After months of ads telling Republicans to call on President Trump to eliminate the “Biden Pill Penalty,” it seems the message is getting through. President Trump issued an executive order this month aimed at reducing prescription drug prices while eliminating the Inflation Reduction Act’s “pill penalty” that makes lower-cost small molecule drugs subject to Medicare price controls.

I wrote about this subject in an earlier post called Biden’s Pill Penalty, which explained that the Inflation Reduction Act  (IRA) of President Biden passed in 2022 threatens to distort innovation by pushing investment towards expensive biological products. Trump’s order aims to reverse all this and restore the incentives to increase research and development of new drugs.

The Wall Street Journal editorial board calls on Republicans to fix this in the tax bill – “even if they can’t muster the courage to repeal the IRA’s price controls, which have done nothing to reduce overall drug prices.” Prescription drug prices have increased more since the IRA passed in August 2022 than in the five previous years, in part owing to market distortions caused by price controls.

The controls have also led to cuts in pharmaceutical research and development. That’s one reason investors have sold off pharma and biotech stocks. Nasdaq’s biotech index has risen only 10% over the last five years while the Nasdaq is up more than 100%.

Declining biotech investment has some Republicans fretting about the U.S. losing its competitive advantage to China. “We lost our leadership in semiconductors, and we are close to losing that position in biotech if we don’t act now,” said Indiana Sen. Todd Young last week.

The WSJ editors say, “One way to act would be to stop Mr. Trump’s mooted 25% tariff on imported medicines. Most generics and active drug ingredients are made in India or China because of lower manufacturing costs. The U.S. doesn’t want to depend on China for critical drugs, and many manufacturers have been shifting production to other low-cost countries.”

Clearly, the WSJ editors are not fond of Trump’s tariffs, but they don’t seem to understand that tariffs are a weapon in the negotiations that makes change possible. The elimination of the Biden Pill Penalty is a good start and I believe the tariffs will come down when fair trade practices are achieved. The goal has to be security for our country by encouraging pharmaceutical companies to manufacture their drugs in the U.S. We will all be better off in the long run when that happens.

We’ve all been to the doctor and been told our cholesterol is too high. For years a good cholesterol was considered anything below 220, then it was 200, and now it’s less than 200. The bar seems to be changing as doctors learn more about the science of good and bad cholesterol.

We’ve been told for a long time that LDL (low density lipoproteins) are “bad cholesterol” and HDL (high density lipoproteins) are “good cholesterol.” A blood test showing our HDLs are high and our LDLs are low has always been considered ideal. But all that seems to be under scrutiny as new information becomes available.

Jennifer Sweenie, writing for The Epoch Times, tells us emerging research is painting a new picture: Focusing solely on “bad” cholesterol misses pivotal pieces of the puzzle. Factors such as the size and composition of particles of high-density lipoprotein (HDL) cholesterol—the so-called good cholesterol—along with triglyceride levels and overall metabolic health, are equally, if not more, important in preventing heart disease. This new understanding is reshaping how we assess heart health, shifting the lens to a more comprehensive, preventive, and personalized approach that prioritizes lifestyle changes such as diet and exercise,

Cholesterol is a fat-associated substance essential for building healthy cells and producing vital hormones such as vitamin D. It’s not inherently bad. Your liver produces most of the cholesterol circulating in your body. The real issue lies in how cholesterol is transported.

“Your liver makes most of the cholesterol that’s circulating around, and your body’s pretty good at maintaining a homeostasis, “ said Nick Norwitz, a Harvard medical student and Ph.D. in physiology from Oxford University.. ”So if you eat more cholesterol, your liver makes less. If you eat less cholesterol, your liver makes more.”

Since cholesterol doesn’t dissolve in blood, it’s transported by lipoproteins, which resemble tiny “delivery buses” on the highway of your bloodstream. LDL primarily carries cholesterol to cells, and excess LDL—especially small, dense particles—can contribute to plaque buildup. HDL helps remove excess cholesterol from the bloodstream and returns it to the liver. In short, cholesterol is the cargo, and LDL and HDL are the vehicles that transport the cargo.

LDL gets its reputation as bad cholesterol because excess amounts can contribute to plaque buildup in the arteries. These smaller particles are more likely to damage the artery wall and cause inflammation. Davis compared them to tiny buses that zip in and out of traffic, increasing the chance of crashes. These “crashes” represent inflammation, which can lead to “traffic jams” or plaque accumulation.

Conversely, larger, “fluffy” LDL particles are less likely to cause problems. HDL helps clear excess cholesterol from the bloodstream and transport it back to the liver for disposal, reducing the risk of buildup. In other words, the real concern lies in how LDL and HDL behave. It’s not the cholesterol itself but the actions of its carriers that can yield plaque buildup.

For years, we’ve been told that lowering LDL cholesterol is the primary way to protect our hearts, but the reality is more nuanced. While elevated LDL can contribute to risk, its impact is conditional, as it’s inextricably linked to overall metabolic health and other factors.

One factor is the amount of apolipoprotein B (ApoB) in your blood, a protein that transports cholesterol and other fats. This can be measured with the ApoB test. “The risk associated with ApoB and LDL counts is context-dependent,” Norwitz said. This context involves an intricate interaction of lipids, metabolic factors, and lifestyle.

Without getting too much farther into the weeds with this discussion, the point is we have more to learn about cholesterol and our current way of measuring good and bad cholesterol is probably inadequate. Stay tuned for more as we learn how we can live longer through a balance of exercise, sleep, and stress management along with controlling our cholesterol levels, good and bad.

You can’t believe everything you read. That’s a simple statement we all need to be reminded of when reading anything in the media. I was reminded of that recently while reviewing an article published in The Epoch Times.

Author George Citroner leads his article with these words: “Patients who undergo anterior cruciate ligament reconstruction (ACLR) surgery to repair torn ligaments may be at an elevated risk of developing early-onset knee arthritis, particularly because of issues related to the kneecap, according to a new study.”

According to the study, findings show that those who received ACLR surgery had a shift in the positions of their knee bones and joints, causing a change in load on their knees. ACLR surgery, common among athletes, aims to repair torn ligaments—but has also been linked to long-term complications, with more than 50 percent of patients developing arthritis within 20 years.

The study, recently published in the Journal of Orthopaedic Research, included 15 participants around the age of 26 years who had undergone ACLR, and compared their knee movements with those of 10 people with no knee problems. The kneecap, or patella, in those who had surgery moved up by 4.4 to 5.6 millimeters more than the nonsurgical group’s kneecaps, and this changed the way the knee joint moved. The patella was also pushed forward by 5.4 to 6.3 millimeters more during walking, indicating a change in knee structure that could stress the joint. The study also noted that the tendon connecting the knee cap to the shinbone was an average of 8.9 millimeters longer in ACLR patients than in the healthy group.

Among the ACLR participants, nearly half had an abnormally higher knee cap, also known as patella alta, which may put excessive stress on parts of the knee that are not used to handling load. According to researchers, a higher-riding patella may contribute to the development of knee osteoarthritis by shifting the load-bearing areas between the patella and the femur to regions of cartilage unaccustomed to load and leaving previously loaded regions unloaded.

“If this condition existed prior to the injury, then it may be a predisposing factor for ACL injury,” corresponding author Marcus G. Pandy, of the University of Melbourne in Australia, told The Epoch Times. “Alternatively, if the condition arose as a result of surgery, then it may help to explain the high rate of knee osteoarthritis seen after ACLR.” According to Pandy, the key takeaway is that people who have undergone ACLR have an abnormally longer tendon in their knees, causing a higher-than-normal kneecap position.

What’s wrong with this study?

Dr. James Penna, chair of the Department of Orthopaedics and Rehabilitation at Stony Brook Medicine, disagreed that ACLR surgeries could be causing a longer knee tendon. The angle of the knee upon impact with the ground varies between individuals who have had an ACL injury and those who haven’t, Penna said.

The researchers who conducted the study raised the question about whether it’s the injury or reconstruction that can lead to elongation of the patellar tendons. Penna disagreed that the longer tendon in the knee could be caused by the surgery. “It doesn’t, it can’t,” he said. He believes the researchers simply happened to have patients with naturally longer tendons in their sample.

Pandy and team wrote that further research is needed to determine the cause of the longer knee tendon in individuals who have undergone ACLR surgery. The researchers didn’t compare those who received ACLR surgery with those who didn’t—this would be the next step, according to Pandy.

My Opinion

It has been well known for nearly fifty years that individuals who sustain ACL injuries are susceptible to developing post-traumatic arthritis in that knee for multiple reasons. The rupture of the anterior cruciate ligament (ACL) is a significant trauma to the knee and is usually associated with other injuries such as a torn medial and or lateral meniscus, collateral ligament injuries, as well as articular cartilage damage. Such injuries will lead to traumatic arthritis in most patients whether or not they ever have ACL reconstructive surgery.

The premise of the Pandy team study that ACL reconstructive surgery leads to alteration of the length of the patella tendon is not credible. Although there are several different methods used for ACL reconstruction, I know of no methods that alter the pre-injury length of the tendon. That means the observation in their study that patients with longer tendons were more likely to develop arthritis is simply an indication that those individuals were at higher risk for developing arthritis, regardless of whether or not they had ACL reconstruction.

The limited size of their study, only 15 patients, means little can be learned from the results of such a study. The only possible conclusion of this study is that patients with longer patella tendons may possibly be more vulnerable to sustaining ACL injuries that those with normal length patella tendons. However, a much larger study group would be needed to draw any meaningful conclusions.

If you are facing ACL surgery, the main thing you should realize is that you are at higher risk of developing traumatic arthritis than individuals without ACL injuries. The surgery is done to stabilize your knee, which should reduce, but not eliminate, your risk of developing arthritis.