Robert Goldstone

A difficult and often fatal disease in older adults, idiopathic pulmonary fibrosis (IPF) is one of a spectrum of diseases called interstitial lung disease.  The title accurately describes the process: Idiopathic (cause is unknown), pulmonary (affecting the lungs) and fibrosis (the normally expansive tissue in the lungs becomes hardened and fibrous).  The disease can be localized or generalized, with generalized findings having a particularly poor prognosis.  Usually not found until its later stages, CT scanning (particularly for lung cancer screening) has shown IPF to be more prevalent than previously thought.

IPF is a progressive disease, and generally only affects the lung as opposed to involving other organs as well.  It is characterized by inflammation, thickening, and scarring of lung tissue.  While the idiopathic part of the name infers the exact cause is unknown, there appears to be a process of abnormal and persistent wound repair, resulting in chronic scarring.  Eventually the normal lung tissue is replaced by non-functioning scar tissue and symptoms then become evident.

The most common presentation of idiopathic pulmonary fibrosis is progressive shortness of breath, generally without a cough.  Risk factors appear to be male sex, older age, and a history of smoking.  Many initial cases present to a doctor (particularly in those with a smoking history or past exposure to chemicals or asbestos) for a decreased ability to breathe comfortably or to exert oneself and are treated empirically as chronic obstructive pulmonary disease.  However further testing differentiates IPF.

Breathing tests show distinctive abnormalities, most coinciding with a restrictive lung disease pattern.  Because the fibrosis prevents the lung from expanding optimally, the FEV1 (ability to get as much air out of the lungs in a one second period) is low.  Likewise, the FVC measurement of capacity is also lowered.  Gas exchange testing also shows a decrease in the effectivity of exchanging air.  This results in the symptoms described.

Chest X-rays and CT scanning then help to make the definitive diagnosis.  The chest x-ray will show patches of fibrosis discernable from normal lung tissue.  CT scanning shows a more detailed picture with coarse reticulation and a pattern called honeycombing, with rows of cysts stacked over one another whose appearance worsens as the scanner moves toward the interior of the lungs.  A lung biopsy at that point is quite definitive for the pathologic changes of fibrotic lung tissue and the honeycomb-like picture.

Lab testing is important to rule out other diseases that may mimic IPF, especially as the treatments may be quite different.  Scleroderma, mixed connective tissue disease and Sjogren’s syndrome may show similar lung findings early in the disease.  Rheumatoid arthritis that affects the lungs, chronic active hepatitis, and inflammatory bowel disease may result in similar early findings.  Blood testing, other physical findings (such as in rheumatoid arthritis for example), and eventually the biopsy results will make a more definitive diagnosis of IPF.

Idiopathic pulmonary fibrosis progresses in several ways.  Some cases are rapidly progressive and the prognosis is dire, with death in a few short months to years.  Others have a slower progression, with periods of acute worsening followed by periods of relative stability. Some have a slow enough stepwise progression of symptoms that the affected individual may die of another condition.  Lung function testing becomes the usual way to follow the progression of the disease along with CT scanning when there is an abrupt change in condition.

Most drug therapy is able to slow the progression of IPF or improve symptoms but is not curative.  Two medicines, pirfenidone and nintedanib, slow the growth factor that is continually repairing and replacing normal tissue with fibrotic one.  Steroids were a treatment of choice but are no longer used routinely because of the possibility of immunosuppression out of proportion to their benefit.  Lung transplantation is considered in selected patients.

When small areas of fibrosis on CXR with a question of IPF are found, but the insured is asymptomatic and the condition is stable, coverage can be considered, and the longer the period of time of non-progressive findings then the closer to a standard issue the case becomes.  In cases of confirmed and more generalized idiopathic pulmonary fibrosis cases are usually declined.

Things should certainly be looking up in terms of bronchogenic carcinoma (lung cancer).  The number one cause of preventable disease and death in the United States, less and less people are smoking than ever before.  According to the Center for Disease Control (CDC) 2016 statistics, the percentage of smokers in the period since World War II has dropped from over 43 percent to under 16 percent of U.S. adults.  And newer treatments for lung cancer are being broadcast on television advertisements regularly.  It should certainly mean improved underwriting with this disease by all standards.

Lung cancer however still carries a dire prognosis.  It is the leading cause of death in both men and women, and what had been a predominately male incidence has been shifting rapidly toward a 50-50 proposition.  Cigarette smoking still causes between 85-90 percent of lung cancers, and the debility of second hand smoke incidence has been duly recognized.  Newer drugs are certainly increasing survival in certain kinds of lung cancers, but often that difference is limited to months and is not universal in its beneficial effects among lung cancer sufferers.

Newer studies are helping to identify which individuals are more prone to lung cancer.  Obviously, not everyone who smokes develops the disease, and some types are more virulent than others.  Both length of time smoking and amount (number of pack-years) are contributing factors.  Newer evidence indicates genetic factors play a role in the development of the disease.  Those with exposure to asbestos or certain types of atmospheric pollutants have higher risks of developing cancer.  As mentioned, those who don’t smoke but are exposed to high levels of second-hand smoke are also at risk.

Four main types of cancer account for over 90 percent of the subtypes of bronchogenic carcinoma.  Squamous cell carcinoma (about 20 percent) arise from the bronchial lining and spread locally at first.  They are most often diagnosed with bloody sputum and examination of cytology from bronchial secretions. Adenocarcinoma (up to 40 percent) arises from mucus glands and is most diagnosed as the results of constitutional symptoms and an abnormal chest x-ray.  Large cell carcinoma (a particularly aggressive type) and small cell carcinoma (which begins centrally and first causes obstructive symptoms) make up most of the rest.  Spread occurs first by local extension into the lung and then into local and distant lymph nodes.  Spread via the bloodstream is also common.

Lung cancer is graded by stages—Stage 1 being the earlier stage where the tumor is small and there is no distant invasion.  Stage 4 is the most ominous and indicates the presence of distant metastasis.  Earlier stages are the most amenable to surgical removal but unfortunately, a minority of affected people have localized enough cancer to where removal of the mass or even of the affected lung itself will prove curative.  More often than not systemic disease is present and treatment is initiated with radiotherapy or chemotherapy.  Small cell cancer is the most chemo sensitive type and the use of chemotherapy is usually the first treatment in these cases.    

Newer and more optimistic findings have occurred with newer therapies designed for first line treatment of patients with locally advanced or metastatic non-small cell lung cancer in those who test positive for the PD-L-1 biomarker and do not have EGFR or ALK genetic tumor aberrations.  Known as pembrolizumab (Keytruda) and nivolumab (Opdivo) among others, these medications have been shown to extend survival.  This survival is not always prolonged however and can be measured in months rather than years in many individuals.

Underwriting for lung cancer is still quite difficult in terms of insurability.  Those with even treated Stage 1 disease have a waiting period of years followed by a significant temporary flat extra premium.  Most advanced cases even with positive initial results may have waiting periods of over five years for any type of insurability, again with high added premiums.  Those that have gone a significant period without disease recurrence may qualify for standard insurance assuming the smoking or causative agent has not left their lungs damaged in any other way (chronic obstructive pulmonary disease, or COPD, for example).  Those who continue smoking after diagnosis are generally declined in any event. 

Is it true, as stories suggest, you can die of a broken heart?  Likewise, can you have suffered a broken heart and get a standard life insurance policy?  The answer to both questions is yes.  The entity is known as Takotsubo cardiomyopathy, or as stress cardiomyopathy, and is very real.  

Takotsubo is actually a Japanese word that translates to “octopus trap.” It was used to characterize the syndrome after the heart took on the shape of a Japanese fishing pot during an acute episode.  Broken heart syndrome is triggered by stressful situations, both physical and emotional ones.  Surgery and serious illness are some on the physical scale; death of a loved one, emotional memories, or constant anxiety—even the breakup of a relationship—can be a cause.  You can even suffer it during a usually joyful event—like the shock of a surprise party!  

The syndrome generally begins with acute chest pain.  An EKG in about half the cases shows the typical signs of having an acute heart attack.  All the signs of an acute event occur: Chest pain, shortness of breath, nausea and the patient in an emergency situation is treated with heart attack protocol.  Cardiac enzymes, which acutely rise during an event, are mainly normal to somewhat elevated but not in  proportion to the symptoms.  An angiogram and cardiac catheterization used to find the site of narrowing or affliction of the coronary arteries though comes back negative and indicates an absence of significant cardiac disease.

So how is the diagnosis made?  Stress cardiomyopathy has very distinctive wall motion abnormalities in the heart, particularly in the large left ventricle which is the chamber charged with getting blood out of the heart to the rest of the body. The base of the left ventricle appears normal while the remainder of the chamber has very disordered or even absent movement.  There is ballooning of the mid left ventricle, and that classical “octopus trap” look that accounts for the Takotsubo name.  The main criteria then are a stressful event to cause the symptoms, EKG changes different from the normal tracing, an absence of any cardiac blockage on perfusion or catheterization testing, and a return to normal in a relatively short time.

The etiology of stress cardiomyopathy is still debated and there is no uniform agreement on what the actual mechanism is.  A tightening of the vessels (spasm) that is temporary has been proposed.  A rush of catecholamines for the severe emotional or physical stress is another hypothesis. Dysfunction on a microvascular basis that the angiogram doesn’t identify is yet another thought.  In any case the symptoms and results from the event are quite real.       

How does someone die of Takotsubo if the findings are temporary and seemingly without any significant coronary blockage?  During the event, heart failure is a real concern with the important left ventricle not functioning properly.  Low blood pressure and shock are very real risks.  Cardiac arrhythmias can cause a stoppage of the heart that may not be treatable.  In cardiogenic shock, coronary care and even mechanical support of the heart is a mainstay of treatment.

What happens after the event has been successfully treated and the storm weathered?  Most people go on to live completely normal lives with no cardiac compromise at all.  The heart returns to its normal function without any signs of permanent damage.  The average age for stress cardiomyopathy is 60-75; a high majority of the affected individuals are women.  A broken heart can occur more than once, but the majority of Takotsubo events are singular.

In those that are affected, a reasonable time period must go by without any cardiac complications for favorable consideration. At that time, if heart function is normal and the stressor (whatever it may have been) has been removed, the heart is considered normal in function and a standard issue may be considered as if the event was fully and successfully treated. A broken heart truly can be mended… 

Every year Webster’s dictionary approves new entries of words that have become part of the accepted American dialect and language over time and through regular use.  One of those is destined to be “amazonization,” which can have several meanings.  In part, it refers to the complete disruption of commerce and business by the behemoth company Amazon.  In theory, it is the depersonalization of the consumer experience and process in search of the cheapest and easiest alternative in doing business.  Life insurance is unfortunately one of those entities subject to these forces, whether by Amazon or by other methods insurers are now using to amalgamate the process.

Life insurance was a people business, much more so than other purchases and processes.  Whether for the personal interaction of providing protection for survivors and loved ones, or sitting with down with a client to best assess his or her personal or business needs and proceeding from there, the key word was personal.  The process involved a one-on-one interaction and mutual exchange of ideas to best meet the client’s needs, or an interactive discussion of what a policy really meant and what it was protecting.  How much insurance did a person or business entity need discussed by people who knew the business and took the time to know the client. What was a policy guarantee and was it realistic for goals down the road?  What new riders could help a client get value added that would not have occurred during a purchase over the internet?

The questions are being kicked down the road to an eventuality of doing business without people and without contact.  People cost money and a streamlined process can be cheaper.  Spreadsheets on the internet compare bottom line prices, without a minute’s consideration of understanding the person with whom  they are doing business. The bottom line is basically: Can the process be made “easy” and can it be made cheaper.  And without the annoying event of actually having to meet a person to have it done, or making that necessary interaction as brief as possible.   

It’s not just insurance that is being affected.  All these processes making up an ”amazonization” of business by other companies besides Amazon constitute supposed “progress.”  The cellphone is progress, and now people don’t need to get together and see each other.  Netflix is progress, and now the bother of having an interactive experience at the movies is a dying concept.  Texting is progress, so why have to speak to someone in person when a few lines of text with an emoji will do?  And, ironically, this entire concept has spread to underwriting, where a personal process is evolving into a statistical correlation.

In underwriting, both medical and personal, the idea was to paint a picture of the insured and assess individual risk as accurately and as comprehensively as possible.  It may involve a personal exam by a physician, Attending Physician Statements from doctors who know the client best, and requirements that more often than not helped identify preferred risks and separate an uninsurable one from the pricing pool.  A medical director huddled with the underwriter and a complete picture of medical, financial and social combination was obtained.  There was the opportunity for the broker and agent to have input into the process and to share thoughts that often had favorable risk applications and considerations.  Something that couldn’t be obtained from paper applications alone.

Now, however, biostatistics have entered the field in a big way.  In summary, it’s closest to the law of large numbers.  If there are enough applicants with similar characteristics with the same variables inputted, the outcomes will be close enough to allow similar processing with minimal expense.  This includes the cost of looking at each of the facets of a case, decreasing the number of people who would have to do it, and minimizing the paperwork as well as the individualization of each application.  The number of medical directors helping to underwrite cases is markedly decreasing. The restriction of requirements no longer permits the details painting the picture of a risk.  Oftentimes, with newer products, brokers and agents are being told upfront there will be no appeals or interventions, and that the actions are final no matter what the contributing or extenuating circumstances.  Like ordering from Amazon, the process is neat, contained, and with no loose ends.  Financially, it’s a success.  

It’s a success if you know exactly what you want and have no individual circumstances or requests that add to the mix.  A friend told me his daughter needed dog food and was ordering it online from Amazon where it was two dollars cheaper.  The father asked, “What if you needed the dog food now?  Or had a question about the suitability of the food for your dog?” The in-person store that helped her would no longer be in business.  Ditto with books—wanting to read a book or determining its usefulness requires a look at several in order to pick the best one.  Needing that, the daughter went to the Barnes and Noble next to the pet store, only to find it had gone out of business.  Enough said…

The shrinking of the life insurance process into a cheaper, easier, winner-take-all approach completely bypasses the reason that made the field what it is today.  Perhaps a container of milk is close enough in quality and sustenance that it can be bought anywhere, likely where the price is minimal and convenience is maximal.  Life insurance takes into account so many personal aspects of need that the process is a necessary component.  And likewise, risk assessment is personal enough from an underwriting standpoint to need to know who you are insuring and to answer the questions that the client would not even have thought to ask.  The process of loss which life insurance provides for is so much more than dollars and cents and convenience; one only needs to ask someone in the process for confirmation.

Webster’s defines progress as the process of improving or developing something over a period of time.  Losing the personality and the individuality of a process that was developed with exactly those functions in mind in favor of cheaper and easier mass production does not quite meet that definition.  It does however define “amazonization,” a process that hopefully never overtakes the individual consideration in the purchase of life insurance.

A tumor with a very serious prognosis, mesotheliomas are primary neoplasms that arise from either the pleura surrounding the lung or the peritoneum.  Most mesotheliomas are diffuse and malignant, while a minority (less than 25 percent) are localized and benign in activity. It’s important to recognize these growths as they have serious and rapid progressions when diagnosed in many cases.

Mesotheliomas are usually tumors of men, and are strongly associated with exposure to asbestos. Up to 10 percent of workers with asbestos exposure through work may develop this disease over their lifetime, and almost three-quarters of mesothelioma development can be traced back to exposure to asbestos within factories or industrial settings. Thanks to modern times there are now companies like Air Quest Environmental Inc. and others, that can offer asbestos testing services within different workplaces to decrease the risk of asbestos exposure to employees in such environments.  There is a slow insidious course to cancer development-the period of exposure can range from 20 to over 40 years previous.  Asbestos workers have a significant risk of developing lung cancer, especially when coupled with a smoking history, but there is not a correlation in itself between smoking and mesothelioma.

Generally, the first sign of mesothelioma is shortness of breath.  There is generally about a 2-3-month lag before the symptoms are evaluated and the cause is pinpointed.  Weight loss and chest pain accompany the shortness of breath, and many times the initial screening is for suspected lung cancer. Mesothelioma is not a disease of the young; in fact most cases are diagnosed right around the age of 70.  

A chest x-ray is generally the first test on suspicion, and shows irregular, nodular thickening generally on one side of the chest.  There is often a collection of fluid (pleural effusion) that is outlined.  A CT scan is then done to differentiate benign from malignant disease, and which cases may benefit from early surgery.  Fluid is removed from the effusion space, is usually bloody, and helps to confirm the diagnosis and differentiate it from lung cancer which is actually the more common investigative outcome.  Special stains are done and microscopy is often definitive at this stage.   

If the tumor is found to be benign, extensive surgery is done.  The pleura is stripped and removed and sometimes the entire lung is removed depending on the extent and position of the growth.  Newer trials also combine chemotherapy as part of the treatment in some individuals.  In malignant tumors, the prognosis is more dire and surgery is not considered.  Questions still exist on the best way to treat such cases, whether strong chemotherapeutic agents are used individually or more rarely combined with surgery if the growth is not widespread.  At times the treatment is only symptomatic as there is no cure that can be expected. 

The prognosis of malignant mesothelioma is grim-survival after diagnosis despite the most aggressive treatments is generally between 6 and 18 months.  Five-year survival of such disease in such cases is well under 10 percent.  Certain factors such as the microscopic appearance of the cells and results from plasma chemistries help to define prognosis.  The usual cause of death in these cases is respiratory failure. Invasion of local structures by the tumor can be both painful and cause compression symptoms of other adjacent body organs.

Underwriting mesothelioma is very difficult and generally doesn’t have a favorable outcome.  The disease must be benign to be considered, and a longer waiting period must pass to be sure the tumor does not grow, spread or have aggressive characteristics.  Underlying lung cancer, particularly in ex-smokers, must be ruled out. Declining use of asbestos in construction materials will decrease the  incidence of mesothelioma, but there is still a population at the target age group that is expected to suffer with this disease.

You’d have to be young or have millennials as children (I do) to have heard of the rock band Rage Against the Machine, popular enough to have entered balloting for the Rock and Roll Hall of Fame this year.  Medical underwriting (and underwriting in general) has its own version of “rage against the machine”: Increasingly, computer templates are making binding underwriting decisions through information that is programmed in with final decisions virtually unappealable.  It’s a frustrating situation that is taking the human element out of a very human situation of health and risk assessment.

The equally famous: “Just the facts, ma’am” (Jack Webb, Dragnet) is what is going into final premium determinations for many insurance products.  Low margin term insurance and long term care riders are at the forefront of this.  A decision is made, and the agent or broker is essentially informed in advance there will be no appeals, oral, written or otherwise.  The problems however arise from the information that goes into the machine—or just as likely—what doesn’t go in.  Sometimes it’s an error, sometimes a misjudgment, sometimes an omission, and often a critical piece of information for which  there is simply no category in which it can be  input. Either way, the picture is not a true one and its accuracy is correspondingly limited.

Much underwriting experience data is segregated by disease entity, and of course no two individuals express the same disease equally nor have it with the same severity.  Entering the degree of disease or severity of aggressiveness is often a subjective judgment.  In a connective tissue disease, a determination between mild and moderate, or moderate and severe, can mean a complete difference in underwriting classification.  Sometimes there are objective measurements (in a disease affecting kidneys there are lab measurements that are quite accurate in determining how severe the disease is).  In just as many other cases (sometimes judged only by symptoms) the correlation does not mirror the ultimate morbidity of mortality.  You know how the client looks and functions, the machine does not, and in a difference of opinion it’s obvious who the victor is.

Misclassification is another area where the automated system fails, or likely it is the in-putter that fails the system.  Either way, the result is inaccurate.  Objective signs such as a pathology report of a cancer or direct lab correlation of control of diabetes are clear-cut. In rheumatologic or even neurologic disease, much less so.  A challenge can persist when assessment is not made to the best of actual ability—when an attending physician can step in and make the most accurate call on his or her patient.  In non-appealable cases, that ability is lost.

Dates are key in assessment of rating for individual policies.  There are definite and stringent divisions, particularly in cancer ratings, of what an individual rating will be after a defined waiting period. When dates are even a little off, relative to dates of treatment, the rating can change or even a declination can exist when a policy could otherwise be placed.  Not the machine’s fault in this instance—here the rage is more accurately focused on the hands of the in-putter.

Medication lists are a source of action on the part of the automated program that are certainly left open to interpretation and often modified by doctor prescribing habits for which no allowance can be made by the program.  Particularly in long term care underwriting, certain meds are “rule-outs” for consideration from the beginning.  There are many cases however where a doctor uses an off-label use for a medicine or tries it for a use of its side effects for a patient condition not associated with the disease the program feels is an uninsurable one.  In fact, so many medications nowadays are given not for the conditions for which they were originally developed (antidepressants for nerve pain or sleep or bladder problems, or anticancer medications for GI and rheumatologic disease as an immunosuppressant) that the rule-out doesn’t hold at all.  When a decision is not appealable, all those cases fall by the wayside for the wrong reasons.

One other area the machine fails is in incorporation of other factors necessary for accurate risk assessment that are not included in the equation.  This is displaced rage against the machine, as there is truly no way the automated decision can include factors of which it has no knowledge.  Everything about the individual you know, such as activity, social involvement, activities of daily living, chronicity of disease and how well the individual copes and compensates for it.  These are positives that tip a situation from gray to black and white, but that the program decides on without the benefit or consideration of same.

The trend to newer products that are lower margin, more easily underwritten without the hands-on of an underwriter, lower cost in providing and administering, and more competition friendly (where lower costs are passed on to consumers and spread-sheeted more competitively) make the process one where it works for the healthy (lowest cost), and markedly impaired risk (declined while limiting acquisition and administration costs) but falls short at the shades of gray in between.  The appeal of such cases can’t be lost or the rage against the machine will lead brokers and agents to places where their voices can be heard.

Thyroid testing has become more sophisticated and much easier to interpret as the state of the art has progressed.  Whereas much of the old testing required a reference test in addition in order to correct for different individual body protein status, newer testing is much more sensitive and spot-on as a single reported value.  Each condition has one or two tests that make the best diagnosis as a primary test and tell the best story for diagnosis and treatment.

Hypothyroidism is a low functioning thyroid state.  It affects more than one percent of the general population and a much larger percentage in individuals over 60.  Weakness, fatigue, anemia, electrolyte abnormalities and heart problems are some of the manifestations of a low thyroid.  As the pituitary gland is the most sensitive in detecting a low thyroid and stimulating the thyroid gland appropriately, a serum TSH (thyroid stimulating hormone) is the most sensitive.  An elevated level indicates a low thyroid state.  Rare conditions such as complete pituitary failure can make an individual hypothyroid without a high TSH, but that is quite an unusual occurrence.  

It makes logical sense that just drawing a serum thyroid level can be just as effective—in fact, a free thyroxine level (T4) does exactly that.  Older T4 measurements used to need to be accompanied with a resin uptake test so the level could be corrected for protein binding abnormalities.  Now, Free T4 is done by dialysis which makes the test accurate on its own.  So why is the T4 a somewhat less sensitive test?  The range of thyroid levels is quite a wide one amongst normal individuals.  A level, for example, of total T4 can be from 5-11ng/dl, a normal free T4 from 0.8-1.8ug/dl.  The TSH helps determine what the right level is for an individual.  So, a free T4 of 0.8 for instance with a TSH of two is fine, but one with a TSH of 10 indicates a low thyroid state.  Thus, the TSH is the most sensitive test for hypothyroidism.

Hyperthyroidism is a condition where too much thyroid is produced in the body.  Sweating, weight loss, high heart rate, tremor, and heart disease may occur from this condition.  Intuitively, a high T4 or free T4 level should seem to indicate a high thyroid state and that is the case.  How about when the thyroid level is high normal and the diagnosis is suspected clinically?  In those cases, the pituitary gland has been fed that signal and it attempts to turn off stimulation of the gland.  As such, TSH is suppressed and almost negligible.  Ultrasensitive TSH measurements are quite good in making this diagnosis,  especially when the thyroid levels may still be in the upper normal ranges.

T3 is another thyroid test used on occasion to diagnose both hyper and hypothyroidism.  T3 is the active form of thyroid hormone.  Think of thyroid as a compound with four iodine molecules attached.  When one is cleaved off it activates the compound and becomes T3.  Even done by dialysis method it is a tougher test to interpret, since so many normal and abnormal body states influence it.  A condition called T3 toxicosis can exist where T3 is inappropriately high relative to T4, and a completely suppressed TSH helps makes the diagnosis.  Likewise, an opposite condition called “euthyroid sick” is another condition that is unique—it is when the body is critically ill and T4 (although maybe even normal) is not converted to T3 but the body’s demand for thyroid is lower (almost conserved).  It is usually a problem where treating the primary condition in the body normalizes the thyroid status with no specific therapy needed.

Other thyroid tests that are noteworthy are antibody and immunoglobulin testing.  Antithyroglobulin and antithyroperoxidase antibodies are usually elevated in Hashimoto’s thyroiditis, where the gland is enlarged and normal thyroid cells are replaced by non-functioning cells.  Most cases of Hashimoto’s go on to hypothyroidism and need thyroid replacement.  Antithyroglobulin antibodies and thyroid stimulating immunoglobulin may be elevated in high thyroid states such as Graves’ disease, where the body’s immune system causes unregulated overproduction of thyroid hormone that speeds up the metabolic process in the body continuously and over-taxes the heart.  These cases need more expedient treatment with antithyroid drugs, radioactive iodine or surgery.

Underwriters use thyroid testing to assess the current state of thyroid disease in the body—in hypothyroidism whether adequate replacement of thyroid hormone is being given (and taken by the applicant), or if overproduction is being adequately treated so no marked and long-lasting cardiac complications develop.  Most internists and general practitioners can handle uncomplicated thyroid disease, but endocrinologists are generally involved when more definitive and urgent treatments are required.  In either case, adequate treatment of disease generally does not result in anything but a standard or preferred policy unless permanent damage to other body organs (most commonly the heart) has occurred.

Getting insurance for individuals with cancer has its challenges.  What was the cancer, how was it treated, how long has it been since therapy, what has the follow-up treatment been?  The keyword in these scenarios is treatment.  What if there has been no treatment at all?   Prostate cancer is one of those processes where both doctors and patients may opt to defer treatment because of the slow-growing nature of the disease, but the unknown outcome makes getting insurance even more problematic. Sadly, a lot of prostate cancer cases are spotted very late because so many people don’t really know or understand their prostate. Those who regularly engage in prostate milking might be more likely to spot the early signs of cancer. You can learn more about this here.

Anyway, the terms “watchful waiting” and “active surveillance” are often used interchangeably, but in fact are somewhat different.  Watchful waiting generally refers to cases where treatment of the disease might result in a series of life-threatening complications that an individual might succumb to or where the treatment of the disease might not confer any added mortality benefit given the person’s overall health (or lack of it).  Active surveillance is the choice to carefully monitor disease status with testing with the understanding that a definitive treatment may be undertaken if the disease advances.  This generally is an understanding between doctor and patient where the natural tendency to advance to treatment is tempered by the morbidities that treatment might bring, especially if the disease may not advance at all or can be treated later on without mortality consequences.

Prostate cancer is perhaps the most controversial of the waiting/surveillance scenarios, since there isn’t universal agreement on its use nor on the exact set of circumstances when it is employed.  In fact, even the simple act of screening for prostate cancer is quite controversial.  Whereas many doctors include it in their cancer screening tests and the insurance industry requires it in the examination bloodwork, The U.S. Preventative Task Force (USPSTF) actually (and bluntly) recommends against prostate specific antigen (PSA blood testing) screening for prostate cancer.  The reasons behind it are enough for a separate article in and of itself, but the Task Force concluded that the benefits of PSA screening do not outweigh the harms.

What are these “harms”?  The Task Force stated that the primary goal of prostate cancer screening is to reduce deaths due to prostate cancer and increase length of life.  It stated that the risk of overdiagnosis of prostate cancer was significant.  That prostate biopsies cause “a moderate or major problem” in terms of complications in many men.  That treatment such as surgery, radiation, and hormone therapy cause a set of symptoms that are unacceptable to men, especially if their prostate cancer is early stage and there is a likelihood that they would have eventually died of another unrelated cause.  Prostate surgery or radiation may result in impotence, incontinence, erectile dysfunction, gynecomastia, and other local complications.  All are fair points, excepting the outcome of death from prostate cancer is significant and the American Cancer Society estimates one in 39 males overall will die from the disease.  

All that said, underwriting comes across cases where active surveillance has been the chosen path.  Are all cases of untreated prostate cancer declined?  If not, which cases are the most amenable to a life insurance offer?  What is the underwriter looking for in such cases?  And which characteristics are the most favorable ones to obtaining an offer?

The American Society of Clinical Oncology (ASCO) has a detailed recommendation for the use of active surveillance.  But it is more limited to pathology.  Let’s go through the things a doctor (and secondarily an underwriter) looks at one point at a time:

• Localized prostate cancer.  The recommendation pertains to cancer located entirely within the prostate gland (no spread or outside invasion) and a Gleason score of six or less.  (Gleason score is based on aggressiveness of the pathology of the tumor).  Some Gleason scores of seven (they range from 2-10) may be included, but their risk is greater.
• PSA levels.  Higher PSA levels generally indicate a higher suspicion the disease is a more aggressive cancer.
• Age.  In older males (such as age 70 or older), the odds increase that a man will “outlive” his prostate cancer, meaning the progression is slow enough that death will occur from an unrelated cause or illness.  In males under 60, that likelihood decreases.
• Stage.  Cancers should be stage 1 or stage 2a.  Rarely 2b is considered.  
• Stable testing.  PSA levels that are serially drawn should not be elevating.  When prostate biopsies are done, they show no advancement of disease (the ASCO suggests serial biopsies).
• Regular follow-up, digital rectal examinations, and continuous assessment.

When all is said and done, there is not universal agreement on which cases can be taken and at what rates by insurers.  The best cases are older males who have stable PSAs, a favorable biopsy result, and overall good health.  Those cases with several years of stability may be taken standard in certain cases.  The most difficult to insure are the men who have higher Gleason scores, are younger, and with higher PSAs.  Insurers will likely postpone or outright decline these cases, as the risks are too high to assume.  

The universal agreement in watchful waiting/surveillance is the need for frequent and comprehensive follow-up.  Regularly scheduled exams, blood work, and biopsies if indicated are what make this method work, whether clinically or from an underwriting perspective.   

Liver diseases can range from mild fatty liver disease to complete decompensation and loss of liver function,  Some are acquired by virus, some due to diet and alcohol use, some secondary from other body illnesses, and some are primary arising directly in the liver and bile ducts.  Two such primary diseases of a very serious nature are primary sclerosing cholangitis and primary biliary cirrhosis.

Primary sclerosing cholangitis (PSC) is a somewhat uncommon disease that is characterized by a diffuse inflammation of the bile tract in the liver, leading to fibrosis, hardening and strictures of those tracts.  It is more common in men than in women, mostly from the ages of 20 to 50.  The disease can be associated with ulcerative colitis (a much more common gastrointestinal disease) and, in fact, nearly two thirds of people with PSC have ulcerative colitis.  It is somewhat genetic in origin, as PSC is associated with several genetic loci that are identifiable.  It also occurs after biliary surgery in some cases.

Most PSC patients have obstructive jaundice, which is progressive.  Before symptoms, an elevated blood alkaline phosphatase of several times normal may be the first indication of disease. Late in the course, osteoporosis, malabsorption, and bleeding veins in the esophagus are ominous signs.  The diagnosis is made by a procedure called magnetic resonance cholangiography, which is like an MRI of the bile ducts and structures.  When smaller rather than larger bile ducts are involved, the life expectancy is longer.  Treatments may include antibiotics when infection coexists, stents to bypass the closing ducts, and liver transplant when the disease has a more relentless course.  Survival from the time of diagnosis averages about 15 years, but can be much shorter when a cancer called cholangiocarcinoma (occurring in as many as 20 percent of cases) is diagnosed.

Primary biliary cirrhosis (PBC) is a chronic disease of the liver where there is autoimmune destruction of liver bile ducts.  It is slow in onset and mainly affects females ages 40 to 60.  Like PSC, the first finding is an increase in blood alkaline phosphatase and, also like PSC, it is associated genetically with certain definable loci.  Many times PBC is associated with other autoimmune diseases such as Sjogren syndrome, thyroid disease and Raynaud’s.

An enlarged liver is the first finding, followed by skin lesions, jaundice, and in late stages cognitive dysfunction.  Blood tests may diagnose the disease, but a liver biopsy allows quantifying how far the disease has progressed.  Survival in PBC generally averages between seven to 10 years, but a medication called ursodeoxycholic acid helps those who are younger live longer.  Liver transplantation is again a necessary therapy, but disease may recur in the transplanted liver as well.

Both primary sclerosing cholangitis and primary biliary cirrhosis are progressive and often unremitting diseases.  If the diagnosis is a proven one, generally even earlier stage patients are not eligible for life insurance coverage.  Those with a successful liver transplant and a healthy course without disease progression for years afterwards are eligible for individual consideration, but no known medical therapies at this time have been able to cure these diseases.

Generally we think of lymphoma as a blood cancer (like Hodgkins and non-Hodgkins disease)—diagnosable diseases from blood testing and lymph node involvement.  Occasionally, the lymphomas may arise from primary skin disease.  Such is the case with mycosis fungoides, which is more ominous than its name suggests.  Mycosis fungoides in not a fungal disease as it sounds but a Cutaneous (skin) T cell lymphoma that actually begins on the skin.

 Mycosis fungoides (MF) may involve the skin for years or even decades without a diagnosis being made.  It begins as a local (or less commonly generalized) red patch or plaque that is usually identifiable on the trunk.  The only presenting complaint to someone affected with it is most commonly itching.  Early skin biopsies may not identify the disease until it is more advanced, and that can be up to 10 years after its appearance.  Tumors appear in more advanced cases, and lymph node swelling also occurs in more progressive disease.  Sometimes the lymph node swelling is benign and is from local pressure from the lesion on nearby nodes, but sometimes MF extends directly into the nodes by itself.

 Skin biopsy is the usual means of diagnosis.  Often a non-healing lesion is biopsied by the dermatologist, who has no idea that MF will be the diagnosis on pathology.  The findings don’t spread to the bloodstream until more advanced disease occurs—the circulating T cells are called Sezary cells and are detectable in blood samples.

 Mycosis fungoides is a difficult differential diagnosis for doctors, who may actually treat lesions with other causes in mind before a biopsy shows the definitive characteristics of the disease under the microscope.  Psoriasis is one commonly confused disease.  So are drug eruptions, eczema, and even ringworm.  The only way to diagnose it is through an adequate biopsy of the lesion or lesions.

 Treatment of mycosis fungoides is not only difficult but complex.  Some cases are slowly progressive and in older individuals will not affect mortality.  Early and even aggressive treatment doesn’t appear to prevent progressive disease.  Corticosteroids are applied to the skin early, with medications such as mechlorethamine, bexarotene and ultraviolet phototherapy.  As the disease becomes more relentless, PUVA therapy, interferon, interleukin, and even total skin electron beam treatments are used.  Chemotherapy (like in more systemic lymphomas) is given if the disease does not respond to more local therapies or is quickly progressive.

 Mycosis fungoides does take time to develop into a malignant and fatal disease, and not every case does.  Those who have just patch or plaque involvement do better than those whose lymph nodes are involved early.  Those with limited plaque disease do the best, and many times their eventual survival is not compromised.  The disease is treated in these slower progressive stages because overly aggressive treatment early in disease doesn’t always influence prognosis and complications and premature death may actually befall the individual before the end stages of MF does.

 Mycosis fungoides used to be a universally uninsurable disease, but that has changed somewhat.  Those who have what is called mycosis fungoides stage 1A (where less than 10 percent of the skin is involved) and in whom there is stable remission for at least three to five years are insurable at a low substandard range.  Cases are reconsidered if the original diagnosis was in error, and indeed one of the more benign causes is identified on a repeat biopsy.  Again the small lesion/plaque form of limited extension is prognostically the best variety.