Robert Goldstone

Carotid artery stenosis is a narrowing or constriction of any part of the carotid arteries, generally caused by atherosclerosis. One of the body’s largest arteries, the common carotid artery is the one you can generally feel pulsations of on each side of your neck. It comes off of the aorta and divides into the internal carotid artery (which supplies blood to the brain) and the external carotid, which supplies the face. The area where it divides is a common site for atherosclerosis, which is a buildup of plaque that narrows the vessel or provides the tendency to rupture and shoot through the bloodstream.

In most cases the cause of carotid artery stenosis is a degeneration of the wall of the artery, usually from fatty or cholesterol deposits. Sometimes the plaque is stable, and causes a narrowing of the blood flow through the brain and face. Other times, a part of the plaque may break off and travel through the circulation to the brain or other body organs. When the emboli shut off blood flow to a given cerebral area, a TIA (if it is temporary) or a full blown stroke can ensue.

The characteristic signs of carotid stenosis are a bruit (rumbling sound) over the carotid artery or the end result—a TIA or stroke. In those with risk factors (high cholesterol, HTN, obesity, diabetes) carotid artery screening may be done in the absence of a precipitating event. This has become quite controversial as we will discuss shortly. A Doppler ultrasound can determine the extent and the degree of the stenosis. Cerebral angiograms were a diagnostic tool but are used less frequently now with the advent of very sensitive MRI and MRA (angiogram) testing.

Treatment is generally aimed at the prevention of problems, including strokes and other complications of atherosclerosis. Anticoagulants (blood thinners like Coumadin or Eliquis) may be given as well as antiplatelet drugs to retard clotting. Surgery (usually a carotid endarterectomy), an open removal of carotid plaque, has been less used because of the risks of preoperative angiography and surgery, however angioplasty and stenting are still the main procedure used for significant symptomatic carotid stenosis.

Recently the USPSTF (US Preventative Services Task Force) reviewed evidence for screening for carotid artery stenosis in asymptomatic individuals and gave it a “D” or unnecessary recommendation. They focused on cost of testing relative to positive findings, false positive testing requiring further work-up which proved to be negative, and potential harm from the angiography, surgery and other interventions. Their position is very controversial, especially in those who have been spared potential life threatening stroke or sudden death.

Prognosis of carotid artery stenosis depends on the degree of stenosis and the contributing co-morbid conditions that may cause progression not only in the carotid arteries but in other major blood vessels in the body. With stenosis less than 50 percent there is a small risk of stroke. At 70 percent or higher the risk becomes quite significant and intervention becomes a consideration (surgical or medical). Risk factor modification such as lowering blood pressure, using cholesterol lowering drugs, smoking cessation and weight loss are important preventative steps.

Most applicants will be rated with stenosis over 50 percent or if significant stenosis has occurred at younger ages (less than 50 for example). Aggressive medical therapy and intervention may be credited in these circumstances. When TIA, stroke or carotid intervention has occurred, the ratings increase. As mentioned active risk modification and close doctor follow-up is necessary, as carotid artery dissection (tearing) and major stroke are distinct causes of mortality.

As I write this, my home state of California has reported over 2.3 million cases of COVID-19, and recorded over 26,000 deaths. The United States has already seen over 20 million recorded COVID cases, and the death toll stands at over 350,000. These are only “so far” numbers, and the slow vaccine roll out to date ensures we are nowhere near the final count on these statistics. And these numbers are only the cases we know about, not the equally massive number of cases where there was a recovery without a laboratory diagnosis or deaths where COVID may have been a major unreported factor—particularly in the elderly.

Thankfully, the number of COVID affected individuals has resulted in a large amount of recovered cases. Or what we assume are recovered cases. Many have gone back to their lives and situations with residual symptoms, even if mild. A small but significant amount who have “recovered” from the acute phase of the illness still have a degree of disability which affects their day-to-day living. These are the “long haulers”—those in whom COVID has spared in the short term but in whom we have truly no idea of what the long term prognosis will be, either morbidity or mortality wise.

Disease-impacted underwriting depends on estimating life expectancy (for life insurance), degree and duration of disability, and long term costs of care for health, disability and long term care. Much of this is based on experience of watching the course of illnesses in multitudes of people and understanding both the process and course of the disease. COVID however is a horse of a different color—we have no experience in how this has played out at other times and only guesstimates of how it will work in the future. Cases followed in the United States have barely reached the one-year point. It has become obvious, even in that short time, that recovery is not always complete, and that remaining objective signs and symptoms have potential to cause continued decompensation in the long run.

Cases of regular exposure where a COVID test is positive and there are minimal symptoms and a return to work without problems are still standard to preferred cases as they were before the infection. Those who were admitted to the hospital but required no ICU care or intubation and had a recovered course likewise don’t appear to date to have recurrent symptoms or compromise. Where it gets more difficult are three categories where more intensive treatment was necessary. Those include admission to the hospital with symptoms and the need for more than routine treatment (remdesivir, oxygen support, etc.), those who were hospitalized for a significant amount of days and whose course required an ICU admission (even not intubated), and those with an ICU admission where other medical problems surfaced with a prolonged hospital stay and where rehabilitation was needed.

Underwriting these cases requires much more care toward these latter classes. Besides perhaps a postpone period to see how symptoms persist or progress, additive testing may be required. Repeat chest X-rays and even chest CTs may be required. Laboratories in follow-up visits must be reported. Face-to-face follow-up care may be required above and beyond tele-visits. Exercise echocardiograms may be particularly helpful in assessing any long lasting cardiac compromise or continued decompensation. And even psychometric testing to screen for PTSD, continued severe anxiety and depression and failure to cope post infection may also be important to assess.

Maybe most perplexing are the long haulers still affected after what seem to be mild or moderate symptoms from the initial infection. Many patients haven’t fully recovered their normal activity level, and remain incapacitated or house bound. Coronavirus may leave patients with a condition called POTS (postural orthostatic tachycardia syndrome), where heart rates can double or triple on standing, blood pressure can drop precipitously, and just about all conditions that are dependent on normal regulation of blood pressure and pulse go out of whack. Dizziness, headaches, shortness of breath, chest pain and “brain fog” (where periods of time without clear thinking occur) cause short term problems and may worsen other body functions. The long effects of this on the heart, the autonomic nervous system, and pulmonary and brain functions are truly unknown. What is the course of COVID induced POTS? We truly don’t know with this limited time experience.

Underwriting is going to be a lot tougher and with a lot more caution in COVID cases and certainly in long haulers where the infection continues to cause symptoms and impairments well into months after infection. Careful examination of medical records and longer periods waiting for in-person visits may be necessary. Testing, whether as routine as for blood, or with scanning and testing cardiac and lung function, may be required. Return to work for a defined period of time without decompensation may need to be demonstrated. And in long haulers, an indefinite period of postponement may be required until we are best able to evaluate the long term effects of this pandemic virus which has caused so much disruption and harm in our lives as a people.

An aortic aneurysm is a dilatation of the aorta which predisposes itself to rupture, hemorrhage and death in short order. The aorta is the largest vessel in the body carrying blood out to the rest of the other organs. There are three layers in the aorta—intima, media and adventitia. A true aneurysm is a dilatation of all three of these layers. When an aortic aneurysm ruptures, there is only a short time frame to emergency surgery to repair it before death ensues.

Aortic aneurysms are usually silent killers in that most (almost all that involve the abdominal part of the aorta and half that involve the upper or thoracic part) are generally asymptomatic. A physical exam may detect a pulsatile mass in the abdomen that corresponds to an aneurysm that hasn’t yet ruptured, but the majority of aneurysms are discovered on more routine imaging. Chest X-rays or ultrasounds are the most common detection methods. Symptoms of a large aneurysm may include low back or mid-abdominal pain or trouble swallowing when the aneurysm compresses the esophagus. Once the aneurysm ruptures, chest pain is sudden and severe along with a sharp drop in blood pressure and throwing up or coughing up blood. Death is common when there is not proximity to a hospital or operating room, and even surgical morality in an acute situation may be as high as 50 percent.

Risk factors for aortic aneurysms are many. Men over age 65, hypertension, smoking and high cholesterol are a few of the major ones. Others include weight lifting, trauma, a bicuspid aortic valve or any other kind of aortic valve disease. Genetic causes including Marfan’s syndrome (a particular offender), Ehlers-Danlos syndrome and Turner’s syndrome are widely recognized. Inflammatory diseases such as ankylosing spondylitis, giant cell arteritis and Takayasu arteritis cause weakness in the aorta through their underlying inflammatory component and screening for an aneurysm may be part of the disease for these conditions work-up per se.

How to treat an aneurysm when discovered in an asymptomatic person has undergone changes in recent years, but is still designed to get to the aneurysm and surgically repair it before it is too late. That said, not every discovered aneurysm is referred immediately for surgery. Things that go into when to make the repair are time since discovery, size of the aneurysm, underlying conditions (like atherosclerosis, hypertension and smoking) and the rate of growth of the lesion. Clinical problems are rare when the aneurysm is 4 cm in size or less. Between 4 and 5 cm, the mortality rate increases but again surgery is not an immediate consequence. Once the aneurysm measures 5.5 cm (this is an increase from the previously accepted 5.0 cm) or the growth is marked in between radiographic evaluations, surgery to accomplish repair is undertaken. As mentioned, this is not an operation with trivial surgical risk, so repair is accomplished in those with larger lesions. The annual rate of rupture is highest in the larger lesions and a rupture may be fatal in up to 80 percent of these cases.

Surgery is usually accomplished as an open repair of the aorta. It must be done in skilled hands as the aorta then certainly is a weakened vessel subject to further problems if not done effectively. As it is a problem in older individuals, a procedure called EVAR (endovascular aortic aneurysm repair) is done in older individuals who are considered high operative risks due to the presence of other complicating diseases or circumstances. It requires indefinite surveillance to monitor for leaks, closing of the vessel or re-expansion even though it is safer for high risk individuals.

Underwriters who assess aortic aneurysm look for various factors in assessing its future morbidity and mortality. The location of the aneurysm is important, as well as the size, cause, treatment, and rate of growth if unoperated. Monitoring control of other contributing conditions is important as well, both in the operated and unoperated individuals. Follow-up is also key— those who do not have adequate medical follow-up with this condition increase their mortality several fold.

Smaller aneurysms may be taken with a small rating as long as follow-up is good. Larger ones have to be followed with care to assess stability, as their rate of growth may pre-dispose them to acute injury and death if a rupture occurs and an operating room is not immediately in reach. There may be a waiting period of six months to a year before insurance is considered after surgery, and the longer time goes by without a recurrence the better. Those with EVAR as treatment are rated more severely as the procedure for repair is not as complication free and there are generally other health problems that were significant enough to have chosen that approach over the more tested open repair.

The Alzheimer’s Association estimates that about one in 10 people over the age of 65 has some degree of Alzheimer’s dementia. I think about that every time I misplace my keys or wonder where my reading glasses are (it helps to have 10 pairs…). There was the old axiom that said if you think you might have it you don’t, but if things are happening to you that you don’t recognize a problem then you just might. Either way recognizing the disease is important and management of it even more so.

In clinical practice differentiating Alzheimer’s from other conditions whose treatment is far different is important. Can early Alzheimer’s be no more than sleep deprivation? Treatable depression? Metabolic disorder? Structural problem in the brain? Even vitamin deficiency? Many of the above conditions can rather easily be reversed with a positive outcome. Would it help to know these conditions in medical underwriting? Just as much. Diagnosing true dementia, particularly early in its course, remains a challenging endeavor.

Diagnosing Alzheimer’s disease, particularly early in the process, is important in that intervention could occur before a patient becomes clinically impaired, and decisions about care and financial and custodial issues can be addressed while a person’s faculties are still intact. But diagnosis of early Alzheimer’s, even when suspected, is still challenging. MRI scanning, touted as a first line of investigation, does not reliably detect Alzheimer’s disease. PET scanning is quite expensive and often does not distinguish Alzheimer’s from mild cognitive impairment of normal aging. And since the medications for Alzheimer’s are not curative and there are no known regimens at present that reverse the findings, one can speculate that having an early diagnosis (besides in advance planning) doesn’t really change much.

All that said, there is substantial interest in blood biomarkers to screen for the disease. An argument that drug development in Alzheimer’s treatment could be improved if the disease is reliably diagnosed earlier is one reason that has been advanced in their favor. The ability of an affected person to plan their life and communicate their wishes before being incapacitated mentally certainly is another. It makes the biomarker question a relevant one.

There are three major biomarkers that have shown promise. Circulating amyloid beta is one. Plasma total tau is a second. And studies with plasma phosphorylated tau 181 and 217 are additional ones. They are in early stage development and large scale studies are still needed to confirm their usefulness, but they are a start.

More than casual questions center on their potential use in insurance if and when they become more commercially available. First, would they be useful to insurers who might incorporate them as part of an age and amount related blood profile? Certainly they would, somewhat to life insurers (as Alzheimer’s does have a relatively longer life expectancy and slower course) but indispensable to disability insurers, long term care product offerings, health insurers and to the availability of many associated riders. Would they ever become just as routine as any of the other blood testing we access, like PSA for instance?

Most prospective insureds understand what insurance blood testing is measuring for and accept the use in order to price a risk and hopefully offer better rates for favorable results. Can the same be said though for an Alzheimer’s blood marker? The first logical question to ask is that if a sensitive test became available to diagnose Alzheimer’s before it became a clinical finding, would you have it run on yourself? Even more concerning, what if an insurer ran the test and then used it in their underwriting? The thought of having a blood test you didn’t want and then having an insurer use an adverse result against you is alarming. Just as concerning is getting a decline for a “confidential” reason and then figuring out by process of elimination what the cause was even though you never wanted to know the result in the first place. You could argue that this already happens with the aforementioned PSA—not all men choose to have it run on themselves (and even the United States Preventative Services Task Force does not recommend the test as part of routine men’s health screening) but insurers run it anyway and can take adverse action on an abnormal result…

We get a lot of blood testing that gives us information on an insured, some that would be considered routine (and a normal part of a doctor’s physical exam) and some that aren’t (like a CDT to screen for alcohol abuse). Genetic testing out of the realm of what normal testing would be and testing that can be considered sensitive information (as in Alzheimer’s) that an insured may choose not to know pushes the limits of what information an insurer should be entitled to. The hope is always that insurance medicine doesn’t kill the goose that lays the golden eggs and that one day even accepted information that we rely on for risk assessment will become unavailable if things get pushed too far.

We’re used to seeing hypercholesterolemia as a known risk factor, but high triglycerides are also associated with an increased risk of cardiovascular disease. High triglyceride levels are additive to risk factors such as diabetes, hypertension, obesity and smoking. Hypertriglyceridemia is also contributory to metabolic syndrome, and it may cause pancreatitis through toxic effects from free fatty acids released by the enzyme pancreatic lipase. So there are significant effects that have to be accounted for in underwriting when elevated levels are encountered.

Hypertriglyceridemia is defined as a fasting serum triglyceride level of 150 mg/dl or more. Levels to 200 mg/dl may be considered normal, but it is important to recognize that triglyceride levels are distinctly affected by fasting. High levels are generally reported as up to 500 mg/dl, and severe is classified as levels over 500 mg/dl. It is important to counsel clients to take their blood draw under fasting conditions. It is also helpful to remove alcohol from the diet prior to blood sampling as well, as it has a deleterious effect on triglyceride levels.

There are five recognized hyperlipoproteinemias recognized by the Fredrickson WHO classification and the American College of Cardiology. The ones that affect triglycerides most are type 2b and type 4. 2b is the commonest one seen in clinical practice and is often associated with a high serum cholesterol as well. Hypertriglyceridemia may result from a genetic or familial predisposition, but is of course affected strongly by diet and lifestyle management.

Lifestyle management is key in managing hypertriglyceridemia. Weight loss, nutritional changes and structured physical activity are the key triad. Reducing carbohydrate intake, and increasing fat or protein intake both lower fasting triglyceride levels. Intake of any fat (saturated or unsaturated) lowers serum triglycerides—an increased intake of unsaturated fats actually increases HDL, the “good” cholesterol fraction. Mediterranean diets have been studied and found to effectively lower triglyceride levels, as do diets designed to lower blood pressure. Exercise on a regular basis has also been found to favorably affect triglyceride levels.

When these measures fail, medications may be prescribed to lower both cholesterol and triglycerides to more favorable levels. Statins are still the mainstay of therapy, and are used in those over age 40 with triglyceride levels of 500 or less and a borderline to intermediate risk of heart disease. Fibrates were more commonly used in years past, but are generally reserved for combination therapy with statins currently. Newer medications including omega free fatty acids (Icosapent, or Vascepa is the newest approved one) may also be added. These of course have to be combined with dietary measures and exercise.

Generally, in considering cases of hypertriglyceridemia, overall cardiovascular risk and the presence or absence of demonstrated cardiovascular disease and/or diabetes is taken into account. Hypercholesterolemia and hypertension are also additive risk factors. While not causing a rating in and of themselves, they can be a multiplier of risk in the presence of other contributing conditions. Cardiovascular disease is the more important of the two.

Hypertriglyceridemia can sometimes be an unpleasant source for a rating when discovered on bloodwork because an insured is generally unaware of it. It can also be a cause of eliminating preferred consideration for an applicant who has already been shown this likely outcome on an illustration. Preferred consideration is generally reserved for levels of triglycerides under 200mg/dl (fasting) or under 400 mg/dl (non-fasting), the absence of cardiovascular risk factors (build, blood pressure, smoking, diabetes) and no diagnosis of metabolic syndrome. This still bears repeating: If there is any question of cholesterol, lipid or triglyceride problems, be sure that the potential insured has his or her blood sample drawn fasting. Preferred categories are tight enough so that even a small difference or elevation in triglyceride levels can have an unfavorable outcome in policy pricing.

Most cases of bronchial asthma are not an underwriting worry. It is a common disease, affecting between five to 10 percent of the population. But asthma is also becoming more concerning than it was ten or twenty years ago. Prevalence, hospitalizations, and fatal asthma cases have all increased, and there were close to 4,000 asthma deaths in the United States last year. Knowing which cases are the most concerning is the key to successful underwriting and case placement.

Asthma specifically consists of airway obstruction (usually acute), airway hyperresponsiveness and airway inflammation. A specific response to an allergen is the most common presentation, but exercise, respiratory tract infections, sinusitis, GERD, stress, and even a change in the weather can precipitate an attack. The commonest allergens on an external basis are usually house dust mites, upholstered furniture and carpets, animal fur and dander and seasonal pollens. Tobacco and smoking of any kind from exposure to products of combustion increase asthma symptoms and are common precipitants of an attack.

Clinical findings can vary widely among patients. Most common is episodic wheezing, chest tightness, difficulty breathing and cough. The attack may come on suddenly or just increase slowly over a period of time. Asthma symptoms are frequently worse at night, and the shortness of breath may initiate an emergency room visit. In older individuals asthma may be mistaken for signs of congestive heart failure, and testing must be done to differentiate the two conditions.

The underwriter first looks at asthma and determines whether the condition is mild, moderate or severe. The National Asthma Education and Prevention Program Expert Panel Report is a good reference for this. Mild asthma is not a daily occurrence, a chest examination is generally clear, inhaled corticosteroids help greatly in control, and there is generally no morbidity or time off of work. Moderate asthma may occur daily, wheezing will be heard on physical examination, asthma medication is generally used on a regular basis, and time off work is minimal. Severe cases will occur throughout the day, hospital admission is not uncommon, wheezing or chest tightness does not readily respond to bronchodilator medication, and there is significant morbidity.

Testing the underwriter may reference involves the evaluation of pulmonary function testing. FEV1, which is the amount of air expelled by the lungs in one second of forced expiration, is generally decreased proportionally to the severity of the attack. Peak expiratory flow is a measurement many patients measure with a flow meter at home to assess when they are getting into trouble with an attack. An FEV1/FVC ratio measures the degree of airway obstruction. Abnormal results and the degree of abnormal findings generally dictate the measures of treatment needed.

Certain rules of thumb help in the evaluation and assessment of the asthma patient when evaluating an insured. How often are the attacks, and what is their severity? What medications are needed to control an attack—generally the use of inhalers is a lot more benign than the use of systemic corticosteroids taken on a regular basis. How often does an individual need to go to the emergency room—the severity of an attack is a predictor of possible adverse mortality in those affected. And also, what other comorbid conditions exist in an asthmatic—obesity is a poor coexisting factor as well as diseases such as diabetes, sleep apnea and chronic smoking.

Asthma may not be ratable at all and considered for preferred classification if the symptoms are infrequent (less than twice/month), they are low intensity, there is no time off work, control is with minimal medication, and the applicant is a non-smoker. When the symptoms are moderate, pulmonary function tests are abnormal, there is use of chronic bronchodilator medication and/or corticosteroids and there are co-morbids, a rating is generally applied. When attacks are frequent, require regular trips to an emergency room setting, or require hospitalization for control, a decline is the more usual outcome.

Particularly difficult situations may be encountered at either end of the age spectrum—in the very young and the elderly. In infants and young children, acute shortness of breath can be quite severe and intervention is more difficult when instructions can’t be followed and the small anatomy of the child is considered. In the elderly, co-morbids often significantly contribute to problems in control and diseases like congestive heart failure have to be considered and co-managed. Those with asthma of long duration may have more severe asthma that is associated with irreversible airway obstruction which leads to a much more difficult prognosis.

Endometriosis is a condition where normal tissue that lines the uterine cavity is found outside the uterus, mainly in the area of the pelvis and the ovaries. It is a common source of pelvic pain in women, and is an increasingly diagnosed entity in workups for infertility. Some more unusual places for endometrial tissue to be found are anywhere in the abdominal cavity, lungs and even reported in the lining of the nose. Thankfully it is normally confined to the pelvic region however.

Endometriosis is a relatively common disorder, occurring in between five percent and 10 percent of all women. The prevalence is four times greater in infertile women. The true cause has not been established, and the course in most women is quite variable. Endometriosis is associated with a higher risk of coronary artery disease, which makes its identification more important in overall health treatment.

Endometriosis is variable both in its presentation and in its course over time. More often than not it is found during a work-up for chronic pelvic pain or for identifying the cause of pain during intercourse. It is also found commonly as an incidental finding in workups for infertility. In those cases, there are no symptoms but aberrant endometrial tissue is found obstructing or altering the normal pathways for ovulation and pregnancy.

Endometriosis has to be differentiated from other female conditions and pathology. They include pelvic inflammatory disease, ovarian cancers, and uterine fibroids. The latter conditions, like endometriosis, cannot be disregarded. For example, uterine fibroids can cause heavy menstrual bleeding, and pain, making it a cause for concern. Many tend to consider fibroid removal without surgery as an option when it comes to abnormal growths in the uterus. As for the endometrial tissue, it can invade the neighboring bowel wall causing blood in the stool. Workups must rule this potentially serious condition out before moving on to the treatment of the primary condition.

Non-invasive imaging is not all that helpful in the diagnosis of endometriosis except if there is a larger tissue mass that can be identified. The diagnostic procedure of choice is a transvaginal ultrasound. Surgery and biopsy is the only way to definitively make the diagnosis. MRIs help in cases where the tissue may be invading on bladder space.

As often endometriosis is a cause for intervention when pregnancy is desired, hormonal manipulation and surgery are generally part of the treatment. Many of the regimes for pain relief involve the use of low dose oral contraceptives, progestins, and GnRH agonists. The courses of treatment are designed to inhibit ovulation over a defined period (six to nine months) and lower hormones, thus hoping that the extra endometrial tissue atrophies and disappears without hormonal stimulation. These treatments unfortunately are not uniformly effective.

Surgical treatment of endometriosis can be more effective in promoting fertility and in decreasing pain. Using a laparoscope, endometrial tissue can be surgically removed or ablated. When this occurs, local blockages can be relieved and successful pregnancies may occur. In very severe cases of pain where pregnancy is not desired, removal of the uterus, ovaries and tubes (hysterectomy and salpingo-oophorectomy) can be a definitive treatment. It is more beneficial in postmenopausal women-in premenopause hormone replacement therapy may lead to a recurrence of symptoms where the endometrial tissue is outside the field of the surgery.

Thankfully most cases of endometriosis have effects on symptoms and morbidity but not mortality. The increased incidence of cardiac disease found on retrospective studies is not significant enough to cause a rating in most cases. When other more serious pathology has been ruled out, preferred ratings are usually the rule.

It is a long way from Bob Dylan’s realistic prophecy of what was happening and what was to come back in 1964 when he wrote the song. No one can disagree with the state of the world protests and the COVID pandemic that the times certainly are a-changin’. This is also the phenomenon happening in underwriting and risk selection, and we have to be prepared to meet the changes to insure a positive outcome no matter our underlying feeling about what those changes are.

While I can’t take my experience in underwriting back to the 60s, I can to the 1980s—where the role of the medical director and underwriters as a whole was taking big progressive steps. The relationship of brokers, agents and insurance underwriters was an interactive one, where give and take helped to build a common ground. Where back and forth for a mutual benefit was not avoided but actually welcomed. The more information on an individual case a doctor and underwriter could gather, the higher the comfort in taking a risk became. Each individual case stood out on its own idiosyncrasies, and every diabetic, rheumatology case, or even mental health issue was judged on an individual basis. Additional information such as lifestyle, social connection and self-care was weighed into an individual situation to make the most positive offer. Producers often were very involved with their clients, and knew so much more under the surface of the application that made for an individual client presentation. Everyone’s handprints could be seen on the application and a collaborative effort was made to do the best for each client.

Medical directors were often involved in more ways than just being a walking textbook for underwriters. They analyzed each case, looking for positives and negatives. They asked questions, even spoke to individual health care providers at times. Most physician medical directors came out of extensive practice situations, so they were able to judge clinical aspects more astutely and read into the nuances of what an Attending Physician Statement said. I could look at my notes from 10 or 15 years previously and know how I felt about a patient’s level of self-care, prognosis, and long term outcome of any particular problem. They were “must reads” for any of us looking for the favorable aspects of approving a case.

Most importantly, the interactions were collaborative. Underwriting manuals give a good idea of combined experience of potential insureds with a combined average of outcomes. Individual underwriting defined a general prediction into an individual assessment. Insurance companies wanted to provide the best offer to as many people as they could, and really only separate the outcomes that would be catastrophic and take them out of the equation. It was not unusual for broker, agent and underwriter/medical director to go back and forth with each other looking for what materials could be added that would provide a more favorable situation for the client. While not waxing poetic for “the good old days,” the situations have changed and we all need to know what to expect in today’s climate.

Much more underwriting is done on a total mortality of insured lives basis. A much larger database is available to companies now to do predictive underwriting. Impaired risk underwriting is being left behind, for more preferred type result cases where a series of algorithms is calculated on personal data and a more predictable set of outcomes. Many companies have impaired retention limits where those who are not in excellent health are basically excluded before the process starts.

Facility of application is becoming the buzzword of application. The relationship oriented business is being left behind for the client-friendly online submission that may take 10 minutes of an individual’s time. Hubs where a client can submit a general application and have it immediately shopped out to ten different companies, particularly for term insurance, are becoming the norm. The playing field shifts from medical underwriting to pricing, and companies who were more client intensive may be left at the starting gate in the eternal search for the lowest price. It is the “Amazonization” of purchasing insurance, and it appears likely to be the new standard going forward.

Medical colleagues of mine to whom underwriting was as much an art as a science are being replaced with physicians (and even non-physicians) who have backgrounds in epidemiology, predictive health and genetics. An insurance policy in the future may be judged as much on zip code of residence, credit history, profession and even facial recognition technology as any medical or social data. Blood samples now can be tested for anything, even genetic tendencies toward any number of possible diseases and testing and analysis that isn’t part of any personal physician’s database. Insureds will sign consents online and truly not know what data they are providing to an insurer and, through the application process, as well to the future database of insurance predictive analysis.

Where this “progress” takes us is unknown at present. Change isn’t always progress, and not all change ends up as a positive outcome. Certain things seem more likely than others based on experience to date. Impaired risk underwriting is dying, or at least being minimized. Price is superseding relationship in the application process. Insureds are being asked to make decisions on product and need more and more based on their own research and without the experience of a professional. Price has risen to the forefront of the application process as well as ease of application. Many Attending Physician Statements are being farmed out to medical personnel in foreign countries to translate and summarize for underwriters without the benefit of understanding of what underlies a doctor’s notes, terminology and expression. The industry runs the risk of people (and legislators) deciding too much personal data is being given and shared and the whole process may be shaved back to using a minimum amount of medical information in order to make an insurance decision.

Once a very relationship oriented business, the immediate future of underwriting and even of insurance in general appears headed to treating the product and the whole application process as a simple commodity, as available online as it is through a professional. It’s clear that the personnel and decision makers of insurers are headed in that direction. It’s being done at the expense of a personal experience and benefit of individuality and the expertise involved with it. It may be that it is the way of the new world. But it may end up, in the words of another 60’s icon, Joni Mitchell: “Don’t it always seem to go, that you don’t know what you’ve got till it’s gone.” Here’s hoping that both the art and the science of underwriting is never lost.

Quite simply, hematuria is defined as the presence of blood in the urine. It can be obvious to the clinician (frank hematuria) or not visible to the naked eye (microscopic hematuria). The large majority of instances in insurance underwriting are picked up incidentally from the submitted urine sample. The critical question then is which cases are significant, which have benign causes, and which need additional investigation before underwriting can continue.

An upper tract source of bleeding (in the kidneys and the ureters) accounts for about 10 percent of cases of hematuria. These can include medical kidney disease (such as glomerulonephritis or medullary sponge kidney), but the most important cause to rule out is urological cancer. Hematuria can basically come from anywhere, from the top of the organ chain (kidneys) to the bladder and the prostate, so an identification of the source is key. Sometimes the cause is obvious and benign (urinary tract infection) and sometimes quite ominous (cancer, kidney failure) so the results on the insurance exam are rightfully taken quite seriously.

Frank blood that can be seen in the urine generally has been worked up by the attending physician. The timing of the hematuria helps the doctor identify the source before tests are ordered. When blood is present at the start of urination but then disappears, the urethra or prostate gland are likely suspects. When blood is mixed in throughout urination, kidneys, bladder or ureter are more likely involved as sources. Symptoms (like pain on urination, back pain, or other constitutional symptoms that are part of more generalized disease) are taken into account as well.

Underwriters treat known and unknown causes differently. Some chronic microscopic hematuria has benign causes, including interstitial cystitis, prostatitis, and urinary tract infection. One common quite benign cause of blood in a urine sample is a woman who is on her menses. If that is suspected, the urine sample is then repeated at a different time. Sometimes “menses” is noted on the lab slip, when it is then the underwriter’s discretion to repeat the sample or consider it benign. A urinary tract infection is generally suspected when numerous white blood cells (infection fighters) and/or bacteria are noted in the sample. Again that is up to underwriter discretion whether to consider the findings “accounted for” or to have the sample repeated after treatment.

Urological cancer is the main “rule out” when known causes (kidney stones, benign hematuria) have been accounted for in a doctor’s work-up. This occurs more often in men than in women, and smoking, exposure to chemical dyes, excessive use of phenacetin and previous treatment with medications for other causes all have to be investigated. CT scans, IVP (intravenous pyelogram), ultrasound, and cystoscopy are used in coming to a diagnosis. Systemic investigation may also be undertaken for diseases like vasculitis, systemic lupus, and congenital diseases such as polycystic disease of the kidneys, which leads to hypertension and eventual renal failure.

Prostate cancer and prostatitis are often causes of hematuria in males. Cystoscopy, biopsy, and examination of cells are important to rule out these causes which are not at the level of the kidney itself but a lower tract cause. Generalized bleeding disorders also have to be ruled out, but the cause is generally more obvious. Hypertension and polyps of the bladder are also causes that are significant.

The most difficult part in underwriting however is the sample that comes back incidentally as positive for blood in the absence of a cause. When found in an insurance exam with no known cause or pending investigation, two repeat urinalyses are generally ordered to rule out transient causes. Two negative samples after a first is positive generally allows underwriting to proceed. The degree of hematuria is important—lesser is treated more favorably than higher amounts of red blood cells found. The presence of either white cells or casts (other degraded kidney cells) helps to implicate a source. Kidney function tests (BUN and creatinine) on the blood sample help to indicate an acute or chronic source of the problem.

Cases may have to be postponed when hematuria is found and no causes have been identified or accounted for. Most chronic conditions can be considered under the umbrella of the underlying condition. Thankfully most cases end up with a benign cause or one that is accounted for in the causative condition, but all cases are considered seriously since cancer is a condition that cannot be missed.

Nonalcoholic steatohepatitis (NASH) is a more aggressive form of liver disease. It is inflammatory in nature, is much quicker in disease progression than the standard type and may result in liver cirrhosis and failure. Both in clinical practice and in underwriting, NASH is under-recognized in its incidence. It actually affects up to five percent of the United States population and its prevalence is on the rise.

NASH often goes along with other diseases such as metabolic syndrome, diabetes, obesity and lipid disorders. It’s generally first suspected with abnormalities in liver function tests. More benign causes, such as fatty liver disease, generally cause only mild signs and symptoms over time and it is the secondary disease that causes more of the morbidity. NASH however may have one in five of those affected go on to develop cirrhosis of the liver, and it is predicted to become the number one indication for liver transplant within the next decade. The mortality rate from NASH far exceeds that from fatty liver disease, and certain subtypes have worse outcomes than others.

Most people who are affected with NASH have no symptoms or the ones that do occur are mild (fatigue or mild abdominal pain). Liver function tests are abnormal in many types of fatty liver disease, so additional testing such as a right upper quadrant ultrasound or CT scan may be needed to differentiate the types. Those whose testing shows more marked fatty liver infiltration will go on to have a more aggressive work-up. Since liver biopsy is the only accepted method to reliably identify NASH from uncomplicated disease, it is often the recommended next step.

Biopsies are not without complications however, and their use is somewhat controversial. Bleeding, pain, infection, bile leak and damage to other organs are not infrequently reported. Additionally, not all pathologists read the slides the same way, and an adequate biopsy sample has to be obtained for it to be of any diagnostic use. There is not a magic bullet yet for NASH treatment either, so obtaining the biopsy as a routine part of the fatty liver work-up is not universally accepted.

There is certain testing however that favors the NASH diagnosis over the milder forms of fatty liver disease. Highly elevated ALT levels lean toward the more inflammatory NASH (although normal levels don’t necessarily rule it out). Cytokeratin 18 is another more specific marker but it is not widely commercially available at present. Noninvasive scoring systems that include patient age, body mass index, glucose levels, liver function test ratios, albumin levels and platelet counts correlate with a NAFLD fibrosis score and a fibrosis 4(FIB-4) score. The higher scores lean more to the need for a liver biopsy to assess how aggressive treatment should become.

Treatments are similar for all subtypes of fatty liver disease, but as mentioned are accelerated once a diagnosis of NASH is made. Lifestyle modification is at the top of the list for therapy, and weight loss is a key component for the majority who are overweight. Sadly, that majority isn’t often able to meet weight loss criteria through diet and exercise, and bariatric surgery may become a recommendation. Bariatric surgery is the most effective weight loss therapy and also improves co-morbid conditions. As it is not an uncomplicated procedure though, it is done when conventional attempts at weight loss fail and co-morbids exist. Studies show the surgery has a very beneficial effect on NASH, with regression and sometimes disappearance of the disease on biopsy.

Pharmacotherapy for NASH is a very promising area for pharmacologic research, but no one so far has come up with a medication that has produced consistent clinical trial results. Randomized trials suggest a diabetes medication (pioglitazone) and Vitamin E have had the most favorable results. A second trial with a different diabetes medication (liraglutide) looks promising but the side effects have precluded its universal use in treatment.

NASH types three and four are insurable but often rated. A liver biopsy is a must for consideration, and has to show mild fibrosis for favorable rating. In those where there is bridging fibrosis or cirrhosis, the ratings are very high or a decline. Concurrent use of alcohol worsens the picture and significantly impairs the overall outcome. 