemistry and health of the average schlubby American.

They then gave three different groups of mice varying doses of oral manganese while a placebo group was allowed to lollygag for the duration of the experiment.

While the manganese-treated mice didn’t lose (or gain) any weight after a month, their blood lipid levels exhibited a remarkable bell-shaped response (where increasing the dosages led to increased efficacy up to a point, after which larger doses led to decreased efficacy). That means that mice that received 5 mg. of manganese per kilogram of bodyweight retained the highest lipid levels while those receiving 40 mg. per kilogram (the highest dose) exhibited a decrease in levels of LDL-cholesterol (the major contributor to atherosclerosis) of about 50%.

The mice were then euthanized, their aortas removed, and then stained and examined under a microscope. Those that were treated with the lowest dosage of manganese exhibited a plaque reversal of 8.71% (over the placebo group) and those that received the highest dosage exhibited an incredible 75.63% reduction in atherosclerotic plaques. Yeah, 75.63%.

Dr. Wang, no doubt rubbing his fingernails on his lab coat and blowing on them, explained it thusly: “Manganese is considered the least understood essential element, mainly playing supporting roles in enzymatic reactions. Yet, we’ve uncovered an active, signaling role of the manganese in controlling lipid delivery into the blood.”

In case you want to know how it works, bulk lipids, including cholesterol and triglycerides, are transported into the blood by specialized carriers called lipoproteins. However, these carriers rely on the biomolecular “condensation” (where two molecules are combined to form a single molecule, usually with the loss of water) of a cellular machinery called the coat protein complex II (COPII). Manganese, it seems, directly binds to the COPII complex and enhances condensation, which results in the bell-shaped regulation on blood lipids seen in the mice.

What’s This Mean for You?

There’s one big problem with this study. Here it is: If you were to do the math and use the same dosage on humans as they did with the mice, you’d scare the hell out of any sane nutritionist or doctor. After all, the maximum suggested dosage for a human is only about 11 mg. a day while the lowest dosage used on the mice (5 mg/kilogram) would translate to between 300 and 400 milligrams, depending on the human’s weight. Granted, none of the mice, even at the highest dosage, exhibited any negative side effects, but still…

HOWEVER, there have been at least a couple of observational studies of manganese on humans and atherosclerosis. The National Health and Examination Survey 2011-2018 found that among 12,061 participants, those that had the highest levels of manganese in their blood had significantly lower risks of cardiovascular disease.

Another study, this one with 334 subjects, found that the serum level of manganese was “significantly lower in severe atherosclerosis patients than mild and moderate coronary artery disease groups.”

Do you see what’s apparently going on? None of the people in these studies were taking humongous, lab-animal sized doses of supplemental manganese. At best, maybe some of them were popping a solitary manganese capsule a day. More likely they just ate a lot of foods that contained manganese (shellfish, nuts, legumes, etc.).

Personally, I’ve bought into the whole concept. After all, it seems I’ve got nothing to lose. Since side effects are negligible, if non-existent, the worst-case scenario is that it just doesn’t work and I’m out a few bucks every month. However, if this study doestranslate to us human-types, then I’ve hit the health/longevity motherlode.

So, I now take ONE 10 mg. capsule of chelated manganese a day (in addition to the umpteen other pills/tablets/capsules I’m taking) a day, but for those of you who have adopted the “if one is good, 400 must be better” philosophy, I urge caution because manganese toxicity is a real thing and you don’t want to develop tremors or Parkinson’s like symptoms.

Addendum: A Few Words on Animal Studies in General

I report on a lot of scientific studies and much of the time the studies I write about were conducted on rats or mice, and that’s often when the rat/mouse turds hit the cage-ventilator fan.

I invariably have to field a few deprecating or patronizing remarks in the comments section about how “rats and mice have been on their own evolutionary path for tens of millions of years, and as such, the studies involving them don’t apply to humans.”

Thank you, intellectual heir of Charles Darwin and Gregor Mendel.

I KNOW rodents aren’t genetically the same as humans. It’s why my Uncle Todd only looks a little bit like Rizzo the Rat from Sesame Street. You are, after all, talking to a nerd who tried to duplicate (unsuccessfully) some of Gregor Mendel’s experiments with pea plants when he was 10. You, are, after all, talking to a nerd who told schoolmates that he wanted to be a geneticist when he was 13: “You know, someone who messes around with your genes.” (Only they heard it as “jeans” instead of “genes” and I was mercilessly teased and bullied and my family had to move to Aurora, Illinois where I was home-schooled and got much of my education from public access TV.)

Well, maybe that last part about moving to Wayne’s World isn’t so much true, but the rest of it is, and while I didn’t pursue genetics, I went to college and studied microbiology, of which, surprise, genetics play a big part.

So, while my knowledge of genetics is still rudimentary compared to the people who work in the field, I understand that g-damn rats and mice are not genetically identical to humans; that we can’t marry them (in Northern states anyhow), can’t produce offspring with them, and can’t compete in ballroom dancing contests with them, among other things.

Here’s the crux of it, though: There’s evidence that rats and mice, while not miniature, four-legged, long-tailed, furrier humans, are the most pragmatic tool we currently have to gauge the effectiveness of drugs, supplements, dietary strategies, or almost any medical or biological premise we might want to test.

Despite the many differences, especially appearance-wise, rats and mice have a surprising number of anatomical, physiological, and, yes, genetic similarities to humans. Case in point: Rats, mice, and humans each have about 30,000 genes of which approximately 95% are shared between all three species.

Moreover, the small size, short life cycle, and ease of maintenance with rats and mice make them almost ideal for laboratory testing.

Given the short life spans of mice and rats, scientists can easily develop unique genetic strains of them that model human ailments like diabetes, obesity, or cardiovascular disease. This makes them especially useful in researching those and other human ailments.

But here’s where I appear to contradict everything I wrote above: It’s true that rats/mice and humans have been on their own evolutionary paths for millions of years, and, despite sharing 95% of our genes, the 5% we don’t share counts for a lot. It explains why Remy in Ratatouille probably couldn’t hold down a real-life job in a French restaurant.

Nevertheless, we shouldn’t automatically poo-poo animal studies. After all, the studies of manganese’s effects on atherosclerosis in animals seems to have pointed us in the right direction. Still, as any responsible doctor/scientist/biohacker will say, more research on humans and the functions/effects of manganese is needed.

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Babak Bagheri, et al. The Relationship between Serum Level of Manganese and Severity of Coronary Atherosclerosis, Zahedan Journal of Research in Medical Sciences, Oct. 14, 2013.

Boxuan Pu, Association between blood manganese and cardiovascular diseases among U.S. adult population, Scientific Reports, 28 December, 2024.

Xiao-Wei Chen, et al. Manganese therapy for dyslipidemia and plaque reversal in murine models, Life Metabolism, December, 2023.