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

When Will We Get Something Better?

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The quest for a pharmacological solution to obesity continues—the magic pill to make us thin. While Ozempic and Wegovy, discovered and developed to treat type 2 diabetes, have been successful in helping reduce HbA1c, it has also helped people lose weight; the problem is the side effects. As you might guess, there are receptors for GLP-1 agonists in numerous locations in addition to the brain, and other organs are impacted.

That’s why a press release from Stanford seemed promising: “Naturally occurring molecule rivals Ozempic in weight loss, sidesteps side effects.” This research used a unique approach: they designed a specific algorithm that used artificial intelligence to identify the hormone segments made by an enzyme prohormone convertase 1/3 (PC1/3); basically, it cuts prohormones into smaller segments. Some may have metabolic activity, most would not.

Based on the analysis of 2,600 protein segments, the researchers identified 373 potentials and tested the top 100 most likely to succeed. They identified a hormone segment with 12 amino acids that appears to impact hunger 10 times better than the GLP-1 agonists, which are cleaved from the same prohormone. When they tested it in mice and minipigs by injecting it into the muscles of the animals before eating, it reduced food intake by 50%.

The volume of work done by the specific algorithm using AI probably saved years compared to testing each prohormone by trial and error, but what’s next? When will it be available? I’ll cover that on Saturday.

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

Research Must Go On

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This is the final installment of my Memo series illustrating why research funding for basic and clinical trials should never stop unless the approach is obviously misdirected. Delaying research due to the dogma of the day is bad; delaying it because someone believes in a refuted dogma is worse. This is not a debate on whether vaccines can cause autism. The data is clear to me; autism is the direct or indirect result of genetic mutations, most of which have not been fully researched. But many people still have questions, so let’s say that someone were to direct research to examine vaccinations as a potential cause for autism, specifically the mumps, measles, and rubella (MMR) vaccine. How should it be done?

First, every child should have complete genetic testing that includes every suspected gene that’s been associated with autism—specifically, retrograde autism, the most serious form. The children should also have a complete microbiome examination because a weak immune system may be related to the development of autism. The genetics and microbiomes of both parents should also be tested.

Second, the children should be randomly selected throughout the United States covering all geographic areas.

Third, the parent should decide whether they choose to have their children vaccinated or not; the decision should not be influenced by healthcare professionals.

Fourth, the key time for retrograde autism is within two weeks of the vaccinations; the diagnosis process should begin within that time frame.

Finally, it has to be a blinded study. That means that neither the physicians nor the parents can be told of the purpose of the study other than to agree to monitor the development of the child.

There are hundreds of details and other variables that need to be worked out, but that’s the basic idea. We’ve had numerous studies that included over a million children that were retrospective observational studies, and that’s great information, but doing a study before children are vaccinated is the best way to answer whether vaccinations are related to autism. The side benefit is that we will have genetic and microbiome profiles to compare with those who were and were not vaccinated and those who were and were not diagnosed with retrograde autism. Anything less would not answer the question.

One more thing: The scientific board that controls the funding can have no part in selecting where and how the research is conducted.

If we did all that—and it’s absolutely doable if we have the will to do it—we could finally answer the questions about vaccines and autism. Since we’re talking about the lives of children, I think most of us would agree it’s a great use of research funds because we could finally know that vaccines are safe.

The Bottom Line

Research on health and disease has to continue without political influence. I’ve tried to illustrate the problems with research delayed by professional and personal dogma as well as an idea of the timeline of how long it takes to get answers. When you get right down to it, can we afford to delay even one second? The next solution might just impact you or someone you care about.

What are you prepared to do today?

        Dr. Chet

References:
1. N Engl J Med. 2002 Nov 7;347(19):1477-82
2. Ann Intern Med. 2019 Apr 16;170(8):513-520

What Research Delays Can Cost

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In 1911, a physician named Peyton Rous discovered that a microbe, found in a tumor in chicken, was able to infect other chickens causing the same cancer. His findings were thought to be ridiculous because cancer wasn’t caused by a microbe—so his research stopped. Those microbes were called viruses in later years.

Move forward to the 1950s, when a scientist named Ludwig Gross picked up the research and established that viruses caused cancer in several species of animals. What he did not prove was how that was possible. The problem was that it went against the central dogma: DNA could result in the production of RNA, but RNA could not go backward and interfere with DNA. Without knowing how that could happen, it wasn’t possible to establish that viruses caused cancer in humans.

In the early 1970s, David Baltimore, Renato Dulbecco, and Howard Temin discovered a piece of the virus that could retroactively insert itself into the cell DNA and make it a cancer cell. They called that reverse transcriptase, and it led to the term retroviruses. In 1975, the researchers won Nobel Prizes for that discovery.

Now the science turned to finding a retrovirus in humans. Robert Gallo discovered just such a retrovirus in two different humans and submitted his paper to the Journal of Virology. It was rejected on September 15, 1980.

During the early 1980s, there was a disease that seemed to be impacting primarily gay men; at that time, catching the virus was almost always a death sentence. Dr. Gallo turned his attention to this new virus and co-discovered what became known as the human immunodeficiency virus, or HIV for short, the virus that causes acquired immunodeficiency disorder, also known as AIDS. That was in 1984—four years after Gallo demonstrated that a retrovirus caused a form of blood cancer, leukemia, in humans.

Those lost years delayed the test for HIV, also discovered by Gallo. By 1995, there was a blend of drugs that could arrest HIV and today, while there is no vaccine yet, HIV is blocked by drugs that stops it from replicating itself.

Four years were lost because science stopped. More correctly stated, science didn’t stop, but those scientists who would have been attracted to the research problem didn’t take up the search because there was limited funding for that type of research. Ryan White, a teenage hemophiliac from Indiana, died on April 8, 1990, from AIDS. If you don’t remember him, you may remember Freddie Mercury who died of AIDS on November 11, 1991. Maybe they would have lived if science hadn’t slowed for four years, as would hundreds of thousands of others.

And imagine how far ahead we might be if 114 years ago, scientists had admitted they didn’t know everything and followed up on the research by Dr. Rous. How many lives could have been saved? What major diseases could have been cured?

That’s the price for delaying research. But what about research that is started based on the dogma of the person who dictates where research dollars are spent? I’ll cover that on Saturday.

What are you prepared to do today?

        Dr. Chet

Reference: Revisionist History. Malcolm Gladwell. The Obscure Virus Club provided the basis for the HIV and AIDS timeline. Every scientific article and fact were independently verified by the Memo writer.