Discover how a mysterious woman who drowned in the Seine River in France became known as the most kissed face in the world. MEDICAL HISTORY by Stuart M. Caplen, MD   Charles Bargue drawing of the “L’lnconnue de la Seine”  Anyone who has taken a CPR (cardiopulmonary resuscitation) course has practiced on a Resusci Anne manikin, but the story behind the face used on that manikin is fascinating.  The Drowning in the Seine The most repeated story is that in the late 1880s, a young woman, about 16 years of age, drowned in the Seine River in France.  As was usual at the time, her body was put on display in the Paris mortuary to see if anyone would recognize and identify her.  The pathologist reportedly asked a mouleur, or cast-maker, to make a death mask of the woman, who later became known as “L’lnconnue de la Seine” (the unknown woman of the Seine).   The Birth of a Muse The mouleur started selling copies of the mask at his shop, and soon the woman depicted on it became a muse for artists, writers, and poets due to her half-smile that Albert Camus once compared to Mona Lisa’s.  The mask became very popular and reportedly was hanging on the wall in the drawing rooms (living rooms) of many fashionable Europeans.  Some women of the time apparently even tried to model their looks after her. From Mystery Muse to CPR Icon In 1958, Asmund Laerdal, a Norwegian toy and doll manufacturer using newly formulated plastic materials, was asked to create a training aid for a new resuscitation technique called CPR.  His son had nearly died of drowning a few years before, so he was very receptive to the idea.  He decided on a female manikin, as he thought it would be less threatening to the trainees.  For the face, he reportedly remembered the face he had seen on the wall at his grandparents’ house, the “L’lnconnue de la Seine”, which then became the face of the Resusci Anne.  He had a well-known sculptress, Emma Mathiassen, model the face, and in 1960,  Resusci Anne was introduced to the world. The "Kiss of Life" Supplying breaths by mouth-to-mouth resuscitation during CPR is also known as the “kiss of life”, making the face of the Resusci Anne, which was modeled on the face of the “L’lnconnue de la Seine”, the most “kissed” face in the world.  More Medical News & Trivia Click here to read another interesting article you may enjoy, The History of Heroin, the “Nonaddictive” Substitute for Morphine. References Grange J. Resusci Anne and L'Inconnue: The Mona Lisa of the Seine. BBC News. 16 October 2013. Retrieved from: https://www.bbc.com/news/magazine-24534069 The History of Resusci Annie. LifeSaver Training. 2024. Retrieved from:  https://www.lifesavertraining.co.uk/facts/the-history-of-resusci-annie/ CPR Educators, Inc. 2024. Retrieved from: https://cpreducatorsinc.com/cpr-doll-face/

Explore the history of phrenology, the 19th-century "science" of reading skulls to determine personality and potential. Discover its rise, fall, and surprising uses. by Stuart M. Caplen, MD   Phrenology is the practice of interpreting mental qualities and potential on the basis of the external appearance or bumps in the skull. It was originally called “ Schädellehre ”  or “doctrine of the skull” by its inventor Franz Joseph Gall. It was later called craniology, and cranioscopy, but eventually the term phrenology came into general usage. (From the Greek word phren - meaning mind.)   Gall, a German physician and anatomist, developed his theories around 1790. After starting to publish and lecture on this new science, the Holy Roman Emperor Franz II banned Gall’s lectures in 1801. After that, Gall and his assistant Johann Gaspar Spurzheim started lecturing throughout the rest of Europe.  Gall believed that elites could use phrenology to govern the masses, whereas Spurzheim and George Combe, a London lawyer who helped popularize it, conceived of phrenology as a less coercive means to perfect or reform humanity. One of the strongholds of phrenology was in the United States, where newspapers first reported on it in 1805. However, it really did not take hold in the U.S. until the 1820s, after Spurzheim traveled to the U.S. and lectured at Yale and at various venues in New York City and Boston.  Phrenology in the 1820s and 1830s was primarily a subject for elites, with physicians, college professors, and political figures founding phrenological societies and participating in the popularization of phrenology in the United States and in Europe. Phrenology was considered cutting-edge science, and medical students were taught phrenology in conjunction with anatomy. However, the elite did not think that phrenology should be a subject for the masses and were against “popular” phrenology. What is Phrenology  The “science” of phrenology was based on these tenets:  The brain is the organ of the mind.  The mind is composed of multiple distinct, innate faculties.  Because they are distinct, each faculty must have a separate seat or “organ” in the brain.  The size of an organ, other things being equal, is a measure of its power.  The shape of the brain is determined by the development of the various organs.  As the skull takes its shape from the brain, the surface of the skull can be read as an accurate index of psychological aptitudes and tendencies.  The various “organs” of the brain were each given a name and location on the skull, frequently depicted either through an image or by a phrenological bust. The relative size of the brain’s organs, as determined from the skull’s surface, reputedly allowed a phrenologist to detect an individual’s character, as well as explanations for past behavior and predictions of future behavior. How the skull itself was “read” varied. Some phrenologists used manual examination, with hands applied to the head of a client. Other phrenologists advocated for the use of tools, using calipers or a tool known as a craniometer to make measurements. Phrenologists believed that they could differentiate great men from criminals and those with intellectual disabilities or mental illness on the basis of a phrenological examination. Some Suggested and Actual Uses of Phrenology  During phrenology's era of popularization from the 1820s to the 1840s, some employers demanded a character reference from a local phrenologist to ensure that a prospective employee was honest and hard-working. Examining children to see if an overabundance of one brain organ could be nurtured as a talent to prevent the child from growing up to be a dissolute or criminal adult.  A prison warden might use phrenology to determine which prisoners were the most dangerous and needed more supervision.  It was thought that phrenology, by identifying prominent brain organs, could be used by education, disciplinary, and governmental organizations to guide people to appropriately express those organs rather than fall into antisocial behavior.  The “science” of phrenology was also used by some as reinforcement for racial and social hierarchies with respect to gender, class, and race.  The End of Phrenology’s Acceptance by the Medical Establishment   By the 1840s, most academics had turned against phrenology. A group of French anatomists and physiologists started a movement against phrenology that became increasingly popular. Also, as time went on, there was less belief that phrenology could actually be used to solve social ills. Finally, as phrenology became more popular and used by the general public, intellectuals and professionals became less interested in it. -------------------------------------------------------------------------------------- If you found this article interesting, click here to read The Story of the Most “Kissed” Face in the World. References Thompson CE. Phrenology. Encyclopedia of the History of Science - Carnegie Mellon University. November 2021. Retrieved from:  https://ethos.lps.library.cmu.edu/article/id/482/ van Wyhe J. The History of Phrenology. The Victorian Web. Last modified 2000. Retrieved from: https://victorianweb.org/science/phrenology/intro.html Photograph, forty years in phrenology : embracing recollections of history, anecdote, and experience / [Nelson Sizer]. New York : Fowler & Wells, [1882]. Wellcome Collection. Retrieved from: https://wellcomecollection.org/works/etdksptf/images?id=yk35tr9s Chart from 'The Phrenological Journal' ("Know Thyself"), print from Dr. E. Clark. Wellcome Collection. Retrieved from: https://wellcomecollection.org/works/b6skynug/images?id=nmsxdkgm https://creativecommons.org/licenses/by/4.0/ Photograph: phrenological head by L. N. Fowler. Wellcome Collection. https://wellcomecollection.org/works/vv27ymqn/images?id=ns6hvph9

Prior to the discovery of insulin treatment, type 1 diabetes, with severe insulin deficiency, was a fatal disease with many debilitating symptoms. This article will discuss how this life-saving medication was discovered.  Medical Past by Stuart M. Caplen, MD   History of Diabetes Mellitus  Diabetes was first documented in an ancient Egyptian papyrus, as well as later in ancient Chinese and Indian medical textbooks. The word diabetes was thought to have originated by an ancient Greek physician from a Greek word meaning passing through. The term diabetes mellitus was introduced in 1647 by the British physician Thomas Willis and referred to both the excessive sweetness of the urine (mellitus is Latin for sweet like honey) and the excessive urination (diabetes means passing through) seen in this disease. In 1776, Matthew Dobson, a British physiologist, first documented that a diabetic’s urine sweetness was from an excess of sugar. In the distant past, some physicians actually used to taste a patient’s urine to make the diagnosis. In 1889, German researchers, Oscar Minkowski and Joseph von Mering, discovered that when a dog's pancreas was removed it immediately became severely diabetic. In the pre-insulin era, also known as the “era of frustration,” physicians tried, generally unsuccessfully to control the disease by use of opiates, as well as having their patients  eat more calories. However, some physicians started recommending calorie restriction with some success, although some diets were so low in calories it caused patients to die of starvation. Calorie restriction was more successful in late-onset diabetes (type 2 diabetes), where the person still produces some insulin, although the amount is not adequate to maintain normal blood glucose levels.  Insulin  Insulin is a hormone secreted by beta cells located in the pancreas in the Islets of Langerhans (named after their discoverer Paul Langerhans in 1869). The word insulin comes from the Latin “ insula ” meaning island in reference to the Islets of Langerhans. The word insulin was coined by Sir Edward Albert Sharpey-Shafer, who in 1910 suggested that only one chemical from the pancreas was lacking in people with diabetes. Insulin is released from the pancreas when blood glucose levels increase after eating and causes the glucose to be moved into cells where it can be used as an energy source. Extra glucose is stored in the liver as glycogen, which can be reconverted back to glucose when insulin levels are low, such as when fasting or overnight, to maintain relatively constant glucose levels in the body. Lack of insulin for any length of time causes ingested glucose to be mostly excreted in the urine, and glycogen stores in the liver to become depleted. The low insulin levels act as a stimulus for the body to produce more glucose, and without available glycogen, muscle and fat are then broken down to produce more glucose (even though blood glucose levels may already be very high). This can lead to muscle wasting, potentially a severe acidosis from ketones produced in the breakdown of fats, and severe dehydration from the increased urination produced by the high glucose levels.  The Development of Insulin  By 1912, it was fairly common knowledge that destroying the pancreatic Islets of Langerhans could cause animals to develop diabetes. A number of researchers had taken pancreatic extracts from animals and found they could reduce blood sugar somewhat, but no one was able to get pure extracts solely from the Islets of Langerhans.  In 1921, working at Connaught Laboratories at the University of Toronto, a Canadian surgeon, Frederick Banting, and his assistant Charles Best figured out how to remove insulin from a dog’s pancreatic Islets of Langerhans, which had not been possible before. Colleagues said the material looked like “thick brown muck,” and they called it iletin (later renamed insulin although Eli Lilly initially used Iletin as a brand name for the drug). With iletin, Banting and Best kept a dog with severe diabetes alive for 70 days, the dog dying only when they ran out of Iletin extract. Banting and Best, along with colleagues J.B. Collip and John Macleod, later produced a more refined and purer form of insulin from the pancreases of cattle. In January 1922, a 14-year-old boy named Leonard Thompson, was dying from diabetes in a Toronto hospital and became the first person in the world to receive an injection of insulin. The first dose was not curative, and the patient developed a sterile abscess at the site of the injection, thought to be due to some contaminants in the solution. Eight days later, Collip, using higher concentrations of alcohol in the mixture, found a way to remove much of the extraneous proteins found in the iletin. Four days later, Thompson received the new, more purified extract, and it was an unqualified success. Within 24 hours, his blood glucose levels had dropped to near-normal and his ketoacidosis, which is seen in severe diabetes, had reversed. The news of this advance spread quickly worldwide, and in 1923 Banting and Macleod received the Nobel Prize in Medicine for their work.  Insulin Vial from 1923 Soon after, Eli Lilly and other companies around the world started manufacturing large-scale amounts of insulin. In 1936, slow-releasing versions of insulin were developed with longer half-lives. Initially, insulin was made from the pancreases of cattle and pigs, but in 1978, “human” genetically engineered insulin produced from E.coli bacteria was developed and is still used today. Conclusion In 2017, there were an estimated nine million type 1 diabetics in the world, who, due to a lack of pancreatic insulin, require daily insulin injections or infusions. The work of the medical pioneers who helped isolate and manufacture insulin has improved both the quality of life for diabetics and saved countless lives since the 1920s.  If you found this article interesting, click here to read The History of Leeches in Medicine and the Era of the “Leech Mania”. References The History of a Wonderful Thing We Call Insulin the American Diabetic Association. Updated July 1, 2019. Retrieved from: https://diabetes.org/blog/history-wonderful-thing-we-call-insulin Vecchio I, Tornali C, Bragazzi NL, Martini M. The Discovery of Insulin: An Important Milestone in the History of Medicine. Front Endocrinol (Lausanne). 2018 Oct 23;9:613. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC6205949/ Rutty CJ. The Making of Insulin. Connaught Fund/University of Toronto. Retrieved from: https://connaught.research.utoronto.ca/about/history/article3 Diabetes. World Health Organization. 14 November 2024. Retrieved from: https://www.who.int/news-room/fact-sheets/detail/diabetes#:~:text=Key%20facts,%2D%20and%20middle%2Dincome%20countries . Photo images reference- University of Toronto, Insulin Digital Library. Retrieved from: https://connaught.research.utoronto.ca/about/history/article3

Colorectal cancer, once considered a disease of the elderly, is increasingly affecting younger individuals. This CME article explores the alarming trend of early-onset colorectal cancer. Read Article, Take Test , Get FREE 🎓 CME Certificate with Valid Email We’ll send you occasional updates. Your email stays private—never sold or shared.  😇 The Increasing Incidence of Early Onset Colorectal Cancer by Stuart M. Caplen, MD   Colorectal cancer used to be a disease of the aged.  A recent, dramatic increase in colon cancer incidence in younger individuals has become a notable problem.  This article will review this increasing trend in a younger age group and provide possible explanations for this increase. Increasing Incidence In the United States (US), an annual 2% increase in early-onset colorectal cancer (EOCRC) was noted between 2011 and 2016.[1]  Based on current trends, by 2030, the incidence of colon and rectal cancer, compared to 2010, will increase by 90% for patients 20 to 34 years of age and by 27.7% for patients 35 to 49 years of age.[2]  In contrast, the incidence of colorectal cancer in the elderly has been decreasing, and is thought to be due to screening colonoscopies, which in the past were recommended for people over the age of 50.[2]  However, in 2021, the U.S. Preventive Services Task Force recommended that colorectal cancer screening, either by stool screening or direct observation, should start at age 45.[3]  It is thought that up to 30% of EOCRCs are hereditary in nature, but the remainder may be due to lifestyle or environmental factors.[4] Why is Early-Onset Colon Cancer Increasing?  The increasing incidence of EOCRC may be attributed to behavioral factors such as obesity, physical inactivity, and diet.  Other possible causes are ingestion or inhalation of toxic substances.  Some of these factors are directly toxic, and some are thought to cause dysbiosis (an imbalance of the microorganisms in the gut, which can lead to chronic inflammation), possibly leading to cancer development.[5,6]  Obesity The prevalence of obesity has increased markedly in the United States over time and is a major risk factor for EOCRC.[2]  It is thought that body fat releases inflammatory cytokines and adipokines, as well as increasing insulin levels and growth factors that may predispose to the development of cancers at an earlier age.[7]  The increased risk of colorectal cancer from obesity varies from study to study, depending on geographic location, gender, and body mass index (BMI), with a range of about an 8% to 50% increase in the risk of colorectal cancer in obese individuals.[8,9] Lack of Exercise Lack of exercise may also be a precipitant of EOCRC.  In one study, prolonged sedentary television time, a marker of inactive lifestyle, was found to correlate with an increased risk of colorectal cancer.  In that study, watching 7 to 14 hours of television per week increased the risk of colorectal cancer by 12%, and watching more than 14 hours a week increased the risk by 69%.[10]  Moderate physical activity has been demonstrated to reduce the risk of both colon and rectal cancers.[2,11]  In other studies vigorous exercise reduced the risk of rectal cancer by 40%[11] and a meta-analysis reported that the risk of colon cancer was reduced 19% in those who regularly exercised.[12] Diet The Western diet, which consists of significant amounts of processed meats, red meat, fast food, and low levels of fruits and vegetables is also associated with an increased risk of colon cancer.[2]  One study found that subjects eating the Western diet had approximately twice the risk of developing colon cancer compared with those who ate a diet consisting of more vegetables, fruits, fish, and poultry and less red meat and sugar than the Western diet.[13]  Ultra-processed foods including ready-to-eat or ready-to-heat formulations contribute about 57% of the calories consumed by American adults, and has been increasing for the past two decades.  These foods are typically high in sugar, oils/fats, and refined starch, and have been found to alter gut microbiota composition unfavorably, which is a known cause of intestinal inflammation.  Heating may also cause migration of carcinogenic chemicals from the ultra-processed foods, as well as from the packaging.  Ultra-processed foods can also contribute to an increased risk of obesity, which is another risk factor for colorectal cancer.[14] Ultra-processed foods frequently contain food additives such as dietary emulsifiers and artificial sweeteners, some of which may also increase the pro-inflammatory potential of an imbalanced gut microbiome.[2]  Food emulsifiers are chemically similar to detergents and are added to processed foods to improve texture or extend their shelf life.  Scientists reported that mice fed low levels of common dietary emulsifiers developed altered gut microbiota and had a thinning of the mucus barrier protecting the intestinal lining.  The mice also developed low-grade intestinal inflammation and metabolic syndrome.  In a second experiment mice were either fed plain drinking water or water containing a 1% concentration of two common food emulsifiers.  Mice fed the emulsifiers developed chronic, low-grade intestinal inflammation and impaired glucose metabolism.  These mice were then given a cancer-causing agent and the emulsifier-fed mice developed more intestinal inflammation and cancer development than the mice who were fed plain water.[15] A longitudinal study of over 200,000 health professionals reported that men in the top fifth of ultra-processed food consumption had a 29% higher risk of developing colorectal cancer than men in the lowest fifth.  No association between ultra-processed food consumption and colorectal cancer in women in that study was detected, with one possible explanation being a protective effect from estrogen.[14] Alcohol Alcohol has been found to be a risk factor in EOCRC.  One study of over five million subjects reported that, compared to light drinkers, moderate drinkers had a 9% increased risk, and heavy drinkers a 20% increased risk of EOCRC.  Compared to non-drinkers, there was a dose-related response with a 7% increased risk of EOCRC for subjects who drank one to two days per week, a 14% increased risk for those who drank three to four days per week, and a 27% increased risk of EOCRC for those who drank five or more days per week.  Suggested causes for this include a DNA damaging effect of acetaldehyde (an ethanol metabolite), tissue injury by oxidative stress, and alcohol-induced intestinal microbiome changes.  Heavy drinkers are also known to frequently have a poor diet low in folate and fiber, which may be synergistic with other cancer-causing properties of alcohol.[4]  The U.S. Surgeon General has recently suggested that alcohol warning labels should include a statement about the heightened risk of cancer from drinking alcohol.[16]  Microplastics Microplastics, which are microscopic particles shed from plastic, have been detected in soil, groundwater, and many food products.  Microplastics have been found both in human stool and embedded in human intestinal specimens.  One theory is that microplastics adherent to the intestinal mucus layer may release some of the carcinogenic chemicals used in the manufacturing of plastic into the intestinal wall.  Microplastics adhering to the intestinal wall may also facilitate the development of biofilm, which can change the intestinal microbiome and lead to chronic inflammation.[17]   One study found microplastics in infant stool at higher levels per gram than adult stool, indicating possible lifelong exposure to intestinal microplastics.[18]  A definitive connection between human exposure to microplastics and colorectal cancer has not been proven, but research is ongoing.   Chemicals A meta-analysis reviewed 33 studies for any correlation between herbicide and insecticide exposure and colon cancer and found that significant herbicide and pesticide exposure increased colon cancer risk by 20% to 32%.[19] “Forever chemicals”, such as perfluoroalkyl and polyfluoroalkyl substances (PFAS), that are in the air, soil, and food chain, have been investigated as a possible cause of EOCRC.  Perfluorooctanesulfonic acid (PFOS) is one of the most commonly detected PFAS, frequently found in drinking water samples with an estimated elimination half-life of 3.4 to 4.8 years in humans.  In one experiment, mice were either fed a normal diet or a diet containing PFOS.  They reported that the PFOS-eating mice had downregulation of their HMGCS2 gene in their intestines. (HMGCS2 controls an enzyme for ketogenesis, a metabolic pathway that provides lipid-derived energy for various organs during times of carbohydrate deprivation.)  In the study, reduced HMGCS2 activity resulted in enhanced proliferation of lipids and lipid accumulation.  PFOS exposure induced changes in a number of other genes and increased levels of proteins associated with carcinogenesis in the intestinal tissues of mice.  The authors also reported that a review of human specimens and cancer databases found decreased intestinal expression of HMGCS2 is associated with colon cancer, as well as a decreased survival time in those who develop colon cancer.[20] Toxic Metals  Toxic metals can accumulate in the body over time and are known to disrupt cellular homeostasis, trigger oxidative stress, and induce DNA damage, which can potentially lead to carcinogenesis.[21]  There are some data about toxic metals and human colorectal cancer, but these are not definitive.  In one study, higher lead levels in female factory workers were associated with an increased risk of death from colorectal cancer, but it was only based on three workers who had developed colorectal cancer.  There was no significant difference in colon cancer death rates in male factory workers based on blood lead levels.[22]   Another study calculated mercury ingestion based on the subjects’ dietary intake of fish and shellfish products.  It was reported that higher levels of mercury ingestion via seafoods resulted in greater than a three-times increased risk of colorectal cancer compared to controls who ate much less seafood and theoretically had lower mercury exposure.[23]   One study reported increased levels of lead, chromium, and mercury in human colon cancer samples that were absent in normal tissue.[24]  However, a second study did not find any statistically significant difference between chromium levels of cancerous colonic tissue versus normal tissue.[25]  While aluminum, chromium and cadmium are known to potentially induce inflammatory changes, a definitive connection to colorectal cancer has not been established.[21]  Arsenic is present in the food supply chain and has been shown to have multiple toxic effects.[26]  However, no association to colorectal cancer has been demonstrated as of yet.[21]     Thus, while there is some indirect and weak evidence that ingestion of some toxic metals may increase the risk of developing colorectal cancer, more research and better studies are needed.  Diabetes  In a number of studies, type 2 diabetes has been shown to increase the risk of colorectal cancer to as high as 47% compared to non-diabetics.  This increased risk appears to be more definitively demonstrated in men.  In women with type 2 diabetes, some studies have shown lesser increases in colorectal cancer risk compared to men, while others reported risk increases equivalent to men.  Insulin supplies growth factors for colonic epithelial cells, and higher than normal insulin levels, as seen in type 2 diabetes, may increase the cellular growth of tumors.  Hyperglycemia may decrease the effectiveness of the immune system, which is theorized as another possible mechanism for the development of cancer.[27,28,29,30]   Cigarette Smoking Cigarette smoking is known to increase the risk of colon cancer.  Subjects in one study who smoked for 12 or more years before the age of 30 were reported to have a 37% increased risk of developing colorectal cancer compared to non-smokers. The actual mechanism of how cigarette smoking increases EOCRC is not known, but one theory is that smoking cigarettes in early adulthood may be associated with molecular changes in the colon that may increase the risk of colorectal cancer.[31] Circadian Rhythm Disruption It is known that circadian rhythm disturbances can cause gut dysbiosis, where the normal balance of microorganisms in the intestines is negatively affected, which can lead to chronic inflammation, thought to be a possible precursor to EOCRC.  In a mouse model, induced circadian rhythm disturbances cause increased amounts of bacteria known to cause inflammation and increased gut barrier defects.  The gut barrier is a multilayered system that allows nutrients to pass through the intestinal wall, but prevents pathogens from entering.  It was also reported that circadian rhythm disturbances increased the incidence of cancer found in genetically modified mice.[32,33]  However, findings in humans have not been as clear.  A longitudinal study of over 78,000 nurses reported that nurses who rotated on night shifts more than three times a month for over 15 years had a 35% increased risk of colorectal cancers compared to nurses who did not work nights.  However, a study by some of the same authors 15 years later, using many more subjects, as well as the original database, found no significant differences between rotating night nurses and day shift nurses with respect to colorectal cancer rates.[34,35]  A meta-analysis of 57 studies reviewed this issue and found no increase in colorectal cancers in rotating or fixed night shift workers compared to day shift workers.[36]  Thus, while circadian rhythm disruption in the animal model has demonstrated negative changes to the gut environment, and an initial study with nurses was suggestive of a correlation, further studies have not confirmed the connection of night shift work and colorectal cancer.  Summary It is clear from the scientific data that the incidence of EOCRC is increasing.  As was discussed in this article, there are many possible causes.  These include food additives, microplastics, cancer-causing chemicals from plastics, herbicides, pesticides, forever chemicals, toxic metals, obesity, lack of exercise, alcohol use, and cigarette smoking.  Risk factors such as alcohol use and cigarette smoking, while contributory to EOCRC, are probably not the cause of its recent increase in incidence, as they have been present and used in the population for generations.  Generally, it takes decades to develop colorectal cancer, but there is evidence that some of these substances, such as microplastics in the intestine, are now being ingested from infancy.  Some causes may have a direct carcinogenic effect, and some may increase cancer incidence by changing the microbiome of the intestine, leading to chronic inflammation.  The etiology of the increases in EOCRC appears to be multifactorial.  It may be possible that in the future recommending the first colorectal cancer screening at an earlier age than 45 might need to be considered.  It is impossible for individuals in modern societies to avoid all possible precipitating factors, but exposure can be limited, and the risk of EOCRC decreased.  Simple modifications of lifestyle such as increasing exercise, stopping cigarette smoking, or dietary changes may significantly reduce risk.   Author's Note - Thank you to Dr. Theodor Feigelman for editing this article. 🎓  Want Free CME Credit for This Article? Take the quiz now at www.FibonacciMD.app . It only takes a few minutes! Your certificate will be emailed to you after you pass the quiz and complete a short evaluation We’ll send you occasional updates. Your email stays private—never sold or shared.  😇 Download article PDF: Click the link for more information on The Effects of Plastics on Human Health or The Proven Benefits of Exercise .   References ✅ Earn Free CME Credit for Reading This Article Eligible for 0.5 PRA Category 1 Credit Click the button below to take a short quiz. A valid email is required to send your certificate. We’ll send you occasional updates. Your email stays private—never sold or shared.  😇

Leeches: A Curious Chapter in the History of Medicine Explore the strange and fascinating history of leech therapy—from ancient medicine and 19th-century “leech mania” to their modern medical revival in reconstructive surgery. by Stuart M. Caplen, MD   The use of leeches for bloodletting started thousands of years ago and reached Europe in the Middle Ages.  The word leech comes from the Old English word “laece”, which meant physician.  Bloodletting was supposed to balance the body’s humors.  The body’s humors were blood, black bile, yellow bile, and phlegm, a theory attributed to the Greek physician and philosopher Hippocrates (460–370 BC).  The leech commonly used in medicine, Hirudo medicinalis  , has three jaws with approximately 100 teeth.  The teeth bite through the skin, and the saliva contains an anesthetic so it doesn’t feel painful to the person when they are bitten.  Leech saliva also causes dilatation of blood vessels to bring more blood to the area.  The saliva contains hirudin, a substance that inhibits thrombin and prevents blood clotting.  Hirudin has been synthesized and used in modern medicine as an anticoagulant.  Leeches’ saliva also has been found to have an anti-inflammatory effect.  A leech can drink up to ten times its body weight in blood.  The first reported medicinal use of leeches was by the Greek physician Nicader of Colophon around 200 BC.  Ancient Indian physicians around the time of Christ also used them for bleeding.  A Greco-Roman physician, Galen, who lived from 129-199 AD, popularized the concept of bodily humors, which when out of balance could cause disease, and advocated the use of leeches to draw off blood and restore this balance.  This practice continued for centuries.   At the beginning of the 19th century, a “leech mania or craze” occurred in Europe and America.  François-Joseph-Victor Broussais, a French physician, believed that inflammation caused most disease and that leeching could reverse that process.  Broussais was the chief physician at Val-de-Grâce military hospital in Paris, and to a large extent most of his ill patients received the same therapy, which was the application of 30 leeches.  There had been objections to more standard bloodletting, but Broussais and his followers felt leeches were a kinder and gentler method.  They also could be applied to specific areas of the body that were affected, such as ears, nostrils, the mouth, or even private parts.  British surgeon Rees Price, author of “A Treatise on the Utility of Sangui-Suction or Leech Bleeding” in 1822, wrote that use of leeches led to a “state of relaxation of the nervous energy of the body.” François Joseph Victor Broussais As bloodletting was an accepted form of treatment at the time for many diseases, using the less traumatic leech rather than incisions with lancets to remove blood appealed to both the general public and the medical profession.  The “leech craze”, which started in France, soon spread widely which created an entire industry which was profitable for leech farmers, importers, apothecaries, and both the “legitimate” medical profession as well as medical quacks. Leeches became fashionable in the culture of that time, which inspired poems, leech-shaped patterns on dresses, and ornate leech jars that decorated the windows and counters of apothecary shops and parlors of the wealthy.  At the height of “leech mania”, France imported 33 million leeches in a single year, and demand far exceeded supply.  The U.S. in the mid-1800s was importing almost the same number of leeches per year from Germany.  By the end of the 18th century, leeches were starting to become extinct in certain countries due to their popular use.  Harvesting large amounts of leeches required access to wetland areas and laborers to both act as lures and collectors.  People started breeding leeches, and according to one account, a breeder had 800,000 leeches on his marshland, which he fed by driving 200 cows and dozens of donkeys into the marshes.  Books on how to breed leeches became popular with tips such as adding iron to water leeches lived in helped make the water less putrid and reduced the need to add fresh water as often.  One of the reasons so many leeches were needed for medicinal purposes is that once a leech was fed, it might not need to feed again for six or more months.  19th Century Leech Seller’s Business Card  Leeches were used in a cholera epidemic in the 1830s.  However, they proved not to be very effective, and in Europe leeching began to become less popular.  Leeching also did not fit in with the emerging concepts of modern medicine at the time and became more associated with medical quackery.  However, in the U.S., leeches were regularly used until the end of the 19th century, and even in the early 1900s, jars of leeches could be found in some American bars and barber shops. Leeching became a disrespected practice until the 1960s through the 1980s, when plastic surgeons started reported using them for engorged skin flaps.  In 1985, there was a well-publicized case where an American plastic surgeon, Joseph Upton, treated a five-year-old boy that had part of his ear bitten off by a dog.  Small capillary blood vessels needed to reconnect for the reattached ear segment to survive.  This was made more difficult if extra fluid and blood accumulated in the tissues due to the veins not draining the area adequately.  Upton remembered reading about microsurgeons who used leeches, and when the child’s ear tissue looked like it was not going to survive, he ordered leeches from a company called Biopharm, which was located in Wales.  Biopharm was started by a zoologist who felt that with all the interesting substances in leech saliva, there was a strong possibility of their renewed use in medicine.  Upton attached several leeches to the boy’s ear, which sucked up the pooled blood and extra fluid and allowed the reattached ear to survive.   In 2004, the FDA approved the use of medicinal leeches in reconstructive and plastic surgery to reduce venous congestion in tissue grafts and flaps.    If you found this article interesting click here to read about Dr. Robert Liston and the 300% Mortality Surgery. References Martucci J.  Medicinal Leeches and Where to Find Them-The rise, fall, and resurrection of the humble leech.  Science History Institute Museum and Library. Retrieved from: https://www.sciencehistory.org/stories/magazine/medicinal-leeches-and-where-to-find-them/ Revised and updated by Luebering  JE. Leeching. Britannica. Sep 29, 2023. Retrieved from: https://www.britannica.com/science/leeching Batchelor AGG et al. The salvage of congested skin flaps by the application of leeches. British Journal of Plastic Surgery (1984) 37, 358-360. Retrieved from: https://www.jprasurg.com/article/0007-1226(84)90079-1/pdf Wells MD et al. The Medical Leech: An Old Treatment Revisited. Microsurgery, 14:183-186 1993. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/8479316/ Follow-Up On The News; Rediscovering Medical Leeches. The New York Times. March 15, 1987, Section 1, Page 47, Retrieved from: https://www.nytimes.com/1987/03/15/nyregion/follow-up-on-the-news-rediscovering-medical-leeches.html Poole S. How Leeches Made Their Comeback. New York Magazine. Nov. 11, 2016, Retrieved from: https://nymag.com/vindicated/2016/11/how-leeches-made-their-comeback.html Portrait of Francois Joseph Victor Broussais (1772-1838). Wellcome Collection.  Retrieved from: https://wellcomecollection.org/works/y5385h9n?wellcomeImagesUrl=/indexplus/image/M0009106.html Alcock-type leech jar. Wellcome Collection. Retrieved from: Retrieved from: https://wellcomecollection.org/works/qg89y593/images?id=vvee3weq Business card for cuppers and leechers in Pittsburgh, Pennsylvania. 19th century.  The Museum of Ridiculously Interesting Things. Retrieved from: https://ridiculouslyinteresting.com/2012/05/06/leeches-leeches-leeches-a-small-collection-of-vintage-advertisements-for-medical-leeches/

This exercise CME unveils the science behind exercise as a powerful tool for health. We'll explore key benefits and how to get your patients moving! ✅ Earn Free CME Credit for Reading This Article Eligible for 0.5 PRA Category 1 Credit Click the button below to take a short quiz. A valid email is required to send your certificate. We’ll send you occasional updates. Your email stays private—never sold or shared.  😇 by Stuart M. Caplen, MD General Medicine / Sports Medicine In this article we will examine the positive effects of exercise that have been scientifically proven.  This article will review a sampling of some of the major benefits of exercise and will not be a complete discussion of all of the benefits.   How is the Intensity of Exercise Determined?  One measure of the intensity of physical activity is the metabolic equivalent of task or MET.  One MET is equal to the rate of energy expended by a person sitting at rest.  Light-intensity activities expend less than three METs, moderate-intensity activities expend three to six METs, and vigorous activities expend six or more METs.[1] Examples of light-intensity activities are slow walking and standing light work.  Moderate-intensity activities include brisk walking, mowing the lawn with a power mower, playing doubles tennis and bicycle riding at 10-12 mph.  Vigorous-intensity activities include jogging, hiking, shoveling snow, bicycle riding over 14 mph, and playing basketball, soccer, or singles tennis.[2] The Physical Activity Guidelines Advisory Committee Findings In 2018, the Physical Activity Guidelines Advisory Committee, a U.S. government advisory committee, after reviewing the science available found that there are health benefits from doing any amount of moderate-to-vigorous physical exercise.  However, to obtain substantial health benefits, it was recommended that adults should do at least 150 to 300 minutes per week of moderate-intensity, or 75 to 150 minutes per week of vigorous-intensity aerobic physical activity, or a combination of the two.  They also recommended that adults should do muscle-strengthening activities of moderate or greater intensity involving all major muscle groups on two or more days a week, as these activities may provide additional health benefits.   The committee reported that health benefits of exercise in adults included: Lowered risk of death, heart disease, stroke, high blood pressure, type 2 diabetes, and elevated cholesterol.  They also noted that the risk of cancers of the bladder, breast, colon, uterus, esophagus, kidney, lung, and stomach were lessened.  Dementia and falls in the elderly were also reduced in exercisers.  Exercise improved cognition, quality of life, sleep, bone health, the ability to lose weight and also reduced anxiety.[3] Cardiovascular and Mortality Benefits A 30-year study of 116,221 adults reported that the group who did moderate-intensity physical activity for 150 to 299 minutes per week had a 19% to 25% decrease in mortality.  Moderate-intensity physical activity of 300–599 minutes per week resulted in a further 3% to 13% decrease in mortality.  The group that had a history of vigorous-intensity physical activity of 75 to 149 minutes per week had a 31% decrease in cardiovascular mortality and a 15% decrease in other causes of mortality.  Those who reported vigorous-intensity physical activity of 150 to 299 min per week had a further decrease in mortality of 2% to 4%.  Vigorous-intensity physical activity of more than 300 minutes a week and moderate-intensity physical activity of more than 600 minutes per week did not lower mortality any further in this study.   The authors concluded that the decreased mortality effect of exercise was maximally achieved by performing approximately 150 to 300 minutes per week of long-term leisure-time vigorous physical activity or 300 to 600 minutes per week of long-term leisure-time moderate physical activity, or an equivalent combination of both.[4] A meta-analysis of 196 articles and over 30 million participants comparing leisure-time moderate-to-vigorous exercisers to controls found the following: Reduction in All-Cause, Cardiovascular Mortality and Cancer Incidence in Leisure-Time Moderate-to-Vigorous Exercisers Compared to Controls It was reported that even as little as 11 minutes of moderate-to-vigorous a day could produce some health benefits, although higher amounts of exercise of up to 300 minutes per week were more beneficial.  The authors also calculated that about 10% of premature deaths could be prevented if everyone in the population did 75 minutes of moderate-to-vigorous exercise per week, with increasing premature death prevention at increasing levels of exercise.  Predicted Reduction in Premature Deaths if Everyone in the Population Exercised [5] Gender Differences in Exercise Effect on Mortality Reduction  In a study of over 400,000 adults, it was reported that regular leisure-time aerobic exercise reduced all-cause mortality 24% in women and 15% in men compared to non-exercisers.  For cardiovascular mortality, regular aerobic exercise was associated with a risk reduction of 14% for men and 36% for women. Men reached their maximal survival benefit of a 19% reduction in mortality from approximately 300 minutes of exercise per week while women, to get the same benefit, only needed to perform 140 minutes of exercise per week.  However, women’s maximal mortality benefit of a 24% reduction occurred at approximately 300 minutes of exercise per week.[6]  Cancer Risk and Exercise Exercise in many meta-analyses has been shown to decrease cancer risk.   The risk of bladder cancer was 15% lower for individuals with the highest level of recreational or occupational physical activity than in those with the lowest levels.  A study which included over 1 million individuals found that leisure-time physical activity was associated with a 13% reduced risk of bladder cancer.  For breast cancer it was reported that the most physically active women had a 12–21% lower risk of breast cancer than those who were the least physically active.  Individuals who engaged in the highest level of physical activity had a 19% lower risk of colon cancer than those who were the least physically active. Highly physically active women had a 20% lower risk of endometrial cancer than women with low levels of physical activity.  Individuals who were most physically active had a 21% lower risk of esophageal adenocarcinoma than those who were least physically active.  The most physically active people have been found to have a 12% lower risk of renal cancer than those who were the least active.  Another analysis of over 1 million individuals found that leisure-time physical activity was linked to a 23% reduced risk of renal cancer.  Individuals who were the most physically active in another meta-analysis had a 19% lower risk of stomach cancer than those who were least active.[1] Dementia and Alzheimer’s disease A systematic review reported that high physical activity individuals compared to very low physical activity individuals had a 28% decreased risk of dementia, and a 45% decreased risk of Alzheimer’s disease.  It is postulated that exercise is neuroprotective due to reducing inflammation, improving cerebral blood flow, lowering blood pressure, reducing lipids and increasing the body’s production of neuroprotective substances, such as brain-derived neurotropic factor.[7]  Type 2 Diabetes and Exercise After eating, insulin is secreted and increases glucose storage as glycogen and fatty acid storage as triglycerides.  During exercise, fuel stores need to be mobilized. The pancreas decreases insulin secretion, and the body increases other processes that help mobilize glucose and fatty acids needed for energy.  After exercise is completed, there is a need to refill the fuel depots mobilized during the exercise, mainly glycogen stores in the muscles.  This is facilitated by an increased sensitivity of muscles to insulin post-exercise. The increased insulin sensitivity allows lower levels of insulin to be secreted from the pancreas.  Insulin sensitivity is higher in people who exercise regularly which decreases the amount of insulin the pancreas needs to produce.[8] Many studies have demonstrated that exercise can increase insulin responsiveness and decrease the risk of people developing type 2 diabetes.[9]  In one study, people who exercised and had an impaired glucose tolerance (prediabetes) had a 46% percent decreased incidence of progressing onto clinical diabetes compared to a control group.[10]  In other studies, there was a 30% risk reduction in subjects who exercised, with a history of impaired glucose tolerance, progressing onto type 2 diabetes.[9] Lipids and Exercise There have been mixed results in some meta-analyses as to the effect of aerobic exercise on lipid values.  One reported that only triglycerides were reduced,[11] while another found statistically significant decreases in total cholesterol (TC), triglycerides (TG), low-density lipoprotein(LDL), with an increase in high-density lipoprotein (HDL) when compared to a control group.[12] In a meta-analysis with female subjects, exercise led to statistically significant reductions of approximately 2%, 3%, and 5%, for TC, LDL, and TG respectively, whereas HDL increased by 3%.[13] In a meta-analysis with male subjects, exercise led to significant decreases of 2% for TC, 9% for TG and an increase of 2% for HDL.  There was a 3% decrease in LDL which was not found to be statistically significant.[14] Although the effects of exercise on lipids seems to be small, there are some data that even a 1% decrease in TC reduces the incidence of coronary heart disease (CAD) by 2%.[15]  Each LDL decrease of 1% reduces the risk of major coronary events by approximately 1.7%.[16] It appears that most of the medical literature points to exercise producing a small decrease in lipid levels, which while helpful, may also require alterations in diet as well as lipid-reducing medications for adequate treatment.[14]  Decreased Inflammation with Exercise It has been reported that leisure-time physical activity reduces levels of high-sensitivity C-reactive protein (CRP), a systemic marker of inflammation.  Inflammation can have a multitude of deleterious effects on the body.[17]  Some studies have reported a lowering of CRP with exercise, as well as lowering of other inflammatory markers including tumor necrosis factor alpha and interleukin-6.[18]  Theoretically, the anti-inflammatory effects of exercise may be related to a reduction of visceral fat (fat deep in the abdominal cavity) which in turn decreases the release of adipokines which activate inflammatory pathways.[19] Interleukin-6 (IL-6) has been found to have both inflammatory and anti-inflammatory properties.  IL-6 is released both by adipose tissue when at rest and by muscular activity during exercise.  It is felt that there may be different forms of IL-6 [20] with the one produced in muscles having anti-inflammatory properties.[21]   Depression and Exercise Data from a number of meta-analyses have found that exercise can reduce depressive symptoms.  Theories about why this occurs include: increased endorphin release, increased brain neurotransmitters, distraction from worries, and positive self-efficacy (the positive feeling one gets from completing a task with the desired outcome).[22]    Bone Health and Exercise Bone mass peaks at approximately 20 to 30 years of age, then plateaus and later starts to decrease with age in both men and women.  There is more bone loss in women due to estrogen reduction at menopause which may lead to osteoporosis.   Bone adaptation occurs when bone tissue deforms from muscle contraction and other stresses such as tortional force that occur during exercise.  Those forces affect biological sensors that lead to osteogenesis (new bone formation) at the site. This process is seen in tennis players, fencers and baseball players who have all been found to have higher bone densities in their active arm than their less active arm.[23,24]   In men there is evidence that exercise late in life will increase bone density, however the results of exercise in post-menopausal women in some studies showed no effect on bone density.[23,24]  It is possible that women who start exercising at younger ages and increase their bone mass might be able to mitigate some of the bone loss of aging.[24] Hip Fractures and Exercise in the Elderly  In a study of 77, 206 postmenopausal women, with a mean follow-up of 14 years, researchers reported that both walking activity and moderate to vigorous recreational physical activity reduced the risk of hip fractures.  There was a 1%, 8% and 12% decrease in hip fractures in subjects that did little walking, moderate walking or a lot of walking respectively, compared to a control group of non-regular walkers.  It was also reported that the risk of hip fracture was reduced 8% in moderate exercisers and 18% in vigorous exercisers.[25]  This occurred despite the lack of proof that exercise increases bone density in post-menopausal women.[23,26]   Another study of 13,987 elderly individuals compared the hip fracture incidence in subjects who engaged in more than one-half hour of daily exercise versus a control group who daily exercised less than one-half hour or did no exercise.  It was reported that compared to the control group, exercising an hour or more a day resulted in a 38% decrease in females and a 49% decrease in males in the risk of sustaining a hip fracture.  Exercising one-half hour to one-hour a day reduced the risk of hip fracture 28% in both males and females compared to the control group.[27] DNA Changes from Exercise  In an interesting experiment, 23 young subjects engaged in vigorous one-leg exercise for three months.  Muscle biopsies were taken before and after the training in both legs.  The researchers found 4,919 changes in DNA methylation in sites on the trained leg.  DNA methylation can facilitate or inhibit gene expression with respect to RNA transcription and the proteins synthesized.  Areas where DNA methylation was increased were mainly associated with muscle remodeling and glucose metabolism.  Areas with decreased DNA methylation were associated with inflammatory or immunological processes and transcriptional regulation.  This suggested to the authors that the changes in methylation seen with exercise training is not random, but rather a controlled process that may help skeletal muscle adapt to endurance training.[28]  Is There a Difference Between Leisure-Time and Occupational Physical Activity? In a study of 104,046 subjects, it was reported that there was a significant reduction in major adverse cardiovascular events and all-cause mortality risk in subjects who exercised moderately or more when compared to low leisure-time physical activity subjects.  However not all exercise is necessarily equal, and in what was called the “physical activity paradox”, occupational physical activity at all levels was found to increase both major adverse cardiovascular events and all-cause mortality risk.[29]  In another study it was reported that moderate-to-vigorous levels of occupational physical activity were found to have significantly higher CRP levels than leisure-time moderate-to-vigorous exercisers.[17]   The explanation for this confusing result is that occupational physical activity is possibly of a too low intensity or too long a duration for improving cardiovascular health.  Improvement of cardiorespiratory fitness requires a high intensity of physical activity for a short period of time.  Leisure-time exercise is for a short period with a recovery period where occupational physical activity is often performed throughout the entire day.  It has been found that occupational physical activity elevates 24-hour heart rate, and if there is frequent heavy lifting or standing without moving much, muscle contractions can occur which can elevate 24-hour blood pressure.  In addition, work stresses may contribute to the detrimental effects of occupational physical activity.[29,30]  Although the authors controlled for socio-economic class and felt it was not an issue in their conclusions, there was a much higher percentage of workers in the upper income group who did low amounts of manual labor.[29]  Thus, it is possible there still might be other lifestyle or socioeconomic class issues that might partially explain the “physical activity paradox”. Conclusions There is abundant scientific evidence that regular leisure-time exercise can reduce systemic inflammation as well as the reduce the incidence of premature mortality, arteriosclerotic heart disease, some cancers, diabetes, dementia, Alzheimer’s disease, hip fractures, and improve bone health and depression.  There is some evidence that occupational related exercise may not have the same protective effects as leisure-time exercise.   As little as 11 minutes of moderate-to vigorous exercise per day may result in health benefits.  People with health problems or middle aged and above should consult a doctor before embarking on an exercise program to ensure safety.     Author’s Note :  The photo at the beginning of the article was used because of the unbridled joy of exercise it depicted.  However, it is recommended that a helmet be worn whenever you ride a bicycle to prevent serious head injury.  Thank you to   Dr. Theodor Feigelman for editing this article. 🎓  Want Free CME Credit for This Article? Take the quiz now at www.FibonacciMD.app . It only takes a few minutes! Your certificate will be emailed to you after you pass the quiz and complete a short evaluation We’ll send you occasional updates. Your email stays private—never sold or shared.  😇 Download PDF: References [1] Physical Activity and Cancer. National Cancer institute. Last reviewed: February 10, 2020. Retrieved from: https://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/physical-activity-fact-sheet [2] Examples of Moderate and Vigorous Physical Activity Harvard, T.H. Chan School of Public Health. 2024. Retrieved from: https://www.hsph.harvard.edu/obesity-prevention-source/moderate-and-vigorous-physical-activity/ [3] Piercy KL, Troiano RP, Ballard RM, et al. The Physical Activity Guidelines for Americans. JAMA. 2018;320(19):2020-2028. doi:10.1001/jama.2018.14854 Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9582631/ [4] Lee DH et al. Long-Term Leisure-Time Physical Activity Intensity and All-Cause and Cause-Specific Mortality: A Prospective Cohort of US Adults. Circulation. August 16, 2022, Vol 146, Issue 7. Retrieved from: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.121.058162?cookieSet=1 [5]Garcia L et al. Non-occupational physical activity and risk of cardiovascular disease, cancer and mortality outcomes: a dose–response meta-analysis of large prospective studies. British Journal of Sports Medicine 2023;57:979-989. Retrieved from: https://bjsm.bmj.com/content/bjsports/57/15/979.full.pdf [6] Ji H et al. Sex Differences in Association of Physical Activity With All-Cause and Cardiovascular Mortality. Journal of the American College of Cardiology. Volume 83, Issue 8, 27 February 2024, Pages 783-793. Retrieved from: https://www.sciencedirect.com/science/article/pii/S0735109723083134?via%3Dihub [7] Hamer M, Chida Y. Physical activity and risk of neurodegenerative disease: a systematic review of prospective evidence. Psychological Medicine. 2009;39(1):3-11. Retrieved from: https://www.cambridge.org/core/journals/psychological-medicine/article/abs/physical-activity-and-risk-of-neurodegenerative-disease-a-systematic-review-of-prospective-evidence/5FB109E05E85CF701F11FB6DBA9AE9B3 [8] Richter EA et al. Interactions between insulin and exercise. Biochem J 12 November 2021; 478 (21): 3827–3846.  Retrieved from: https://accessapps.amdi.usm.my/reqba_uploads/article/bcj-2021-0185c.pdf [9] Peirce NS. Diabetes and exercise. Br J Sports Med 1999;33:161–173. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1756173/pdf/v033p00161.pdf [10] Pan XR, Li GW, Hu YH, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care. 1997;20(4):537-544. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/9096977/ [11] Kelley GA et al. Comparison of aerobic exercise, diet or both on lipids and lipoproteins in adults: A meta-analysis of randomized controlled trials. Clinical Nutrition. Volume 31, Issue 2, Pages 156-167. 201. Retrieved from: https://www.sciencedirect.com/science/article/abs/pii/S0261561411002238 [12] Tran CV et al.   The effects of exercise on blood lipids and lipoproteins: a meta-analysis of studies. Med Sci Sports Exerc, 1983. Retrieved from: https://www.researchgate.net/profile/Zung-Tran-2/publication/16550198_The_effects_of_exercise_on_blood_lipids_and_lipoproteins_A_meta-analysis_of_studies/links/564b7e0008ae020ae9f82835/The-effects-of-exercise-on-blood-lipids-and-lipoproteins-A-meta-analysis-of-studies.pdf   [13] Kelley GA et al. Aerobic exercise and lipids and lipoproteins in women: a meta-analysis of randomized controlled trials. Journal of Women's Health, 13(10), 1148-1164,  2004. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447858/ [14] Kelley GA, Kelley KS. Aerobic exercise and lipids and lipoproteins in men: a meta-analysis of randomized controlled trials. J Mens Health Gend. 2006;3(1):61-70. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475654/ [15] Consensus Development Panel. Lowering blood cholesterol to prevent heart disease. J Am Med Assoc; Consensus conference; 1985. pp. 2080–6. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/3974099 [16] Pedersen TR, Olsson AG, Faergeman O, et al. Lipoprotein changes and reduction in the incidence of major coronary heart disease events in the Scandinavian Simvastatin Survival Study (4S). Circulation. 1998;97(15):1453-1460. Retrieved from: https://www.ahajournals.org/doi/10.1161/01.cir.97.15.1453?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed [17] Lee J, Kim H, Jang T, et al. Occupational physical activity, not leisure-time physical activity, is associated with increased high-sensitivity C reactive protein levels. Occupational and Environmental Medicine 2021;78:86-91. Retrieved from: https://oem.bmj.com/content/78/2/86.long [18] Beavers KM, Brinkley TE, Nicklas BJ. Effect of exercise training on chronic inflammation. Clin Chim Acta. 2010 Jun 3;411(11-12):785-93. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629815/ [19] Gleeson M, Bishop NC, Stensel DJ, Lindley MR, Mastana SS, Nimmo MA. The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol. 2011;11(9):607-615. Published 2011 Aug 5. Retrieved from: https://www.nature.com/articles/nri3041 [20] Rose-John S. IL-6 trans-signaling via the soluble IL-6 receptor: importance for the pro-inflammatory activities of IL-6. Int J Biol Sci. 2012;8(9):1237-1247. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491447/ [21] Pedersen BK, Steensberg A, Schjerling P. Muscle-derived interleukin-6: possible biological effects. J Physiol. 2001;536(Pt 2):329-337. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278876/    [22] Craft LL, Perna FM. The Benefits of Exercise for the Clinically Depressed. Prim Care Companion J Clin Psychiatry. 2004;6(3):104-111. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC474733/ [23] Barry, Daniel W. MD; Kohrt, Wendy M. PhD. Exercise and the Preservation of Bone Health. Journal of Cardiopulmonary Rehabilitation and Prevention 28(3):p 153-162, May 2008. Retrieved from: https://journals.lww.com/jcrjournal/abstract/2008/05000/exercise_and_the_preservation_of_bone_health.1.aspx [24] Santos, L., Elliott-Sale, K.J. & Sale, C. Exercise and bone health across the lifespan. Biogerontology 18, 931–946 (2017). Retrieved from: https://link.springer.com/article/10.1007/s10522-017-9732-6 [25] Lamonte WJ et al. Association of Physical Activity and Fracture Risk Among Postmenopausal Women. JAMA Netw Open. 2019;2(10):e1914084. Retrieved from: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2753526 [26] Kohrt, WM et al. Physical Activity and Bone Health. MEDICINE & SCIENCE IN SPORTS & EXERCISE. American College of Sports Medicine. 2004. Retrieved from: https://www.corsi.univr.it/documenti/OccorrenzaIns/matdid/matdid600016.pdf [27] Exercise and Other Factors in the Prevention of Hip Fracture: The Leisure World Study. Paganini-Hill a et al.  Epidemiology. Vol. 2, No. 1 (Jan., 1991), pp. 16-25.Retrieved from: https://www.jstor.org/stable/20065660 [28] Maléne E Lindholm Me et al.  An integrative analysis reveals coordinated reprogramming of the epigenome and the transcriptome in human skeletal muscle after training, Epigenetics, 9:12, 1557-1569. 2012. Retrieved from: https://www.tandfonline.com/doi/epdf/10.4161/15592294.2014.982445?needAccess=true [29] Holtermann A, Schnohr P, Nordestgaard BG, Marott JL. The physical activity paradox in cardiovascular disease and all-cause mortality: the contemporary Copenhagen General Population Study with 104 046 adults. Eur Heart J. 2021;42(15):1499-1511. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8046503/ [30] Holtermann A, Krause N, van der Beek AJ, et al. The physical activity paradox: six reasons why occupational physical activity (OPA) does not confer the cardiovascular health benefits that leisure time physical activity does. British Journal of Sports Medicine 2018;52:149-150. Retrieved from:  https://bjsm.bmj.com/content/52/3/149.long

Discover the sweet and tart truth about cherries! These ruby-red powerhouses, in season late spring to early summer, are packed with nutrients and phytochemicals offering heart, cancer, and sleep benefits. by   Mary B Grosvenor, MS, RD   and Lori A Smolin, PhD   Life may or may not be a bowl of cherries, but they can certainly make it a little bit better. Fresh cherries offer a sweet, sometimes tart, juicy treat in late spring and early summer. Frozen and dried cherries are available year-round. This ruby-colored fruit is low in calories and high in nutrients and other health-promoting substances, providing a  guilt-free indulgence that  can boost your nutrient intake and benefit your health. Cherries originated in Mesopotamia and were first cultivated by the ancient Greeks. They were carried  throughout Europe by the Romans as their empire expanded. Cherries were brought to America by English colonist in the 1600s and were later introduced in California by Spanish missionaries. [1]  On average, Americans eat about 2.2 pounds of cherries per year. [2] Cherry Botany Cherries are classified as a stone fruit, named for the single hard pit, or stone, in the center. The pit is surrounded by fleshy fruit and a thin skin.  Stone fruits, also called drupes, include peaches, plums, and apricots as well as cherries. Of the more than 1,200 varieties of cherries, the most popular are Bing, Rainer, Black, Queen Anne, and Montmorency.[3] Generally, they are placed in two categories, sweet cherries and sour or tart cherries. Dark red Bing cherries are the most popular sweet cherry. Rainier and Queen Anne are also common sweet cherry varieties, with a yellow and orange color distinctive in the cherry world. Sweet cherries are typically eaten fresh, whereas tart cherries are used in pies and juices. Bright red Montmorency are the most popular tart cherry.[4] Nutritional and Health Benefits Cherries have been called a superfruit because of the nutrients and phytochemicals they contain. One cup, or about 20 cherries, provides about 85 Calories, over 3 grams of fiber, and a gram and a half of protein along with over 10% of the recommended intake of vitamin C and copper, 300 mg of potassium, and  small amounts of calcium, iron, folate, and vitamin A. Cherries are high in polyphenols, in particular anthocyanins, which give them their red color. These phytochemicals, along with vitamin C,   give cherries antioxidant and anti-inflammatory properties, which has led to the suggestion that they may help reduce the risk of heart disease, cancer, and other inflammatory diseases, as well as improve exercise performance and sleep.[5,6] Cherries may protect heart health by helping to manage blood pressure and because the polyphenols they contain  reduce cellular damage and inflammation.[ 5,6 ]  The phytochemicals in cherries have been found to guard against cancer by acting as antioxidants and anti-inflammatory agents as well as by helping to regulate cell death and proliferation, and the invasion and migration of cancer cells .[7] Cherries and their juice have been shown to be beneficial for arthritis and gout.[6,8]   One study found that subjects eating fresh cherries for two days had a 35% lower risk of gout flare-ups compared with those who didn’t eat cherries. Those who combined cherry intake with  medications for gout  had a 75% reduction in flare-ups.[9]  Tart cherry concentrate has been shown to benefit endurance exercise performance by improving muscle function and reducing muscle damage, oxidative stress, inflammation, and muscle soreness.[10,11]   Tart cherry juice concentrate can also help you sleep better because it provides the antioxidant phytochemical melatonin, which improves sleep duration and quality.[12] Yet even a bowl of cherries can have its downsides. Eating too many can cause bloating, cramps, and diarrhea in some people because cherries are high in the sugar alcohol, sorbitol. This is a particular problem for those with irritable bowel syndrome.  And make sure to spit the pits. Cherry pits contain small amounts of poisonous cyanide. But don’t panic if you swallow one – whole cherry pits are unlikely to be toxic. The cyanide is not released unless the pit is chewed or crushed; you would need to chew about 5 pits to release enough cyanide to cause a reaction.[13] Enjoy Some Cherries Cherries are delicious fresh from the grocery store, farmer’s market, or pick-your-own orchard. Be sure to wash them before eating because they may have been sprayed with pesticides.  They can sweeten breakfast cereal or yogurt, or top an ice cream treat.  Cherries both sweet and tart are baked into pies, cobblers, and crisps. They can also be made into sauces, salsas, and dressings served with savory dishes. While most often eaten cold they can be roasted with sugar or with some salt and olive oil. So, enjoy a bowl of cherries. They contribute color and flavor to our food and provide health benefits to our bodies. References [1] Agclassroom.org . Cherries Published 2025. Accessed June 7, 2025. https://cdn.agclassroom.org/ca/factsheets/cherry [2]  Top 20 Fruits and Vegetables Sold in the U.S. 2020. International Fresh Produce Association. Published November 12, 2021. https://www.freshproduce.com/resources/consumer-trends/top-20/ [3]  Austin, A. People with sensitive stomachs avoid eating cherries. Here's why. USA Today. April 6, 2024. https://www.usatoday.com/story/life/health-wellness/2024/08/06/are-cherries-good-for-you/74503368007/ [4] Southern Living.  Our 6 Favorite Types Of Cherries. Published 2021. Accessed May 31, 2025. https://www.southernliving.com/food/fruits/types-of-cherries [5] Kubala J. 7 Impressive Health Benefits of Cherries. Healthline. Published June 19, 2019. Accessed May 31, 2025. https://www.healthline.com/nutrition/cherries-benefits#healthier-heart [6] Kelley DS, Adkins Y, Laugero KD. A Review of the Health Benefits of Cherries. Nutrients. 2018;10(3):368. Published 2018 Mar 17. `` [7] Fonseca LRS, Silva GR, Luís Â, et al. Sweet Cherries as Anti-Cancer Agents: From Bioactive Compounds to Function. Molecules. 2021;26(10):2941. Published 2021 May 15. doi:10.3390/molecules26102941 [8] Chen PE, Liu CY, Chien WH, Chien CW, Tung TH. Effectiveness of Cherries in Reducing Uric Acid and Gout: A Systematic Review. Evid Based Complement Alternat Med. 2019;2019:9896757. Published 2019 Dec 4. doi:10.1155/2019/9896757 [9] Zhang Y, Neogi T, Chen C, Chaisson C, Hunter DJ, Choi HK. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis Rheum. 2012;64(12):4004-4011. doi:10.1002/art.34677 [10] Gao R, Chilibeck PD. Effect of Tart Cherry Concentrate on Endurance Exercise Performance: A Meta-analysis. J Am Coll Nutr. 2020;39(7):657-664. doi:10.1080/07315724.2020.1713246 [11] Levers K, Dalton R, Galvan E, et al. Effects of powdered Montmorency tart cherry supplementation on acute endurance exercise performance in aerobically trained individuals. J Int Soc Sports Nutr. 2016;13:22. Published 2016 May 26. doi:10.1186/s12970-016-0133-z [12] Howatson G, Bell PG, Tallent J, Middleton B, McHugh MP, Ellis J. Effect of tart cherry juice (Prunus cerasus) on melatonin levels and enhanced sleep quality. Eur J Nutr. 2012;51(8):909-916. doi:10.1007/s00394-011-0263-7 [13] Are Cherry Pits Safe to Eat? Cyanide Content and More. Healthline. Published April 14, 2021. https://www.healthline.com/nutrition/cherry-pits ‌ Photo Credits to   Mary B Grosvenor, MS, RD

The debate over fluoridated water has resurfaced amid new legislation. This article explores fluoride sources, its effects on oral health, the history and current state of water fluoridation, and potential risks, particularly to children's cognitive development. by Lori A Smolin, PhD   and Mary B Grosvenor, MS, RD In 1999 the Centers for Disease Control and Prevention declared fluoridation of drinking water one of the ten great public health achievements of the 20th century.[1] Twenty six years later, in March of 2025, the Governor of Utah signed a law banning the addition of fluoride to drinking water.[2] Bills to ban fluoridation have also been introduced in several other states. Controversy around the safety of water fluoridation has existed since its inception but has intensified recently due to research suggesting a link between high intakes of fluoride and IQ.[3,4] Where Do We Get Fluoride? Fluoride is a mineral found in small amounts in almost all soil, water, and foods, including tea and marine fish consumed with their bones.[5] Tea contributes significantly to fluoride intake in cultures where large amounts are consumed. In the United States however, most of the ingested fluoride comes from fluoride in toothpaste and other dental products and from fluoride added to the water supply. Because food readily absorbs fluoride from cooking water, the fluoride content of foods can be significantly increased when it is prepared using fluoridated water. Based primarily on studies done in the 1970s and 80s, the typical fluoride intake in the U.S. from food and beverages, including fluoridated water, is estimated to be 2.2 mg/day for young children and 2.9 mg/day for adults.[5] Swallowed toothpaste adds - depending on how much is swallowed - about 0.1 mg per day in adults and over twice this in young children. [5,6] Fluoride and Oral Health While fluoride is not an essential nutrient, nutrition guidelines do make daily intake recommendations based on the amount consumed by healthy individuals that benefits oral health. This amount is 0.05 mg/kg body weight/day for everyone over 6 months of age, or about 1.1 mg/day for a 6-year-old and 3.8 mg/day for an adult. [7]  Because fluoride has a high affinity for calcium most of the fluoride in the human body is found in bones and teeth, where it strengthens bone and makes teeth more resistant to decay. Tooth decay, also known as cavities or dental caries, is the most common noncommunicable disease in the world. It occurs when bacteria in the mouth form colonies, known as plaque, on the surface of the teeth. If not removed, the bacteria in the plaque metabolize dietary carbohydrates, producing acids that dissolve tooth enamel and the underlying tooth structures. Cavities may seem like a minor issue, but left untreated, they can cause incapacitating pain, reduce the ability to eat, lead to tooth extraction,  and cause systemic infection . [8,9] Fluoride consumed early in life, during tooth development, is incorporated into tooth enamel, making it more resistant to the acid that causes decay. After the teeth are formed, fluoride is no longer incorporated into the enamel, but ingested fluoride is secreted in saliva. This continually bathes the teeth reducing the amount of acid produced by bacteria, inhibiting the dissolution of tooth enamel by acid, and increasing enamel remineralization after acid exposure.[10] Fluoride in toothpaste and mouth rinses has the same topical effect but remains in the mouth for only a few hours after use. Fluoridation of Drinking Water Fluoride is added to community water supplies to reduce the risk of tooth decay. This intervention had its beginnings in the early 1900s, when it was observed that people in areas with naturally high levels of fluoride in the water had fewer cavities, but also often had stained teeth, a condition originally called Colorado Brown Stain and now known as dental fluorosis. [9] By the 1940s, studies that added low levels of fluoride to drinking water found tooth decay to be reduced by 50 to 70% among children in communities where fluoride was added to the water compared to those in communities without added fluoride. [9] B y 1950, the American Dental Association and the U.S. Public Health Service endorsed fluoridation of community water supplies. Continued evidence of the benefits of fluoridated water to dental health led to the development of the first guidelines for the addition of fluoride to water in 1962. [11]   Currently, the U.S. Public Health Service recommends an optimal water fluoride concentration of 0.7 mg/L; an amount that maximizes dental health and minimizes the risk of fluorosis. This is not a mandate but a guideline for state and local governments to use in deciding whether to implement water fluoridation.[12] To reach this level, communities add fluoride when water fluoride levels are low, remove fluoride where levels are too high, or just monitor the concentration when the water already contains the recommended amount of fluoride.[12] Currently about 63% of Americans are served by community water systems that fluoridate their water.[13] When compared to non-fluoridated communities, these fluoridation programs have been estimated to reduce tooth decay by about 25%.[12] T he difference in effectiveness between current studies and those reported in the 1940s has been attributed to the consumption of foods and beverages processed or bottled with fluoridated water in areas without fluoridated water and to the widespread use of fluoride toothpaste, which was first marketed in 1956 and now accounts for about 95% of the toothpaste sales in the U.S. [9,11,14] Is Fluoride Harmful? The potential for fluoride to cause harm depends on the amount that is consumed. Single doses in the range of 3 to 5 grams are fatal, although this has only been reported from accidental poisoning.[15]  Much smaller fluoride doses, such as might be obtained from water that exceeds 4 mg/L, carries a risk for changes in bone structure.  [16] This amount is uncommon in natural water supplies, and 4 mg/L has been set as the limit allowed by the Environmental Protection Agency   in public water systems.[16] The most common adverse effect, dental fluorosis, occurs at even lower doses.[15] During tooth development, which takes place in children 8 years and younger, fluoride intakes of only a few milligrams per day can cause the symptoms of dental fluorosis, which range from white  or brown stains on the teeth to pitting of the tooth enamel. To prevent dental fluorosis, nutrient guidelines recommend that fluoride intake be limited to no more than 1.3 mg/day for children ages 1 to 3 years and no more than 2.2 mg/day for those 4 through 8 years.  Dental fluorosis does not occur in those older than 8 years but an upper limit of 10 mg/day has been set to protect bone health.[7]  While these recommendations set clear guidance for protecting dental and bone health, they do not address some of the newer research suggesting a link between higher fluoride intakes and lower IQs in children. Several recent large studies have evaluated the impact of fluoride intake on IQ in children. A National Toxicology Program Monograph and corresponding systematic review and meta-analysis concluded with moderate confidence that at fluoride exposures that exceed 1.5 mg/L of drinking water there is a dose response association between higher fluoride level and lower IQ in children.[17,18] When childhood exposure to fluoride levels below 1.5 mg/L of drinking   water was examined, no association was found.[18] Thus far, however, studies examining fluoride and IQ have only looked for an association between the two. An association does not mean that high fluoride is the cause of lower IQ; a mechanism whereby fluoride might affect IQ has not been determined. Factors other than, or in addition to fluoride, could be contributing to the reductions in IQ. Questions have also been raised about the impact of fluoride on the gut microbiome, but reviews of the current literature show that fluoride at levels typically consumed (less than 2mg/L) have no impact on the gut microbiome. [26] Weighing the Risks and Benefits The risk that high fluoride intake in children may result in reductions in IQ is the focus of current concerns.  Data from populations around the world have found lower IQ scores in children exposed to fluoride levels above 1.5mg/L of drinking water. [18,19]   But in the United States, where water is a major dietary source of this mineral, fluoride is added to water at a level that is less than half of the lowest amount associated with IQ reductions.[12] Based on this, it could be assumed that the risk to children is low. However, there is no recent data on total fluoride intake in U.S. children  and no studies have examined the relationship between fluoride intake and IQ in the United States, so it is difficult to accurately evaluate risk.  We do know that there are areas in the U.S. where the natural water supply contains fluoride levels greater than 1.5 mg/L.[18]  Individuals whose water comes from a community water supply can request information on the fluoride in their drinking water by contacting the supplier. Those whose w ater comes from a well can have it tested for fluoride content. Another major source of fluoride in the U.S. is fluoride-containing toothpaste and dental rinses. The American Dental Association recommends fluoridated toothpaste but also recognizes that the ingestion of too much fluoride while teeth are developing can cause dental fluorosis. [20] Therefore, it is recommended that children begin using fluoride toothpaste at age 2 years, and until age 3 should use just a smear the size of a rice grain. Children aged 3 to 6 years should use no more  than a pea-sized amount. Following these standards and making sure older children do not swallow fluoride-containing toothpaste or dental rinses can help maximize the benefits and minimize the risks. [20] A majority of Americans consume fluoridated water and use a fluoride-containing toothpaste. Researchers have expressed concern that for some, particularly children, total fluoride intake may reach levels comparable to that associated with reduced IQ [21]. But is the solution to end water fluoridation for everyone? There is evidence that cessation of fluoridation will cause a decline in dental health, particularly in those without the resources to access fluoridated oral care products or good dental care.  Seven to eight years after the city of Calgary stopped water fluoridation the incidence of tooth decay was 10% greater than in Edmonton, where fluoridation remained in place; the lack of fluoride had a greater impact in those without dental insurance. [22,23] Bottom Line Fluoridation of community drinking water is the most cost-effective method of delivering fluoride to the American public. The recommended level of fluoride in drinking water in the United States reduces the risk of tooth decay and saves billions of dollars in annual dental costs; and there is no evidence that it affects children’s IQ.[24] However, more research is needed to determine the actual intake of fluoride in U.S. children including that in the food and water supply as well as that ingested in swallowed toothpaste and dental rinses.[18]   More research is also needed on how and if fluoride affects brain development, its effect on the microbiome, and the oral health impact of stopping water fluoridation. [25] References [1] CDC. Ten Great Public Health Achievements -- United States, 1900-1999 . CDC. Published April 2, 1999. https://www.cdc.gov/mmwr/preview/mmwrhtml/00056796.htm‌ [2] Moyer MW. Utah Becomes First State to Ban Fluoride in Public Water. The New York Times. https://www.nytimes.com/2025/03/28/well/utah-fluoride-ban.html . Published March 28, 2025. [3] Hicks, J. .Pipe Dreams: America’s Fluoride Controversy. Science History Institute. Published December 4, 2024. Accessed May 9, 2025. https://www.sciencehistory.org/stories/magazine/pipe-dreams-americas-fluoride-controversy [4] Grandjean P. Developmental fluoride neurotoxicity: an updated review. Environmental Health. 2019;18(1). doi: https://doi.org/10.1186/s12940-019-0551-x [5] National Institute of Health. Office of Dietary Supplements - Fluoride. ods.od.nih.gov . Published April 26, 2022. https://ods.od.nih.gov/factsheets/Fluoride-HealthProfessional/ [6] U.S. Environmental Protection Agency Fluoride Risk Assessment and Relative Source Contribution 2010 https://www.epa.gov/sdwa/fluoride-risk-assessment-and-relative-source-contribution [7] Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington (DC): National Academies Press (US); 1997. 8, Fluoride.Available from: https://www.ncbi.nlm.nih.gov/books/NBK109832/ [8] World Health Organization. Sugars and Dental Caries. World Health Organization. Published November 9, 2017. https://www.who.int/news-room/fact-sheets/detail/sugars-and-dental-caries [9] CDC. Achievements in Public Health, 1900-1999: Fluoridation of Drinking Water to Prevent Dental Caries. Published 2019. https://www.cdc.gov/MMWR/preview/mmwrhtml/mm4841a1.htm [10] CDC. About Fluoride. Oral Health. Published May 9, 2024. https://www.cdc.gov/oral-health/prevention/about-fluoride.html [11] CDC. Timeline for Community Water Fluoridation. Community Water Fluoridation. Published May 23, 2024. https://www.cdc.gov/fluoridation/timeline-for-community-water-fluoridation/index.html [12] CDC. About Community Water Fluoridation. Community Water Fluoridation. Published May 15, 2024. https://www.cdc.gov/fluoridation/about/index.html [13] CDC. 2022 Water Fluoridation Statistics. Community Water Fluoridation. Published 2024. https://www.cdc.gov/fluoridation/php/statistics/2022-water-fluoridation-statistics.html [14] American Dental Association. Fluoride: Topical and Systemic Supplements. www.ada.org . Published June 14, 2023. https://www.ada.org/resources/ada-library/oral-health-topics/fluoride-topical-and-systemic-supplements ‌[15] Guth S, Hüser S, Roth A, Degen G, et al Toxicity of fluoride: critical evaluation of evidence for human developmental neurotoxicity in epidemiological studies, animal experiments and in vitro analyses. Arch Toxicol. 2020 May;94(5):1375-1415. doi: 10.1007/s00204-020-02725-2. [16] National Primary Drinking Water Regulations | US EPA. US EPA. Published November 30, 2015. https://www.epa.gov/ground-water-and-drinking-water/national-primary-drinking-water-regulations#Inorganics [17] NTP Monograph on the State of the Science Concerning Fluoride Exposure and Neurodevelopment and Cognition: A Systematic Review. Published online August 1, 2024. doi: https://doi.org/10.22427/ntp-mgraph-8 [18] Taylor KW, Eftim SE, Sibrizzi CA, et al. Fluoride Exposure and Children's IQ Scores: A Systematic Review and Meta-Analysis. JAMA Pediatr. 2025;179(3):282-292. doi:10.1001/jamapediatrics.2024.5542 [19] Kumar JV, Moss ME, Liu H, Fisher-Owens S. Association between low fluoride exposure and children’s intelligence: a meta-analysis relevant to community water fluoridation. Public Health. 2023;219:73-84. doi: https://doi.org/10.1016/j.puhe.2023.03.011 [20] Thornton-Evans G, Junger ML, Lin M, Wei L, Espinoza L, Beltran-Aguilar E. Use of Toothpaste and Toothbrushing Patterns Among Children and Adolescents — United States, 2013–2016. MMWR Morbidity and Mortality Weekly Report. 2019;68(4):87-90. doi: https://doi.org/10.15585/mmwr.mm6804a3 [21] National Academies of Sciences, Engineering, and Medicine. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. https://doi.org/10.17226/11571 . [22] McLaren L, Patterson SK, Faris P, et al. Fluoridation cessation and children's dental caries: A 7-year follow-up evaluation of Grade 2 schoolchildren in Calgary and Edmonton, Canada. Community Dent Oral Epidemiol. 2022;50(5):391-403. doi:10.1111/cdoe.12685 [23] McLaren L, Patterson SK, Faris P, et al. Fluoridation cessation and oral health equity: a 7-year post-cessation study of Grade 2 schoolchildren in Alberta, Canada. Can J Public Health. 2022;113(6):955-968. doi:10.17269/s41997-022-00654-4 [24] CDC. Facts About Return on Investment of Oral Health Interventions. Oral Health. Published August 14, 2024. https://www.cdc.gov/oral-health/data-research/facts-stats/fast-facts-return-on-investment.html [25] National Toxicology Program. Fluoride Exposure: Neurodevelopment and Cognition. National Toxicology Program. Published August 22, 2024. https://ntp.niehs.nih.gov/whatwestudy/assessments/noncancer/completed/fluoride [26] Yasin M, Zohoori FV, Kumah EA, Subramanian M, Dean P, Orr CH. Effect of Fluoride on Gut Microbiota: A Systematic Review.  Nutrition Reviews . Published online March 10, 2025. doi: https://doi.org/10.1093/nutrit/nuae202

Grilled chicken, fresh strawberries, and crisp mixed greens make a light, healthy meal. Creative Cooking for the Health-Conscious Gourmet FibonacciRECIPES  | Culinary Medicine   Recipe These sweet and tangy chicken slices, served with strawberries and mixed greens, is a spring delight. You can also enjoy the marinated grilled chicken warm with rice. Ingredients: 1 pound (4) boneless skinless chicken breasts 2 ½ cups whole strawberries, divided 4 cups mixed salad greens 1 garlic clove, diced 1 tsp Dijon mustard 1/8 tsp black pepper ½ cup crumbled blue cheese ¼ cup balsamic vinegar ¼ cup canola or grapeseed oil ¼ cup sliced almonds ¼ tsp salt Fresh ground pepper and sea salt for garnish Lite balsamic salad dressing Instructions: Stir together vinegar, garlic, mustard, salt, pepper, and canola oil in bowl Dice ½ cup of the strawberries and add to vinegar marinade Pour marinade over chicken, stir, cover, and refrigerate for at least 4 hours or overnight, mixing occasionally. When ready to prepare, remove chicken from marinade and grill, about 3-5 minutes on each side until internal temperature reaches 165 degrees. Discard marinade Allow to chicken to cool and then slice thinly against the grain Wash and slice the remaining strawberries Wash salad greens For each bowl of salad, add 1 cup greens, 1 sliced chicken breast, ½ cup sliced strawberries, 2 tbsp blue cheese, and 1 tbsp almonds Garnish with almonds, Drizzle with lite balsamic dressing. Sprinkle with sea salt and fresh ground pepper to taste Nutritional Information Makes 4 Servings Nutrients in a serving:   Calories  265, Total Fat 8g, Saturated Fat 1.4 g, Cholesterol 90mg, Total Carbohydrate 8g, Dietary fiber 4g, Protein 37g, Potassium 565mg, Sodium 350mg Nutrition Chef Authors : Mary B Grosvenor, MS, RD Lori A Smolin, PhD Medically Reviewed by FibonacciMD editors. Editor's Note:  This recipe is appropriate for a low-calorie, low cholesterol, low saturated fat, low carbohydrate, high protein dietary regimen and a good source of fiber. Learn about some of the health benefits of strawberries in our article about Sweet Science: Unpacking the Health Benefits of Strawberries

Understanding Adenomatous Polyps as Precursors to Colorectal Cancer Adenomatous polyps are common precancerous lesions linked to colorectal cancer and frequently detected through colonoscopies. This post explores their causes and risk factors, histology, diagnostic screening, and follow-up detection to reduce cancer risk. Adenomatous Polyp By   Devon Drew, Nancy Mills , and Richard Strongwater Adenomatous polyps are dysplastic lesions resulting from  APC  gene mutation that cause increased intestinal crypt cell proliferation. They are considered to be precancerous and are the precursor lesions to ~70% of colorectal cancers. They are the most common finding in screening colonoscopies, with a prevalence of ~30% in average-risk individuals. Typically, these polyps are asymptomatic and discovered only on routine colonoscopy, but they may cause bleeding. Adenomatous polyps that are small and contain only low-grade dysplasia have limited clinical significance, but they are nonetheless removed to prevent the possibility of progression to cancer. Such progression is believed to take ~10 years. The risk of progression is low in non-advanced lesions < 5 mm in size; it is present in < 1% of lesions 6-9 mm in size. Causes and Risk Factors Increasing age, male gender, family history of colon cancer, family history of advanced adenomatous polyps, and inherited polyposis syndromes increase the risk of developing adenomatous colon polyps. Diagnostic Evaluation Colonoscopy is the gold standard for discovering adenomatous polyps.  It has a high sensitivity for their detection. Polyps are removed and sent to pathology for further evaluation. Upon microscopic evaluation, adenomatous polyps can be subclassified into tubular, villous, or tubulo-villous types, depending on their histology. The majority are tubular, but if they contain > 25% villous architecture, they are then designated tubulo-villous; > 75% villous architecture classifies them as villous. Most lesions contain only low-grade dysplasia, but increasing lesion size increases the likelihood of finding invasive cancer or villous elements within the lesion. Adenomatous polyps > 1 cm in size or containing high-grade dysplasia and/or villous elements are considered to be advanced; these carry a higher risk of progression to cancer. Polyps may also be classified as elevated, flat, or depressed, depending on their morphology. A depressed morphology increases the likelihood of adenocarcinoma occurrence even in smaller lesions. Computed tomography colonography and capsule colonoscopy have a high sensitivity for the detection of adenomatous polyps > 1 cm in size but less sensitivity than traditional colonoscopy for small polyps. Additionally, patients with polyps measuring > 6 mm that are found during these procedures are advised to undergo traditional colonoscopy for polyp removal. Fecal immunochemical testing (FIT), FIT-fecal DNA testing (see below), flexible sigmoidoscopy, and Septin9 screening are additional tests that aid in the detection of colorectal cancer but that have limited utility in the detection of precancerous adenomatous polyps. Treatment and Recommended Follow-Up Screening colonoscopy or other detection methods should begin at age 45 in average-risk individuals. All polyps are endoscopically or surgically removed upon detection. However, depending on the size and morphology of the polyp, complete resection may not always be achieved. Between 19%–27% of colorectal cancer that occurs between colonoscopy screenings appear at the site of a previously removed polyp where residual tissue has been left behind. Generally, patients with no polyps may undergo follow-up colonoscopy at 10-year intervals if not considered high risk. Individuals having 1–2 tubular adenomas < 10 mm in size are considered to be at low risk, and the recommended follow-up colonoscopy can be performed in 5-10 years. Individuals having either adenomas containing villous architecture, polyps > 10 mm in size, three or more adenomas, or high-grade dysplasia are considered to be at high risk and should be followed up with colonoscopy in 3 years. Individuals with a relative who had colorectal cancer or advanced/high risk polyps are at higher risk and should be screened with colonoscopy beginning at age 40 or 10 years younger than the age of the relative at diagnosis. If the relative was < 60 years of age, the screening should occur every 5 years; it should occur every 10 years if the relative was older than 60. CDC Screening recommendations The US Preventive Services Task Force (Task Force) www.UsPreventiveServicesTaskForce.org   recommends  that adults age 45 to 75 be screened for colorectal cancer. The decision to be screened between ages 76 and 85 should be made on an individual basis. For patients at an increased risk of getting colorectal cancer, screening should be made on an individual basis- considering when to begin screening, which test is right for them, and how often to be tested. Most patients should begin screening for colorectal cancer soon after turning 45, then continue screening at regular intervals. However, the patient may need to be tested earlier than 45, or more often than other people, if they have: Inflammatory bowel disease  such as Crohn's disease or ulcerative colitis. A personal or family history of colorectal cancer or colorectal polyps. A genetic syndrome such as  familial adenomatous polyposis (FAP)  or  hereditary non-polyposis colorectal cancer (Lynch syndrome). Stool tests The  guaiac-based fecal occult blood test (gFOBT)  uses the chemical guaiac to detect blood in the stool. It should be done once a year.  The  fecal immunochemical test (FIT)  aka iFOBT checks for blood generally from the lower intestines and uses antibodies to detect for blood in the stool. It is also done once a year in the same way as a gFOBT. Unlike the guaiac-based fecal occult blood test (gFOBT), the FIT test does not have any drug or dietary constraints because vitamins and foods do not affect the test outcome.  Multitargeted stool DNA or RNA tests with fecal immunochemical testing (FIT)  look for certain abnormal sections of DNA or RNA from cancer or polyp cells, as well as for occult blood. Colorectal cancer or polyp cells often have DNA or RNA mutations. The  FIT-DNA test  (also referred to as the stool DNA test) combines the FIT with a test that detects altered DNA in the stool. For this test, you collect an entire bowel movement and send it to a lab, where it is checked for altered DNA and for the presence of blood. It is done once every 3 years. The Cologuard brand tests for DNA changes and for blood in the stool. ColoSense  tests for RNA changes and blood in the stool. It is currently approved by the FDA but not yet by the American Cancer Society or the US Preventive Services Task Force (USPSTF). Insurance coverage is not universal. Insurance and Medicare coverage Colorectal cancer screening tests may be covered by your health insurance policy without a deductible or co-pay. For more information about Medicare coverage, visit  www.medicare.gov  or call 1-800-MEDICARE (1-800-633-4227). TTY users should call 1 (877) 486-2048. Check with your insurance plan to find out what benefits are covered for colorectal cancer screening. 📘 More to Read Early-Onset Colorectal Cancer on the Rise More young adults are being diagnosed with colorectal cancer, a trend that has experts concerned. Staying informed is crucial—for patients, families, and healthcare professionals alike. Learn more: https://www.fibonaccimd.com/post/cme-early-onset-colorectal-cancer 🎓 Continuing Medical Education (CME) Opportunity Free CME for Medical Professionals Healthcare providers: Stay current on the rising incidence of early-onset colorectal cancer. ✅ Read the article ✅ Enter your email ✅ Take the quiz ✅ Earn free CME credit Start by reading the article " Early Onset Colorectal Cancer ". https://www.fibonaccimd.com/post/cme-early-onset-colorectal-cancer Sources: Hamilton SR, Aaltonen LA, eds.  World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of the Digestive System.  Lyon, France:IARC Press; 2000:111-112. Heitman SJ, Ronksley PE, Hilsden RJ, Manns BJ, Rostom A, Hemmelgarn BR. Prevalence of adenomas and colorectal cancer in average risk individuals: a systematic review and meta-analysis.  Clin Gastroenterol Hepatol.  2009;7:1272-1278. Lieberman DA, Rex DK, Winawer SJ, Giardiello FM, Johnson DA, Levin TR. Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer.  Gastroenterology.  2012;143:844-857. Rex DK, Boland CR, Dominitz JA, et al. Colorectal cancer screening: recommendations for physicians and patients from the U.S. Multi-Society Task Force on Colorectal Cancer.  Am J Gastroenterol.  2017;112:1016-1030. Colorectal Cancer Screening Tests. American Cancer Society. Feb 28,2025. https://www.cancer.org  › detection-diagnosis-staging Screening for Colorectal Cancer. Centers for Disease Control and Prevention. Oct 17, 2024. https://www.cdc.gov  › colorectal-cancer › screening

by Stuart M. Caplen, MD Rheumatism sufferer in the carcass of a whale in Twofold Bay, town of Eden, Australia. In March 1896, an article in the Australian Pall Mall Gazette described a new cure for rheumatism.  It was republished in The New York Times in 1897.  It related that two-to-three years previously, “a gentleman of convivial habits but grievously affected by rheumatism” was taking an after-dinner stroll along an Australian beach.  He and his friends passed a whaling station where there was a dead whale partially cut open.  The paper noted that “our hilarious friend” decided to plunge into “the huge mountain of decomposing blubber.”  His friends tried valiantly to rescue him but could not.  As the heat and smell were too great, they decided to wait until he sobered up enough to make his own way out.  He “found himself so comfortable that he did not emerge for over two hours.”  When he did, he was “quite sober,” and his rheumatism of many years’ duration had totally disappeared.  (Rheumatism is not a specific disease, but rather a general term used to describe any condition causing pain or inflammation in the muscles, joints, or fibrous tissue of the body.) Word of this miraculous event, now known as the “whale cure,” spread rapidly.  The town of Eden, on the shores of Twofold Bay, became a haven for patients with rheumatism.  The sufferers congregated at a local hotel that benefited from the large influx of guests seeking a cure.  When a fresh whale was caught, the patients took a rowboat over to the whaling station.  The whalers made holes in the whale’s carcass which the patients then immersed themselves “as in a Turkish bath” for two hours with the blubber closing around their bodies.  The whalers did not charge for this service and worked on other parts of the whale while the sufferers partook of the cure.  The article also reported that “many are the cases of complete recovery of people who have hardly been able to use their limbs for years.” It was later suggested that if the sufferer could remain in the whale for 30 hours the cure would last for over a year.  It was believed the heat and gases produced by the dead whale were the reason the cure worked. New York Times - March 7, 1897 In an 1886 article in the Sydney Bulletin, a cured sufferer who stated “he was helpless with rheumatism” wrote of the horrific heat and smell during the two hours he was inside the whale.  He carried an odor that lingered for a number of days and wrote “men I considered true brothers held their noses and bolted,” when he came near them.  Part of his back and his fingernails and toenails had turned black after the treatment.  However, he said that for 12 months his rheumatism was cured, only to return after that period, “as bad as ever”.  He reported, “The smell has never left me : that dead whale still haunts me.“ The whale cure started falling out of popularity after about a decade or so due to a decline in whaling activities, a change in public sentiment as medical science advanced, as well as concerns about the smell and hygiene of the treatment. Illustration of rheumatism sufferers going to Eden for the “whale cure” Click here to read about how Benjamin Franklin discredited the “miracle cure” of  Mesmerism in  Benjamin Franklin, Mesmerism, and the First Use of Placebos in Science. References Photo- Wellings C.E. A cure for rheumatism; Bob Wiles in the carcass of a whale, Twofold Bay. National Library of Australia. Taken between 1900 and 1922. Retrieved from: https://nla.gov.au/nla.obj-148641890/view Barlass, T, Bizarre whale treatment for rheumatism revealed. The Sydney Morning Herald. March 30, 2014. Retrieved from: https://www.smh.com.au/environment/conservation/bizarre-whale-treatment-for-rheumatism-revealed-20140329-35q0w.html Foose N. The Putrefied Whale Cure. Antiquated Antidotes. January 2023 .Retrieved from: https://antiquatedantidotes.blog/2023/01/06/the-putrefied-whale-cure/ Rance C. The Quack Doctor. 'Horrible bubbles': the whale bath for rheumatism. Jan 19, 2024. Retrieved from: https://thequackdoctor.substack.com/p/horrible-bubbles-the-whale-bath-for A New Cure for Rheumatism. The New York Times - March 7, 1897. Retrieved from: https://www.nytimes.com/1896/03/07/archives/a-new-cure-for-rheumatism.html The Whale-Cure for Rheumatism. Sydney Bulletin Volume LIII, Issue 9516, 8 September 1896, Page 6, Retrieved from: https://paperspast.natlib.govt.nz/newspapers/CHP18960908.2.45 Ralston W.   The Whale Cure for Rheumatism in Australia .   The Graphic . 31 May 1902. From the Australian National Maritime Museum.  Retrieved from:  https://collections.sea.museum/objects/41892/the-whale-cure-for-rheumatism-in-australia

In an article published February 2025, researchers compared arsenic content and human consumption of arsenic in brown rice compared to white rice. It is commonly thought that brown rice is more healthy than white rice.  Brown rice is less processed, contains rice bran and germ and has more nutrients than white rice.  However, the bran and germ contain higher concentrations of arsenic than found in white rice.  Arsenic can be  found naturally in water and soil. There are two types of arsenic compounds; organic which contains carbon, and inorganic which does not.  The inorganic form is considered the more toxic of the two types.  Chronic arsenic exposure has been linked to cancers and cardiovascular disease.  There are some studies that have linked higher arsenic ingestion to decreased IQ and cognitive functioning in children. The authors, through a literature review, estimated the amount of arsenic contained in white and brown rice.  Then using average consumption data from a large U.S. government data base, estimated the average amount of rice Americans consume.  Combining the two they estimated the arsenic load people were exposed to. They reported that U.S. brown rice had 48% higher levels of inorganic arsenic than white rice.  Brown rice from around the world was found to have 18% higher levels of inorganic arsenic than U.S. brown rice.  Rice bran (the outer coating of rice that makes brown rice brown), contained more inorganic arsenic than were found in entire grains of either white or brown rice.  They also found children under 5 years of age were the highest consumers of rice per body weight. They estimated that children 0 to 6 months of age who ate brown rice on a regular basis might be ingesting higher than recommended amounts of inorganic arsenic by body weight.  It was also reported that if brown rice products were eaten daily, children 6 months to 2 years might exceed recommended amounts of arsenic ingestion.  Arsenic ingestion in 2-year-olds to 5-year-olds was not over the recommended safe level but was a higher amount per body weight than in adults. The authors suggested that there was a potential of elevated arsenic exposure from brown rice, especially in infants 0 to 2 years of age, but caution might be used with respect to brown rice ingestion up to 5 years of age.  In other age groups those who only ate brown rice had higher arsenic intake than those only eating white rice, but arsenic ingestion did not exceed what is considered a safe range based on body weight. Comments: Brown rice is more nutritious than white rice but unfortunately contains more arsenic. While the amount of arsenic ingested is below current safety levels for most age groups, in the very young it may exceed safety levels.  Arsenic levels in rice may differ by geography, water supply, strain of rice and how the rice is processed. Consumer Reports has reported finding arsenic in many rice products including rice cereals.  In 2012 they reported elevated arsenic levels in brown rice compared to white rice and found arsenic levels in some infant rice cereals at levels five times higher than oatmeal. Arsenic in food is not just a problem limited to rice.  In 2012, Consumer Reports tested apple and grape juice and found 10% of the samples contained elevated levels of arsenic that exceeded federal drinking-water standards. In 2025, Consumer Reports tested powdered baby formula for contaminants.  With respect to arsenic, they found levels of arsenic in seven out of 41 brands over what was considered a safe daily limit, and two brands were near the limit. Consumer Reports suggested in 2012 that industry and governmental agencies should accelerate efforts to reduce arsenic levels in rice by: Developing types of rice that take up less arsenic, and using rice with the lowest possible arsenic in products for young children, such as infant rice cereal Phasing out use of pesticides containing arsenic Ending the use of arsenic-laden manure as fertilizer Banning the feeding of arsenic-containing drugs and animal byproducts to animals While regulations for manufacturers and farmers will help decrease the issue of toxins in food, parents need to be aware of the issue and stay informed about the safety of food products ingested by their infants or young children. Unfortunately, arsenic is not the only contaminant in the food chain.  Click here to read about how plastic products have entered the food chain and their effects on health in the article, The Effects of Plastics on Human Health. References Scott CK, & Wu F. Arsenic content and exposure in brown rice compared to white rice in the United States. Risk Analysis, 1–14. 28 February 2025. Retrieved from: https://onlinelibrary.wiley.com/doi/10.1111/risa.70008 Arsenic in your food. Consumer Reports. November 2012. Retrieved from: https://www.consumerreports.org/cro/magazine/2012/11/arsenic-in-your-food/index.htm#recommendations Kirchner L. We Tested 41 Baby Formulas for Lead and Arsenic. Consumer Reports.  March 18, 2025·Updated March 21, 2025. Retrieved from: https://www.consumerreports.org/babies-kids/baby-formula/baby-formula-contaminants-test-results-a7140095293/ Wasserman, G.A., Liu, X., LoIacono, N.J. et al. A cross-sectional study of well water arsenic and child IQ in Maine schoolchildren. Environ Health 13, 23 (2014). Retrieved from: https://ehjournal.biomedcentral.com/articles/10.1186/1476-069X-13-23#citeas Tian Y et al. Exposure to arsenic and cognitive impairment in children: A systematic review. PLoS One . 2025;20(2):e0319104. Published 2025 Feb 26. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC11864541/ Wasserman GA et al. Water arsenic exposure and children's intellectual function in Araihazar, Bangladesh [published correction appears in Environ Health Perspect. 2004 Dec;112(17):A980]. Environ Health Perspect. 2004;112(13):1329-1333. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC1247525/