Blood tests are the cornerstone of laboratory monitoring for patients in the intensive care unit but can result in significant blood loss. Modern laboratory analyzers require smaller volumes of blood than previous analyzers but most ICUs still use large volume blood tubes. A new study shows that ICUs can safely switch to smaller volume tubes that can reduce blood loss.
In the past, most collection tubes used for blood testing were made of glass with rubber stoppers and interior vacuum to facilitate blood filling. Currently, most hospitals primarily use plastic collection tubes that are safer than glass tubes. In the United States, the Becton Dickinson Corporation’s Vacutainer® is the dominate blood specimen tube used in most hospitals. Blood collection tubes are taken to the hospital’s clinical lab where tests are run on laboratory analyzers. The original analyzers required several milliliters of blood to perform testing, however the current generation of analyzers generally require only 0.5 ml of blood (or less) for testing. But blood specimen tube size has changed little over the past 40 years. As a consequence, most blood sent to the lab for testing is unused. Blood tubes come in a variety of sizes and each hospital determines the size of each type of tube to stock. The typical standard-sized Vacutainer® tubes used in most U.S. adult hospitals are as follows:
When drawn directly from a peripheral vein, no blood needs to be discarded for most laboratory tests. However, when drawn from a central venous catheter or a tunneled catheter, the initial aliquot of blood removed should be discarded since it can be diluted by electrolyte-containing IV fluids or catheter flushes used to maintain catheter patency. The recommended discard volume varies between hospitals but is typically 5 or 6 ml.
Let’s take a typical example of a patient with a central venous catheter admitted to the ICU with sepsis requiring regular blood draws consisting of a chemistry panel, CBC, and lactate every 6 hours plus a PTT/INR every 12 hours and a vancomycin level daily.
Discard x 4 = 20 ml
Chemistry x 4 = 28 ml
Lactate x 4 = 16 ml
Hematology x 4 = 12 ml
Coagulation x 2 = 9 ml
Drug level x 1 = 7 ml
TOTAL DAILY VOLUME = 92 ml
The average 70 kg healthy adult has 5.3 liters of blood (5,300 ml). Therefore, blood loss for laboratory test specimens in this patient would be 1.7% of the blood volume per day. For a 5-day ICU stay, this would add up to 8.7% of the blood volume or 460 ml. This is also the volume of 1 donated unit of blood. Many critically ill patients are already anemic at the time of ICU admission and thus start off their ICU stay with a much lower amount of red blood cells than a normal healthy person, thus compounding the effect of blood removal for lab testing. This is a significant amount of blood and can affect oxygen carrying capacity of the blood to target tissues. It can also mean the difference between whether or not a patient needs a blood transfusion. The unfortunate irony is that most of this blood gets wasted.
In the past, the threshold hemoglobin level in the ICU to order a blood transfusion was 10.0 g/dL. More recently, that threshold has dropped to a hemoglobin level of 7.0 g/dL for most ICU patients based on clinical studies indicating that ICU patient outcomes are better when using the lower hemoglobin value. The effect of blood loss for laboratory testing will be greater for patients who are already anemic in whom lab testing-related blood loss is more likely to push the hemoglobin below the 7.0 g/dL level and thus require transfusion.
Reducing blood collection tube size
A study in this week’s JAMA examined whether ICU patient outcomes can be improved by changing to smaller Vacutainer® tube sizes. This was a large study involving 21,201 patients in 25 ICUs in Canada. Patients had specimens drawn into standard-size blood collection tubes (4 -6 ml) or small tubes (1.8 – 3.5 ml). Red blood cell transfusion was less common in patients assigned to the small volume tubes (10 units of RBCs fewer per 100 patients). The drop in hemoglobin level was also lower in small volume tube patients. The frequency of specimens with insufficient quantity of blood for analysis was not higher using low volume tubes (in fact, it was statistically significantly lower when using the smaller-size tubes).
The implication of this study is that ICUs can safely shift to use of small volume blood collection tubes without risk of an insufficient quantity of blood to perform laboratory tests. By changing to small volume tubes, ICU patients have a smaller ICU-related drop in hemoglobin and require fewer units of transfused blood during their ICU stay. This should come as no surprise to pediatricians who have successfully used smaller volume blood tubes for many years to perform the exact same blood tests ordered in adult ICUs.
Reducing blood discard volume
A 2021 study in the Journal of Laboratory Physicians examined whether a 3 ml blood discard volume was as good as a 5 ml blood discard volume in patients with central venous catheters. There was no significant difference in chemistry lab test results between specimens obtained after the two discard volumes. The implication is that ICUs can shift to using smaller discard volumes, thus further reducing ICU-related blood loss.
A typical triple lumen central venous catheter has 3 lumens that are each either 18 gauge (1 mm) or 16 gauge 1.3 mm) in diameter. The catheter length is selected based on which central vein is chosen for insertion and is either 15 cm or 20 cm. The volume of each lumen can range from 0.12 ml to 0.27 ml, depending on lumen gauge and catheter length. PICC line lumens are typically 18 gauge and are 50 – 60 cm in length. This equate to a lumen volume of 0.47 ml. Thus, even using a 3 ml blood discard volume allows for several times the volume of fluid contained in the catheter to be removed before obtaining venous blood through a triple lumen central venous catheter or a PICC line.
Implications for ICU policies
When it comes to blood draws for lab testing in the intensive care unit, less is more. We can reduce ICU-related blood loss and reduce blood transfusions in ICU patients with several policy changes.
Reduce standard central venous catheter blood discard volume to 3 ml.
Change to small volume Vacutainer® tube sizes. The vast majority of laboratory tests can be performed using 1.8 to 3.5 ml tubes.
Consolidate blood draw time intervals. Avoid ordering some blood tests at 6 hour intervals and others at 8 hour intervals – this results in six or seven blood draws per day, wasting excessive blood for discards and occupying valuable nursing time.
De-escalate lab testing as soon as clinically indicated. The need for lab tests and test frequency should be reassessed on a daily basis and incorporated into multidisciplinary rounds checklists.
Simply reducing the blood discard volume to 3 ml and changing to smaller volume blood collection tubes should reduce ICU-related blood loss from lab testing by 50%. These policy changes should not be made unilaterally by any one hospital leader. Ideally, these should arise from a consensus of the laboratory medical director, the ICU medical director, the ICU nurse manager, and the director of hospital supply. The reasons for the change should also be communicated to all of the nurses and physicians who practice in the ICUs in order to ensure a consistent message to the hospital staff. Smaller volume blood collection tubes can also be well received by patients and families who in the past have frequently raised concern about the volume of blood regularly removed from ICU patients for lab test purposes.
There is always resistance to change in our intensive care units. We get comfortable with certain practices because that is the way that we have always done things and because we fear that any change could have deleterious effects on patient outcomes. Change in the ICU should be steered and not forced. New findings in the medical literature now make reducing blood loss for lab testing a change that will be much easier to steer.
When physicians hear the words “antibiotic stewardship”, they think of inpatient programs to control antibiotic use. However, more than 80% of antibiotics are prescribed in the outpatient setting. The Joint Commission mandates that hospitals have an inpatient antibiotic stewardship program but there is no national requirement in the outpatient setting and consequently, better stewardship of outpatient antibiotic use is essential to control multi-drug resistant bacteria.
Emergence of drug-resistant bacteria
The story of drug-resistant bacteria is the story of evolutionary biology and that story dates back more than 2 centuries ago.
It was the fall of 1827 and Charles Darwin was bored. He was in his second year of medical school at the University of Edinburgh but was neglecting his medical studies as he was more interested in studying the biology of oysters than of humans. So, his father sent him to Cambridge to study to become a county parson instead. There, he was more interested in studying entomology than religion. However, he did manage to graduate in 1831. But with no employment opportunities that interested him, he decided to sign on as a naturalist on a 5-year expedition to chart the coast of South America on the HMS Beagle. His observations of during the voyage served as the foundation for his theory of natural selection that later became the central tenet of evolutionary biology.
Perhaps nowhere has natural selection been more easily observed than in the emergence of antibiotic resistant bacteria over the past 80 years. In 1928, Alexander Fleming discovered penicillin, purely by accident. In 1941, police constable Albert Alexander became the first person treated with penicillin when he scratched his face with a rose thorn and developed a flesh-consuming infection caused by Staph aureus. After 5 days of treatment with the new drug, his infection was under control but he then relapsed when his doctors exhausted their supply of penicillin. When penicillin was initially rolled out, it killed essentially all Staph aureus bacteria. But by 1942, penicillin-resistant Staph were identified and by 1946, 12.5% of all Staph aureus isolates were resistant to penicillin. One year later, the incidence of penicillin resistant staph had tripled even further.
To fight the rapidly emerging resistance of Staph aureus to penicillin, a new semi-synthetic penicillin derivative was created in 1959 called methicillin. It was first marketed in September 1960 but only one month later, a public health lab in London identified isolates of Staph that were resistant to the new antibiotic and these were called methicillin resistant Staph aureus, or MRSA. Thirty years ago, 2% of all Staph infections were due to MRSA. Today, in the United States, most staph infections are caused by MRSA and one-third of all healthy Americans are colonized with MRSA in their noses. To treat MRSA infections, the medical community turned to vancomycin. But in 2002, the first case of vancomycin-resistant Staph aureus was identified in a diabetic patient in Michigan. Today, vancomycin-resistant Staph aureus has replaced MRSA as the bacterial bogyman in our nation’s hospitals.
Currently in the United States, there are 2.8 million infections caused by drug-resistant infections and 35,000 deaths due to antibiotic resistance every year. There are additionally 12,800 deaths each year due to Clostridium difficile that arises as a complication of antibiotic use. Antibiotic overuse and misuse is fertilizer for antimicrobial resistance. To slow the emergence of drug-resistant pathogens, it is necessary to more judiciously prescribe antibiotics, especially in the outpatient setting.
The problem of outpatient antibiotic use
In the U.S., three are 211 million outpatient antibiotic prescriptions written every year. The CDC estimates that 72% of these are necessary but 28% are unnecessary. Even when antibiotic prescriptions are necessary, we have opportunities to improve drug selection, improve drug dosing, and shorten the duration of administration. Taking all of this into consideration, about half of all outpatient antibiotics are either unnecessary or prescribed incorrectly.
All of us who practice outpatient medicine have been guilty of antibiotic misuse at one time or another. A patient comes to the office with a viral upper respiratory infection and the doctor prescribes an antibiotic that was never needed in the first place. Maybe the doctor was not aware of clinical practice guidelines for managing upper respiratory infections. Maybe the doctor wanted to make the patient happy by prescribing an antibiotic. Maybe the doctor was afraid of complications of the URI. Maybe the doctor figured he or she could bill a higher level of service for the office visit by prescribing an antibiotic. Maybe the doctor thought that it would be faster to prescribe an antibiotic than to explain why an antibiotic was not necessary. Regardless of the reason, the next time that the patient has a cold, that patient will believe that an antibiotic is necessary and expect the physician to prescribe one. This results in a vicious cycle of antibiotic misuse.
The 4 components of outpatient antibiotic stewardship
The Centers for Disease Control has an excellent on-line resource for outpatient antibiotic stewardship. This resource identifies four key components that can be incorporated into any outpatient practice: commitment, action, tracking, and education.
Not only must the physician be committed to appropriate antibiotic use but the entire office staff must be committed. This implies that a consistent message will be given to patients, from the nurses, from the schedulers, from the medical assistants, and from the physicians. For example, when a patient calls in with a sore throat, the nurses can set the stage for antibiotic stewardship by saying “The doctor needs to evaluate you in person to determine if an antibiotic is necessary” rather than simply calling in an antibiotic prescription. The schedulers can help by telling the patient that the office has the ability to do on-site rapid strep screens during the patient’s office visit. The medical assistants can reinforce the message by telling the patient that a negative rapid strep test means that the sore throat is not caused by a bacteria.
Ideally, each medical practice should have a leader for the practice’s antibiotic stewardship program. This could be a pharmacist, nurse or medical assistant. This individual would be responsible for ensuring that all of the office staff know their roles in antibiotic stewardship and that the office’s commitment to antibiotic stewardship is communicated to patients. A simple way of doing this is with posters in the waiting room or in the examination rooms stating the practice’s commitment. The CDC has a down-loadable poster that can be used by any medical office. A 2014 study found that inappropriate antibiotic prescriptions were reduced by 19.7% simply by hanging commitment posters in exam rooms.
Incorporation of evidence-based guidelines for management of common outpatient infections can help ensure that the right antibiotic is prescribed for the right duration of time for any given bacterial infection. Guidelines can also help ensure that antibacterial antibiotics are not prescribed for viral infections. One of the challenges with use of evidence-based guidelines is that many national organizations publish their own guidelines for any given infection and these guidelines can differ depending on the decisions of different guideline writing committees and how long in the past the guidelines were written. Large medical centers can develop their own practice guidelines based on distillation of available literature. In smaller outpatient practices, it is best for all of the providers to agree on the use of one guideline or another – it can be confusing to staff and patients if different providers in the practice utilize different clinical guidelines. When possible, the power of the electronic medical record should be harnessed to prompt clinicians regarding test ordering or antibiotic prescriptions for any given infection based on the ICD-10 diagnoses.
A useful action plan is the use of the “over-the-counter prescription pad” to use for common viral infections – essentially a printed checklist of non-antibiotic recommendations by the provider for such items as acetaminophen, NSAIDs, decongestant nose sprays, guaifenesin, dextromethorphan, etc. Often, a printed paper to given to the patient that is customized to include the patient’s name, date, and diagnosis can be a powerful way to reinforce that antibiotics are not necessary and that the physician is invested in treating the patient (just not with an antibiotic).
For hospital-employed physicians, most compensation plans incorporate some kind of quality metric into each physician’s annual bonus. In our medical center, over the years these have included metrics such as percent of patients getting mammograms or colonoscopies, percent of patients getting influenza vaccinations, and patient satisfaction scores. Antibiotic stewardship is in many ways an ideal quality metric for outpatient and ER practices. This is because appropriate antibiotic prescription is a physician behavior whereas when a patient refuses a flu shot, is a no-show for their scheduled colonoscopy, or writes a bad patient satisfaction survey, it is a patient behavior. As a result, using these latter types of metrics for physician bonuses tends to financially reward physicians who have a “desirable” patient panel as opposed to those physicians who care for a lot of uninsured, lower income, or lower education level patients. By using a physician behavior in the bonus equation, the practice can avoid penalizing physicians for patient behaviors that are beyond the physicians’ control.
The electronic medical record can be utilized to track and report antibiotic stewardship quality metrics such as use of order sets derived from the organization’s clinical practice guidelines, use of rapid strep testing in patients given antibiotics for pharyngitis, and appropriate duration of antibiotics for uncomplicated urinary tract infections.
This requires both education of physicians and education of patients. Physician education can take the form of grand rounds and other CME events about antibiotic stewardship. But on a smaller scale, can include distribution of the organization’s clinical practice guidelines for common infections. Successful distribution can be a challenge, however – many hospitals that maintain a “clinical practice guideline” website on the hospital’s intranet find that physicians rarely access the website. Successful adoption of guidelines usually is most effectively done on a local basis, such as at medical staff meetings, at department meetings, or by incorporation of the guideline into the electronic medical record.
Patients need to be educated about the difference between viral and bacterial infections and why viral infections do not require an antibacterial antibiotic. They also need to be educated about the risks of antibiotics, including costs, side effects, development of drug-resistant bacteria, and C. difficile. Patient education materials can again include posters for the examination rooms but can also include text pasted into the patient’s after visit summary. Whenever possible, after visit summaries should be printed and handed to the patient at the end of their office visit rather than simply loaded onto the patient portal in the electronic medical record – few patient actually open up their patient portal after they leave the office but a piece of paper will tend to stick around until the patient actually reads it.
The Centers for Disease control has several excellent patient education handouts that can be printed as posters for the office’s exam rooms or as paper handouts to be given to patients. These are available in both English and Spanish language versions. These can be downloaded from the CDC’s website or you can click on the images below for the English language handouts.
Penicillin allergy deserves a special mention. Fully 10% of patients report having an allergy to penicillin but only 1% of the population actually has penicillin allergy when tested for IgE-mediated reactions. In other words, 9 out of 10 patients who think they have a penicillin allergy do not actually have an allergy. One of the reasons for this is that 80% of patients who truly have a penicillin allergy lose their IgE responsiveness after 10 years. But presumption of penicillin allergy drives the use of more broad-spectrum antibiotics and the development of drug-resistant bacteria. Patients reporting penicillin allergy should be asked about the specific symptoms they had when taking penicillin in the past. When uncertainty exists, patients should undergo penicillin skin testing. In the past, this required consulting an allergist but now there are easy-to-perform penicillin allergy skin tests that can be done in the primary care office. Importantly, if the test is negative, then not only does the patient need to be informed that they are not allergic, but penicillin allergy should be removed from their electronic medical record.
The special case of dentistry
Dentists account for 10% of all outpatient antibiotic prescriptions. But dental practices generally fall outside of the purview of our nation’s hospitals. As a consequence, dental practices are largely on their own when it comes to antibiotic stewardship support. Physicians can help by participating in dental continuing education programs and by sharing effective programs and practices with local dentistry colleagues. One of the important changes over the past 20 years has been a move away from indiscriminate use of prophylactic antibiotics prior to dental procedures in patients with heart murmurs and limiting prophylactic antibiotics to only those cardiac patients that truly benefit from them. There are also CDC guidelines for when to prescribe antibiotics for common oral infections such as pulpitis, periodontitis, and pulp necrosis.
An ounce of prevention
The most effective way to reduce antibiotic misuse and development of drug-resistant pathogens is to never get infected in the first place. Keeping patients up to date with vaccinations is essential. Chief among these for bacterial infections is pneumococcal pneumonia – the new PCV20 vaccine should be given to all adults over age 65. Similarly, viral infection can mimic bacterial infections or lead to secondary bacterial infections that can result in antibiotic prescriptions. Preventing these common viral infections can thus reduce antibiotic use. All Americans should receive an annual influenza vaccine and COVID update vaccine. All people over age 60 and all pregnant women should be vaccinated against RSV.
We are fortunate to be living in an era when we have more effective vaccines for deadly diseases than ever before. Vaccine recommendations change frequently as new vaccines are developed. The CDC lists the current vaccination recommendations on their website. You can also click on the images below for the 2024 child and adult vaccine schedules.
We don’t have to lose the war…
I have watched patients die of bacterial infections that were untreatable with any known antibiotic. I have taken care of patients with such extensive drug allergies that there was only one or two antibiotics that I could use for any infection they came down with. I have taken care of patients who were admitted to our ICU with overwhelming Clostridium difficile due to taking an unnecessary antibiotic or due to taking a necessary antibiotic for longer than indicated. In all of these cases, antibiotic misuse and drug-resistant bacteria were the root causes.
The good news is that initiatives to reduce antibiotic misuse are effective. Since 2013, the CDC reports that there has been a decrease in hospital-acquired infections caused by vancomycin-resistant enterococcal, multi-drug-resistant Pseudomonas, methicillin-resistant Staph aureus, carbapenem-resistant acinetobacter, and drug-resistant Candida. However, other outpatient-acquired drug-resistant pathogens are now on the rise including erythromycin-resistant group A Strep, drug-resistant Neisseria gonorrhoeae, and ESBL-producing Enterobacteriaceae. Outpatient stewardship efforts in our physician offices, urgent care centers, and emergency departments can and will make a difference. To view an OSU MedNet-21 webcast for more information on outpatient antibiotic stewardship, click on this link.
The final 2024 Medicare Physician Fee Schedule was published yesterday in the Federal Register. The fee schedule will impact different specialties differently and as usual, there were some winners and some losers but mostly losers – all physicians will see a reduction in their total Medicare reimbursement. The entire fee schedule is a 1,230 page document. Here are some of the key take-aways.
The conversion factor will drop by 3.4% to $32.74 per RVU
Primary care physicians will get a supplement to outpatient E/M codes by using CPT code G2211
Telemedicine did not get cut
Different specialties will see different changes to their Medicare payments ranging from +3% to -4%
Caregiver training will now be covered by Medicare
There is better clarification of whether a physician or advance practice provider should submit a bill for split/shared encounters
Medicare will provide a $38.55 supplement for 4 different vaccines when given in a patient’s home
Overall lower reimbursement
The single most important item that affects how much physicians get paid is the annual conversion factor. This is the amount that Medicare pays physicians per RVU. In brief, each service or procedure performed by a physician is assigned a number of RVUs (Relative Value Units) that correspond with the complexity and amount of time it takes to perform that serve or procedure. There are 3 subcomponents of the RVU: a work RVU (physician effort), an expense RVU (overhead expense to perform that service or procedure), and a malpractice RVU (cost of malpractice insurance to perform that service or procedure). For example, a level 4 outpatient visit for a new patient is worth a total RVU of 5.44 (2.60 work RVU + 2.61 expense RVU + 0.23 malpractice RVU).
Every year, Medicare adjusts the conversion factor. Because Medicare is mandated to be budget-neutral, in most years Medicare reduces the conversion factor since there is not enough money to increase physician reimbursement while expanding Medicare coverage for new areas of spending. For 2024, Medicare will again lower the conversion factor, this time to $32.74, which is a decrease from 2023’s conversion factor of $33.89, 2022’s conversion factor of $34.61 and 2021’s conversion factor of $34.89. Thus, over the past 3 years, Medicare is has reduced physicians’ pay by 6.2%. During that same time, inflation has risen by 17.62%. To put these numbers in perspective, in 2021, an RVU could buy 9.8 gallons of milk but in 2024, an RVU will only buy 7.8 gallons of milk. This means that the purchasing power of 1 RVU has fallen by 20% since January 2021.
Given this rather enormous drop in the purchasing power of an RVU over the past 3 years, private practice physicians have few options to prevent lower income: spend fewer minutes with each patient or work more hours. Hospital-employed physicians require greater subsidy per physician from the hospital in order to overcome both inflation and the reduction in income generated by Medicare payments to the physicians.
Primary care got a boost
Primary care physicians have to do a lot of work behind the scenes to coordinate care among various specialists, fill out patient paperwork, negotiate with insurance companies for prior authorizations, answer phone calls, and respond to EMR patient portal questions. This additional work has not been compensated in the past. New for 2024 is an add-on CPT code, G2211, that accounts for this extra work performed by primary care practitioners after the patient leaves the office. It can be added onto most primary care office visit CPT codes, thus increasing Medicare payment for primary care services. Medicare estimates that it will eventually be used for 54% of all outpatient office visits that are billed using E/M codes. G2211 will be worth 0.33 RVUs (about $10.91).
Telemedicine did not get cut
The COVID pandemic resulted in Medicare loosening restrictions on telemedicine by allowing most outpatient E/M services to be paid when performed using telemedicine. Prior to the pandemic, telemedicine could only be performed in limited situations, such as when the patient lived in an isolated remote region of the country. During the pandemic, patients and physicians all throughout the country found that telemedicine was convenient, efficient, and in many situations just as effective as in-person office visits. In short, Americans liked telemedicine. As the pandemic has been winding down, there was fear that Medicare would revert to previous telemedicine restrictions, making telemedicine inaccessible to most patients and physicians. For 2024, Medicare has decided to extend the telemedicine waivers and will continue to pay for telemedicine through the end of 2024.
To bill for a telemedicine encounter, there must be both an audio and a video connection between the patient and the physician. This has been problematic for patients who lack high-bandwidth internet connections or lack video cameras on their computers or cell phones. In these situations, the encounter is generally converted to an audio-only telehealth encounter – essentially a phone call. In the past, Medicare would not pay for these phone calls but during the pandemic, Medicare did pay for phone calls when they were done as a telehealth encounter that substituted for an in-person office visit. For 2024, Medicare will continue to pay for audio-only telehealth encounters.
Prior to the COVID pandemic, telemedicine was difficult to perform in teaching settings since the resident and physician needed to be in the same physical location. For 2024, Medicare will permit the resident and the attending physician to be connected by video conferencing during a telemedicine encounter, thus permitting them to be in different locations.
Medicare had originally proposed that if a physician performed a telemedicine encounter from their home (rather than the office), that their home address would need to be registered on Medicare enrollment and billing forms. Presumably this would also apply to telemedicine encounters performed by a physician located in a hotel room, AirBNB, or family member’s home. An implication of this was that all of these various addresses would then need to also be approved by malpractice insurance companies as “medical practice locations”. This would place an enormous burden on physicians and practice administrators by adding a huge volume of paperwork to be completed anytime a physician performed a telemedicine encounter from any location other than their regular medical office. The good news is that Medicare decided to NOT make this requirement for 2024. Instead, when a physician performs a telemedicine encounter from their home, they can use their regular office as the site of service for billing purposes.
Changes in reimbursement for specialists
Every year, Medicare tinkers with the amount that it pays for any given service or procedure. 2024 is no exception and as a result, the RVUs for some services and procedures went up and for others, went down. Because of the budgetary net neutrality requirement, an increase in RVUs for one service must be accompanied by an equivalent decrease in RVUs for another service. The result of this is that some specialties will see an increase in their total annual Medicare allowable charges and other specialties will see a decrease in their allowable charges. Medicare estimates the impact of the 2024 Physician Fee Schedule on various specialties on page 79,468 of the Federal Register. The table below shows these estimates for selected physician specialties.
This table lists the charges by specialty, not the actual reimbursement. The change in charges ranges from +3% (endocrinology and family practice) to -4% (interventional radiology). When added all together, the charges have to total zero due to net neutrality requirements. The effect of the reduction in the conversion factor is on top of any changes to charges. Because the conversion factor will fall by 3.4% ($33.89 to $32.74), all specialities will actually see a drop in reimbursement. To see the actual estimated effect on Medicare reimbursement for any specialty, subtract 3.4% from the percentages in the table above.
New CPT codes
The American Medical Association creates CPT codes and then Medicare decides which codes will be reimbursed and the amount of RVUs assigned to each new CPT code. For 2024, the AMA announced that there will be 230 new CPT codes, 49 deleted CPT codes, and 70 revised CPT codes. This brings the total number of CPT codes to 11,163. It can take a while for a newly created CPT code to work its way through the RVU assignment process. The best resource to determine whether a CPT code is currently reimbursed by Medicare is the Medicare Physician Fee Schedule Look-Up Tool on the Medicare website. By entering a CPT, you can find out what the RVUs are for that CPT code and also the dollar amount that it reimburses. The 2024 data has not yet been entered into this on-line look-up tool but should be available in January 2024.
Although commercial health insurance companies tend to pay for the same CPT codes as Medicare, on occasion, a particular insurance company may reimburse for a CPT code that Medicare does not reimburse for. This adds a layer of complexity to the revenue cycle office of any medical practice. By billing for these CPT codes, the revenue cycle department accepts that there will be denials from those insurance carriers that do not reimburse for a particular CPT code. However, no one wants to leave money on the table from the insurance carriers that do cover that CPT code.
Caregiver training services now covered
New for 2024, Medicare will pay for providers to train caregivers (often family members). Although these codes will likely primarily be used by physical, occupational, and speech therapists, other providers (including physicians) can also bill for these services. These CPT codes should be used to support patients with certain diseases or illnesses (e.g., dementia) in carrying out a treatment plan. This can cover a broad range of skills, from assisting with activities of daily living to more complex tasks such as transfers, mobility, communication, and safety practices. These codes should be used when only the caregiver is present and the patient is not present.
CPT 97550 – first 30 minutes of caregiver training. It is valued at 1.00 work RVUs.
CPT 97551 – each additional 15 minutes of caregiver training. It is valued at 0.54 work RUVs.
CPT 97552 – group caregiver training. It is valued at 0.23 work RVUs.
Spit/shared evaluation and management services
Under Medicare, a service can be billed by only one practitioner, and if non-physician practitioners (for example, nurse practitioners) bill for a service, they receive only 85% of the physician rate. Frequently, a nurse practitioner will do an initial assessment and then the physician will follow the NP later to confirm the assessment and finalize management recommendations. In the past, it has been controversial about whether the bill for the service should go out under the NP or the physician in these situations when the clinical service is considered “split/shared”. In past years, Medicare has stated that it should be whichever of the two providers were responsible for the “substantive portion” of the visit but did not provide a good definition of substantive portion. For 2024, Medicare has defined “substantive portion” of a split or shared service to mean more than half of the total time spent by the physician and the non-physician practitioner. This should eliminate much of the administrative confusion.
The implication is that when physicians bill for split/shared visits, they should document that they performed the substantive portion in their progress note in case of a billing audit by Medicare carriers. Medicare carriers sometimes differ in their documentation requirements so physicians (or their billing staff) should check with their specific Medicare carrier to learn what chart documentation is sufficient. Most likely, it will be something along the lines of: “I personally performed more than 50% of the total time required for this split/shared visit in conjunction with the advance practice provider“. In other words, just one more lengthly phrase to clutter up progress notes in patient medical records.
Vaccinations given in a patient’s home
As a pulmonologist, I have personally given many influenza vaccinations to patients on mechanical ventilators during home visits. I have also given many flu shots to patients during home hospice visits. Those vaccinations were reimbursed at the same rate as if they were given in a physician office. In 2021, Medicare approved paying providers $35.50 extra to give COVID vaccinations in a patient’s home, over and above the usual charge for the vaccinations. This was done to encourage widespread use of the COVID vaccines, particularly in vulnerable patients who were confined to their home due to chronic disease.
For 2024, Medicare will continue to pay the supplemental reimbursement for COVID vaccinations given in a patient’s home and will also expand the list of vaccines that are eligible for this supplement to include pneumococcal pneumonia, influenza, and hepatitis B vaccines. This supplemental payment for 2024 will be $38.55 and will be added to the usual Medicare Part B payment of $32.57 for influenza, pneumococcal, and hepatitis B vaccinations and $43.43 for COVID vaccinations.
It will be harder to maintain a private practice
Over the past decade, it has become increasingly difficult for physicians to fund their salary from billing for professional services alone. Because such a large percentage of physician revenue comes from Medicare, the changes to the Medicare Physician Fee Schedule have played an out-sized role in the inability of physicians to rely on their billings alone. Currently, 33.4% of physician professional billing revenue in the United States comes from Medicare. Medicaid accounts for an additional 8.5%, private health insurance accounts for 38.4%, and out-of-pocket payments account for 7.6%. The remaining 12.2% is from other federal health programs such as the Department of Veterans Affairs, the Department of Defense, the Indian Health Service, and CHIP. The changes that Medicare makes to the annual Physician Fee Schedule are generally also made by other payers, especially Medicaid and the other federal health programs.
When adjusted for inflation, over the past 22 years there has been a 26% decline in Medicare payments to physicians During those same 22 years, there has been a 47% increase in medical practice expense. This reduction in physician income from professional billing coupled with this increase in overhead office expense has led to most physicians now being hospital-employed rather than in a private practice. As hospital-employees, physicians can receive monetary subsidies from the hospital in order to maintain salaries that cannot be supported by professional revenue alone.
Due to inflation during 2022 and 2023, we have seen many unions win contracts with double-digit wage increases for union workers whereas Medicare is reducing payment to physicians for clinical services. This further reduction in physician payments by Medicare in 2024 is likely to push even more physicians out of private practice and into hospital-employed models as private practice becomes increasingly unsustainable.
Next year will be the 80th anniversary of the first description of idiopathic pulmonary fibrosis (IPF). It will also mark 40 years since I graduated from medical school. I spent most of those 40 years specializing in the management of patients with IPF and there have been enormous strides forward in those 40 years. This post will look back on where we have been, where we are now, and where we are going with respect to treating IPF.
First, some definitions.
Interstitial lung diseases are characterized by the accumulation of inflammation or scar or both in the lungs. There are at least 140 different interstitial lung diseases. Pulmonary fibrosis means accumulation of scar in the lungs and many of the interstitial lung diseases can result in pulmonary fibrosis. For most of these, the cause is known, such as rheumatoid arthritis-associated pulmonary fibrosis, radiation-induced pulmonary fibrosis, and asbestosis. Idiopathic pulmonary fibrosis (IPF) is when pulmonary fibrosis occurs without any known underlying cause (“idiopathic” means no obvious cause).
Usual interstitial pneumonitis (UIP) is a pattern of findings on either a chest CT scan or a lung biopsy that is typically seen in idiopathic pulmonary fibrosis. However, the UIP pattern can also be seen in other interstitial lung diseases. For this reason, the radiologist and the pathologist generally do not diagnose idiopathic pulmonary fibrosis – it is up to the pulmonologist who is seeing the patient to diagnose idiopathic pulmonary fibrosis by taking the radiologist’s or pathologist’s finding of UIP in the context of the patient’s history, physical exam, and laboratory test results.
The historical timeline of IPF
There is no one person who discovered idiopathic pulmonary fibrosis. Instead, there has been an evolution of thought about IPF over the past century. Some of the more important points in the timeline of IPF are:
1944. The first clinical description of idiopathic pulmonary fibrosis is credited to Drs. Hamman and Rich from Johns Hopkins in 1944 in their description of 4 patients with interstitial lung disease of uncertain cause. Although the term “Hamman-Rich syndrome” became used as a catch-all term for many interstitial lung diseases (including idiopathic pulmonary fibrosis), their 4 patients likely had acute interstitial pneumonitis, which is a different disease.
1962. Dr. Gross suggested that there were two forms of Hamman-Rich syndrome: an acute form and a chronic form. This article laid the foundation for IPF as a distinct disease (the chronic form).
1964. Dr. Scadding from the United Kingdom proposed using the term cryptogenic fibrosing alveolitis for the chronic form of Hamman-Rich syndrome. For many years, cryptogenic fibrosing alveolitis was synonymous with idiopathic pulmonary fibrosis.
1969. Drs. Leibow and Carrington described 5 histologic subgroups of “chronic idiopathic interstitial pneumonia”, one of which was usual interstitial pneumonitis (UIP).
1976. Researchers at the National Institutes of Health, led by Dr. Crystal, proposed that idiopathic pulmonary fibrosis initiates as inflammation in the alveoli of the lungs that later progresses to fibrosis. The basis of this proposed mechanism was the findings of increased inflammatory cells in bronchoalveolar lavage fluid obtained from bronchoscopies performed on patients with IPF.
1998. Drs. Katzenstein and Myers proposed that usual interstitial pneumonitis is the lung biopsy finding that occurs in idiopathic pulmonary fibrosis. They determined that the disease is due to excessive fibrosis (scar) and that there is little inflammation.
2001. Dr. Hunninghake and colleagues determined that IPF can be often be diagnosed by the finding of usual interstitial pneumonitis on the chest CT scan, allowing some patients to avoid undergoing a lung biopsy.
What causes idiopathic pulmonary fibrosis?
In 2023, idiopathic pulmonary fibrosis is less idiopathic than it was in the past. IPF can be currently thought of as an auto-fibrotic lung disease due to a combination of inherited genes and environmental factors. An “auto-immune” disease occurs when the body’s immune system turns against itself, such as in systemic lupus erythematosis. An “auto-inflammatory” disease occurs when the body’s inflammatory system turns against itself, such as in the VEXAS syndrome. An “auto-fibrotic” disease is when the body’s scarring system turns against itself. Scar results when wounds heal and as such, auto-fibrotic diseases can be thought of as disorders of uncontrolled wound healing.
There is not one single gene that is responsible for idiopathic pulmonary fibrosis but rather there are many genes that can predispose a person to develop IPF. These genes vary in terms of how strongly they predispose IPF. For example, people with abnormal telomerase genes have a very high risk for developing IPF whereas those with an abnormal MUC5B gene have an increased risk of developing IPF that is not as great as with abnormal telomerase genes. For all of these genes, environmental injury to the lungs significantly increases the chance that a person will ultimately develop IPF. The most common cause of environmental injury is tobacco smoking but respiratory viruses, work-related dust inhalation, air pollution, and chronic gastroesophageal reflux can also increase the chance that a person with an abnormal gene will develop IPF.
How do we know if a drug for IPF works?
The only way to know if a drug against any disease works is by scientific research. But some types of scientific research are more convincing than others. Here are the common categories of research that physicians look at when determining a drug’s effectiveness.
Case reports. These are usually publications of one or two patients who appeared to respond to some type of treatment. Case reports are the weakest evidence of a drug’s effectiveness but they can be the justification for doing additional future research about a drug.
Case series. These are publications of numerous patients treated with a drug. Although they can provide stronger evidence than a case reports, they are still overall fairly weak. These are often called “retrospective reviews” meaning that a physician is looking back (retrospective) over a group of patients that the physician has managed in the past.
Open-label clinical trial. This is when a researcher deliberately gives a group of patients a drug and tracks how they respond to it. There will generally be a specific test that the researcher performs to see if the drug has an impact, for example, by performing pulmonary function tests. When a clinical trial is “open-label”, it means that the researcher and the patients know whether or not they are getting the drug. However, this knowledge can lead to bias by either the patients or the researcher who may want to think that the drug is working, even if it is not.
Randomized, double-blind, placebo-controlled clinical trial. These provide the strongest evidence that a drug is effective. Patients are randomly assigned to either receive the drug or a placebo and neither the patients nor the researchers know if a particular patient got the drug or got the placebo. In order for these studies to be statistically significant, the studies have to have a large number of patients, typically in the hundreds or thousands.
There are three “phases” of clinical trials of new drugs. The FDA will grant approval if the final phase of a clinical trial shows a statistically significant benefit of the drug without severe side effects.
Phase 1 trials. These involve a small number of patients and are usually open-label and of short duration. The researchers are primarily interested in drug safety and side effects. Several doses of the drug will be tested in order to find the safest doses and how frequently the drug should be given.
Phase 2 trials. These involve a larger number of patients who are randomized to receive either the drug or a placebo. During phase 2, the researchers will determine if the drug holds the possibility of being effective and will determine the best dose of the drug to use in the next phase.
Phase 3 trials. These involve very large numbers of patients – IPF trials typically require more than a thousand subjects. There are usually many hospitals (study sites) involved from multiple states and often from multiple countries. Patients are randomized to receive placebo or the drug and are tested regularly to determine if the drug is effective compared to placebo. Most IPF phase 3 trials require each subject to participate for 1 – 2 years.
IPF treatment over the years
Prior to 2014, there were no drugs that were approved by the FDA to treat idiopathic pulmonary fibrosis. Therefore, physicians used drugs that were approved for other diseases that were already available on the market. This is called “off-label” use of these drugs. Over time, researchers performed clinical trials to determine if these off-label drugs were actually effective and pharmaceutical companies developed new drugs to test in clinical trials. Clinical trials are expensive to perform and most of the clinical trials involving off-label drugs were funded by federal grants from the National Institutes of Health. Clinical trials of newly created drugs are generally funded by pharmaceutical companies. There has been a steady evolution in the treatment of IPF:
1970’s – The prevailing belief about the cause of IPF was abnormal inflammation resulting in alveolitis. Thus, the drugs most commonly used to treat IPF were anti-inflammatory drugs, such as the corticosteroid, prednisone. There were no clinical trials to determine the best dose or whether corticosteroids even worked at all.
1980’s – After years of watching patients fail to improve with corticosteroids, physicians turned to a more powerful anti-inflammatory drug, cyclophosphamide (Cytoxan) based on case reports and retrospective case series. Cytoxan was largely used as a chemotherapy drug to treat cancer but was also being used to treat auto-immune diseases such as systemic lupus erythematosus (aka, SLE) and granulomatosis with angiitis (aka, Wegener’s granulomatosis). A problem with Cytoxan is that it was very toxic and patients frequently developed low white blood cell counts, bladder hemorrhaging, and bladder cancer.
1990’s – After years of dealing with Cytoxan’s side effects, physicians looked to a different drug that was slightly less powerful as an anti-inflammatory drug but had much fewer complications. That drug was azathioprine, or Imuran. This was often given along with the corticosteroid, prednisone. A third drug as also frequently added: N-acetylcysteine (NAC). Because NAC has very few side effects and is available over-the-counter, it was seen as being fairly innocuous and possibly beneficial due to it’s anti-oxidant properties.
2000’s – A phase 3 study of azathioprine, prednisone, and NAC found that these drugs were not helpful in IPF and if anything, patients who took them did worse than patients who got the placebo. A small study suggested that gamma interferon might be beneficial and so physicians turned to the off-label use of gamma interferon that was already approved by the FDA for use in a rare condition called chronic granulomatous disease.
2010’s – A phase 3 study of gamma interferon showed that it was ineffective in IPF and thus physicians stopped using it. In 2014, large phase 3 trials found that the anti-fibrotic drugs pirfenidone and nintedanib were both effective in IPF, resulting in the FDA approving their use. Presently, these are the only drugs approved for IPF in the U.S. and are considered the current standard of care.
The past 3 decades are littered with drugs that initially held promise but were shown in clinical trials to be ineffective in IPF. A list of the most prominent of these drugs is below:
Current IPF treatment
Pirfenidone and nintedanib have both been shown to slow the progression of IPF compared to placebo, however they do not stop or cure the disease. Think of them as slowing the progression of IPF from 60 miles per hour down to 30 miles per hour. The patients will still ultimately get worse but just more slowly. There has not been a head-to-head comparison of the two drugs but the available evidence suggests that both are equally effective. The choice of which drug to prescribe is generally based on the personal preference of the physician and the patient. These preferences are most commonly based on the differing side effect profiles of the two drugs: pirfenidone cause cause skin rash and sun-sensitivity, nintedanib can cause diarrhea. The drugs also differ in drug-drug interactions – for example, nintedanib interacts with anticoagulants whereas pirfenidone interacts with ciprofloxacin.
Lung transplant is the only curative treatment for IPF. In the U.S., IPF is now the most common indication for lung transplant, accounting for 37%. Not all patients with IPF are eligible for transplant, however. The decision of eligibility is made by each hospital’s transplant team and limiting factors can include active tobacco use, obesity, older age, deconditioning, and presence of other concurrent diseases. Moreover, transplant comes with it’s own risks – 15% of patients with IPF die in the first 12 months after transplant and of those who survive the first 12 months, only 67% are still alive 5 years after transplant. However, post-transplant care is improving and survival rates are expected to improve in the future.
In addition to anti-fibrotic medications and lung transplant, there are other interventions that have been shown to be useful in patients with idiopathic pulmonary fibrosis. Oxygen is effective in improving the quality of life of patients with IPF. It can reduce shortness of breath, improve ability to exercise, and facilitate travel. Pulmonary rehabilitation is also effective in improving quality of life and should be considered for all IPF patients with shortness of breath or exercise limitation. Patients with IPF are at increased risk of obstructivesleep apnea and physicians should have a low threshold for performing sleep studies and prescribing CPAP when indicated. Although treating asymptomatic patients with proton pump inhibitors is ineffective in IPF, whose with symptoms of gastroesphageal reflux should be treated in order to reduce on-going lung injury. Patients with large hiatal hernias may benefit by surgical repair if they are able to tolerate surgery. Smoking cessation is essential to stop on-going lung injury, improve quality of life, and make patients eligible for lung transplant. All patients with IPF should be vaccinated to prevent pneumococcal pneumonia, influenza, respiratory syncytial virus (RSV) and COVID. Patients with IPF are at higher risk of death from respiratory infections and even if they survive the infection, it can result in additional lung injury that can accelerate the progression of IPF. During the first 12 months of the pandemic, 5% of my outpatients with interstitial lung disease died from a COVID infection due to their greater susceptibility.
Although cure of IPF is not yet possible (other than with transplant), it appears that our current treatment approach is making a difference. A recent study from Italy compared patients with IPF over a 15-year period from 2002 to 2016. Over this time, there was an increase in life expectancy, decrease in the rate of hospitalization, and decrease in the rate of acute exacerbations. Correlated with these improved outcomes was an increase in the use of anti-fibrotic drugs (pirfenidone and nintedanib), decrease in the use of anti-inflammatory drugs (corticosteroids, cyclophosphamide, and azathioprine), and increase in the use of bronchoscopic cryobiopsies as opposed to the more invasive surgical lung biopsies.
The future of IPF treatment
Prior to the FDA approval of pirfenidone and nintedanib, most IPF clinical trials compared a promising drug to placebo. Now that pirfenidone and nintedanib are the accepted standard of care, future trials have to either compare new drugs to pirfenidone and nintedanib or have to compare new drugs to placebo in patients who are already taking pirfenidone or nintedanib. Performing clinical trials in IPF is complicated for a number of reasons:
The heterogeneity of IPF makes trial design difficult. Given that there are multiple predisposing genes involved in IPF and given that there are multiple environmental risks for IPF, no two patients with IPF are exactly alike and treatments that work for one patient may not work for another.
Mortality cannot be used as an endpoint. The current average survival of a patient with IPF is 5.5 years based on the Italian study. If researchers were to use death as the endpoint in a clinical trial, that trial would have to last for a decade or more in order to recruit a sufficient number of patients and follow them until death. This is too long of a length of time to realistically perform a clinical trial.
Pulmonary function tests are currently the best outcome measure for IPF clinical trials. We use change in the forced vital capacity and diffusing capacity as markers of the progression of IPF. Although this is appealing from a logical standpoint, PFT changes may not necessarily correlate with life expectancy. But for now, PFTs are the best that we have.
To be statistically significant, trials must include hundreds of patients. The CAPACITY and ASCEND studies that led to approval of pirfenidone enrolled 1,247 subjects. The IMPULSIS studies that led to the approval of nintedanib enrolled 1,066 subjects. To recruit this many subjects, many study sites are required – the IMPULSIS studies required 205 hospital locations in 24 countries, the CAPACITY studies required 110 hospital locations in 13 countries, and the ASCEND study required 127 hospital locations in 9 countries. Because future trials will need to incorporate multiple treatment arms including those taking pirfenidone, those taking nintedanib, and those taking neither, the number of subjects in future trials will need to be even larger than in previous IPF trials.
Clinical trials are costly. The average cost to bring a new drug to market, from initial drug discovery to FDA approval is $2.3 billion. Consequently, for pharmaceutical companies to recoup their drug development costs, any new drug is expensive and IPF drugs are no exception. The retail price of pirfenidone is $16,000 per month ($2,200 per month if using coupons such as GoodRx) and the retail price of nintedanib is similar.
There are a number of new drugs currently in phase 1 and phase 2 trials and several of these hold early promise to add to our treatment options for IPF patients. Some of the questions likely to be answered in future IPF treatment research include:
Is combination therapy more effective than mono therapy? Currently, patients receive either pirfenidone or nintedanib but not both. We do not know if the combination of the two be better than either one alone. The same holds for any new drug that is developed – whether it should be given alone or in combination with one of the two currently approved drugs.
Is inhaled therapy better than oral therapy? Giving drugs to treat lung disease by inhalation is attractive – it offers the possibility of giving relatively high concentrations of the drug directly to the airways with lower concentrations in the blood. This has the potential to reduce systemic side effects while boosting the effect in the lungs.
What are the chemical pathways involved in fibrosis? At present, it appears that transforming growth factor-β (TGF-β) is a key player in fibrosis development. Drugs that specifically target TGF-β may be effective in slowing fibrosis. Because TGF-β is secreted as inactive form that is converted to an active form by αvβ6 integrin, this molecule is another attractive target for future treatments. We need to identify the other proteins in the body that are involved in fibrosis.
Are there biomarkers of IPF that would be better to use in clinical trials than changes in pulmonary function tests? In atherosclerosis, we have a great biomarker in the cholesterol level that allows us to determine if a drug is working without having to wait to see whether or not a patient develops a heart attack or stroke. Measurement of biomarkers that are involved in the chemical pathways of fibrosis would allow us to more quickly tell if a drug is working for a particular patient without having to wait months or years to see if there are changes in pulmonary function tests.
Can genetics direct treatment? The different genes involved in idiopathic pulmonary fibrosis affect different proteins in the body and each of these proteins has a different role in the development of fibrosis. In lung cancer, we use the genetics of a person’s cancer to choose which chemotherapy will be most effective. As we learn more about the genetics of IPF, it is likely that a person’s specific genetic make-up will help us pick the best treatment for that particular individual.
What is the role of gene therapy? Gene editing is in its infancy in medicine but is already showing great promise in muscular dystrophy and sickle cell anemia. As we learn more about the genes involved in IPF, we may be able to edit those genes, not only in patients with IPF but also potentially in their relatives with the hope of preventing the onset of IPF in the first place. Because IPF only affects the lungs, it is possible that only the genes of lung tissues would need to be edited, for example, by inhalational techniques.
When I first started specializing in treating IPF 35 years ago, it was my hope to see effective treatments arise during my career. Not only do we now have effective treatments but we also know which medications can actually make patients worse. For these reasons, our management of IPF is much better today than ever before. The treatment will be even better yet in the future with translational research that results in taking the word “idiopathic” out of idiopathic pulmonary fibrosis and clinical research to bring us more effective therapies for patients with IPF.
Yesterday, Ohioans voted fairly convincingly to keep abortion legal. The reason for most abortions in the United States is because of an unwanted pregnancy. The reason for most unwanted pregnancies is unintended conception. We keep wasting divisive emotional energy, political energy, and money on the end-result of unintended conception when we should be working together to fix the root causes of unintended conception. So, what can we do in Ohio (and in the rest of the country)?
Who gets abortions in the U.S.?
Abortion is common in the United States – nearly 1 out of every 4 (23.7%) American women will have an abortion before age 45. Data from the Guttmacher Institute shows that currently in the U.S., 46% of all pregnancies are unintended and of those, 34% end in abortion. The most recent data from the CDC shows that in 2020, there were 620,327 abortions in the United States. This is an underestimate of the true number because California, Maryland, and New Hampshire did not report abortion numbers to the CDC. The Guttmacher Institute includes data from all 50 states and thus its estimate of annual abortions is higher than the CDC’s. The Guttmacher Institute reported that in 2020, there were 930,160 abortions in the U.S. Every year. Overall, there were 198 abortions for every 1,000 live births – this works out to mean that 16.5% of all pregnancies end in abortion. Although the highest number of abortions occur in women in their 20’s, the highest rate of abortion occurs in adolescents. 1.5% of all women of childbearing age have an abortion. The majority of abortions (59%) are performed in women who already have children. In addition, 85% of abortions are performed in women who are unmarried and 49% are in women living below the poverty level.
Why do women get abortions?
A study in the journal BMC Women’s Health reported the most common reasons cited by women who underwent abortions in the United States. Most women (64%) reported more than one reason for undergoing abortion. The most common reasons were financial (40%), timing (36%), absence of a supportive partner (31%), and need to focus on their other children (29%). A study in the journal Contraception found that half of all women undergoing abortion were using some form of contraception during the month that they became pregnant with condoms being the most frequent method, followed by birth control pills.
So, how do we reduce the number of abortions without making them illegal?
In medicine, the key to curing a disease is to first determine the root cause of that disease and then treat the root cause, so that the disease never occurs in the first place. The same applies to hospital quality initiatives – you determine the root cause of a medical error and then correct that root cause so that the error can be prevented in the future. The problem with abortion in the U.S. is that we have focused most of our attention on the end result (abortions) instead of the root cause (unintended conception). Rather than contentiously facing off against each other over abortion, those who are in the “right to life” camp and those who are in the “right to choose” camp should unite on the common ground of reducing unintended conception. Here are some tactics that can reduce the number of unintended conceptions and thus reduce the number of abortions.
Improve insurance coverage for effective contraception. The most effective methods of birth control are sterilization, hormone implants, and IUDs. These methods are required to be covered by federal law, however, there is a legal exemption for churches, religious-affiliated schools, and religious-affiliated universities who can opt out of health insurance coverage of contraception for their employees. The opt-out initiative was led by the Catholic Church that still decrees that the use of contraception is a sin. Although this decree is largely ignored by U.S. Catholic women (99% of who use some method of contraception), it may contribute to Catholic women having a higher rate of abortion than mainline Protestant women and nearly twice as high of a rate as evangelical Protestant women and women of other religions. Ideally, all health insurance should cover tubal ligation, IUDs, vasectomy, and hormone implants. If health insurance provided by religious organizations does not cover contraception, then women (and men) should have access to alternative health insurance plans.
Improve over-the-counter contraception options. Condoms were cited as the most common method of contraception used by women undergoing abortion. Why were they used? – because they are immediately available to anyone over-the-counter. The problem with condoms is that they just don’t work very well – nearly 20% of women who rely on condoms are pregnant within a year. Fortunately, there is a new over-the-counter oral contraceptive pill (Opill) that will be available in early 2024. Hopefully, this will be followed by other over-the-counter oral contraceptives. The most effective contraceptive methods (sterilization, IUDs, and implants) are not amenable to over-the-counter sales since these methods require a procedure performed by a physician (or NP/PA).
Improve sex education in middle schools and high schools. In the United States, by age 15, 21% of American girls have had sexual intercourse. By age 18, 65% of females have had sexual intercourse. Sex education requirements vary by state and only 39 states require schools to teach sex education. The CDC recommends 20 specific topics be covered in school sex education classes, however fewer than half of high schools and fewer than one-fifth of middle schools provide instruction on all 20 of these topics. The majority of teens reported that they had not had any sex education prior to their first sexual intercourse. In public schools, sex education curricula are usually set by elected school boards and recently, those school board elections have become heavily politicized, especially by ultra conservative groups. In many home-schooled and religious-affiliated schools, abstinence is the only contraceptive method that is taught (if anything is taught at all). But here is the thing: ABSTINENCE AS A PUBLIC POLICY JUST DOES NOT WORK. Parents, if you have 3 kids then statistically, 2 of them are going to have intercourse before they graduate from high school. You may not be very happy about it but that is reality. Clearly, our schools can do better.
Fund organizations that provide sex education and contraception. Many abortion opponents advocate for defunding Planned Parenthood. This makes about as much sense to me as defunding the IRS in order to improve the federal deficit. Teenagers and adults in their 20’s need someplace to go to learn about contraception if they aren’t learning about it in their schools or in their homes. Furthermore, they need someplace to go if they don’t have health insurance, don’t have a regular healthcare provider, or don’t feel comfortable asking their doctor for contraception. If you really want to reduce the number of abortions in the U.S., then fund Planned Parenthood and similar organizations specifically to help prevent unwanted conception in the first place.
Promote the use of “morning after” pills. These are levonorgestrel-based medications that can be taken up to 5 days after intercourse in order to prevent pregnancy. They range in price from about $12 (My Choice Emergency Contraception) to about $50 (Plan B One-Step). Most are available over-the-counter and you can even have them delivered to your door within 30 minutes using DoorDash. We need greater public awareness of these products and greater societal normalization of their use.
Reduce fetal abnormalities. Although fetal abnormalities account for a minority of abortions, they are often sensationalized in the press. There are tangible measures that we as physicians can take to reduce fetal abnormalities and thus reduce the attendant abortions: ensure adequate folic acid supplementation, stop teratogenic medications (preferably before pregnancy), smoking cessation, and promotion of alcohol abstinence.
Optimize the health of the mothers. A minority of abortions are performed because the mother’s life is in danger. Although these conditions are sometimes unanticipated and unavoidable, they are often preventable with good maternal care. Ensure that hypertension is treated. Screen and treat gestational diabetes. Provide regular prenatal office visits. Focus on achieving a healthy weight, a healthy diet, and a regular exercise regimen (preferably before pregnancy). Counsel women of childbearing potential who have chronic diseases about the risks of pregnancy and the timing of pregnancy in the anticipated course of their underlying disease. Support community educational programs for mothers-to-be.
So, where do we go after Ohio Issue 1?
For those who voted against Issue 1, don’t despair, there is still much that you can do to reduce the number of abortions in Ohio by reducing unintended pregnancies. For those who voted for Issue 1, your work is just starting since legalization of abortion means that you now need to focus your advocacy efforts on availability of contraception and sex education. Abortions should not be felonies but they should be fewer. Reducing unintended conception is the way to do it.
A reader recently emailed me to ask how his hospitalist group should negotiate with the hospital to get paid to do extra shifts. It turns out that this is a great question and one that applies to any physician group that provides shift-work care: emergency medicine physicians, anesthesiologists, intensivists, etc.
There are many situations where physicians could be asked to work extra shifts: unexpected inpatient census surges, resignation or retirement of other physicians, maternity or paternity leave, jury duty, illness or injury, FMLA leave, etc. In a private group practice, the physician partners generally just distribute the extra work among each other and pay themselves accordingly. However, for hospital-employed physicians, there is usually a physician contract dictating the expected number of shifts each physician will work each month.
The COVID pandemic put a new wrinkle in work expectations for hospital-employed physicians. Hospitals faced loss of income from cancelation of lucrative elective surgical procedures and diagnostic tests. The hospitals had no money to pay for extra shifts. In addition, most hospitalists, intensivists, and ER physicians felt a moral obligation to work extra shifts to cover the surge in COVID admissions, even if it meant little or no extra pay. But the COVID pandemic is now receding and physicians need to recalibrate expectations for compensation for extra shifts worked. Each hospital is a little different and there are several variables that will affect your best course of action.
This post is directed toward hospitalists who are asked to work extra shifts but could equally apply to any other physician specialty that is employed on a shift-work basis. In preparing to approach the hospital administration about getting paid for extra shifts, there are a number of considerations that you need to think about.
Are there multiple hospitalist groups? If so, the hospital could play the groups against each other so it would be important to have a unified approach to the compensation issue around extra shifts.
Are you hospital-employed or employed by an independent group that then contracts with the hospital? This is essentially who writes your paycheck. If you work for a separate, independent group, then the best approach is to have the group’s CEO, manager, or attorney deal with the hospital executive director or hospital CEO. If you are hospital-employed, then it is usually up to the lead physician to do the negotiation.
When in the calendar year are the contracts up for renewal? If it is January 1st, then insist on including extra compensation for extra shifts as part of the written contract. If it is later in the year, then you’ll have to decide whether to negotiate an addendum to your current contracts or whether to wait until the next contract cycle.
When does the hospital do its budget for the next fiscal year? Most academic hospitals use July 1st to correspond with the academic year and the University’s annual budget but private hospitals may have their budget cycle beginning on January 1st or some other time of the year. It is much easier for hospital administrative leaders to include a line item on the budget for anticipated overtime expenses. If you try to negotiate after the hospital budget is completed, then the administrative leaders would need to use money in their discretionary/emergency funds to pay for it and the hospital leadership will usually be less open to doing this since they get requests from all directions for that money on an almost daily basis
What do the competing hospitals do? Find out what other regional hospitals offer their hospitalists for doing extra shifts. This information often has the greatest impact on how receptive the hospital administration is to paying for extra shifts. Hospital administrators love benchmarks so find compensation benchmarks wherever you can.
How willing/able are you to walk away. This depends on the size of your geographic region – if there are a lot of local hospitals and hospitalists are in high demand, then you have greater negotiation power, particularly if those other hospitals are offering richer contracts. See if other regional hospitals have posted job descriptions for open hospitalist positions that includes payment for extra shifts – presenting the hospital administration with these kind of documents can be pretty persuasive.
Can you re-structure your shifts to make doing extra shifts more palatable? Options could include having some of the day shift hospitalists leave when they get their work done, rather than waiting until a defined shift change-over time (such as 6:00 or 7:00 PM). To do this, you have to have 1 or more hospitalists stay until check out time to cover admissions, inpatient calls, etc. This can have the impact of then having short and long daytime shifts and you can use the hours saved during the short shifts to apply to extra shifts. This is entirely dependent on the preferences of the hospitalists – for many years, we had 2 hospitalist groups – one group wanted to stick with a set 12-hour shift model and get payment for extra shifts required for census surges. The other group wanted to allow some of the hospitalists to leave once their work was done in the afternoon, allowing those hospitalists to get home in time for their kids getting off school and daycare; these hospitalists worked more shifts per month but the average shift was shorter. Also, if you have 2 or more hospitalists covering night shifts, is it possible to convert one (or more) of them into a shorter swing shift – in most hospitals, the majority of the nighttime ER admissions come between 6 PM and midnight so it may be possible to use hours saved by shortening the shifts to use toward extra shifts.
Do you need to get paid to do extra shifts or do you need another hospitalist? If you are dealing with one of your hospitalists being out for 6 months on FMLA, it may make more sense to bring in a locum tenens for 6 months rather than spread the work out among the rest of the hospitalists. If the hospital census is growing, maybe you would be better off hiring a part-time hospitalist. One of our hospitalist groups had several “1099 physicians” who were on our regular medical staff but were independent contractors who the group could ask to do shifts here and there when needed and were then paid per shift worked, rather than a fixed annual salary (thus getting an IRS 1099 form rather than a W-2 form at the end of the year). The hospital administration is likely used to using “traveler nurses” to supplement the nursing staff so the concept of 1099 physicians will not be foreign to them.
How does the hospital deal with extra shifts for other physicians, nurses, and pharmacists? If these hospital-employed professionals get paid for doing extra shifts during patient census surges, then use this as a bargaining point to have a similar arrangement for the hospitalists. Also, how does the hospital deal with other hospital-employed physicians who do shift work (for example, anesthesiologists and ER doctors)? The hospital will likely want to have consistency so if they are already paying ER physicians who do extra shifts, then you can use this to justify your request.
Be sure you know what you are asking for. How much are you asking to get paid for working extra shifts? For example, if the original expectation is that the hospitalists work 15 twelve-hour shifts each month with a compensation of $325,000 per year, that works out to $1,800 per shift. So, will you ask for $1,800 per extra shift worked or ask for time and a half at $2,700 per extra shift worked? Will you want more per shift for undesirable shifts such as night shifts and holidays?
When possible, make extra shift voluntary. Some physicians value money more than time and others value time more than money. Mandating extra shifts can be viewed as punitive whereas monetarily incentivizing extra shifts can be viewed as an employment perk by physicians looking to increase their income by internally moonlighting. At our hospital, we had some hospitalists who were happy to get paid to work several extra shifts per month and some physicians who did not want to work extra shifts, no matter how much extra they would get paid.
How does the hospital manage physician professional income? Know how much money your group brings in from professional billing – few (if any) hospitalists can cover their salary by professional billing alone and so most (or all) require supplemental monetary support from the hospital. Know how much your hospitalists bring in per day shift and per night shift, particularly if the hospital is doing the billing for your doctors and the professional revenue is being routed through the hospital’s finance department. These data will dictate how much you will ask the hospital to pay for extra shifts. If extra shifts are required due to an unexpected inpatient census surge, then there will be additional revenue from physician billing during those shifts and this will offset the amount that the hospital would be asked to compensate physicians who work those shifts. On the other hand, if the extra shifts are due to a hospitalist being out on maternity leave, then the anticipated revenue from physician professional billing would already have been budgeted for and the hospital would need to provide more for physicians who work the extra shifts.
Meet with the right people. This requires you to know who in your hospital administration has the authority to make the decision. This is usually a hospital chief operating officer but could be the hospital CEO. Many physicians think that they need to approach the chief financial officer but the CFO usually just passes those requests to someone else, like the CEO. The titles vary from hospital to hospital so schedule a meeting with the person who can actually respond to your request.
Data, data, data. Go into this meeting armed with data about how many extra shifts are being done per month or per year, how many hours your hospitalists are working, etc. It is useful to have a benchmark for this, such as the annual MGMA physician compensation report that lists the average hours per week hospitalists work.
Beware of becoming a clock-puncher. Physicians have historically been considered professionals when it comes to employment models. That means that their workday ended when they got their work done, rather than at some specified hour of the day. On the other hand, hourly workers clock in and clock out, getting paid for the number of hours that they work per day. Physicians who work shifts fall into a gray zone between these. The danger of too rigidly demanding payment for extra hours worked is that you run the risk of ceding autonomy to the hospital administration. The hospital CEO does not punch in and out of a time clock at work and if the CEO considers you to be employed in a professional model, then the two of you can be on an equal footing in a negotiation. On the other hand, if the CEO considers you to be an hourly worker, then the CEO owns you.
Make the right kind of appeal. Making demands and threats to the hospital administration usually gets their defenses up and makes them resistant to monetary requests. It is better to appeal to their humanity and to preservation of hospital quality. For example, employee burnout is an existential treat to hospitals so consider opening your meeting with the hospital administrative director with something like “We’re really concerned about some of our hospitalists who are showing signs of physician burnout due to the extra shifts that they are required to do and we’re worried that it will affect their performance and affect patient quality of care. We need some help figuring out a way to address physician burnout.” If you’re lucky, the hospital administration will offer extra compensation and think that it was their idea (rather than yours).
Extra payment for shifts done to cover hospitalists who are out due to FMLA or sickness is tricky. If the hospital views the hospitalist group as an independent business entity, then they will view their deal is with the group to provide coverage for a specific number of shifts per month and it is up to the group to figure out how to cover those shifts when a hospitalist is out on maternity leave, illness, or injury. If that is the case, then the group needs to anticipate the average amount of FMLA and sick time per year and build that into the annual contract as a cost of doing business. If the hospitalists are hospital-employed, then you have more power to negotiate FMLA/sick time coverage since the hospital is the “business owner” of the hospitalists. Your hospital likely does not require its nurses to do extra uncompensated shifts when one of the nurses is out on FMLA and you can use that as a point in your favor when meeting with administrative leaders.
Most physicians are uncomfortable asking for additional compensation; we would rather ask for additional patient care resources, such as additional nurse practitioners, a new operating room, or a new MRI machine. Many physicians go through their entire career without ever asking someone for a raise. Consequently, negotiating with the hospital for compensation for extra shifts worked can feel foreign. The key to overcoming this is preparation and the considerations above will help you to be prepared.
One of the concerning observations from the COVID pandemic is that immunity from infection (“natural” immunity) appears to be better than immunity from vaccination. This is often attributed to the fact that when a person is infected with COVID, their adaptive immune system creates antibodies against many different parts of the COVID virus whereas an mRNA vaccine produces antibodies only against one specific site on the exterior of the virus. However, the reason for this difference in immunity may be due to something altogether different – infection results in the immune system producing lots of anti-COVID IgA but mRNA vaccines produce relatively little anti-COVID IgA. To understand why this is important, let’s take a look at the function of the different classes of antibodies (also known as immunoglobulins), including IgA
Current intramuscular COVID vaccines provide good protection against severe COVID infection but offer less protection against mild COVID infection
Secretory IgA antibodies in respiratory mucus is the main antibody that prevents inhaled viruses from getting into our bodies
Intramuscular COVID mRNA vaccines create a lot of IgG antibodies in the blood but create relatively little secretory IgA antibodies in respiratory mucus
Inhaled COVID vaccines offer the potential to create larger amounts of secretory IgA in respiratory mucus and thus provide greater immunity against COVID infection
The basics of immunoglobulins
There are five types of immunoglobulins: IgG, IgM, IgA, IgE, and IgD. Each of them plays a different role in the immune system. All are produced by plasma cells. There is a constant amount of many, many different immunoglobulins in the body but in response to an infection, B-lymphocytes are converted into plasma cells that then make antibodies that uniquely target that particular infection. After the infection is cleared, the number of these plasma cells fall with the result that the level of those antibodies targeting a specific infection also fall.
IgG is the most abundant immunoglobulin in the blood, accounting for 75% of blood immunoglobulins, and is the main workhorse antibody in the blood to fight bacteria and viruses that have entered the body. New IgG is produced about 1 – 3 weeks after the start of an infection. It is the only type of immunoglobulin that crosses the placenta. It has a half-life of 23 days.f-
IgM is also produced by B-lymphocytes and released into the blood. It accounts for 10% of blood immunoglobulins. It is produced faster than IgG after an infection, generally in 5 – 10 days. It is also used to combat bacteria and viruses. It has a hallife of 7 days.
IgA is the second most abundant immunoglobulin in the blood, accounting for 15% of blood immunoglobulins. However, secretory IgA is also produced in the mucosal lining that forms the surface of the airways and the gastrointestinal tract. Because of this, IgA is overwhelmingly the most abundant immunoglobulin in the mucus of the lungs and nose. As a result, IgA is the most abundant immunoglobulin in the body, when considering both the amount found in the blood as wells the amount found in other parts of the body. IgA is used to fight bacteria and viruses and secretory IgA in mucus can fight these pathogens before they enter the body. It has a half life of 5.5 days. There are two types of IgA – IgA1 is found in the respiratory tract and IgA2 is found in the gastrointestinal tract.
IgE is used by the immune system to fight parasites, such as the worm Strongyloides. It is also involved in allergies. It is not involved in the defense against viruses. It has a half life of 2 days.
IgD is only present in very tiny amounts in the blood and its function is not well understood.
Viruses usually enter the body either through the respiratory tract or the gastrointestinal tract. In these tracts, viruses first have to pass through epithelial membranes layered with mucus. The main class of antibodies in mucus is IgA and thus IgA is the more important antibody in the initial protection against respiratory viruses. Mucosal IgA can stop some infections altogether if there is enough IgA to bind all of the individual viruses that are inhaled. Even if a few viruses evade mucosal IgA and get into epithelial cells and into the bloodstream, the numbers of individual viruses are low, giving the adaptive immune system a chance to rev-up blood antibody production and defeat the infection before the virus can replicate into large numbers inside of the body.
IgA levels protect against COVID
One of the ways scientists learn about the roles of different immunoglobulins is by studying people who are born with deficiencies of different immunoglobulins. Selective IgA deficiency is the most common of these immunoglobulin deficiencies and occurs in somewhere between 1 in 200 and 1 in 1,000 Americans. The curious thing about IgA deficiency, however, is that two-thirds of patients are asymptomatic. In about one-third, IgA deficiency confers a greater risk of sinusitis and pulmonary infections. IgA deficiency can also cause increased susceptibility to allergies. However, there is evidence that IgA deficiency plays a role in defending the body against COVID infection. The COVID virus enters the body through the nose and then first infects the epithelial cells lining the respiratory tract by crossing through the airway mucus layer. Because IgA is the most important anti-viral defense in mucus, it follows that lower levels of IgA could increase the risk for COVID.
A 2022 study in the Japanese Journal of Infectious Disease found that patients with selective IgA deficiency were 7.7-times more likely to have severe COVID infection than patients with normal IgA levels.
A 2022 study in the Journal of Clinical Immunology found that patients with severe COVID infection had lower serum levels of IgA than those with less severe COVID infection and healthy persons.
A 2023 study in The Lancet Infectious Disease found that healthcare workers who had detectable anti-COVID IgA in nasal mucus samples after vaccination had a lower risk of later getting a COVID infection than those healthcare workers who did not have detectable anti-COVID IgA in nasal mucus after vaccination.
A 2023 study in the Journal of Allergy and Clinical Immunology Practice found that patients with selective IgA deficiency were more likely to get initial COVID infections and were more likely to have recurrent COVID infections than persons with normal IgA levels.
IgA levels in respiratory secretions falls as people get older. A 2021 study in the Journal of Pharmacy & Bioallied Sciences found that salivary IgA levels fall after age 60. One possible explanation for the greater risk of severe COVID in the elderly could be from low mucosal IgA levels compared to younger persons.
Current mRNA vaccines have less effect on IgA
Given that secretory IgA in mucus appears to be an important component of the immune system’s defense against COVID, it follows that the effectiveness of vaccines against COVID depends in part on the ability of those vaccines to produce anti-COVID secretory IgA in the airways. Although current intramuscular mRNA vaccines are very good at stimulating anti-COVID IgG antibodies in the blood, they are not as effective in producing anti-COVID IgA antibodies in respiratory secretions.
A 2022 study in in the journal Frontiers in Microbiology found that anti-COVID IgA was detectable in throat swabs 4 days after infection with COVID and in the blood 10 days after infection. However, after an intramuscular mRNA COVID vaccine, throat swabs were negative for anti-COVID IgA indicating that COVID infection causes the body to make IgA in respiratory secretions more effectively than COVID vaccination.
A 2022 study in the journal Nature found that anti-COVID IgG and IgA was detectable in the saliva after the first dose of an mRNA COVID vaccine. After the second dose IgG antibody levels were boosted but IgA levels were not boosted. In fact, only 30% of subjects had detectable anti-COVID IgA in the sputum after the second dose of vaccine.
A 2023 study in The Lancet eBioMedicine found that patients with COVID infection had high levels of anti-COVID IgA in both blood and nasal secretions for 12 months after infection. Subsequent vaccination caused an increase in blood IgA but did not cause an increase in nasal secretion IgA.
A 2023 study in The Journal of Allergy and Clinical Immunology: Global found that after intramuscular mRNA vaccination, there was a significant increase in anti-COVID IgA and IgG in the blood but only a minimal increase in anti-COVID IgA in nasal secretions.
A 2023 study in The Lancet Microbe found that anti-COVID IgA levels in nasal secretions did not increase substantially after booster mRNA vaccinations whereas IgG levels did increase.
How can we improve COVID vaccines?
For decades, physicians have written off IgA deficiency as having minimal, if any, clinical significance. But evolutionary science demonstrates that proteins that are unnecessary for the survival of a species eventually go away. It takes a lot of energy and nutrients to produce these proteins and individuals who do not need to expend energy and nutrients for unnecessary proteins can use that energy and nutrients for other functions, giving that individual a survival advantage. Taking into account both blood and secretory amounts, IgA is the most abundant immunoglobulin in the body. Even if we do not fully understand its functions, for the human body to expend so much energy and nutrients on IgA production, it must be important. Given the enormous amount of IgA found in respiratory mucus, it follows that its importance is in defense of inhaled viruses and bacteria.
The lungs have a huge surface area. If you were to lay out the surface of all of the bronchi, bronchioles, and alveoli in a person’s lungs, it would cover an area the size of a half of a tennis court. That surface area is exposed to the outside environment with every breath we take. COVID vaccines that result in a high level of anti-COVID IgA antibodies in the respiratory mucus should give the best protection against COVID infection. These IgA antibodies would be able to bind and destroy COVID viruses before those viruses enter the respiratory epithelial cells and cause infection. Vaccines that only increase antibodies in the blood but not in the respiratory mucus will not reduce the chances of getting infected but only reduce the severity of infection once it occurs.
To use an analogy, if you are trying to defend your country against an invading army, you are better off posting your defensive troops at your border, rather than trying to fight your battles in the interior of the country after the invaders have already crossed your borders.
So, how can we engineer vaccines to cause a robust secretory anti-COVID IgA response? The answer may be to give inhaled vaccines. This would potentially stimulate production of secretory IgA in the airways, where it is needed for the initial defense against COVID. Indeed, it may be that we need both inhaled vaccines to produce secretory IgA to protect against initial infection and intramuscular vaccines to produce blood IgG antibodies to protect against severe infection. The COVID virus enters our bodies in droplets and aerosols – it only makes sense that we should create vaccines that are also administered by droplets and aerosols.
Research is now being done to create inhaled COVID vaccines. At the Ohio State University College of Veterinary Medicine, researchers recently published their work in hamsters using an intranasal live-attenuated mumps virus containing the COVID spike protein. They found that this vaccine was highly effective in generating anti-COVID mucosal IgA and completely protected these hamsters from COVID infection. Subcutaneous administration of this live-virus vaccine was also effective. The MMR vaccine currently in use in pediatrics uses this same attenuated live-virus approach. There are currently phase 1 and phase 2 clinical trials underway in the U.S. and abroad using intranasal COVID vaccines.
The current generation of intramuscular mRNA vaccines have done what was most needed in the first years of the pandemic – they prevented people who were infected with COVID from dying of COVID. The next generation of vaccines should be designed to keep people from getting infected altogether. The key to this goal may be secretory IgA.
Two weeks ago, the new COVID booster vaccines were released and the internet is full of articles titled “Should you get a COVID booster?“. This is the wrong question – the real question is “When should you get a COVID booster?”. We so want the COVID pandemic to be over and gone. Americans are returning to theaters and restaurants, houses of worship are full again, sporting events are sold out, and mask-wearers are a tiny minority at the grocery stores. But COVID is not going away.
For the past 3 years, there have been two peaks of case numbers every year – a large peak in January and a smaller peak in the summer. Data from the CDC this week indicates that the current 2023 summer peak is cresting and cases should begin to fall over the next few weeks (reported case numbers are unreliable but COVID hospitalizations, COVID deaths, and the percent of ER visits due to COVID are accurate measures). If history repeats itself, then we should have a break in cases for the next couple of months until they begin to rise again in the winter.
COVID is a moderately lethal infection – less lethal than Ebola but more lethal than influenza. Immunity is very effective in protecting you from dying of COVID but less effective from protecting you from catching a non-fatal COVID infection. There are two ways to get immunity – either by having a previous COVID infection or by getting a COVID vaccine (or both). On the whole, immunity from past infection is probably more effective than immunity from a vaccine. However, to get immunity from a past infection, you have to first survive the infection. There are a number of advantages to getting immunity from a vaccination compared to getting immunity from an actual COVID infection:
So far, 1,144,539 Americans have died from COVID and most of these were people who had no immunity to the virus and died from their first infection. To understand how our immune system fights COVID, let’s first take a look at the basics of the immune response to viruses.
How the immune system works
Viruses cannot reproduce on their own – they have to get inside of our cells and then hijack those cells’ RNA to produce new viruses. Our defense against viruses takes two forms: the innate immune system and the adaptive immune system. Innate immunity uses parts of the immune system that we are born with to fight any new infection. The innate immune system consists of interferons, natural killer lymphocytes, and macrophages. When a cell gets infected with a virus, that cell releases interferons that then signal natural killer cells to kill any other infected cell before it can produce more viruses. In addition to stopping the infection by killing infected cells, the innate immune system has macrophages that can eat and kill extracellular viruses before those viruses can infect other cells in the body. The innate immune system works whether or not a person has been previously infected with the same virus or has received a vaccine against that virus. Think of the innate immune system working on instinct. The adaptive immune system, on the other hand, can be thought of as working by learning. Of the two, the adaptive immune system is the more powerful.
The adaptive immune system learns from previous infection or vaccination so that when a person is exposed to a future infection, the adaptive immune system can be immediately activated against that virus. The adaptive immune system consists of T-lymphocytes, B-lymphocytes, and antibodies. When a person is first infected with a virus, T-lymphocytes become activated and then in turn activate B-lymphocytes to produce antibodies that are specifically directed against that particular virus. These antibodies are our immune system’s most important weapon against viruses and can defeat viral infections in four ways. First, antibodies can bind to the virus so that the virus cannot get into cells and thus prevent the virus from infecting cells. Second, when antibodies bind to a virus, it signals macrophages to eat and kill that virus. Third, when antibodies bind to an infected cell, they mark that cell for natural killer lymphocytes to kill that infected cell, thus preventing further viral replication. Fourth, when antibodies bind to infected cells, they activate the complement system to punch holes in that cell, thus killing it and preventing further viral replication. Antibodies last for about a month in the bloodstream and after an infection is resolved, the adaptive immune system cuts way back on new antibody production.
The innate immune system works immediately after an infection but it takes the adaptive immune system 1 – 3 weeks to ramp up antibody production after a new infection. However, the second time a person is infected with the same virus, that adaptive immune system can ramp up antibody production much faster, in a matter of days rather than weeks. This is because of memory T-lymphocytes and memory B-lymphocytes that have learned how to make antibodies against that particular virus. These memory cells cause antibodies to be produced much faster than during the first, initial infection with a virus.
Antibodies and COVID
Many people who are now getting infected with COVID are on their second or third infection. For most people, the second infection is not as severe as the first and the third infection is not as severe as the second. This is because the memory T-lymphocytes and memory B-lymphocytes allow the immune system to respond faster and more effectively against repeat infections. Multiple doses of vaccines do the same thing – with each vaccine dose, your body makes new antibodies against COVID variants covered by that vaccine booster and also trains your memory lymphocytes to ramp-up antibody production quickly if you are exposed to the virus in the future.
Because antibodies only have a lifespan of about a month, antibody levels fall after either an infection or a vaccination as the B-lymphocytes start to slow down antibody production. As a result, after vaccination, COVID antibody levels begin to fall after about 3 months. So, you are best protected against a future infection in the first 3 months after a COVID vaccine as well as in the first 3 months after a COVID infection. But what most people do not realize is that it is not just the antibody levels in the blood that protect against COVID infection but it is also the training of the memory T-lymphocytes and memory B-lymphocytes that protect against infection Those memory cells last many years and can sometimes last for a lifetime. We have blood tests that can measure antibody levels but we do not have blood tests that measure memory lymphocyte levels and consequently, this important effect of vaccination is often overlooked.
When you get a COVID mRNA vaccine, you produce antibodies against one small part of the COVID virus. On the other hand, when you get a COVID infection, you produce antibodies against many different parts of the COVID virus. For that reason, a COVID infection will stimulate stronger immunity against another future infection than vaccination does. But because the memory T-lymphocytes and memory B-lymphocytes learn from each exposure to a virus or to a vaccination, the more you stimulate those memory cells, the better they become at fighting infection. Also, because antibody levels eventually fall after a COVID infection, those antibody levels can be replenished if a person gets vaccinated several months after that infection. For these reasons, a COVID vaccination gives you good immunity, a COVID infection gives you better immunity, and a COVID infection plus a vaccination gives you the best immunity.
So, when should you get a COVID vaccine?
Early in the pandemic, the answer to this question was easy – everyone should get a COVID vaccine as soon as possible. However, now that most Americans have at least some degree of immunity from either previous vaccination, previous COVID infection, or both, the answer to the question is a bit more complicated. In order to get the maximum benefit from vaccination, the timing has to be individualized. And the key to individualization is the fact that antibody levels persist for about 3 months after infection or vaccination before those levels begin to drop off. So, here are my recommendations:
No previous vaccination or infection. These are people who are most likely to become severely ill or die if they get a COVID infection. They should get vaccinated immediately. Even if COVID case numbers in their community are low, it is not worth gambling with one’s life that they won’t be exposed to an asymptomatic person at the grocery store, at church, or at work.
Received an older COVID vaccine within the past 3 months. These people should wait until at least 3 months after their last vaccination. Their antibody levels are already high and it is better to wait until their antibody levels begin to fall before re-stimulating their adaptive immune system. However, given the anticipated January surge in COVID numbers, they should not wait long after that 3-month period.
Had a COVID infection in the past 3 months. These people should similarly wait until at least 3 months after their COVID infection. However, they should also get vaccinated before the anticipated winter surge in cases.
Previous vaccination more than 3 months ago and no previous infection. These people should time their vaccine to when they are most likely to be exposed to COVID. For the last 3 years, the winter peak of COVID cases has been in the first week of January. Assuming this year is similar, then get a new COVID vaccine now and by mid-November at the latest.
Previous vaccination more than 3 months ago and had a previous infection. Congratulations – these people already have the strongest immunity. But their immunity will be even stronger with a new COVID vaccine now or by mid-November at the latest.
Moderately or severely immunocompromised. Here is where things get a bit complicated. These people need more vaccine doses in order to be protected. If they have never been vaccinated, they should receive 3 doses of either the new Pfizer or the new Moderna COVID vaccine. If they have previously received 1 dose of either Pfizer or Moderna, then they should receive 2 doses of either of the new COVID vaccines. And if they have received 2 or more Pfizer or Moderna vaccinations in the past, they should receive 1 dose of either of the new COVID vaccines. If you are uncertain, it is better to err on the side of too many rather than too few doses for immunocompromised people.
Planning travel or large family get togethers over Thanksgiving or Christmas. Get a COVID vaccine now (or by the end of October at the latest) in order to ensure that you have protective antibody levels over the holidays. First, because it will protect you from getting infected while traveling and second, because you don’t want to get an infection just before your travel date and have to cancel your trip.
There are three COVID vaccines currently on the market. The Novovax protein subunit vaccine is based on the original strain of COVID and is only approved for primary vaccination in people who have never received any COVID vaccines; it is not available as a booster. Anyone who received the Novovax (or the no-longer available J&J vaccine) still needs to get one of the new mRNA vaccines since neither Novovax nor J&J covers the newly circulating COVID variant. The new Moderna and Pfizer mRNA vaccines are available for anyone for either primary vaccination or as a booster. The new Pfizer and Moderna vaccines are interchangeable so if you have previously received a Moderna vaccine, you can get either a Moderna or Pfizer booster and vice-versa.
The bottom line is that everyone should get a new COVID vaccination
Your body’s immune system is like your muscles – the more you train it the stronger it becomes. Vaccinations both keep your antibody levels high and train your immune system to make new antibodies rapidly and in large quantities. There are really no good reasons to not get vaccinated. Everyone should get vaccinated in the next 6 weeks to optimally protect themselves during the upcoming holidays and the anticipated upcoming winter surge in COVID numbers. The Moderna vaccine or the Pfizer vaccine – either one is fine, no matter what brand of vaccine you have received in the past.
And, oh by the way… get your other protective vaccinations, too. I got my influenza and pneumococcal vaccines together on September 1st and my RSV and new COVID vaccines together on September 18th. This was my 6th dose of a COVID vaccine since December 15, 2020. My immune system will be ready for whatever gets thrown at it this winter.
One out of every two women will develop a pelvic floor disorder at some point in their life. These disorders usually require physical therapy and often require surgery. So, why don’t we hear more about pelvic floor dysfunction?
The pelvic floor is a hammock-like group of muscles and ligaments that drape across the pelvis and support all of the pelvic organs. If these muscles and ligaments become damaged, then they cannot hold organs in the pelvis (resulting in prolapse) and cannot maintain sphincter control (resulting in incontinence). The most common cause of dysfunction of these muscles and ligaments is pregnancy and childbirth. During pregnancy, the weight of the gravid uterus plus changes in intra-abdominal pressure can stretch the components of the pelvic floor. During delivery, the levator ani muscle, pubococcygeus muscle, and pudendal nerve are all susceptible to stretch injury. In addition, more than half of vaginal deliveries result in vaginal lacerations which can involve the pelvic floor muscles and sphincters.
The frequency of these disorders is shockingly common. At one year after vaginal delivery, 41% of women experience stress urinary incontinence, 32% experience nocturia, 23% experience flatus incontinence, and 9% have some degree of prolapse. Age also affects the pelvic floor with loss of muscle and ligament integrity, particularly after menopause. The Women’s Health Initiative study found that 41% of older women with a uterus have some degree of prolapse.
So, why don’t we hear about it?
Pelvic floor dysfunction is a silent epidemic because all too often, women do not bring it up when seeing their doctor and their doctor does not ask the right questions.
Assumption of normal. Many women just assume that symptomatic pelvic floor dysfunction is just a normal and expected consequence of “everything getting stretched out” during labor and delivery. Because of this assumption of normal, women frequently do not discuss postpartum urinary incontinence, anal incontinence, or vaginal bulges with their doctor.
Patient embarrassment. Many women have a hard time bringing up issues regarding their urination or bowel movements, even with their physician. Some women don’t know enough about normal female pelvic anatomy to tell when their pelvic structures are not quite right.
Doctors do not ask the right questions. Obstetricians are generally good at asking about pelvic floor dysfunction symptoms but primary care physicians and other non-obstetricians frequently are not. Sometimes it is because the primary care physician just assumes that the obstetrician will take care of any problems resulting from pregnancy and sometimes it is because of lack of familiarity with the clinical manifestations of pelvic floor dysfunction. When asking women about pelvic floor dysfunction, we should remember the 3 “B’s”: Bladder, Bowel, and Bulge.
Pelvic floor dysfunction symptoms
The most common serious consequences of pelvic floor dysfunction are incontinence and prolapse. Types of urinary incontinence include stress urinary incontinence, urgency urinary incontinence, and mixed urinary incontinence. Bowel control issues include fecal incontinence, flatus incontinence, and fecal urgency.
Prolapse occurs when a pelvic organ herniates. A cystocele is when the bladder herniates into the anterior vaginal wall. A rectocele is when the rectum herniates into the posterior vaginal wall. And a uterovaginal prolapse is when the cervix and uterus descends into the lower vagina. Prolapse can result in urinary incontinence, constipation, pelvic discomfort, and pain during sexual intercourse.
What can be done about it?
Pelvic floor physical therapy. Fortunately, there are effective treatments that can significantly improve the quality of a woman’s life. This generally starts with pelvic floor physical therapy. This is performed by a specially-trained physical therapist who can teach women exercises to strengthen the pelvic muscles and help restore normal pelvic function. Most notably are Kegel exercises when the pelvic muscles are contracted and then relaxed.
A bit of history about Kegel exercises. If I was to then ask you who invented Kegel exercises, you might say American gynecologist Arnold Henry Kegel who published an article about exercises to strengthen the pelvic floor in the Annals of Western Medicine and Surgery in 1948. But that wouldn’t be exactly right. Instead, we have to go back 12 years earlier when a book was published by a professional dancer named Margaret Morris. She was born in 1891 and began her career as a child actress and ballet dancer. By age 19, she was an internationally known choreographer and theater producer. In her 30’s she opened a dance school and became interested in how movement and posture affected health. So, in 1925, she went to London’s St. Thomas Hospital to study physiotherapy. She further developed her ideas about exercises and health that culminated in her 1936 book titled “Maternity and Post-Operative Exercises”. In her book, she outlined 21 exercises for women to perform that could improve urinary incontinence and other consequences of childbirth. Her book was reviewed in JAMA in 1937 where the reviewer stated that he was: “..satisfied with the soundness of Miss Morris’s scheme and believe that their application will yield most beneficial results.” Dr. Kegel then wrote about her exercises more than a decade later and he now gets all of the credit for Margaret Morris’s pelvic floor exercises.
Other non-surgical treatments. When symptoms persist despite pelvic floor physical therapy, there are other treatment options. Diet and lifestyle measures to reduce urinary incontinence include weight loss, avoidance of excessively large fluid ingestions, and avoiding drinking fluids shortly before bedtime. Pessaries and over-the-counter vaginal inserts can also be useful. Measures to reduce fecal incontinence include dietary soluble fiber (but avoid insoluble fiber), ritualization of bowel movements, and over-the-counter loperamide. Avoidance of caffeine and avoidance of vigorous exercising after meals can also reduce fecal incontinence.
Surgical options. When these measures are ineffective, there are a variety of surgical options. There have been many recent developments in surgical procedures for pelvic floor dysfunction. For example, in the past, uterine prolapse was primarily treated with hysterectomy; however, now there are many uterine-sparing procedures that can be performed. Other new techniques include sacroneuromodulation for fecal incontinence and onobotulinum toxin for urinary urgency incontinence. This is where a urogynecologist can be an invaluable resource. Many larger medical centers have comprehensive subspecialty peripartum pelvic floor disorder clinics overseen by a urogynecologist. Physicians at smaller hospitals that cannot support a full subspecialty clinic should be familiar with regional pelvic floor disorder clinics for referral.
The bottom line: talk with your patients
Given the frequency of pelvic floor dysfunction, it is incumbent on every primary care physician to be familiar with the symptoms and to be willing to speak openly about them with patients. If your hospital has a labor and delivery unit, then it needs a pelvic floor physical therapist. As an emeritus faculty, I’ve been doing some pro bono teaching at the Ohio State University and recently guest-moderated an OSU MedNet webcast on pelvic floor disorders by Dr. Lisa Hickman. This webcast is a great resource for physicians, nurse practitioners, nurse midwives, and physician assistants who need to brush up on the diagnosis and management of pelvic floor dysfunction. You can view the webcast by clicking on this link.
I just watched the Netflix series Blue Zones that examined habits of societies of people who were most likely to live more than a century. While I agree with most of the conclusions, there is much left out. The problem with such observational studies is that they are subject to population shift bias, observer bias, and selection bias. Over the last 40 years, I’ve seen hundreds of people die. It is inevitable if you are a critical care physician and even more inevitable if you are also a pulmonary physician specializing in idiopathic pulmonary fibrosis, a terminal disease. So, I have my own thoughts on what it takes to live to be a hundred years old (and what it takes to not die in our ICU). But first, let’s take a look at the three forms of bias.
Population shift bias. On the surface, it would seem to be easy to estimate the life expectancy of a group of people. Just look at all of the death certificates and calculate the average age of death. However, human populations are dynamic, with people constantly moving in and out of a given area. Let’s use an example of a hypothetical group of people living on an island in the Mediterranean. You go to the public records department and pull all of the death certificates for the past 10 years and find that the average age of death is 88 years old. You might then assume that the life expectancy is 88 years. But what if there had been no good-paying jobs on that island for the past 10 years and most of the people under age 65 moved to the mainland to find work? In that case, people born on the island who died before age 65 died somewhere else and this makes the average age of people dying on the island look falsely high. Also, the percentage of people living on the island who are older than 100 (per capita rate of centenarians) will be falsely high.
Population shift bias can also occur if there is a change in the birth rate. Let’s say you are measuring longevity by the average age of people on the same island. Three generations ago, families had an average of 6 children but now, families only have an average of 2 children. As a result, the average age of people on the island at any given time is now higher because there are fewer children. But that doesn’t mean that people are really living long.
Observer bias is a problem with any observational study. Let’s say you find that Seventh Day Adventists have a high percentage of people who live past 100. So, you look at the habits of those people to try to determine why they lived as long as they do. There may be hundreds of variables that make them different than everyone else in the world but if you are trying to prove that it is because of diet, then you will have blinders on and only focus on the observation that Seventh Day Adventists eat a plant-based diet. So, you might conclude that the vegetarianism caused then to live so long while overlooking the fact that Seventh Day Adventists also don’t smoke cigarettes.
Selection bias occurs when you look at a small group of people who have a particularly good or bad outcome and then assume that the group of people is representative of the population as a whole. An example of a selection bias error that is frequently made is nursing homes. It is often said that as soon as a person enters a nursing home, it cuts 3 years off of their life. One might then assume that being admitted to a nursing home causes a shortened life expectancy. However, a 70-year-old who need nursing home care is by definition sick and debilitated. A healthy and active 70-year-old would not be admitted to a nursing home. Entering a nursing home doesn’t make you live shorter, being chronically ill and debilitated makes you live shorter. The same can be said of doctor visits – people who visit doctors ten times a year are more likely to die than people who only visit a doctor once a year. If you fall into the trap of selection bias, then you would assume that seeing a doctor causes you to have a shortened life expectancy whereas the truth is that people who see a doctor more frequently have more serious and complicated diseases than those who see a doctor rarely.
The scientist in me would say that the only sure way to know if a habit will make you live longer is to do a randomized controlled trial, preferably placebo-controlled. But this type of study is impossible when looking at people’s life-long habits. So, everything we hear about the habits of people who live beyond 100 years is affected by these forms of bias. And I freely admit that these biases affect my own thoughts on living to be 100. You’ll see that my list is a lot different than the Blue Zone’s list. But I think you’ll find that my list will give you a better chance of becoming a centenarian. So, here goes:
Be a non-smoker. It is almost unbelievable that it was less than 50 years since the U.S. Surgeon General first reported that smoking was bad for your health. A study in the New England Journal of Medicine in 2013 found that women who smoke a pack of cigarettes a day live 11 years less than women who do not smoke. For men, smoking reduces life expectancy by 12 years. If you do the math, that works out to 14 minutes of life lost on average for every cigarette smoked.
Get rid of your gun. Most of the people who die of firearm injuries did so from their own gun or the gun belonging to someone else in the family. The CDC reports that in 2022, 48,117 Americans died from a gunshot – 58% of those were suicides. In other words, a good guy with a gun is more likely to kill himself than to kill a bad guy with a gun.
Wear a seatbelt. In America, we kill almost as many people with cars as we do with guns. The National Highway Traffic Safety Administration reports that in 2022, 42,795 Americans died in a motor vehicle accident. More than half of the drivers and passengers who died in a car accident were not wearing a seatbelt. In 1984, New York became the first state to legally require people to wear seatbelts – the law was met with outrage by anti-belters who said that it was an encroachment on their personal freedom. Unfortunately, that argument does not fly with widows and orphans.
Maintain a normal BMI. We define obesity as a body mass index (BMI) greater than 30. Overweight is a BMI between 25 – 30. The National Health and Nutrition Examination Survey (NHANES) found that the prevalence of obesity in the U.S. is now 42%. As Americans have become more obese, a cultural taboo on criticizing obesity has emerged with the result that those who say anything bad about obesity can be accused of “fat-shaming”. But the reality is that obesity is not healthy. It increases the risk for hypertension, diabetes, and sleep apnea all of which can shorten life expectancy. It can cause arthritis that reduces physical activity and increases the risk of falls. A 2014 study found that people with a BMI > 40 have a life expectancy 14 years less than those who with a normal BMI between 18.5 and 25. A 2019 study found that even those with a BMI between 30 – 40 had a reduced life expectancy of 5.5 to 7.5 years compared to normal weight individuals.
Don’t use drugs. In 2022, 105,452 Americans died from a drug overdose. That’s one out of every 3,000 people and more than died by both guns and motor vehicle accidents combined. The drug that causes the most overdose deaths is fentanyl. Most drug users do not call their local drug dealer asking for fentanyl. Instead, it is mixed with other drugs to potentiate their effects at a low cost. However, street drugs are not mixed by compound pharmacies and instead are mixed in unpredictable amounts by dealers with the result that a drug user does not really know what he or she is getting in a dose from one day to the next. Consequently, dying from a drug overdose is now easier than ever before.
Get vaccinated. In 2019, 2,854,838 Americans died; of those, 49,783 (2%) died of influenza and pneumonia. In 2021, 3,464,231 Americans died; of those, 416,893 (12%) died of COVID. Last week, for my 65th birthday, I got a flu shot and a pneumonia shot. When they become available later this month, I’ll get this season’s COVID booster. These are some of the best investments you can make in your health. Infections cause inflammation and prolonged inflammation is harmful to the body. Vaccinations also cause inflammation (its how they work) but in contrast, vaccination inflammation is mild and brief – vaccinations stimulate rather than stress the immune system. If you live on a remote island with few visitors, it is easy to avoid respiratory infections since those infections have to be brought to the island by someone who is already infected. But for the rest of us, exposure to infections that have the potential to kill us is unavoidable so our best defense is vaccination.
Choose your parents carefully. Okay, I know that no one can choose their parents but it is true that the genes that we inherit from them have a big impact on our life expectancy. Evolution has genetically engineered us to be able to live long enough to have children and then raise them until they can be self-sufficient. The current average age of menopause is 51 but in ancient times, it was much earlier, around age 40. Allowing for 15-20 years to fully raise and protect a child, our genes needed to ideally get us to about age 55 or 60. There was no natural selection advantage to having genes that let a person live older than that because those genes did not give a greater survival advantage to one’s offspring. Genes that resulted in high cholesterol or breast cancer didn’t really matter 200,000 years ago because people did not live long enough to get the diseases they cause. Consequently, many families carry genes that that result in fatal diseases that occur in the family members’ 60’s or 70’s.
Exercise your body. Many studies have shown that people who exercise regularly live longer. There are a lot of reasons for this: lower risk of obesity; lower risk of dying of cardiovascular disease; lower risk of osteoporosis; and better strength and balance that can reduce the chance of falling. However, the most effective physical exercise is a life-long exercise lifestyle rather than a New Years resolution gym membership. Walking can be great exercise but we have unfortunately engineered our communities to encourage sitting in a car rather than walking to workplaces, stores, restaurants, and places of worship. Rather than retiring and moving to a gated community on the outskirts of town, consider moving to a walkable neighborhood – preferably one with a lot of hills.
Exercise your mind. What allowed humans to become the apex predators on Earth? Some people would say it is the capacity of speech. Others would say the ability to make tools. Yet others would say the dexterity that resulted from opposable thumbs. The reality is that it is verbal communication, tool-making, and complex dexterity were all facilitated by the homo sapiens brain. Every successive branch of hominid evolution has been associated with a larger and larger brain, from homo habilis (640 cc) to homo erectus (1,029 cc) to homo sapiens (1,350 cc). Our brains are like any other organ in our body – they work best when we use them regularly. Ideally, we should be exercising all areas of our brains. Exercise the brain’s motor centers by activities requiring balance and dexterity, for example, tennis or dancing. Exercise the brain’s left cortical areas with reading, creative writing, and conversation. Exercise the brain’s right cortical areas with music and art.
Be engaged with other people.About 400,000 years ago, human ancestors firs started using spears. Ever since then, humans who lived in communities had an enormous advantage over those who lived solitary lives. The more organized the community, the better it’s chance of survival. Communities have propelled humans to the top of the food chain. We need communities as much as communities need us. Social isolation is associated with a higher risk of depression, suicide, dementia, and early death. Keeping connected with other people helps keep us connected with life. There are endless ways to do it: volunteer, be active in your place of worship, speak with family and friends regularly, even use Facebook.
Avoid excessive calorie-dense foods. Everyone has an opinion about the best diet for longevity. Vegetarian, vegan, low-carb, herbal supplemented, more olive oil, less nitrates – the list is endless. The reality is that humans are built to be omnivorous and consequently, there are a lot of ways to have a healthy diet, as long as they are nutritionally balanced. The antithesis of nutritionally balanced diets are those that are dominated by calorically dense foods. These include excessively sweetened foods, fast foods, and high fat “junk” foods. MacDonalds french fries, like heroin and Fox News, have been specifically engineered to be addictive after just one bite and make you want more. Daily calorie needs are determined by age and physical activity but 2,000 for women and 2,500 for men is a good average. Why waste so much of that on a Wendy’s Frosty (393 calories), Burger King large fries (448 calories), and a Chic-fil-A wrap (660 calories)? The advantage of diets that are high in vegetables, beans, and whole grains is that you can eat a lot, feel full, and have balanced nutrition – all without breaking the calorie bank.
Drink in moderation (or not at all). For some people, there is no “safe” amount of alcohol – they are wired for addiction. But one or two glasses of wine a day is OK for most people and may or may not actually be beneficial. However, drinking excessively can unquestionably kill you. Excessive alcohol is involved in one-third of gun-related homicides, one-half of gun-related suicides, and one-third of motor vehicle deaths. In addition, chronic excessive alcohol use can cause cirrhosis, pneumonia, various cancers, and dementia. Overall, alcohol is responsible for 140,000 deaths per year in the U.S.
Avoid poverty. You don’t need to be extremely rich to live a long life but it is really hard to live a long life if you are extremely poor. Poverty is associated with higher rates of smoking, obesity, drug use, and higher death rates for all of the 14 leading causes of death. Poverty results in inability to afford healthcare, living in crowded and unhealthy conditions, and over-reliance on calorically dense foods. Owning a Tesla won’t make you live longer but having to do all your grocery shopping at the Dollar General and being unable to afford a pneumonia vaccine can make you live shorter. Also, it is a lot more expensive to live to age 100 than to live to age 70, simply because you have to pay for more years of living expenses. So, even a middle-income working couple needs to make careful financial planning to avoid poverty in retirement.
See your doctor regularly. A good primary care provider is worth his/her weight in gold when it comes to staying healthy and living longer. Even if you walk 5 miles a day, eat a nutritionally balanced diet, and never smoke, there are still things that can happen that are outside of your control. We can’t always prevent high blood pressure, colon cancer, or high cholesterol, no matter how good our lifestyle is. Five hundred years ago, people rarely died of heart attacks, colon cancer, and dementia for the simple reason that they didn’t live long enough to get them. But these are conditions that early diagnosis by your PCP can result in effective treatment. See your doctor once a year for a routine visit and follow all of the recommendations for health screening and preventive care.
Blue Zones is worth a watch on Netflix. But its conclusions are susceptible to being affected by population shift bias, observer bias, and selection bias. My own personal conclusions about longevity are also affected by these same biases. So, take my recommendations with a grain of salt – just don’t overdue it with too much sodium.