How Magnesium Affects Your Brain

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If there’s one thing we can usually agree on, it’s that we want to retain as many of our important memories as we can along with the ability to learn new things. That’s why a couple of recent studies on the mineral magnesium caught my attention. Both were published in the past two years by the same research group, but the results of one inspired the second.

Researchers used data from the UK Biobank Study to examine the relationship between magnesium intake, blood pressure, and specific brain volumes. Just over 6,000 male and female subjects ages 40–73 completed the 16-month study. Brain volumes were assessed by MRI and included grey matter and white matter lesions. Dietary intake was assessed at least five times over the course of the study via the Oxford WebQ food frequency questionnaire.

The results demonstrated that high magnesium intake was associated with increased grey matter and lower volume of white matter lesions; there was no relationship between blood pressure and magnesium intake. What is also interesting was that brain volumes were stationary if magnesium intake remained stable, but if magnesium levels were low and rose, there was an increase in grey matter. It’s unclear if reducing magnesium intake would decrease grey matter.

The question is why? Prior research showed that low magnesium intake is related to increased blood pressure, but that wasn’t the case in this study. What caused the positive outcomes? We’ll look at the second study on Saturday.

The Insider conference call is tomorrow night. We’ll expand on the magnesium studies, including what supplement forms may be better than others. I’ll also be answering questions from Insiders. Become an Insider before 8 p.m. tomorrow night and you can join the discussion.

What are you prepared to do today?

        Dr. Chet

Reference: European Journal of Nutrition (2023) 62:2039–2051

I’m Alive V2.56

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When I woke up this morning, I knew I had another year to do what I do but with more urgency. If you want to know the story, read last year’s Memo to understand. Why more urgency? Simple: I’m not any younger and while I try to age with a vengeance, the clock keeps ticking and I’ve got a lot to do. Let’s get to it.

My foray into the primary or secondary cause of death stems from a variety of sources: my once-favorite statistician, a comic, self-proclaimed gurus, and many healthcare professionals who should know better. I’m going to try to set things straight with a few examples.

The Cold

Q. Someone has a really bad cold, but a light bulb has gone out and he must get on a ladder to change it. While up on top, he sneezes, falls off the ladder, hits his head, and dies. What is the cause of death?

A. Was it the cold? The light bulb? The ladder? None of those—he died from a fall. Without those first three factors, there would have been no fall, and he’d still be miserably dealing with cold symptoms.

The Car Accident

Q. Let’s say someone is a type 2 diabetic. She is obese, has high blood pressure, and has been diagnosed with cardiovascular disease. She has a car accident; she is severely injured, loses a lot of blood, and while on the way to the hospital, she has a myocardial infarction and dies in the ambulance. What is the cause of death?

A. The loss of blood due to injuries in the car accident. The CVD may be a contributing factor, but with no accident and no blood loss, she won’t die on that day.

The Respiratory Infection

Q. Let’s keep the same person for this scenario only in this case, she catches a respiratory viral infection like the flu or respiratory syncytial virus (RSV), which has been in the news lately. She gets severe symptoms including congestion that require hospitalization. She continues to get worse, has a heart attack, and dies. What is the cause of death?

A. The cause of death is the viral infection. The obesity, the hypertension, the diabetes, and the CVD could have been contributing factors, but again, no infection and she’s still alive. You may be surprised that 6,000–10,000 people per year with CVD die due to RSV this way each year.

More
The rantings of the people I mentioned earlier shouting, “They died of their lifestyle, not of an infection!” is simply wrong. The presence of the pre-existing conditions might kill them in the next 5, 10, or 30 years, but they’d been living with those conditions for some time, and there’s no reason to think they would have died on that particular day—no infection, no death at that time. It was the infection that caused their death.

The Bottom Line

We live in a world where social media and purported health gurus overshadow science, and sometimes, common sense. There are plenty of gray areas in the interpretation of health information. Yes, we should all do better to improve every facet of our health, but we should not change the interpretation of causes of death to fit a specific narrative. That can harm us all because it may raise doubt about preventive steps we can take. In the end, it’s your body and your choice. Choose wisely.

What are you prepared to do today?

        Dr. Chet

References:
1. https://doi.org/10.1111/imj.13377
2. Biomedicines 2023. 11:71

Finding the Cause of Death

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Last week, I left you with a question about a hypothetical situation: What if my grandmother’s bedsores had become infected to the degree that it spread throughout her body; she still had congestive heart failure but didn’t have pulmonary effusion at that time. What would be the primary cause of death?

With so many health experts and influencers that get a lot of attention in social media, causes of death appear to be misunderstood. Let’s cover it as simply as I can, based on the definitions from the CDC, WHO, and other agencies around the world.

  • The primary cause of death is the situation or condition that started the chain of events resulting in death.
  • The secondary cause(s) of death are any conditions that may have contributed to the death.

In the case of the hypothetical situation, the cause of death was the systemic infection from the bedsores. The congestive heart failure was a secondary cause of death. We can’t know for certain, but the infection probably took away the ability to fight back due to the weakened condition of the cardiovascular system.

I’ll give some examples of misinformation in Saturday’s Memo—which is May 10. Long time readers will understand the significance of that day.

What are you prepared to do today?

        Dr. Chet

Why My Grandmother Died

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You may be wondering why the TAP-IT study created that stop-in-my-tracks moment. In the mid-1980s, my grandmother Frances was 80 years old and was always my biggest fan. She had congestive heart failure, so doctors tried the needle procedure, which drained close to 20 lbs. of fluid from around her lungs; you can imagine the pressure that caused on her heart. But congestive heart failure is an unforgiving disease—at least it was back then. Without a real treatment other than thoracentesis, there’s no cure.

Months later, the pulmonary effusion happened again, but she refused treatment because the procedure had hurt too much the first time. She died a couple of weeks later. The study prompted my realization that a medication like a diuretic might have prevented a rather difficult death with multiple bedsores.

The fact that there was never a randomized controlled trial to compare the two approaches until 45 years later just absolutely astounds me. At least now there are treatment options for people with the same condition without the same type of complications.

Just to be clear: there was no coming back from advanced congestive heart failure as my grandmother had. Using either procedure would not have cured her—it would have eventually killed her anyway. But the difference was really in her quality of life. She may have lived longer and certainly less painfully using the diuretic, which as I said was available even back then. But there was no research to support it.

What Was the Cause of Death?

There appears to be a lot of misinformation today about cause of death. I’m going to use my grandmother as an example. I mentioned that she had severe pulmonary effusion due to the congestive heart failure. But she also had bedsores. If they had gone septic, resulting in a whole-body infection, what would have been the official cause of death? That’s what we’ll explore next week. Please share your thoughts.

What are you prepared to do today?

        Dr. Chet

Reference: Circulation. 2025 Apr 1;151(16):1150–1161

TAP-IT to Stop It

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Have you ever had a moment where you were reading something, listening to an audio, or watching a video where you just had a moment of realization and absolutely stopped in your tracks? The reason is that you got hit with a discovery of some fact that you didn’t know. More than that, you realized what it meant. That’s what happened to me while listening to a podcast from a cardiologist about pulmonary effusion and how to treat it.  Let’s start there.

Pulmonary effusion (PE) is the buildup of fluids in the connective tissue surrounding the lungs and the chest cavity.  If enough fluid builds, it’s going to push on the lungs and ultimately push on the heart and make it very hard to breathe. To restore function, the fluid has to be removed. This happens to people who have congestive heart failure.

The TAP-IT study, formally called Thoracentesis to Alleviate Cardiac Pleural Effusion–Interventional Trial, was recently published in a leading heart journal. The researchers selected subjects who were 80+ years of age with less than a 25% ejection fraction. This population was chosen because they are the ones most likely to suffer from pleural effusion. They compared subjects who took diuretics to alleviate the fluid with subjects who got thoracentesis. The goal was to determine if there were any differences in outcomes as assessed by the number of days lived after beginning treatment.

The results? There were no differences in outcomes between the two groups. That’s amazing! Both reduced the pleural effusion, but there were differences in patient comfort and quality of life. As you might imagine, sticking a 2- to 5-inch needle through the rib space and into the pleural cavity to drain the fluid is going to be uncomfortable if not downright painful. There were also 20 out of 80 pneumothoraxes with the needle approach, while there were no complications noted in the group that took the medication.

The realization? This was the first randomized controlled trial that compared thoracentesis with diuretics, even though diuretics have been available for 75 years and thoracentesis for 175 years! Why did that matter to me? I’ll tell you on Saturday.

What are you prepared to do today?

        Dr. Chet

Reference: Circulation. 2025 Apr 1;151(16):1150–1161

The Bottom Line on Red Yeast Rice

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If you remember the last Memo, I said that the active ingredient in red yeast rice (RYR) was monacolin K, which is chemically identical to a current statin medication: lovastatin. The problem with RYR in supplements is that the amounts of monacolin K varied depending on the exact type of Monascus mold used—it could be high enough to mimic the actual medication, or it could have none. You wouldn’t know because it wasn’t standardized.

As a result, the FDA declared that RYR could not be sold in the U.S. because of the lack of information on the amount of monacolin K in the supplements and because lovastatin had already been approved as a drug. Mostly the latter.

The next logical step would be to see if the FDA set a limit on the amount of monacolin K allowable in RYR products in the U.S. They have not; they consider it a drug that shouldn’t be sold in the U.S. at all. You can still find RYR as a dietary supplement, but it should not contain enough monacolin K to really do anything to lower cholesterol. On the other hand, the European equivalent of the FDA has set a limit of no more than 3 mg of monacolin K in a daily serving. You can buy it from a European company, but technically, it’s illegal in the U.S.

In this case, it makes no sense to obtain a product in the U.S. that may or may not have monacolin K in it and which could actually contain lovastatin in it as product analytics have shown. By the way, the side effects from both forms, monacolin K and lovastatin, are identical with muscle pain and the like. Doesn’t happen to most people, but it can happen. Obviously, if you’re taking a statin, don’t add RYR without your doctor’s approval.

The Bottom Line

That’s the deal with RYR in 2025. If you don’t want to take a medication, change your lifestyle to naturally lower your cholesterol. Check with your doctor to find out the limitations that he’s putting on you as it relates to exercise intensity and then get after it. Not to lose a whole bunch of weight. Not to win the next 5K. Not every day.  But to make your heart stronger and fitter. You want natural? That’s the most natural solution to high cholesterol for most people.

What are you prepared to do today?

        Dr. Chet

References:
1. Methodist Debakey Cardiovasc J. 2019 Jul-Sep;15(3):192-199.
2. NIH NCCIH 2024. Red Yeast Rice.

It’s Back: Red Yeast Rice

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I still get questions about using red yeast rice (RYR) instead of a statin to lower cholesterol. About 15 years ago, I looked up the data, wrote about it, and tucked it away. The answer was yes—but. What does that mean? Time to review it again in case you’ve been thinking about it.

Red yeast rice is actually not a yeast, it’s a mold that is produced by the fermentation of a fungus in the Monascus family that grows on, as you may have guessed, red rice. The genera Monascus purpureus is technically a mold—a fungus that produces filaments that include many cells rather than a yeast, a single-celled fungus. From a marketing perspective, you can understand why supplement manufacturers wanted to use red yeast rice rather than red mold rice.

Did RYR as a supplement work to lower cholesterol? Yes, based on several studies done in the late 1990s. There was only one problem. The RYR contained monacolin K, a by-product of fermenting the mold on the red rice. Why is that a problem? Because monacolin K is chemically identical to lovastatin, a pharmaceutical that lowers cholesterol. While no one wants to take medications any more than they have to, the RYR was a “natural” alternative. Is it still available and moreover, is it the same RYR? I’ll let you know on Saturday.

What are you prepared to do today?

        Dr. Chet

References:
1. Methodist Debakey Cardiovasc J. 2019 Jul-Sep;15(3):192-199.
2. NIH NCCIH 2024. Red Yeast Rice.

Specificity of Training

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The concept of training to attain specific performance is called specificity of training. The simplest example is that if you want to run a marathon, you run long distances for training, not 10-yard sprints. I think it’s more than that: the objective is to train the body to use physical activity, food, and rest in a way that creates better performance during specific tasks. Remember prepping for surgery or taking kids to the amusement park? It doesn’t have to be just an athletic event. You also have to be mentally ready for the task as well.

I define energy as the mental clarity to focus on any given task along with the physical energy to complete it. On Tuesday, I talked about a marathon speech that made it. Here’s an example of an effort that didn’t succeed.

Amazing Misses

Paula and I were watching The Amazing Race, which combines travel with completing tasks requiring focus as well as endurance. On top of that, this episode took place in a climate that was extremely warm. When one competitor who looked very fit was asked why he had to stop and rest while completing the tasks and was barely able to stay in the competition, he said he misjudged what would be required physically and mentally.

I don’t agree. I’d say he didn’t train properly to make sure he had enough energy to complete the tasks by manipulating exercise, diet, mental challenges, and physical challenges in his training. He had to know what it would be like; there are dozens of prior seasons he could have watched. Even though he said he was especially sensitive to heat, there are ways to prepare for that. He and his partner could have trained, anticipated the worst, and designed the training to sustain the ability to perform. That would include eating and sleeping during the competition.

The Bottom Line

Two extraordinary performances, one successful and one not so much. If you want to perform at a high level, regardless of the task, you have to train specifically for that task—an important speech, a road trip, even a vacation. If you want some help figuring that out, review your copy of the Optimal Performance program or purchase yours today.

What are you prepared to do today?

        Dr. Chet

An Amazing Performance

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This week, I’m going to talk about a couple of amazing examples of physical feats; it all comes down to training to perform. I’m telling you in advance that the Optimal Performance training program provides the why and the how. When I’m done with the Memos, decide if you want to revisit it if you have it or buy it if you don’t.

A week ago, Senator Cory Booker of NJ spoke on the Senate floor for over 25 hours without taking a bathroom break or eating anything. I don’t care what your political persuasion may be, that’s an extraordinary physical task. According to reports, he prepared by not eating solid food after the Friday before he began speaking and limiting his water intake starting Sunday. What he probably did not train for was staying on his feet for that amount of time, but we know he wore his most comfortable shoes. That aside, this was the absolute correct way to prepare for this kind of effort.

This applies to you as well. If you’re going to have a shoulder or a knee replaced, how are you getting ready? If you’re not doing rehab exercises and building the supporting muscle a couple of months before—if you’re not preparing—it’s going to take longer in rehab to get back to full function.

How about those of you taking kids or grandkids to a giant theme park? You don’t want to disappoint the kids by wimping out halfway through!

What if you know your business is going to be exceptionally busy on a certain date? How about going on a week-long business trip? What if you’re getting ready to take the LSATs or MCATs or any other seven-and-a-half-hour test? There are also ways to manipulate what you eat and when you eat that can lead to maximal energy levels when you need it most; and if you have the energy to do whatever it is, you’re likely to perform better and enjoy it more.

We typically think of athletes when we think of serious preparation for physical challenges, but we all need it at some time. I’ll give you the scientific principle behind this in Saturday’s Memo. Until then, remember to check out the Optimal Performance program.

What are you prepared to do today?

        Dr. Chet

It’s Going to Be a While

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In the last Memo, When Will We Get Something Better?, we looked at research on a new drug to counter obesity. But don’t hold your breath.

The researchers developed a sophisticated algorithm and used AI to find the process and the potential obesity-protein hormone to help combat obesity. What’s next? Several years or longer of clinical trials to test its effectiveness and safety in human beings. If it works, it will be another pharmaceutical solution to obesity and a step better than the GLP-1 agonists currently available. Two of the researchers hold the patent for the process and the protein itself, but there are no shortcuts on the science.

In my opinion, the problem is this: that’s not really the solution. They’re looking for a pharmaceutical solution. This protein, called BRG for short, will still have to be regulated like a pharmaceutical, made like a pharmaceutical, and prescribed as such even though it’s a natural hormone made in the body.

Where the research should focus is on a natural way to stimulate the body to upregulate (turn on) the gene or genes with diet, exercise, or some other natural means. Turning specific genes on and off is where we want to be, not creating companies and chemicals that will create a single molecule. It’s just the wrong approach to me. It may very well work, but it’s not natural in any way. I’m not suggesting that people with massive obesity won’t benefit from it, but it’s treating the symptoms of the problem, not the problem itself.

The problem is that because we overeat the wrong foods while not moving enough, genes have become upregulated and stay that way. We need solutions that help us get to downregulating those genes so that weight loss can become permanent.  Eat less. Eat better. Move more. For life.

What are you prepared to do today?

        Dr. Chet

References:
1. https://med.stanford.edu/news/all-news/2025/03/ozempic-rival.html
2. Nature (2025). https://doi.org/10.1038/s41586-025-08683-y