3 strikes, you’re out? (Part III)
Now for the second strike. After the debacle of torcetrapib, I for one felt that the class, if not the concept, was in deep trouble. Not only did the drug not benefit, it seemed to harm people. It is believed this is because the drug activated the aldosterone system in the body to raise blood pressure, among other things.
The next batter up was dalcetrapib. This drug was produced and studied by Roche. I participated in one of the six studies for a brief period of time, and the research facility at Holy Cross participated in a study called Dal-plaque, which was a two-year intravascular ultrasound study of the drug. This study was being done to evaluate whether plaque was removed from the coronary artery system by the drug.
Early on the results of the studies were favorable. As reported at the European Society of Cardiology meeting in Paris last April (remember I have written that the European meeting is where all the new information is presented, and anyway, Paris is way better than Dallas) dal-Vessel was a report on the 600 mg dose of dalcetrapib. It reported that the drug was less potent than torcetrapib, raising HDL by 31% compared to placebo and did not increase inflammatory markers or markers of oxidative stress. There was no change in LDL levels as there was in the use of torcetrapib. There was no change in systolic or diastolic blood pressure. There was immediate discussion that maybe less is more in this case. Hope springs eternal.
The true data would again come from the outcome study of 16,000 patients. The data were expected in 2013. Well guess what? I know that you my readers can guess at this point that things didn’t go so well. Last week the outcomes study was halted. It was not stopped because of increased deaths as was torcetrapib. It was stopped because there was no benefit, and the drug would not become beneficial no matter how long the study was continued. This is not the approach that the Zetia outcomes trial has taken as I have written. They keep going and going…
The knower of all things came out and stated that this result was “not a surprise” because dalcetrapib was too weak and didn’t additionally lower LDL. Now they tell us. Someone should have told Roche before they wasted $500 million dollars. What now?
There are two more batters. The next up is anacetrapib from Merck, which is deep into their outcome trial. Anacetrapib increases HDL by 100% and decreases LDL by 35-40%. There is one more batter in the batter’s box named evacetrapib by Lilly. The evacetrapib outcomes trial has not started yet, and the question remains whether they will step up to bat.
We may just be wrong about all of this. There is a considerable amount of money that changes hands here to do the monitoring and running of these trials. Many millions of dollars. Sometimes the science gets lost in the mix. We cannot lose sight of the very real need for improvement in the treatment of cardiovascular disease. But, one has to be cognizant that things are not going well for this class of drugs after close to $2 billion has been spent.
Maybe we should go back to the drawing board?
3 strikes, you’re out? (Part II)
Let’s talk about torcetrapib. Like Madonna, Dunkirk and other things that are known by one name, torcetrapib has taken on more than just the name of a failed drug.
As I wrote in my last blog, this class of drugs (the CETP inhibitors) followed from the observation of a human genetic abnormality, which led to very high levels of HDL. It is urban legend in cardiology that for every 1% rise in HDL, a 3% reduction in mortality occurs. This data, however, was in the era before statins and was primarily the result of using niacin by itself. See my past blog post, Aim high and Fail, for the debacle of adding niacin to a statin. As I have stated in the past, statins reduce cardiovascular death by about one-third in those that take the class of drugs. What about the other 66%? If we could just find a drug to raise HDL, then all would be right with the world.
The development of the drug torcetrapib began in 1990 and was first given to humans in 1999. According to Pfizer’s press release, they began full-scale production of the drug in 2005. Large scale studies began in 2004. I and my research group participated in one of them. The large-scale clinical trial that the FDA required was named ILLUMINATE or Investigation of Lipid Level Management to Understand Its Impact in Atherosclerotic Events.
In this trial, and the others in the program, the combination of atorvastatin and torcetrapib lead to a decrease of 20% in LDL and an increase of 61% in HDL compared to the group that took atorvastatin alone. I need to point out that this study is not a placebo study. Further, an increase in HDL of 60% was unheard of. The excitement that this compound generated was epic. The hope was that this combination would lead to an impressive reduction in cardiovascular mortality.
Nothing of the sort happened. In fact, on December 2, 2006, it was revealed that the combination of atorvastatin and torcetrapib resulted in a 60% increase in cardiovascular deaths, and the study was halted. In fact, every study of the drug was halted, and the compound was done. Pfizer was also done. After spending close to $1 billion on the drug and betting the “farm”on it, Pfizer withdrew from cardiovascular disease management entirely.
How did this happen? No one knows for sure, but two pieces of information were brought forward. The first was that there was an increase in the mean blood pressure of the study group of 4.6 mm Hg. I for one don’t understand the implication of this, but a big deal was made of it. Patients with cardiovascular disease are often hypertensive and are on medication. Couldn’t a small increase in meds have avoided this? The second piece of information was published in The NEJM on March 29, 2007 (N Engl J Med 2007; 356:1304-1316).
This article was concerning a study known as ILLUSTRATE or the Investigation of Lipid Level Management Using Coronary Ultrasound to Assess Reduction of Atherosclerosis by CETP Inhibition and HDL Elevation. Briefly, the two groups (one on atorvastatin and one on atorvastatin and torcetrapib) underwent intravascular ultrasound at baseline and two years later. The expectation would be that the study group would have a reduction in their atheroma burden. At the end of the study, there was no appreciable difference. If anything is learned, it is that it is better to prevent this illness than try to “Drano” it out.
I for one believed that this was the end of this class of drugs. Three other companies had agents in the same class, and after review of the data, each believed that their compound would succeed where torcetrapib failed.
Strike one…
3 strikes, you’re out? (Part I)
Is it really possible that statins as a class of drugs are so powerful that no new drug can fill an acknowledged need? Why is it that drugs such as niacin, Zetia, Lopid, etc. alter the amounts of the components of cholesterol, HDL and LDL but do not lead to better outcomes?
As I have blogged about, the FDA previously used what is known as surrogate markers for measures of success. If a compound could lower LDL or raise HDL and it didn’t kill you or make you sick, then it could be approved. Rightly so, this has come to be viewed as incorrect, and to be approved, a compound now actually has to do something. In the case of atherosclerosis, that means that you need to reduce death and illness in the form of less unstable angina, myocardial infarction and stroke.
One would think this would be easy. One would be wrong, and this week we physicians and you my readers were faced with the end of another compound that did not make the cut.
Cholesterol and its components are treated by doctors at a truly elemental level. In fact, the metabolism of cholesterol is extremely complicated as illustrated by this diagram from Wikipedia:
I bet you are glad that you don’t have to memorize this. The part that we have down is the part in the upper left corner of the diagram showing the class of drugs known as statin, which blocks the metabolism of cholesterol early on by blocking the enzyme HMGCR. The part that has now failed again is in the center of the diagram labeled CETP, which interferes with the movement of HDL to LDL.
The saga of CETP will now be described because like any good story, the story itself is a reflection of how things in the world of research are going, and like much of what goes on today, represents the need for new models of progress.
CETP stands for cholesteryl ester transfer protein. This protein helps in the movement of cholesteryl esters and triglycerides from very low density lipoproteins to high density lipoproteins. Although the diagram above is static on paper, in the human body it is constantly moving, and a single cholesterol test is just a snapshot in time. This is the reason doctors want fasting levels of cholesterol; it provides a “level” system of following someone. At different times of the day your cholesterol numbers are different, so for a comparison, fasting is often used.
However, since you are not fasting during the day, this has never made much sense to me. My goal in the majority of my patients is to drive their cholesterol numbers to a LDL of 70 mg/dl or less, so I want to see their “random” numbers. I want to see your worst cholesterol numbers, not your best.
CETP is coded on the 16TH chromosome. Remember genes on our chromosomes code for proteins, which run us. When these genes are damaged or mutated, the amount of CETP varies. A family in Japan was found to have exceptionally low amounts of CETP, and this caused them to have very high levels of HDL and very long lives. The light bulb went off, a drug was developed to block this enzyme and then poof! A new drug class was formed.
The first in class was torcetrapib. This drug is a long story in itself and was, and is, responsible for Pfizer getting out of the cardiovascular business after losing close to a billion dollars on it.
Interested? Read on…
And now for the other shoe (Part II)
On April 19, 2012 Pauline Chen, who is a surgeon and writes for the New York Times, penned an article about a program that is gaining more traction and may become the new “norm” in third year medical education.
Beginning in 2004 at Harvard, third year students were given a panel of 100 outpatients who they then followed for the year in clinic. The clinic is akin to an office setting. These students followed their patients into the hospital and into the OR, if that is where they went. They also had preceptors in the major specialties in clinic for didactic learning. What was found was that these students “had a more rewarding and humanizing learning experience.” They were able to reintegrate themselves into the fourth year of medical school and maintain their knowledge and ethical outlook.
Somehow the “powers that be” feel that the grind of hospital learning needs to be replaced by the clinic setting. Somewhere along the way, medical students have been deemed to have a lack of empathy and that “patients are reduced to their disease.” This is sometimes how we physicians communicate amongst ourselves. It is a shorthand that is developed and often easier to remember than names.
Is this really the same education? Clinic is not the hospital. The daily grind and responsibility of hospital patient care, even though as students we really aren’t responsible, teaches us something. There was and should be a pride in accomplishing things that are difficult. Even as students, we shared in the successes of patients and in their difficulties. It speaks to one of the rules of The House of God, that book I have blogged about in the past. One of the rules is “the patient is the one with the disease,” This is because as students, house staff and when we are released to be on our own, we physicians feel the anguish of suffering and the occasional death. We feel the happiness of a successful operation. We share in the recovery from a heart attack. I am doing something to you, the patient, and I am responsible. I take it personally. I am making a decision, and I am responsible for it.
Maybe the problem is not with the students but with the doctors. Maybe the students are picking up our subtle, and not so subtle, anguish at the ever-increasing change of our beloved profession. The constant interplay of government in what we do. The constant interference in patient care. What other profession has 100% of its work reviewed by the government as ours does? Are the reviewers doctors? No. They are people trained to look for whatever the government is looking for at the moment.
Let me give you one example. The LDL goal for patients with coronary disease is 70 mg/dl. If you were on simvastatin 80 mg (when we could use it) and you the patient were not at goal, then you had to move to Lipitor. Before Lipitor was generic, this often resulted in having to have a full-blown conversation with the insurance company as to why I needed to spend more money for you the patient.
I believe that this education pathway will further erode the medical education of our next generation of physicians. It further engenders what I see as an accelerating trend of patients who are admitted to the hospital by “hospitalists,” being cleaved from their long-term physicians. It’s said that this is to shorten hospital stays and save money, but I have yet to see any real data on this. When long-term patients need us the most, we are relegated to social visits. Social visits are all well and good, but when someone I have cared for continuously for 20 years is in the hospital, they have the right to expect more from me at that point in their lives.
I will continue to practice how I was taught.
And now the second shoe (Part I)
I have spent the last several blogs on the new MCAT exam and whether it will allow the medical schools to admit a class of “better doctors.” There is another change which is occurring which will also alter the scope and magnitude of medical education.
This change is in the third year of medical school. The third year has traditionally been when students leave the classroom for good and enter the world of medicine. There is usually an early introduction into medicine in the courses that teach us to examine patients.
Some training is done on simulators but much is done the old fashion way — with live patients who graciously let medical students paw them as we feel livers and listen to heart murmurs. Medicine is a “hands on” effort, and it takes some time before students become able to exam (touch) patients properly. In the new environment, this is often done with gloves on. In some cases this is absolutely necessary, but in others, I feel that it demeans the human touch.
Some schools advance students into hospitals early, and some are more traditional. I don’t believe that it is as rigid as it was when I was a student.
Now there is a movement to change the third year. In the past it consisted of learning all the sections of medicine. Even if you didn’t want to or were appalled at the thought, you were dragged through medicine, surgery, ob/gyn, pediatrics, psychiatry and the occasional specialty. You are assigned patients, and you must learn everything about them. These patients are then presented to attendings who teach you about the illness and help you learn.
In addition to the attending, each patient also has a fourth year student, an intern, and a junior or senior resident who actually have ultimate responsibility for the patient. As a medical student, you get to think about it but not actually do it. You can write an order, but it has to be signed by a more senior member of the team. These are the checks and balances of medical training. The senior residents are grilled and supervised by the chief resident and the professors who are constantly around. The hardest thing I ever did was when I signed my first real order the first day of my internship. This is when no one had to check anymore, and you are petrified that you will make a mistake.
These are some of the fondest memories I have of training. Seeing patients and trying to figure out what is wrong with them and hoping that you can help them get over their illness. The people I trained with were so smart that they made you want to be better and smarter. You would work the same shifts as the house staff, and when you got home, you were just as tired but felt compelled to go home and learn.
One problem that became evident was that after a month, you gave “your ” patients to another third year student, and you moved on. Sometimes you were in the same hospital and could go and check up on them. Often, though, in the Emory system of four hospitals, you were at a different hospital and so you lost touch. You never had the completion of the care and often did not know how things turned out.
This approach to medical training is changing. I’m not sure if it is better or worse than the concept in which I was trained. I will describe it in my next blog.
A roughly 43% chance (Part III)
In my last blog, I reviewed the history of the MCAT test. Now I will discuss why a 153-page preview guide is needed to explain the new test.
In the fall of 2008, the “powers that be,” and we know who those people are, gathered to decide what the next generation of medical students, and by extension, the next generation of doctors should look like. I guess they didn’t like my generation or the one behind me. In 2011, the results of their meetings were released, and in 2015 the MCAT will be changed.
This timeline is important because it will change the course work required for students to learn the information necessary for the exam. This information isn’t the kind of information you learn by flashcards.
The new test will be biochemistry, multicultural/behavioral concepts (I’m not kidding), critical analysis/reasoning from the humanities, along with the usual suspects: biology, chemistry, math and physics.
Can we make “renaissance physicians?” Do we need to? Colleges and Universities will now have to design courses that will prepare the “Pre-Med” student for this test. In the past, it was easy, and the path was well- documented and tested. I took all the science courses I could and then all my other courses were English and Greek mythology. I have a soft spot for Greek mythology. This will need to start for the Class of 2013 so that they will be ready in 2015 for the new test.
Can you really test for empathy? Can you teach people to be empathic in a classroom setting? What do patients want from their physicians? Empathy or knowledge ? Can you have both?
There are countless stories of physicians who were changed by being sick. The grind of having a chronic illness is certainly overwhelming. Just dealing with the paperwork of insurance and the routine of the hospital can get you down.
When I was in training at Emory University in Atlanta, I was taught by example. The mostly men who taught me were by and large from the South, and their manners and beliefs were from that era. Everyone was treated the same, with respect and compassion. I was trained across the spectrum of patients from inner city, to Veterans, to University and Community hospitals. That is one of the strengths of the Emory program. In all settings, patients were treated the same. Woe to you if any attending heard a remark about a patient that was deemed disrespectful. I know people who were dismissed from the program for it.
Along with this example was an acquisition of knowledge. If physicians don’t understand what is wrong, we cannot attempt to correct it. Some of what we do is technical. The skill set I have to perform angioplasty was honed over 30 years and over 20,000 procedures. The next generation of practitioners will not have that experience because the nature of the procedure and our understanding of the illness has changed. The same holds for the next generation of cardiac surgeons.
I see this change already. The students that I see don’t seem as motivated, and the talk mostly revolves around a different lifestyle than I have experienced. I believe that change is good, and we should strive to improve medical education. We need to enhance physicians’ ability to communicate, but all around us are reports that people communicate less and less in person and more and more via technology. In the office, I now have to enter and create a computer document. I have chosen to use a laptop so I can at least look at my patients. Some doctors now have to face away to use the computer. The hands-on nature of medicine moves further and further away from us, and technology intervenes. This is good and bad, and we must learn how to control it.
Sometimes all it takes is holding someone’s hand.
A roughly 43% chance (Part II)
Photo from mcat-bookstore.com
The first change I would like to discuss is the MCAT or Medical College Admission Test. As discussed in an article in the New York Times by Dr. Elisabeth Rosenthal on April 13, 2012, this rite of passage is again being updated to reflect what the authors believe to be a flaw in current students.
Any test that needs a 153-page preview guide can’t be all good. As discussed on Wikipedia, the MCAT started it’s life in the 1920′s as a response to the high dropout rate of students entering medical school. By 1946, the dropout rate was 7%. In 1946, a new test was composed of four sections which included english, math, science and what was called “understanding modern society.” Although the scores were combined into the famous “3200,” the only score that really counted was the science score.
In 1962, the understanding modern society became “general information.” This continued until 1977. This is the test that I took when I sat for it in 1975 as a junior in college. The test was, and is, a focal point in the passage into medical school. Colleges and Universities differ, and an “A” in one is a “B” in others. The test serves as an independent source of information to admissions officers. You are being tested against the whole pool of applicants, so my score can be – and was – compared to everyone else’s.
The test can make or break you.
Schools are interested in the person who went to Africa for two years to dig wells for water. Those that spent considerable effort in developing inner city healthcare and on and on. When it comes down to it, however, the admissions committees believe that a certain score guarantees that the holder of that score will complete medical school, and that is their goal.
That score is generally the science score. If you can’t do the science, your chances of acceptance and “success” are small.
In 1977, this emphasis on science doubled down. General information was eliminated, and the scoring changed. Now each component of science was scored individually. The sections were scientific knowledge, science problems, reading skills analysis and quantitative analysis (math). Biology, chemistry and physics scores were separated and scored 1-15.
In 1992, this changed again. In an interesting experiment, but one doomed to failure as most of us are unable to speak or write in complete sentences, a section was placed in the test where two essays were written in an hour and scored with the letters J-T. Don’t ask me, it wasn’t my idea. The other sections were verbal reasoning (English), biological sciences, physical sciences (physics and chemistry) and the written part. Maximum score was 45.
Well the test is again changing. Starting in 2015, a new MCAT will be offered. How did we get to this point? Will this time be the charm? Is science going to take a back seat? Can you create a test to predict what is perceived to be a better doctor in the current environment of too much information? What kind of doctor is the “facebook generation” going to produce. Will they communicate with their patients by Twitter? Post your X-rays on Tumbler?
What is a pre-med student to do?
A roughly 43% chance (Part I)
If you apply to medical school, your chance of being accepted is around 43%. Can we “make” better doctors? Will the doctors of tomorrow be prepared for the challenges of today?
Tip O’Neil, the former speaker of the house from 1977-1987, was from Massachusetts. He once famously said that “all politics is local.” What he meant was that people hate politicians but generally like theirs. Most people like their doctors even when they are being treated very poorly by them. They are comfortable with them.
I spend a considerable amount of time talking with my patients about all sorts of things. I am genuinely interested in their lives and former activities. Many have historical stories that I am very interested in, especially the veterans from World War II.
I also spend a considerable amount of time talking to patients about other doctors. There are physicians who are going to take care of you for a long time, and there are physicians that you need for about 3 hours. Some physicians are “one shot deals” and then you never see them again. Patients rightfully expect that all physicians will take the time to explain what need to be done and why. At times, decision making is complex, and a considerable amount of time needs to be spent solving patients’ needs. This is obviously not always the case.
Medical care is changing. All of these changes are not for the better. My uncle was an Internist from “the old school.” He made house calls. He had a little black bag. He knew patients for years and cared deeply for them. He was an honored and respected man who was a leader in his hospital and oversaw a huge expansion of it. He is the reason why two of his sons and I entered the medical profession.
He didn’t have a job; he had a lifestyle. That lifestyle for better or worse was that his patients came first and his family was second. He knew everything about each patient and was there to intercede in their needs with other physicians.
This is no longer the case. Now, more likely than not, you will not be admitted to the hospital by your doctor but by the “hospitalist.” That physician may or may not call your doctor to determine if that “scar”on your lung has been worked up before. The theory is that with the Electronic Medical Record your data will be there, and they can figure it out for themselves. In the near future, even if your doctor wanted to see you in the hospital, it would be for social reasons only as they will not be reimbursed for hospital visits. This is the direction that things are going and the direction that the government is driving it.
Further, these doctors — like many others – are now shift doctors. They work a shift and then “sign out” to the next shift like we did in training. This is also seen in the clinic visits that patients see in large health plans. You may see any of several physicians and not necessarily “your” physician. The difference was that in training, I did not go home until my work was finished. The powers that be didn’t care if it took me all week. This trained me to work efficiently and put long hours in. Today’s trainees are limited in their work hours, and this is reflected in the career paths they pick and the kind of nine to five jobs they want.
Next…how doctors are being chosen and trained.
The next frontier: Gene-based therapy (Part II)
A study was published in Lancet recently and can be found at Lancet 2012; DOI:10.1016/S0146736(12)60161-5. This study is titled “Point-of-care genetic testing for personalization of antiplatelet treatment (RAPID GENE): A prospective, randomized, proof-of-concept trial” (it’s a real page-turner). What this study did was identify carriers of the CYP2C19*2 allele with a bedside test that uses a swab of your mouth and can be done by any individual. The information was then used to treat patients. Carriers were randomized to prasugrel (Effient). Non-carriers and those randomized to standard treatment received Plavix. At follow-up, 23 patients in each group had at least one allele CYP2C19*2. Platelet reactivity was low in the group treated with prasugrel, and seven in the standard group had high levels of platelet reactivity. This was taken by the authors to show that these patients should have been switched to prasugrel. I would ask “if there were 23 patents who had alleles, how come only seven had an effect?” Do you swab everyone and change everyone who has the allele? Is there any clinical benefit? We have been using Plavix for almost 10 years. It will be generic next month.
If this was, and is, such a big problem, how come so few patients are troubled by it? Do we have to make everything complicated to improve care? Are we improving care? As I have blogged about before, no study has shown that by measuring platelet reactivity a clinical benefit can be obtained. Certainly this study does not show clinical benefit. It shows a test benefit. That, however, is not good enough to warrant the extra expense of medicine and the test. Dr Sanjay Kaul of Cedars-Sinai in Los Angeles put it best, ” The unbridled (and uncritical) enthusiasm for genomics revolutionizing personalized medicine has often blurred the distinction between hope, hype and reality. While the progress in DNA sequencing technology and bioinformatics is undeniably breathtaking, the translation of this knowledge to clinical practice has lagged behind. Genomics will get there, but it cannot be expected to move faster than the speed of science.”
The FDA will not allow a drug on the market unless a clinical benefit is found. This benefit must be statistically significant but that is often in the eye of the beholder or the drug sales rep. Treating 200 patients to avoid one event to me is not anything to be excited about. But, in my world, it gets you an entrée into the world of drugs. Crestor had a new indication for its use by showing a benefit of 1 event reduction in 500 treated woman who had low LDL but high hs-CRP’s. Doesn’t sound like much to me, but it was good enough.
Likewise, a test has to have a reason. The reason needs to have a clinical benefit. The study on clinicaltrials .gov was called TARGET-PCI and was enrolling 1,500 patients using the genotyping assay and attempting to find a clinical benefit. It was stopped, according to the site, because of lack of financial support. That probably translates to futility for finding the “right” answer. You have to ask the right question. As we study the subject, platelet function, it becomes more complex. The beauty of nature and the interactions in a human being is astounding to me on a daily basis. I am in awe of what the body can do and how resilient it is. Believe me, we rely on that.
The next frontier: Gene-based therapy (Part I)
One of the lures of becoming a physician is the intersection of science and humanity. Everyday I am allowed to bring science to my patients in an attempt to impact upon their problems or attempt to improve their health conditions. This is a constantly changing environment and one which seems to be accelerating everyday. These changes require understanding them and then awaiting recognition that the changes are of clinical value. This is where “the rubber meets the road.” It is all well and good that X + Y = Z, but there has to be a clinical value to what is being offered. One such “advance” is gene-based therapy. The fact that we are as far along in this field as we are is astounding. Physicians didn’t know the structure of genes until the work of Watson, Crick and Franklin in the 1950′s as I have blogged about before. Only recently was the human genome mapped. This project was supposed to take years and was accomplished in a much shorter time. Now we have therapies available that match genes with function, which is always the production of a protein that can aid in the treatment of specific problems.
One such match is a gene that codes for the protein that metabolizes the prodrug Plavix into the active drug. As I have blogged about before, patients take this and other drugs like it to prevent stent closure or thrombosis after angioplasty. I have blogged about this concept and the issues of Plavix before. When first developed, physicians thought that one size fits all and that Plavix was metabolized in the same way in everyone, hence only one 75 mg dose was offered. Then came work showing a specific protein resided in the liver and that patients had variable amounts of this protein depending on their genes. This results in a variable response to Plavix and its important effect. The process of stent closure or thrombosis is often devastating, and it can have up to a 30% mortality. Out came the companies to sell machines that would be used to test various aspects of this process. Some of the machines tested the platelet function after Plavix was given and active. Some test the genes themselves to predict what will happen to the patient. None of these tests seem to have any effect on the clinical outcomes of patients. In other words, no matter what we test and what we do, it doesn’t seem to matter in the end. Some of this seems to be who you ask. There are some doctors Like Eric Topol who are building whole second careers on this concept. Others are not so sure. As always in my blogs, two recent studies provide a counter point to this discussion.
The first is not an actual published study but an observation. The government has a web site which I have mentioned before. It is clinical trials.gov. To perform an FDA sanctioned study in the United States, the study must be listed on this site. This now allows individuals to see studies that were done and never reported. The general consensus is that the ones not reported did not prove the theory and as such may “harm” the drug or concept being studied, and this reporting keeps companies “more honest.” The trend now is to expect that every study done is reported, but this still is not always the case. Next…what was found on the site.
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