Cholesterol Management 101

By Michael Richman, MD, FACS

Nearly one year ago, in a blog published on WebMD, I addressed the concerns of medical training that interns and residents endure while on their journey to gain board certification as a physician or a surgeon. Now, new information collected from a recent study of 215 interns in 11 general surgery residence programs outlines the efficacy of the new standards. I felt that the former study hampered the ability of newly trained doctors to deal with real-world medicine after they completed their training. Required residency hours were lengthy and medical professional communities recognized the potential dangers that excessive work hours under stressful situations posed on several levels, including sleep deprivation and the resulting increased rates of medical errors due to fatigue.

In 2003, in an effort to further regulate, the Accreditation Council for Graduate Medical Education (ACGME) looked at the current residency programs. This included studying the amount of time residents were required to spend at the hospital, patient safety issues, resident wellness, and the resident training experience. In 2007 medical residents were restricted to 80 hours per week, overnight call frequency could be no more than one overnight every third day, straight shifts were a maximum of 30 hours, and residents had 10 hours off between shifts. Although these rules were voluntary, adherence had been mandated for the purposes of accreditation of the residency. Moreover, first-year residents, also called interns, were limited to shifts no longer than 16 hours straight due to these newly regulated standards effective on July 1, 2011.

While patient safety advocates and surgeons themselves voiced objections and trepidation, the ACGME still implemented the new standards in an effort to protect residents from sleep deprivation, fatigue, and the medical errors that can follow. Second-year resident schedules allowed up to 24 straight hours of work, with 4 additional hours permitted to ensure proper patient hand-off, as opposed to the previous standards in which 24-hour shifts were the maximum for all residents, with 6 hours acceptable for patient hand-off.

With all the debate and protest, David Farley, MD, of the Mayo Clinic in Rochester, Minn., and his colleagues conducted a thorough study and his findings were published in the June 18, 2012 edition of the Archives of Surgery, along with statistics that caused alarm within the medical community and indicate potential adverse effects on patient care.

The investigation found that 80% of the surgical interns believed that the time restrictions would decrease continuity of care with patients, and nearly 58% believed that it would impact overall patient care. Furthermore, even greater concern was expressed when interns were asked about the effect the reduced hours would have on their expertise in the operating room, with 67% reporting apprehension. On average, 50% of the interns believed their general medical knowledge, surgical skill set, and educational experience would suffer, even if their fatigue would lessen.

Farley’s findings reiterate my opinions regarding the deficiencies in medical training in the United States since I was a medical resident. After four years of medical school and nine more years of surgical training after that, I went into private practice as a heart surgeon in 1999. I did my general surgery training at Los Angeles County-USC Medical Center, which is probably the busiest hospital in the U.S. I performed over 1300 cases as the primary surgeon in four years and often spent 130 hours a week at the hospital. I did my heart surgery training at University of Miami-Jackson Memorial Hospital, which also is one of the busiest hospitals in the United States. Today, the graduating residents from the same general surgery program I trained at finish with around half the number of cases that I performed in the same time frame of training.

There is a reason that surgical training is accordingly extensive and complex. The first reason is to purge those doctors that can’t perform under such extreme conditions. The second reason is that in order to develop an excellent technical skill set in the operating room, there needs to be a graded approach to learn how to operate such that residents can care for patients independently at the end of residency. In most residency programs today, residents are only allowed to do a portion of the case because the attending surgeon completes the surgical procedure. In addition, many procedures that were done “open” in the past are now done using minimally invasive techniques. Therefore, when a complicated procedure mandates performing it in an open fashion, future surgeons may not have had any experience learning how to do an operation in this manner. Operating on simulators is not the same as operating on the human body. After graduation, how are these surgeons going to face a sick patient “alone” if they haven’t successfully performed the required procedures for board certification with great frequency and using all the techniques?

As I stated in my previous WebMD article, “What Kind of Doctors Are We Training for the Future?” many times operative procedures and the care of sick patients are performed under exhausting conditions, and mistakes may be made. I believe that fatigue is not the primary cause of mistakes, but rather mistakes are due to insufficient experience performing surgical procedures and caring for a large number of critically ill patients at one time. Furthermore, since residents no longer have to make many decisions independently, they are not equipped to enter real-world surgery where there may not be anybody to help with complicated decision making. Finally, the new rules that have been put in place have turned the surgical field into a “shift” mentality, which minimizes accountability and goes against the fundamental reasons why one decides to pursue a surgical career.

As I stated in my prior article, “With a shortened work week, now at 70 hours, there can be no accountability on the part of residents, since as soon as the ‘going gets tough,’ they’re allowed to go home. In the real world, sick patients are not on a 9 to 5 schedule. Does anybody ever think why it takes so long to become a navy fighter pilot? Does one ever think that mistakes are made due to pilot fatigue? The answer to the last question should be obvious, but the difficult, grueling, repetitive training minimizes this, as it does in surgical training.”

So what kind of doctors are we training for the future? It is imperative that current surgical training be rigorously scrutinized. Unless we individualize the training that is required of each specific specialty, the future of medicine, as we currently know it, is doomed to failure. Surgical care has many shades of gray and cannot be made into a black-and-white issue. To limit work hours and allow future surgeons to believe that delegating responsibility is the norm assumes that all residents are created equal and does not allow any flexibility in the way surgery residents are trained. This makes further specialized post-residency training almost mandatory in a narrow surgical field just so a future surgeon can master the skills that should have been taught during their general surgical residency. Unless we confront the reality of current medical training and the future of health care, we are heading for a health care system that is inferior to that of many other countries. The current health care law was supposedly made to provide excellent care to all Americans while cutting costs. Unfortunately, this notion actually creates a dichotomy because poorly trained surgeons will rely on more and more testing on more people who now will have insurance in order to make a diagnosis that could be made by simple examination, if only the doctor knew how to perform that examination properly. The art of physical diagnosis by examining the human body has been replaced by tests that are often unnecessary and are very costly. Residency training needs to be extended if the current system remains and surgeons need to be compensated appropriately after spending a majority of their life studying, training, and making little or no money.

By Michael Richman, MD, FACS

In my last article, I wrote about the HS- Omega-3 Index. In simple terms, this index is a measure of the amount of the two major omega-3 fatty acids, EPA (Eicosapentaenoic acid) and DHA (Docosahexaenoic acid), in the membrane of a red blood cell. The HS-Omega-3 Index has many features that qualify it as not only a biomarker of omega-3 intake, but also as a cardiovascular risk marker and, most importantly, a risk factor and target for therapy. Substantial evidence suggests that correcting an omega-3 insufficiency by increasing the omega-3 index reduces coronary heart disease risk and this can be accomplished quickly, safely, and inexpensively.

People often ask what brand of omega-3 fatty acid is the best to consume, and whether they should take krill oil instead to raise their EPA and DHA levels. I have talked before about how not all brands of omega-3 fatty acids are equal in terms of the amounts of EPA/DHA in each 1000 mg capsule and one needs to be an educated consumer before buying any brand. The easiest way to determine whether krill oil is better is to understand one simple fact: The industry producing these supplements is not well regulated and anyone can make any claim about a product. Many people say that krill oil is the best way to get omega-3 fatty acids, but krill oil is more expensive than the standard omega-3 fatty acid supplements. Although there is some evidence that krill oil many increase omega-3 levels more efficiently, it is at very best only two times more effective than standard omega-3 fatty acid pills. Considering the much higher price for krill oil, the potentially small increase in bioavailability may not be worth it. Until data exists comparing fish oil to krill oil on intermediate markers of risk and actual disease endpoints, it will be difficult to say one is better than the other.

By Michael F. Richman, MD, FACS, FCCP

In 2008, I wrote a two-part series about Omega-3 Fatty Acids and discussed the most important components of O3FA’s — EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid). Almost daily, I discuss with my patients the fact that there are different amounts of EPA/DHA in every O3FA tablet, which makes it difficult to know how much EPA/DHA one is ingesting and if the levels are meeting the goals suggested by the American Heart Association. The AHA recommends O3FA intake in the form of routine fatty fish such as salmon for patients without Atherosclerotic Coronary Artery Disease (CAD), fish oil supplements in patients with CAD, and high-dose O3FA (about 4000 mg/day) in patients with high triglycerides.  Until recently, it has just been a guessing game, but now doctors can use a new test called the HS-Omega-3 Index, which was developed by Dr. William Harris, to measure the amount of EPA and DHA within the membrane of a red blood cell.

The HS-Omega-3 Index has many features that qualify it as not only a biomarker of omega-3 intake, but also as a cardiovascular risk marker, and, most importantly, a risk factor and target for therapy. The optimal level of the HS-Omega-3 Index, based on the consensus of several studies, is currently 8% or greater, with a high-risk zone being less than 4% and an intermediate-risk zone of 4-8%. Ongoing research will further refine the target values for the HS-Omega-3 Index. At present, there is no compelling evidence for safety concerns at RBC omega-3 levels above the target level of 8%.

Few other cardiovascular biomarkers are as easily (and safely) modified as the HS-Omega-3 Index, and once modified, have as much potential to impact important clinical outcomes. If the HS-Omega-3 Index is ≥ 8% (low risk), there is no present need to change the diet or supplement with omega-3 fatty acids. If the Index is between 4.1-7.9% (intermediate risk range) and especially if it is ≤ 4% (high risk range), increasing the intake of EPA+DHA from oily fish and/or fish oil supplements (0.5-1g per day if intermediate; 1-2g per day if high risk) is advised. Retesting after 4-6 months is recommended for titrating the omega-3 dose because it takes about this long for membrane composition to reach a new steady state47.

Randomized controlled trials of Omega-3 FA have provided guidance for their use in clinical medicine. In the largest study to date (the Japan EPA Lipid Intervention Study, JELIS), 1.8g per day of EPA ethyl esters reduced the risk for major adverse cardiac events over 5 years in over 18,000 patients with high cholesterol, all of whom were taking statins. Sub-analyses of this study showed that treatment with EPA reduced risk in patients with pre-existing coronary disease, impaired glucose metabolism, peripheral artery disease, a history of stroke, and with the abnormal lipids characteristic of the metabolic syndrome. At present, the substantial evidence suggests that correcting an omega-3 insufficiency (i.e., increasing the omega-3 index) reduces coronary heart disease risk and can be accomplished quickly, safely, and cheaply. Of all the coronary heart disease risk factors currently known, none is as amenable to correction nor is as potentially impactful once corrected as the omega-3 index.

By Michael F. Richman, MD, FACS, FCCP

A few weeks ago, FDA announced that cholesterol-lowering drugs known as statins would have to carry warnings that side effects can include, among other things, possible memory loss. The news appeared in many papers and on news channels. Unfortunately, FDA’s complete statement regarding statins and memory loss was not revealed to the public.

It seems hardly a day goes by that I don’t wake up and see some negative press regarding statins. On various news channels, I once again heard that some “expert” said that statins make people lose their memory. It would be nice to hear that statins have changed the face of cardiovascular disease by reducing morbidity and mortality dramatically — 40-50%. Despite this, we still have a long way to go to eradicate cardiovascular disease, which still remains the number 1 killer of men and women in the United States.

I have been busy seeing patients, but I felt I needed to take the time to address the new comments. Back in 2006, the Statin Safety Task Force of the National Lipid Association formed a Neurology Panel and examined the evidence-based literature, a 22 million-person HMO database, and the FDA adverse event reporting system to assess the effects of statins on the nervous system. This was an independent body of experts that included the top thought leaders in the world in their specific field of expertise.

They asked some fundamental questions, including whether or not statins impair cognition and memory. Their conclusion, drawn from controlled studies and meta-analyses of cohort studies, was no. First of all, there is no evidence that statins are a common or significant cause of cognitive decline or memory loss. This is supported by large, randomized clinical trials, including the Heart Protection Study (HPS) and the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). The HPS was a large statin trial and included 20,536 participants who were followed over a 5-year period. Also, the Jupiter Study, which involved approximately 18,000 patients on Crestor 20mg, had absolutely no data to suggest that a statin has any effect on the neurologic system, including loss of memory.

I would never say that a medicine of any kind does not cause some type of problem in a patient. It is true that probably any medicine can cause any symptom in any patient. I like to think of this as a kind of allergy called an idiosyncratic reaction. It is always possible that a rare case of impaired memory or cognition could occur, but this would most likely represent an idiosyncratic reaction. There is no evidence of a causal relation between impaired memory and/or cognitive dysfunction. In fact, statins may actually benefit some patients’ memories: A paper published last year in the journal Experimental Neurology, which is one of the premier journals focusing on neuroscience, stated that there is evidence statins may have a beneficial effect on the progression of Alzheimer’s disease.

This information was not part of the general news coverage of FDA’s decision, even though FDA’s communication further reports, “Data from the observational studies and clinical trials did not suggest that cognitive changes associated with statin use are common or lead to clinically significant cognitive decline.” Similarly, the 2006 NLA expert paper on statin safety addressed raised anxieties on the potential reports regarding cognition, but investigators were unable to conclusively establish the clinical relevance or pathologic mechanism of these outcomes.

I think the best way to approach a patient with peripheral neuropathy or impaired cognition while on statins is to first recommend a thorough exam by a neurologist in an attempt to find a cause. If this is not possible, it is certainly appropriate to stop the statin to see what happens. Due to the length of time it can take to resolve reversible peripheral neuropathy, the patient should remain off the statin for 6 months. Patients with impaired cognition should wait about 3 months. If symptoms improve then it is certainly possible that the statin the patient was taking was causing or contributing to the memory loss. One might want to consider switching to a different statin, as the benefits of statins in reducing cardiovascular morbidity and mortality have been proven. If the neurologic symptoms do not improve, the problem may be categorized as unrelated to the statin and one should restart therapy based on a risk-benefit analysis. One must remember that there are many reasons a patient taking statins may experience impaired cognition and/or peripheral neuropathy, including vascular disease, diabetes mellitus, and advancing age. Before stopping any statin altogether, it’s important to exhaust every possibility.

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By Michael F. Richman, MD, FACS, FCCP

Today, I write to you about a new cutting-edge biomarker that can be measured in the blood and may be a predictor of cardiovascular events, including heart attacks, strokes, and cardiovascular deaths. The marker is called Cytastin C.

I first heard about this protein in college biology but really never paid much attention to it at the time, but recently it’s become a hot topic in cardiovascular disease prevention. It is a small protein that is produced at a steady rate by virtually all the cells in your body. It’s measured in the blood and is currently used as a biomarker of kidney function and may become the gold standard test when looking for early kidney disease. New research has indicated that Cytastin C serum marker test results may also be a better indicator of a person’s potential for new onset or worsening cardiovascular disease.

Doctors use several biomarkers to figure out a patient’s risk of heart disease just like a mechanic would look at several items under the hood of your car to diagnose a problem. For heart disease risk, your doctor may look at LDL-P, Apo-B, Lp(a) concentrations, and myeloperoxidease levels, to name a few.  Presently, a patient’s creatinine level is measured and is the most widely used test to determine kidney function. Why is a kidney test important, you ask?  Medically speaking, even moderate kidney dysfunction increases the risk of a patient having a heart attack, stroke or other cardiovascular event, including death. So measuring Cytastin C is emerging as a method of predicting cardiovascular events and also a decline in the function of one’s kidneys.

While the medical community has been looking at renal function by use of creatinine-based test results for many years, it’s not as accurate as we would like.  This has led many physicians and researchers to search for other markers of kidney disease through renal function.  Again, this is important because an interruption of renal function is a hallmark sign of early CVD.  Because Cytastin C is produced by many cells of the body, it’s a slightly better predictor and discriminator than just looking at creatinine.

Many of you write to tell me that you bring these ideas directly to your doctor.  So, I want to give you some information.  In 2004, a German researcher, Wolfgang Koenig published a paper in the Journal of Clinical Chemistry evaluating the impact of Cystatin C against other markers, including creatinine on a large amount of patients with coronary heart disease (CHD).  Since his paper was published, researchers have been consistently showing that Cystatin C is superior and it’s my professional opinion that it should be part of a checklist of items your doctor looks at to help predict your risk of cardiovascular disease, including heart attack and stroke.  Currently, there is an abundance of new research in progress to better understand the role of Cytastin C in cardiovascular disease prevention and this exciting new topic may add to better ways to prevent death from the number 1 killer of men and women in the United States.

By Michael F. Richman, MD, FACS, FCCP

So, your doctor looks at your blood test and says, “You have high homocysteine levels.” What does that mean? And what should you do about it?

Homocysteine is a common amino acid (one of the building blocks that make up proteins) found in the blood and is acquired mostly from eating meat. I have written before about the possible role of elevated homocysteine levels in causing heart attacks or strokes. High levels of homocysteine are related to the early development of heart and blood vessel disease. In fact, it is considered an independent risk factor for heart disease. High homocysteine is associated with low levels of vitamin B6, B12 and folate and kidney disease.

Research has shownthat both folic acid and B vitamins lower homocysteine levels, and many researchers and physicians believed that this would lower a patient’s overall cardiovascular risk. Not so.  Recently, a study called the Women’s Antioxidant and Folic Acid Cardiovascular Study found that supplemental folic acid and B vitamins do not lower the risk for important vascular events in women who are otherwise at high risk for such events, even though these supplements lower homocysteine levels.

What is high risk?  A minimum of three “cardiac risk factors” puts anyone at high risk.  They are:  high cholesterol, hypertension, metabolic disorder,  a family history of heart disease and a prior heart-related event, such as heart attack or stroke. Lifestyle indicators include obesity and cigarette smoking.

The study was a randomized, double-blind, placebo-controlled trial conducted in Boston that  began in 1998 with 5,442 women, age 40 and older with a history of cardiovascular disease, and studied them over the course of seven years.  Study participants received either a folic acid/B vitamin combination or a matching placebo.  What they found was startling to the medical community.  Over the course of 7.3 years, there was a similar incidence of heart attacks and strokes between the group that received the vitamins and the one that didn’t.  In fact, 406 women in the treatment group and 390 in the placebo group experienced at least one “event” of heart attack or stroke.

These findings  are identical to those seen in the Heart Outcomes Prevention Evaluation trial, the Norwegian Vitamin Trial and the Vitamin Intervention for Stroke Prevention trial, among others (which enrolled mostly men), even though the therapy is successful in reducing homocysteine levels. While numerous observational, epidemiological studies have confirmed that elevated homocysteine is a predictor of cardiovascular risk, it has become very clear that lowering homocysteine levels has little to no outcome for men or women at high risk of cardiovascular disease.  So, why are people with elevated homocysteine levels at high risk for cardiovascular disease?  Medical researchers are working on this one.  As a heart surgeon, I see clogged arteries every week, up close and personal.  It makes you wonder, is homocysteine really the culprit?  Or, is it just the result of something else that is going on in the body?   I will keep you updated as new trials and information are released on this important subject.

By Michael F. Richman, MD, FACS, FCCP

In the October 18, 2011 issue of the Journal of the American College of Cardiology, Dr. Susanna Larsson of the National Institute of Environmental Medicine in Stockholm, Sweden stated in a news release that women who ate up to two bars of chocolate per week showed a significantly reduced risk of stroke. Those women who ate up to a half of a bar or even smaller amounts also had a reduction in the stroke rate.

The study included 33,372 women who were asked to report how often and how much chocolate and other foods they consumed over the course of a year.  Investigators listed the women into categories ranging from those who never ate chocolate to those who indulged three or more times a week and examined the risk of stroke over a mean follow-up of 10 years, adjusting for major risk factors associated with stroke. Women who reported having been diagnosed with hypertension did not show any significant benefit; however, those without hypertension and higher chocolate consumption seemed to show a decrease in strokes. The researchers identified 1549 strokes in their study.

I know this sounds great to chocolate lovers, but there’s a problem with the way the study was conducted. The gold standard of any trial is to have what is called level 1 evidence. This means that the study was randomized, blinded to the researchers, controlled, and resulted in a statistically significant primary endpoint. An example of this would be a study comparing two drugs or a drug versus a placebo in which neither the patient nor the investigator knew what the patients were being given. The study is rigorously controlled and the goal of the study (primary endpoint) is clearly reached with statistical significance. This study did not appear to follow such strict standards.

First, the women were given a food frequency questionnaire and from this these wonderful results were reported. I don’t remember what I ate yesterday let alone keeping track of everything for an entire year. Then, a statistician was brought in to adjust the data and was somehow able to exclude anything else that may impact stroke rates. The result is a study saying that Swedish women who ate a certain amount of chocolate had lower stroke rates than those who did not. The association between chocolate consumption and stroke was stronger the higher the concentration of cocoa in the chocolate.

So, what are the health properties of chocolate? Researchers have long thought that cocoa, the main ingredient in chocolate, may have cardiovascular benefits due to the flavonoids in cocoa and their antioxidant properties. Antioxidants protect the body from damage caused by free radicals and can suppress oxidation of low-density lipoprotein particles, which are the carriers of the bad cholesterol in the blood. Dark chocolate consumption has also been shown to reduce blood pressure, which is a major risk factor for stroke, but the data is limited at best.

Now the question from chocoholics is: how much should one eat? Chocolate, and especially chocolate bars, are high in sugar, fat and calories and should therefore be consumed in moderation if at all. Dark chocolate, with a concentration of greater than 50% cocoa, is usually lower in sugar and has higher flavonoid content. Indulgence in chocolate in moderation remains a reasonable approach to satisfy a craving. Eating a healthy diet, controlling blood pressure and cholesterol levels, and modifying other risk factors for stroke is the best approach for now.

In early September, the results of a study known as the SATURN statin trial were released. Since that time, I have had several patients ask me which statin drug is the best to remove cholesterol plaques. Plaques lead to blockages from the arteries of the heart. This is a very interesting question that I have been asked before by many patients. The simple answer is that to date, there are no published studies that have looked at whether or not being able to remove plaques from arteries in the heart, also know as atheromas, can lower the chances of having a heart attack. This is known as outcome data.

I find myself spending more and more time with patients trying to explain what they heard or didn’t hear or read on television or the newspaper regarding cholesterol studies. There are many studies published every day on many different topics. The majority of the papers are not published in journals that are reviewed by doctors who practice in the same field as the paper’s author. These are what as known as “throw away” journals as the often lack credibility. Articles that are published in “peer-reviewed” journals are generally regarded as those that have undergone rigorous scrutiny before being accepted for publication.

With that as a background, I want to talk about SATURN. This trial compared two different statin drugs in 1,300 patients. It looked at how the drugs removed some plaque from the atheroma. Specifically, they looked at the change in atheroma volume before being treated with drugs and then after two years on treatment. They put a catheter in the heart arteries and used ultrasound to measure the change in the volume of the plaque.

The two statins compared were high dose Crestor and Lipitor. The results showed that the two statins were the same in the amount of plaque reduction, but a numerical result was not given. The information will be presented at the American Heart Association meeting in November.

The main reason I brought up this trial is because this study was just “a pretty picture”. What does this mean? It means that the authors had no outcome results to report. Although the plaque volume decreased, there is no data looking at if there was a reduction in non-fatal heart attacks, fatal heart attacks, or overall cardiovascular death.

So how does the information from the SATURN trial help us? In my view, it does’t provide us with any useful information until we can show that removing plaque will result in an outcome that will provide useful data which will result in a treatment that will change an outcome and benefit patients.

NBC Nightly News recently featured a story about C-reactive protein as a “simple blood test that could save women’s lives.” As WebMD’s medical expert on cholesterol and a heart surgeon, I want to explain the role of C-reactive protein as a so-called biomarker of heart disease. While the use of this blood test may be useful in helping to determine one’s risk of a possible heart attack or a stroke in the future, it is simply one of many new and emerging biomarkers that your doctor can use to help determine your risk.

C-reactive protein (CRP) is found in the blood. Its levels rise in response to inflammation. The more inflammation, the higher the CRP.

Now lets talk about inflammation and its role as a cause of events like heart attacks and stroke. It’s been well documented that both inflammation throughout the body as well as inflammation specific to the blood vessels play a prominent role in events leading to the build up and rupture of plaques in a person’s arteries. Exactly how this occurs is under great debate and being widely studied.

While CRP and its role in inflammation was discovered in the 1930s, it has received more attention in medical journals and in the media over the past 10 years. At some points, experts thought CRP was a more important test that the traditional cholesterol panel that looks at levels of good and bad cholesterol. They also thought that CRP testing alone was a better indicator than measuring LDL-C (the bad cholesterol) in predicting heart attacks and strokes.  

More than 25 studies published during the last 10 years have provided strong evidence that C-reactive protein predicts heart risk in various scenarios, not only in initially healthy subjects, but also in those who have established atherosclerosis (clogging of the arteries). However, two years ago, in July 2009, The Journal of the American Medical Association analyzed data from approximately 100,000 people and concluded high levels of C-reactive protein does not cause heart disease. 

Researchers have also found out that lowering C-reactive protein does not protect people from developing heart disease. Many patients who had “low cholesterol” but had high CRP were treated with statin drug therapy to try to lower CRP. It was hoped that this would lower the rate of heart attacks and strokes. As of today, we do know that lowering CRP has not altered the rate of strokes or heart attacks.

A large study authored by more than 35 noted MDs and PhDs showed there are people who produce more C-reactive protein throughout their lives and others who produce less. The theory goes, if C-reactive protein causes heart disease, those who make more would have more heart disease. The study did not find this. There was no association between CRP and heart disease rate. So, in other words, the association between C-reactive protein and heart disease must reflect something else. In short, C-reactive protein is simply a marker of inflammation and NOT an accurate predictive test for heart disease risk. 

 The U.S. Preventive Services Task Force announced recently supported this finding, saying that CRP alone was not enough to determine heart disease risk. 

Every day I have patients who read news articles, or see news stories on a new test. Many are now asking about their C-reactive protein. Thanks to misleading and often half researched news articles and reports, many think that this single test is absolutely critical to prevent a heart attack. I explain to them, as I have done here, that while it is important, it is only one biomarker used to help determine their risk. Despite multiple attempts to develop drugs to target and lower C-reactive protein, many experts now feel that it is time to abandon that search and concentrate on finding better drugs to prevent the build up of cholesterol in the artery wall.

Medical training is one of the most difficult times a new doctor has to endure in their quest to become a licensed and board certified physician or surgeon. Medical residencies traditionally require lengthy hours of their trainees. The American public and the medical education establishment increasingly recognized that such long hours were counter-productive, since sleep deprivation increases rates of medical errors.

In 2003, the Accreditation Council for Graduate Medical Education (ACGME — the society that accredits training programs) addressed the current residency training and duty hour requirements. The elements highlighted include patient safety, resident wellness, and the resident training experience.

After lengthy debates among various medical societies, in 2007, regulations capped the work-week at 80 hours for medical residents in training. The ACGME also mandated that overnight call frequency to no more than one overnight every third day, 30-hour maximum straight shift, and 10 hours off between shifts. While these limits are voluntary, adherence has been mandated for the purposes of accreditation of the residency. (more…)