Note: This story is based on facts and is true. However, the patients in this story are hypothetical, created from inferences drawn from published reports.
In the sweltering heat of the summer of 1983, a medical student or dermatology resident working in the Calcutta School of Tropical Medicine and Hygiene, Department of Dermatology would have the great privilege of caring for many, many patients. The dermatology outpatient clinic sees over 100,000 patients a year. The rashes seen in this clinic often represent the dermatologic manifestations of severe infectious diseases such as sexually transmitted infections, leprosy, and tuberculosis are handled there. Add to that the myriad of patients with scabies and fungal infections such as ringworm, as well as all manner of eczematous dermatitis and one can see that the list of potential diagnosis of complaint of “rash” can become quite long.
When you are a student learning dermatology or any specialty, your main job is to obtain a thorough history, perform a detailed physical examination, and create a list of potential diagnosis for each patient. This all-important list is referred to as the differential diagnosis. Diseases on this list will have any number of overlapping features and may require further investigation. Tasks such as drawing blood for testing for syphilis, obtaining a skin scraping and examining it under the microscope, performing a biopsy, etc. are often needed to achieve a definitive or final diagnosis. However, it also might require the skills of a more highly trained and experienced attending physician. This is the story of one such very skilled physician, how his keen mind discovered an epidemic of poisoning, and how our minds work for and against us.
In the clinic, once the resident or student has seen the patient, they “present” the patient’s clinical history and physical examination to the supervising attending physician. Generally, the medical student will see the patient first and develop a list of possible causes for the patients presenting problem, called the “chief complaint.” A resident in dermatology will then review the case with the student and repeat the process. The resident re-examines the patients, reviews and clarifies elements of the history, and endeavors to focus on the more salient aspects of the case. The resident and the student then put their plan together and present the case to the attending physician, their supervisor, who is ultimately responsible for considering the differential diagnosis and laying out the next steps to achieving a definitive diagnosis, whenever possible.
In the beginning of training, this process is a daunting task for the student and the resident. Generating this list is a challenge because each case seems like it could have a myriad of causes. Over time, the patterns begin to emerge – even for the novice trainee. Soon, the list begins to repeat itself and although the repetition makes the task easier, the mind starts to create cognitive shortcuts that can result in bias. Research has shown that a variety of these cognitive bias are the outcome of the functional characteristics of the information processing of the human brain. They are insidious and take many forms. A physician might gather enough evidence to seem to support one diagnosis (search satisfaction) and decide, incorrectly, that the patient has a condition that fits that diagnosis (premature closure). That decision might be based on an unconscious stereotyping (attribution error) of a patient and the possible diseases or conditions. These biases can be very powerful and resistant to correction. The fact that, well into the 1950s, the leading journals of dermatology had titles like American Medical Association (AMA) Archives of Dermatology and Syphilology and Indian Journal of Dermatology and Venereology demonstrates how common it was to have difficult to diagnose and treat rashes caused by sexually transmitted infections like syphilis. Thus, a resident or student in the clinic might enter each exam room with the preconceived notion that the rash is a form of a sexually transmitted disease. However, even though syphilis is on the differential diagnosis of every single patient that walks into the outpatient dermatology clinic, the treating physician needs to be aware of and reflect on other causes each and every time.
Thus, it was in the heat of July 1983, amongst hundreds of patients in the Calcutta School of Tropical Medicine and Hygiene Department of Dermatology that a newly married young man arrived with his wife seeking help for the following chief complaint, “my skin is getting darker.” He otherwise felt well and had recently married. His worried wife was there with him, but she could not provide any further insights. The patient’s skin had simply started to become darker since they had been married. The darkening manifested itself as large and small patches and spots all over his body. As is the custom, it is typically the medical student who first sees the patient.
For a medical student, this would be a puzzling case. How does one’s skin suddenly get darker? The pigment of the skin is determined by the amount of melanin pigment in the skin cells. The simplest explanation was that since melanin is affected by simple things like sun exposure, the patient had an unrealized sun exposure. After all, it was summer. However, the darkening was also present in areas that had no sun exposure, and so sun exposure was crossed off the differential. Melanin is also affected by hormones. Perhaps the patient had Addison’s disease? Addison’s disease is a condition caused by insufficiency of the adrenal glands. The adrenal glands produce the stress hormone cortisol, which helps modulate much of our normal functioning such as fighting infections, regulating the heart and blood pressure, and the ability of the kidneys to maintain proper hydration and electrolyte function. Patients with Addison’s Disease will have fatigue, low blood pressure, low blood sugar, depression, craving for salty foods, and intolerance of cold and heat. In other words, they can appear like every other patient who comes to the clinic feeling ill – save for one manifestation – their skin begins to darken. The hormones released by the brain to try to jump start the adrenals also jump start skin cells to produce melanin – the pigment that darkens the skin. President John F Kennedy suffered from Addison’s Disease and, despite his suffering, it is thought that the skin darkening which gave him the perpetual appearance of being tanned helped his political career. Having developed some possible diagnosis, the student would now have to review these diagnoses with the resident – confident that it was not sun exposure but concerned that it might be Addison’s disease.
The first thing the resident who reviewed the case with the student would do is dismiss the possibility of Addison’s disease. Partly because that is what residents do – they convince medical students that rare diseases rarely happen. The old medical axiom that “common things occur commonly” rules the resident’s world. For them, diagnosing the common things comes easily and is job one. A resident with aptitude, good training, and a little effort can handle most diagnoses and, by adding a little precautionary testing, pickup the occasional unusual case. However, “common things occur commonly” also can be a cognitive trap – easy to fall into and hard to escape.
The resident would conclude that, in this case, Addison’s disease could be pushed to the bottom of the differential diagnosis list because of the patient’s general good health. Upon examination, the skin did not seem to be that dark and had to be compared to the patient’s wife to even appreciate the difference. It seemed to hardly be a concerning rash except for the fact that the darkening of the skin was also seen on the patient’s palms and soles – an area usually spared from general dermatologic diseases except for one common culprit – syphilis. In this newly married young man with a concerned wife, syphilis had to be the major concern.
On this day in 1983, presenting the attending with only one diagnosis on the differential would not be good enough, for today’s attending physician was Chair of the Department of Dermatology. A good resident trying to impress the attending learns to consider at least four causes for a patient’s illness – one serious, one probable, one interesting, and one treatable. One serious demonstrates that the resident is aware of the worst possibilities, one probable indicates the resident has a grasp on what typically causes these symptoms, one interesting gives the attending something to wax eloquent about, and one treatable keeps everyone feeling like something can be done. The abbreviation S.P.I.T. reminds them to include these four types of condition in the differential. Always “SPIT” the differential out on teaching rounds. So, what about this patient with darkening skin? Well they could have Addison’s disease (serious) or syphilis (probable). Leprosy was a common problem but often resulted in patches of skin that felt numb and were lighter in color – not darker. The resident added xeroderma pigmentosum (interesting), or phytophotodermatitis (treatable). Xeroderma pigmentosum is a condition where the patient lacks the ability to repair sun damage and sustains a severe sunburn after only a few minutes in the sun, with freckling, dry skin and changes in skin pigmentation. However, the medical student was correct – the darkening was occurring in areas without sun exposure. Phytophotodermatitis is a condition where exposure to certain compounds in plants sensitive the skin to sunlight, resulting in spotty skin burns resembling a suntan. Cutting or handling citrus fruits such as lime or lemon, as well as exposure to weeds such as wild carrot often used as home remedies are the typical cause. These changes can definitely occur on the hands – but generally not the palms. With a good differential in hand, and a plan to break the bad news to the newlyweds that they needed to be at least tested, if not treated for, syphilis, the resident and student would discuss the case with their attending physician – Professor K.C. Saha.
Professor Kshitish Chandra Saha, popularly known as KC, was beloved by his residents and trainees. He had a brilliant mind and a delightful disposition. Born on New Year’s Day in 1930 in Mirpur, Dhaka in Bangladesh, Dr Saha excelled in medical school and received the highest marks in his class in Medicine and Pathology. He went on further to receive a Diploma in Tropical Medicine and Hygiene. In 1957, he joined the West Bengal Health Services and devoted himself completely to his trainees and his patients. Brilliant physicians, like KC Saha, excel at the particular skill of creating and refining a differential diagnosis. Osler once said that there are no boring patients, only boring doctors. Dr. Saha never met a boring patient – each patient was a chance to teach his residents and students about the art and science of medicine. He would pleasantly probe the trainees’ knowledge-base with questions. Never mind what you think it is – tell me what it could be? What have you missed? What other piece of information have you overlooked that might transform this simple rash into something of concern? For Dr. Saha, the common things which occurred commonly were only the start.
Dr. Saha’s research and interest in the field of dermatology, at that time, was in two main areas – dermatoglyphics and dermatological manifestations of nutritional deficiencies. Dermatoglyphics was a scientific form of palm reading. Certain diseases, especially congenital ones, have very identifiable patterns of skin folds in the palm. Patients with Down’s syndrome will have a single crease that is present across the entire palm. Appreciating these patterns, especially in pediatric patients, could guide their care early in life. The latter interest involved understanding how deficiencies in elements like zinc and phosphorus could lead to diseases with dermatologic manifestations. As a busy clinician who saw many patients, Dr. Saha was well versed in the variety and frequency of dermatologic diseases that affected his patients in this region of India. This made him aware that, by sheer statistical probability, a patient at the outpatient dermatology clinic with skin problems had a 1out of 3 chance of having an infection as a cause. These infections ranged from syphilis, leprosy, to an endless variety of viral and fungal infections.
When Dr. Saha entered the room and introduced himself to the patient and his new wife, the patient was sitting with his arms folded and hands tucked under his elbows. A habit the patient had developed to hide the lesions from view. After the usual pleasantries, Dr. Saha asked the patient to show him the rash. The patient unfolded his arms and extended his hands outward and displayed his palms.
Prof KC. Saha was silent as his practiced eye was immediately drawn to the peculiarity of the pattern of this rash. His mind was so preoccupied with processing the visual information he was gathering that he was unaware of the eyes in the room fixed upon his face. Everyone was looking at Dr. Saha, but Dr. Saha was engrossed in this patient’s palms. The skin on the palms showed a number of dark patches that were rough and thick. The thickening of the skin was not uniform, like one would expect from the calloused hands of hard work. Rather, it was an amalgamation of many patches of thickening. A few areas remained relatively normal. In addition, the thickened patches of skin were darkened relative to the normal skin. Dr. Saha looked up over his glasses at his resident and said without smiling “Did you examine the soles of his feet?” The resident had not – a major blunder on his part. Rashes that fell into patterns which involved both the palms and the soles were of a unique variety. Syphilis being the most likely infectious cause. Dr. Saha kneeled down and had the patient remove his sandals. The pattern of the rash was identical on the soles.
Dr. Saha became suddenly and demonstrably animated. His questions came rapidly and with some urgency. Have you had this all your life? Even a milder form? Where did it start? What did it look like when it started there? Did you feel ill at the beginning of the rash? Do you have stomach pains? Diarrhea? When were you married? Where do you live? What do you do for work? Does anyone else have this rash? Do you use any home remedies? Drink alcohol? Smoke? The patient became visibly anxious. Dr. Saha then turned to the wife – Where are you from? Where did you live before you were married? Where does your family live? Are there rats in the house? Do you have a garden? Do you eat the same food he does? Drink the same water? Are you happily married? The couple, now visibly distressed, gave their answers but with some bewilderment. Dr. Saha paused, looking briefly at the patient’s wife, smiled weakly, and said “We will be right back…” and left the room, resident and student in tow.
At the desk in his office, Prof KC Saha sat down with his trainees. He paused. First, he turned his attention to the student, complimenting the differential diagnosis with a smile. Then he gave a raised eyebrow to his resident and a reminder that for a dermatologist, not examining the entire skin is like never examining the patient. The student and the resident both braced for what came next, expecting directions to treat the patient for syphilis now that the lesion was seen so obviously on the palms and soles and a parting lecture on thoroughness. Instead, Dr. Saha asked an unusual question, “Have you ever heard of the phrase, “raindrops on a dusty road?” The student and resident’s eyes widened – they had heard of that particular rash and knew it’s worrisome cause but had never seen a case. When rain falls on a dry dusty road, each drop hits the ground and makes a dark wet crater with a mound of light-colored dust around it. This is the phrase that is used to describe a particular type of rash associated with one condition only – poisoning by arsenic!
Dr. Saha’s urgent questioning of the patient’s wife now made sense. Arsenic poisoning was a fairly rare event, and usually associated with either being a target of homicide or exposure at the workplace. The patient’s occupation excluded exposure to typical arsenical chemicals such as pesticides, herbicides, and insecticides. The occasional mouse was seen in the home, but they had not used an arsenic containing poison. The wife and the patient both consumed the same food and water and lived in a village just east of Calcutta (now called Kolkata). They had been only recently married. Neither of them had previous illnesses. The patient had never had rashes as a child and felt fine until the rash began a few months ago. Since then he had occasional upset stomach and diarrhea. Neither had any rashes on the genitals or problems with their genitourinary system. The husband smoked a little and drank alcohol socially, but not the wife.
Dr. Saha returned to the room to discuss his plan. He wanted to test and treat them both for syphilis as a precaution, although he was highly doubtful that this was the cause. He wanted them to keep a careful diary of what they ate and drank. He told them he was concerned about a nutritional deficiency or some contaminant in their food or water, without saying that it was arsenic poisoning. That diagnosis would require confirmatory testing that was expensive and difficult to obtain. He reviewed his recommendations for good nutrition. He wanted them to keep a careful eye out for the use of chemicals around the home or work. The husband agreed to be tested but refused treatment for syphilis, stating emphatically that he and his wife were monogamous. Dr. Saha conceded on the need for treatment but insisted that they both be tested and return in 2 weeks’ time to review the results. They agreed. Dr. Saha eyed the wife for her reaction, she seemed bewildered. He took note of it.
At home later that evening, KC relaxed and wondered about the potential arsenical keratosis patient he had seen. He relaxed by sitting down with some Hindi lyrics he was writing for a musician. KC was an accomplished musician, composer, and an approved lyricist for Akashvani – the Indian governments All India Radio. His mind wandered and he wondered – how would he manage the workup of the patient? Testing would be fairly expensive and might lead to a dead end. He could get a urine specimen tested for heavy metals, but this could lead to false positives that would cloud the diagnosis. Arsenic attaches itself to sugar molecules and, in this particular state, is harmless. Patients who eat fish will have arsenic detected on a screening test of their urine, but it is of no consequence. He would need to send samples to a more sophisticated lab than the hospital. He worried. Perhaps he let a murderer escape the clinic! Was the wife poisoning the husband? Maybe she was not happy to be in the marriage? He would wait for their return, hoping that some clue would arise in the meantime.
Two weeks later, as Dr. Saha walked through the waiting room to start his day, he saw the patient and his wife. They had indeed come back and this time had brought another patient along with them – a neighbor from the same village. Dr. Saha greeted this trio in the waiting room and hastily signaled to the clerk to pull the patient and their neighbor back to the exam room.
The story unfolded. Things had worsened dramatically. The husband’s rash had spread. He now had a similar rash on his torso, in patches. The wife had the rash as well, just beginning on the palms and soles. Furthermore, they had brought a neighbor who was developing the same rash. Dr. Saha examined the husband’s hands and noticed a faint white horizontal line forming at the base of the fingernail. A line of this sort was first identified by physicians nearly 80 years ago and described in detail by a Dutch physician named R.A. Mees. These lines were clear evidence of poisoning by some heavy metal – arsenic, thallium, or selenium. Given the pattern of rash on the palms and soles it all but confirmed arsenic as the source. Dr. Saha was confused. Why did the wife’s rash suddenly start now – was she poisoning herself to cover up her homicidal work? Dr. Saha did what the best physicians do best – he went silent and listened to the patient. As this group began to urgently share their concerns and random bits of information about themselves, a story emerged. The wife only moved to this West Bengal region after she was married, and so she had not been in the home for very long when the husband first developed the rash. Now that she too had the rash of arsenic poisoning, and a neighbor with the same rash, Dr. Saha’s concern shifted from suspicion of murder to arsenic toxicity from some common source, as yet unknown.
Dr. Saha’s demeanor relaxed a bit, and he sat down in a chair in the room and began to talk to his patients, explaining that he was concerned that they were being exposed to arsenic in some way. He gave the usual list of sources, but again everyone in the room denied any exposure to them. He reviewed the diary that the patient had kept. Things were silent for a while as he read through the details of food and meals, locations of establishments where they ate, and travel. Then finally, the neighbor spoke up – could this be caused by the new well for the village? Dr. Saha’s eyes widened, “What new well?”
In the 1980’s in the West Bengal region of India, in the area surrounding Kolkata, access to clean drinking water was the major determinant of health, especially in children. Deep wells that did not contain the harmful viruses and bacteria that caused cholera, hepatitis, dysentery, and the like were rare and only located at great distance. Walking a few miles every day to get water was part of daily life. Hand dug wells, although often closer and more convenient, were especially contaminated by these same organisms. Sanitation in small villages often consisted of pit latrines that further contaminated the water source. Even areas that had piped treated water and sanitation were at risk for waterborne illnesses. In the 1970’s, UNICEF launched a major campaign to improve the health in this region in India and in Bangladesh to the east. They financed the drilling of numerous wells called “shallow tube wells”. These wells were drilled further than a hand dug well could be, but not so far down as a deep well. As a result, they bypassed the contamination of the surface wells. They were much less expensive to construct because they took advantage of innovations in plastic piping “tubes” of that era. It seemed like a perfect solution. Testing by the British Geologic Survey reported the water to be safe for human consumption. Fewer children were dying from infectious diarrheal illnesses as result of this effort. The water problem seemed to be solved. In a very short period of time, UNICEF, WHO, governments, non-governmental organizations, and individuals and families began the ambitious task of drilling tube wells throughout the region. There was only one problem, the British Geologic Survey and other testing authorities did not include a test for arsenic in their testing panel. “You don’t find, what you don’t think to look for” goes the old saying on how our thinking can yet again lead us astray.
Arsenic often exists tightly bound to other particles or compounds. Seafood contains a good deal of arsenic, but it is bound to other compounds such as arsenical sugars and thus ingestion does not result in arsenic poisoning (although a urine arsenic test might be falsely positive). In India and the surrounding areas in south east and west Asia, particles of iron oxide bound to arsenic flow from the mountains to the rivers and surface waters. When the water sits on the surface in marshes and swamps, the bacteria break down the compound and free the arsenic into the underground water in a form that can be absorbed by the body. This arsenic gets into the aquifer and settles in the exact strata from which a tube well draws. Deep wells bypass this layer. Rice fields irrigated by tube well water will lead to high concentrations of arsenic in the rice, further increasing the arsenic exposure. When these wells were being dug, no one appreciated the complex interplay between inorganic arsenic compounds from the Himalayas and surface bacteria – hence arsenic was excluded from the water testing panel.
At the end of his session with his patients, Professor KC Saha had grim news for his patients. They should not drink the water from the tube well. Sadly, that prescription was difficult to follow. The deep well was impossibly far away. The patients negotiated – what if we drank less of the tube well water? What if we only bathed with it or cooked with it? These were good questions, but Dr. Saha first needed to know the concentration of arsenic in this water to even begin to answer. The patients were relieved that they did not have syphilis and left thanking Dr. Saha for his help. He smiled cheerfully and accepted their thanks – but knew that this situation was very serious. He asked them to spread the word about the well water and ask if others had the same rash.
Dr. Saha left the exam room, now realizing that he needed some serious assistance from the Health Department. If he was correct, a large number of patients could be poisoned from arsenic from the tube well in this village. Furthermore, it became important to spread the word to his dermatology colleagues to consider tube well water as a source for patients presenting with a rash consistent with arsenical melanokeratosis – the medical term for this particular rash.
As the word spread, Dr. Saha’s colleagues reviewed cases initially attributed to other causes and reconsidered the diagnosis. Over the summer, Dr. Saha catalogued the villages where patients with arsenic poisoning lived. He contacted colleagues at the All India Institute of Hygiene and Public Health, Calcutta and arranged for water samples to be tested for arsenic. When he could, he collected finger nail clippings containing the white lines typical of arsenic poisoning for testing. The number of arsenic poisoned patients in his clinic quickly grew to 18 cases. He sent water from 5 villages for testing, carefully identifying the type of well and location. Of the tube wells (less than 200 feet deep), 62% showed arsenic levels above the permissible limit. The highest concentration was found in the water sample consumed by the family of the first case. The arsenic levels in the ponds generally corresponded to the arsenic levels of the nearby shallow tube wells. None of the deep wells (more than 300 feet deep) had elevated arsenic.
Dr. Saha reviewed the world’s literature and found three other epidemics of chronic arsenic poisoning. One in Taiwan in 1961, Northern Chile in 1971, and the third from Chandigarh, India in 1971. He and his colleagues wrote a paper describing their experience with these initial cases and submitted them to the Journal of the Indian Medical Association. The paper, entitled “Chronic arsenic poisoning from tube-well water”, was accepted and published in January 1984.
Although there were only a few cases in their report, the authors hoped that the discovery of a serious health threat to thousands of people in the West Bengal region would trigger concern, a call for action, or a thorough investigation by authorities. Local newspapers did pick up on the story and published articles reviewing the problem. Shockingly, even after this publication indicating the problem with tube wells, more were dug without being tested for arsenic. The enthusiasm of the WHO, NGO’s, and governments across the region for this solution to the fresh water supply problem was unbridled and unstoppable. They were convinced that tube wells were a force for good.
By nature, thorough and committed, Dr. Saha was undaunted by the unresponsiveness of authorities. Determined to demonstrate the widespread impact of the contamination, he traveled the villages going door to door over the next few months. He was able to see many other patients with arsenical melanokeratosis, raising the final count of poisoned patients to 127. Complete examinations of these patients revealed that the arsenic poisoning had progressed past the point of merely an unsightly rash – patients also had advanced forms of arsenic toxicity such enlargement of the liver and spleen, as well as motor weakness and loss of nerve function. Villagers who escaped the disease were often individuals who worked a great distance from their home and mostly drank water at their place of work or had just migrated to the new area and had not consumed the tube well water for a long enough period of time. When the chemical analysis of nail clipping tests were complete – they confirmed elevated arsenic levels in all the patients.
Dr. Saha carefully wrote up the results of his extensive work and submitted them to the Indian Journal of Dermatology. It was published in October of 1984 and entitled, “Melanokeratosis from arsenic contaminated tubewell water.” Within two years, Dr. Saha had published more papers on the topic and the total cases of arsenic poisoning that he treated was well over 1000. In the 35 years since, his original article has been referenced repeatedly as the quintessential work that first identified the spreading epidemic of arsenic poisoning. Sadly, in those same 35 years, 1.3 million more tube wells have been drilled and are in use in West Bengal region of India alone. In neighboring Bangladesh, 10 million tube wells were drilled. The great majority these are producing arsenic contaminated water.
If you discovered that tube wells pump water that contains toxic levels of arsenic, why wouldn’t you stop? Why would you drill another – let alone drill 10 more, 100 more, or millions more? Would you stop after a year of drilling tube wells, 10 years of drilling tube wells? To diagnose the first case of arsenic poisoning by tube well water, Dr. Saha had to overcome a variety of cognitive biases. The reasons that organizations like the WHO continued to drill tube wells can be answered by exploring a different form of cognitive bias known as optimism bias.
By nature, we humans believe that we are more likely to experience good things and avoid bad things. Optimism bias is furthered influenced by our mental health. “Happy” people underestimate the risk of bad outcomes and exaggerate the likelihood of good outcomes, whereas people with depression can experience the reverse – pessimism bias. Our mind plays other tricks on us as well. Although we know much about our own lives, we take the truly limited information we have about others and think of them in generalized groups. This reinforces our optimism bias. When we drive by a car accident, our mind assumes that the drivers in the accident were reckless, speeding, or distracted because we have grouped “bad drivers” into a category called “people who have car accidents.” Furthermore, our personal experiences greatly influence our perception of risk and whether our outlook is optimistic or pessimistic. If you don’t know anyone who developed lung cancer from cigarette smoking, you are less likely to believe that you will develop lung cancer smoking cigarettes. When you hear that your friend developed colon cancer, you don’t assume that it was some random gene mutation – you assume that it was from their diet or some unknown family risk factor. More to the point, If you are drinking water from a tube well that someone told you was contaminated with arsenic, but no one you know has been made sick by drinking arsenic contaminated water, you will be unrealistically optimistic about your risks and continue to use the water. Finally, if you are the WHO and believe you are eliminating childhood diseases and lowering mortality by digging tube wells – you don’t stop when you hear of an outbreak of arsenic poisoning in West Bengal, India. After all, your bias tells you it’s a poor area in a poor country with poor health – tube wells are helping these poor foks! You keep digging wells because it is impossible to imagine that an entire subcontinents water supply could be contaminated by arsenic and that your well-intentioned solution could be slowly poisoning them.
Even as of this moment, we can find evidence of how cognitive bias is affecting our ability to manage a threat to our health in the global pandemic caused by the Covid19 virus. Epidemiologist say that it will continue to spread until either we develop a vaccine or until 75% of us get the virus and confer a herd immunity for the uninfected. The elderly and the infirm suffer greatly and have a greater chance for death. The young and healthy have very mild symptoms, and so, function as vectors for transmission. Masks, social distancing, and hand washing greatly reduce the chances of infection. We know the virus spreads from one person to the other. And yet, all around us we can watch as cognitive bias plays out in real time. We see the optimism bias of people not wearing masks and gathering in groups believing they are somehow immune from contracting the disease or experiencing a bad outcome. Less visible is pessimism bias of individuals who won’t even venture out of the house into the fresh air. The attribution error that assumes that someone else who contracted Covid19 had any number of “bad” behaviors that were the cause. Unhitching our minds from these biases is a difficult task and requires a combination of self-awareness and self-reflection – two things often in short supply in the human brain.
Meanwhile, less you think the problem with the human condition is only this complicated, we can go back in time to the 1930’s and another clinic in southern India, where the manifestations of fluoride poisoning, or fluorosis, were first identified in patients in their 20’s and 30’s. The bones begin to harden with excess calcium while joints stiffen and become inflexible, muscles atrophy, and patients lose their appetite and waste away – and yet the mind remains intact. The cause? Drinking water from those “safe” deep wells throughout India and Asia that are, in fact, extensively contaminated with fluoride! These wells are so contaminated, and have been for over a hundred years, that fluorosis is considered a disease endemic to the entire continent of Asia, with India and China having the greatest number of affected individuals.
One well contains arsenic, the other fluoride, and a third dangerous levels of bacteria. It’s no wonder our minds provide us, for better or worse, with the cognitive tricks to make these choices.
Remember, it’s a dangerous planet, we only survive it.
Arsenic found in tube well water. The Statesman, December 4, 1983.
Is it being examined why Arsenic is being found in tube-well water? Anandabazar Patrika, December 6, 1983.
Arsenic in Nabadwip tube-well water also. Anandabazar Patrika, December 7, 1983.
J Indian Med Assoc. 1984 Jan;82(1):34-5 Chronic arsenic poisoning from tube-well water. Garai R, Chakraborty AK, Dey SB, Saha KC.
Gold, Ron S.; Sousa, Phillip N. de (2012). “When does event valence affect unrealistic optimism?”. Psychology, Health & Medicine. 17 (1): 105–115.
Professor and Chair of Emergency Medicine at Drexel University College of Medicine and a Medical Toxicologist
Views are my own created for the purposes of furthering medical education using #FOAMED