References for CME Article " What Is SIBO, and How Is It Diagnosed and Treated?" References [1]   Reynolds KH. Small intestinal bacterial overgrowth: a case-based review. J Patient Cent Res Rev. 2015;2:165-173. Retrieved from: https://institutionalrepository.aah.org/cgi/viewcontent.cgi?article=1209&context=jpcrr [2] Pimentel, Mark et al. Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of Irritable Bowel Syndrome. American Journal of Gastroenterology 95(12):p 3503-3506, December 2000. Retrieved from: https://journals.lww.com/ajg/abstract/2000/12000/eradication_of_small_intestinal_bacterial.26.aspx [3] Kiow LC et al. Predictors of Small Intestinal Bacterial Overgrowth in Symptomatic Patients Referred for Breath Testing. J Clin Med Res. 2020;12(10):655-661. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC7524565/ [4] Achufusi TGO et al. Small Intestinal Bacterial Overgrowth: Comprehensive Review of Diagnosis, Prevention, and Treatment Methods. Cureus. 2020;12(6):e8860. Published 2020 Jun 27. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC7386065/ [5] Ghoshal UC, Shukla R, Ghoshal U.  Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy.  Gut and Liver 2017;11:196-208. Retrieved from: https://www.gutnliver.org/journal/view.html?doi=10.5009/gnl16126 [6] Redondo-Cuevas L et al. Do Herbal Supplements and Probiotics Complement Antibiotics and Diet in the Management of SIBO? A Randomized Clinical Trial. Nutrients. 2024;16(7):1083. Published 2024 Apr 7. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC11013329/ [7] Systematic review with meta-analysis: the prevalence of small intestinal bacterial overgrowth in inflammatory bowel disease. Shah A, Morrison M, Burger D, et al. Aliment Pharmacol Ther. 2019;49:624–635. Retrieved from: https://onlinelibrary.wiley.com/doi/10.1111/apt.15133 [8] Meta-analysis: proton pump inhibitors moderately increase the risk of small intestinal bacterial overgrowth. Su T, Lai S, Lee A, He X, Chen S. J Gastroenterol. 2018;53:27–36. [9] Pimentel M et al. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. The American Journal of Gastroenterology 115(2):p 165-178, February 2020. Retrieved from: https://journals.lww.com/ajg/Fulltext/2020/02000/ACG_Clinical_Guideline__Small_Intestinal_Bacterial.9.aspx [10] Rezaie A et al. Hydrogen and Methane-Based Breath Testing in Gastrointestinal Disorders: The North American Consensus. Am J Gastroenterol. 2017;112(5):775-784. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC5418558/pdf/ajg201746a.pdf [11] Takakura w et al.  A Single Fasting Exhaled Methane Level Correlates With Fecal Methanogen Load, Clinical Symptoms and Accurately Detects Intestinal Methanogen Overgrowth. The American Journal of Gastroenterology 117(3):p 470-477, March 2022. Retrieved from: https://commdx.com/wp-content/uploads/2022/02/A_Single_Fasting_Exhaled_Methane_Level_Correlates.211-2.pdf [12] Emery C & Massey BT. Scintigraphy Demonstrates High Rate of False-positive Results From Glucose Breath Tests for Small Bowel Bacterial Overgrowth. Clinical Gastroenterology and Hepatology 2016;14:203–208. Retrieved from: https://www.cghjournal.org/article/S1542-3565(15)01047-2/pdf [13] Lim J, Rezaie A. Pros and Cons of Breath Testing for Small Intestinal Bacterial Overgrowth and Intestinal Methanogen Overgrowth. Gastroenterol Hepatol (N Y). 2023;19(3):140-146. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10496284/ [14] Losurdo G et al. Breath Tests for the Non-invasive Diagnosis of Small Intestinal Bacterial Overgrowth: A Systematic Review With Meta-analysis.  J Neurogastroenterol Motil 2020;26:16-28. Retrieved from: https://www.jnmjournal.org/journal/view.html?doi=10.5056/jnm19113 [15] Tansel A, Levinthal DJ. Understanding Our Tests: Hydrogen-Methane Breath Testing to Diagnose Small Intestinal Bacterial Overgrowth. Clin Transl Gastroenterol . 2023;14(4):e00567. Published 2023 Apr 1. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10132719/#R3 [16] Grace E, Shaw C, Whelan K, Andreyev HJ. Review article: small intestinal bacterial overgrowth--prevalence, clinical features, current and developing diagnostic tests, and treatment. Aliment Pharmacol Ther. 2013;38(7):674-688. Retrieved from: https://www.immuron.com.au/assets/files/Grace%202013.pdf [17] Saffouri et al. Small intestinal microbial dysbiosis underlies symptoms associated with functional gastrointestinal disorders. Nature Communication 10, 2012 (2019). Retrieved from: https://www.nature.com/articles/s41467-019-09964-7#citeas [18] Shayto RH, Abou Mrad R, Sharara AI. Use of rifaximin in gastrointestinal and liver diseases. World J Gastroenterol . 2016;22(29):6638-6651. Retrieved from:  https://pmc.ncbi.nlm.nih.gov/articles/PMC4970477/ [19] Scarpellini E et al. High dosage rifaximin for the treatment of small intestinal bacterial overgrowth. Aliment Pharmacol Ther . 2007;25(7):781-786. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/17373916/ [20] Low K et al. A Combination of Rifaximin and Neomycin Is Most Effective in Treating Irritable Bowel Syndrome Patients With Methane on Lactulose Breath Test. J Clin Gastroenterology.  Volume 44, Number 8, September 2010. Retrieved from: https://web.archive.org/web/20190303045212id_/http://pdfs.semanticscholar.org/a7d9/babf8f1187d0eb57ef118b4c7453f3bf763a.pdf [21] Zhong C et al. Probiotics for Preventing and Treating Small Intestinal Bacterial Overgrowth: A Meta-Analysis and Systematic Review of Current Evidence. J Clin Gastroenterol. 2017;51(4):300-311. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/28267052/ [22] Rao SSC, Rehman A, Yu S, Andino NM. Brain fogginess, gas and bloating: a link between SIBO, probiotics and metabolic acidosis. Clin Transl Gastroenterol. 2018;9(6):162. Published 2018 Jun 19. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC6006167/ [23] Mitten E et al. Recent Probiotic Use Is Independently Associated With Methane-Positive Breath Test for Small Intestinal Bacterial Overgrowth: 1151. American Journal of Gastroenterology 113():p S660, October 2018. Retrieved from: https://journals.lww.com/ajg/fulltext/2018/10001/recent_probiotic_use_is_independently_associated.1151.aspx [24] Smolin LA & Grosvenor MB, What is a Low FODMAP Diet?, Fibonacci Medicine and Nutrition.  Sept. 1 2023, Retrieved from: https://www.fibonaccimd.com/post/what-is-a-low-fodmap-diet [25] Bellini M, Tonarelli S, Nagy AG, et al. Low FODMAP Diet: Evidence, Doubts, and Hopes. Nutrients . 2020;12(1):148. Published 2020 Jan 4. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC7019579/#B25-nutrients-12-00148 [26] Pimentel M et al. A 14-day elemental diet is highly effective in normalizing the lactulose breath test. Dig Dis Sci. 2004;49:73–77. Retrieved from: click here [27] Chedid V et al. Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Glob Adv Health Med. 2014;3(3):16-24. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4030608/ [28] Rastgoo S et al. Glutamine Supplementation Enhances the Effects of a Low FODMAP Diet in Irritable Bowel Syndrome Management. Front Nutr. 2021;8:746703. Published 2021 Dec 16. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC8716871/ [29] Redondo-Cuevas L et al. Do Herbal Supplements and Probiotics Complement Antibiotics and Diet in the Management of SIBO? A Randomized Clinical Trial. Nutrients. 2024;16(7):1083. Published 2024 Apr 7. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC11013329/ [30] Xu F et al. Clinical efficacy of fecal microbiota transplantation for patients with small intestinal bacterial overgrowth: a randomized, placebo-controlled clinic study. BMC Gastroenterol. 2021;21(1):54. Published 2021 Feb 6. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC7866462/ [31] Wang L et al. The impact of small intestinal bacterial overgrowth on the efficacy of fecal microbiota transplantation in patients with chronic constipation. mBio. 2024;15(10):e0202324. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC11481539/ CME article: " What Is SIBO, and How Is It Diagnosed and Treated?"

Easy Caprese Chicken Skewers Say goodbye to dry skewers! Mary B. Grosvenor, MS, RD shares her secret to perfect Caprese Chicken en Brochette, ensuring tender chicken alongside fresh tomatoes and mozzarella. It's an ideal dish for a light yet satisfying meal. Creative Cooking for the Health-Conscious Gourmet FibonacciRECIPES  | Culinary Medicine   Recipe This recipe makes a beautiful appetizer or main dish. Caprese combines tomatoes, basil and mozzarella, this dish adds chicken. Cooking the chicken before skewering allows it to remain tender and juicy. This also eliminates the challenges of cooking skewers that combine meat, vegetables and cheese. Ingredients: 1 lb grape or cherry tomatoes Balsamic glaze Skewers Chicken 2 lb boneless skinless chicken  breast ¼ cup olive oil ¼ cup balsamic vinegar 1 tbsp honey ½ tsp dried oregano ½ tsp onion powder 2 gloves garlic, crushed (1/2 tsp garlic powder 3 tbsp fresh parsley ¼ tsp salt ¼ tsp pepper Marinated Mozzarella 2 oz Mozzarella pearls 2 Tbsp prepared basil pesto 1.5 tsp Italian dressing Instructions Prepare a marinade using olive oil, balsamic vinegar, garlic, onion, oregano, parsley, salt, pepper, and honey Add chicken breasts and marinate for 30 minutes to 24 hours in the refrigerator Meanwhile, combine pesto and Italian dressing and add mozzarella pearls, refrigerate Preheat grill to high heat.  Add chicken and grill for 3-5 minutes per side, alternating sides until chicken reaches 165 degrees. Remove from grill and cool slightly. Cut  into 2-inch cubes To prepare brochette, slide ingredients onto skewer alternating chicken, tomatoes and mozzarella pearls Plate and drizzle with balsamic glaze, or sauce of your choice. Honey, soy or maple glazes pair well. Makes 18 skewers or 6 servings Nutrition information per 3 skewer serving Calories  275, Total Fat 10.5g, Saturated Fat  2.7g, Cholesterol 110mg, Total Carbohydrate 8g, Dietary fiber 1g, Protein 36g, Potassium 665mg, Sodium 170mg Nutrition Chef Authors: Mary B Grosvenor, MS, RD Medically Reviewed by FibonacciMD editors. Editor’s Note- Editor’s note: Appropriate for low-calorie, low-carb, high-protein dietary regimen. more health-conscious recipes

Zika, Dengue, Chikungunya, and West Nile Infectious Disease and Emergency Medicine ✅ Earn Free CME Credit for Reading This Article Eligible for 0.75 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 The Aedes Aegypti Mosquito[1] No other animal infects and causes disease as effectively as mosquitos, which are the deadliest animals in the world to humans. Infections caused by mosquitos kill over 700,000 people a year.[2] In this article we will look at four mosquito borne viral diseases; Zika, dengue, chikungunya, and West Nile. Currently West Nile is endemic in the continental US, but clinicians may see the other three diseases in travelers who are either from, or who have visited endemic areas. It is also possible that like Zika a few years ago, these diseases may become endemic in the U.S. at some time in the future. Zika Virus In 2015 and 2016 Zika was a front-page news story due to surging infections in the Americas, with the threat of severe fetal brain defects occurring if pregnant women were infected. Since then, Zika has almost disappeared.[3] In 2016, there were 5,168 reported cases in the U.S. and 36,512 cases in U.S. territories, with widespread transmission in Puerto Rico and the U.S. Virgin Islands, and limited local transmission in Florida and Texas.[4] Brazil had 200,000 reported Zika cases in 2016, and infants born with microcephaly increased 10-fold from prior levels in late 2015 to early 2016.[5] By 2019, there were only 27 reported U.S. cases in travelers and 74 cases in U.S. territories.[6] There are currently no countries with a large outbreak of Zika. Some experts do not think pesticide spraying has caused the decline, and it is possible that a form of herd immunity in endemic areas has occurred, limiting the ability of mosquitos to spread Zika to humans.[3] Zika virus is an RNA Flavivirus transmitted by Aedes aegypti and Aedes albopictus mosquitos. Human to human transmission also occurs, and potentially it can be transmitted by blood transfusion and sexual contact. Zika virus was first discovered in 1947 and is named after the Zika Forest in Uganda. The first human case was reported in 1952.[7] Zika Clinical Disease[8] Zika virus infection[10] Most people infected with Zika virus are asymptomatic. Clinical findings typically are acute onset of fever with maculopapular rash, arthralgia, and/or conjunctivitis. Myalgias and headaches are common. The illness is usually mild with symptoms lasting from several days to a week. Severe disease requiring hospitalization is uncommon, and fatalities are rare. There have been some cases of Guillain-Barré syndrome reported after a Zika infection. Zika virus infection during pregnancy can cause fetal microcephaly, decreased brain tissue, and damage to the back of the eyes.[9] Treatment No specific treatment is available for Zika virus disease, other than supportive care. As dengue presents similarly, and in the same geographic areas as Zika, aspirin and other non-steroidal anti-inflammatory drugs(NSAIDs) should be avoided until dengue can be ruled out, to reduce the risk of hemorrhage. People infected with Zika, should be protected from mosquito exposure during the first few days of illness to reduce the risk of further human to mosquito to human transmission. Sexual relations should be curtailed to prevent passing on the infection.[8] A vaccine has been developed, but gaining approval by testing it in an environment of decreasing cases has proved difficult.[3] Sexual Transmission [11] Zika can be sexually transmitted by sharing sex toys, and by vaginal, anal, and possibly oral sex, even if asymptomatic. Zika virus has been detected in semen, vaginal fluids, saliva, urine, and breast milk. There is no evidence however, that Zika can be transmitted through saliva during kissing. Zika virus has been reported to persist in semen for up to 69 days. It is recommended that pregnant women with sexual partners who live in, or have traveled to, an endemic Zika area, use condoms during sex, or abstain from sexual relations for the duration of the pregnancy. Condom use is recommended after travelling to an endemic area for two months for nonpregnant females, and three months for males, due to the longer survival time in semen. Testing [12] Zika testing of symptomatic male and female non-pregnant patients is not currently recommended by the CDC based on current epidemiology, but this guidance may change in the case of a renewed outbreak of cases. However, these patients should be tested for dengue virus, which is more common, and has similar presenting features. Testing asymptomatic males and non-pregnant females for either dengue or Zika viruses is not currently recommended. Zika testing involves a very complex algorithm for pregnant women. Recommended testing is different if the woman is symptomatic, asymptomatic, has had an abnormal fetal ultrasound consistent with a congenital Zika infection, or has had sexual relations with someone suspected of having the disease. If you are interested in learning more about the complete CDC Zika testing guidelines algorithm for pregnant women, follow this link: https://www.cdc.gov/zika/hc-providers/testing-guidance.html Dengue Structure of a dengue virus[13] Dengue viruses in tissue[14] Dengue viruses are Flaviviruses, transmitted through the bite of infected Aedes aegypti or Aedes albopictus mosquitos. Dengue is caused by one of four related viruses: Dengue virus 1, 2, 3, and 4. For this reason, a person can be infected as many as four times with the different dengue viruses.[15] The history of dengue is not well known, but a dengue-like outbreak in humans was recorded in a Chinese medical encyclopedia in 992. In the 1700s dengue was known as breakbone fever. Queen Luisa of Spain used the word dengue while writing about her recovery from it in 1801. No one is sure about dengue’s etymology, but the word dengue in Spanish means affectation, or careful, and may have described the stiff, painful movements of people with dengue fever. Another theory is that the name came from a Swahili phrase “Ka dinga pepo”, or “disease caused by an evil spirit”.[16] Dengue is common in more than 100 countries around the world. About three billion people live in endemic areas, and every year up to 400 million people get infected with dengue, approximately 100 million people get symptomatic illness, and 22,000 die from severe dengue.[15] Dengue is common in the U.S. territories of Puerto Rico, the U.S. Virgin Islands, and American Samoa. Nearly all dengue cases reported in the U.S. mainland are from travelers infected elsewhere. In 2019, there were 1,203 cases of dengue reported in the U.S., and 56 cases reported in U.S. territories.[17] Dengue is a frequent cause of infection in Central and South America, East Africa, Southeast Asia and the Pacific Islands.[18] Global Dengue Risk Map[18] World Health Organization(WHO) Clinical Dengue Definitions[19] Dengue is defined by a combination of ≥2 clinical findings in a febrile person who traveled to, or lives in a dengue-endemic area. Clinical findings include nausea, vomiting, rash, aches and pains, a positive tourniquet test, leukopenia, or the following warning signs which may predict severe dengue: abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy, restlessness, and liver enlargement. Severe dengue is defined as dengue with any of the following symptoms: severe plasma leakage leading to shock or fluid accumulation with respiratory distress; severe bleeding; or severe organ impairment such as elevated transaminases ≥1,000 IU/L, impaired consciousness, or heart impairment. Dengue Clinical Disease and Treatment[19] Most dengue infections are asymptomatic, with only 25% of dengue virus infections estimated to be symptomatic. It commonly presents as a mild to moderate, nonspecific, acute febrile illness. Approximately 5% of patients with dengue progress to severe dengue, a life-threatening disease. The early clinical findings of severe dengue are nonspecific, but recognizing early signs of shock, and promptly initiating intensive care unit therapy can reduce the risk of death to <0.5%. A study of antibody dependent enhancement of dengue in children found that the level of serum antibodies from a first infection determined the risk of severe dengue disease on reinfection. The presence of high dengue antibody titers in an individual are protective, but people with intermediate antibody titers had a much higher likelihood of developing severe dengue, even greater than those with low antibody titers. In that study the chances of getting severe dengue during a second infection was 1.6% in the high antibody titer group, 11.4% in the intermediate antibody titer group, and 6.6% in low antibody titer group. It is thought that particularly with intermediate dengue antibody titers, some binding of antibodies to the dengue virus occurs, but the antibody does not necessarily neutralize the virus. This creates a virus-antibody complex that appears to facilitate viral entry into host cells, and can trigger an immune cascade that leads to severe dengue. This is felt to be the reason why a dengue re-infection with a different strain, or first infection after dengue vaccination, may increase the risk of contracting severe dengue.[20 Clinical Course of Dengue[21] Dengue begins abruptly after a typical incubation period of five to seven days, and has three phases: febrile, critical, and convalescent or recovery. Febrile Phase The febrile phase lasts two to seven days and can be biphasic. Other signs and symptoms may include severe headache, retro-orbital eye pain, muscle, joint, bone pain, and/or a macular or maculopapular rash. Some patients have an injected oropharynx and facial erythema the first 24–48 hours after onset. Bleeding may occur from thrombocytopenia, or in more ill patients from a coagulopathy. Thrombocytopenia results from transient bone marrow suppression, and increased peripheral destruction of platelets in dengue.[22] In this phase, patients may have minor hemorrhagic manifestations such as ecchymosis, purpura, epistaxis, bleeding gums, or hematuria. Petechiae may occur, and a positive tourniquet test may aid in the diagnosis of dengue. A positive tourniquet test result is ten or more petechiae per one square inch in the arm, after inflating a blood pressure cuff halfway between the systolic and diastolic pressures for two minutes.[23] Positive Tourniquet Test[23] Critical Phase The critical phase of dengue begins at defervescence, and typically lasts 24–48 hours. Most patients clinically improve during this phase, but there can be substantial plasma leakage due to a marked increase in vascular permeability. Patients with severe plasma leakage and third spacing may have pleural effusions, ascites, hypoproteinemia, or hemoconcentration. Liver enlargement may occur.[22] Once hypotension develops, irreversible shock and death may ensue despite resuscitation. Patients can also develop severe hemorrhagic manifestations such as hematemesis, bloody stools, or menorrhagia. Increased activated partial thromboplastin time (APTT), and a reduction in fibrinogen levels may be seen in severe dengue.[22] Uncommon complications include myocarditis, pancreatitis, and encephalitis. Convalescent/Recovery Phase[19] In severe dengue, as plasma leakage and third spacing subsides, the patient enters the convalescent or recovery phase, and begins to reabsorb extravasated intravenous fluids, pleural effusions and ascites. As a patient’s hemodynamic status stabilizes there is a significant diuresis of the excess extracellular fluid. The patient’s hematocrit stabilizes, or may fall because of the dilutional effect of the reabsorbed fluid, and the white cell count usually starts to rise, followed by a recovery of platelet count. In the convalescent-phase rashes may desquamate and become pruritic. Dengue and Pregnancy [15] There is limited data about dengue during pregnancy. Perinatal transmission can occur, and maternal infection may increase the likelihood of symptomatic infection in the newborn. Of 41 perinatal transmission cases to fetuses described in the literature, all developed thrombocytopenia, most had evidence of plasma leakage typically with ascites or pleural effusions, and 39 were febrile. Nearly 40% had a hemorrhagic manifestation, and 25% were hypotensive at some point. Perinatally infected neonates typically become ill during the first week of life. Placental transfer of maternal dengue IgG antibodies from a previous infection does occur, but when the protective effect of these antibodies wanes, infants 6–12 months of age are at risk for severe dengue. Laboratory Findings and Testing [24] Course of a Dengue Infection[25] Laboratory findings commonly include leukopenia, thrombocytopenia, hyponatremia, elevated aspartate aminotransferase and alanine aminotransferase, and in the majority of cases, a normal erythrocyte sedimentation rate.[26] During days one to seven after symptom onset, dengue virus RNA can be detected with molecular tests, such as an RT-PCR(reverse transcriptase polymerase chain reaction). NS1 is a dengue virus protein that also can be detected by some commercial tests. An IgM antibody level should also be drawn. A negative result from a molecular, NS1, or IgM antibody test is not conclusive. After seven days post symptom onset, patients with initially negative RT-PCR, NS1,and IgM antibody tests from the first seven days of illness should have a convalescent sample tested for IgM antibodies. During the convalescent phase, IgM antibodies are usually present and can be reliably detected. IgM antibodies against dengue virus can remain detectable for 3 months or longer after infection. If a PCR or NS1 test is positive for dengue, a current dengue diagnosis is confirmed. If the PCR result is negative and the IgM antibody test is positive, the laboratory diagnosis is presumptive dengue virus infection. Cross reactivity with other flaviviruses such West Nile, yellow fever, and Zika, is a limitation of dengue IgM antibody tests. Therefore, a patient with past flavivirus infection(s) may be falsely test positive for dengue virus IgM antibodies. To determine if dengue is causing the infection, IgM positive specimens should be tested for specific neutralizing antibodies by a plaque reduction neutralization test (PRNT). Whenever a pregnant woman is tested for dengue, it is recommended Zika also be tested for using an RT-PCR test, as they may present similarly. Treatment [27] No specific antiviral agents or treatments exist for dengue. Supportive care is recommended and patients should try to stay well hydrated, and avoid aspirin and other NSAIDS because of their anticoagulant properties. Fever can be controlled with acetaminophen and possibly tepid sponge baths. Febrile patients should avoid mosquito bites to reduce risk of further transmission to other people. In severe dengue, ICU care may be required. Prophylactic platelet transfusions in dengue patients are not beneficial, and may contribute to fluid overload. Administration of corticosteroids has not demonstrated any benefit, except in the case of autoimmune-related complication such as immune thrombocytopenia purpura. A vaccine to prevent dengue, Dengvaxia, administered in three doses six months apart, is licensed and available in some countries for people aged 9-45 years old. The WHO recommends that the vaccine only be given to people with confirmed prior dengue virus infection, as previously uninfected people who are vaccinated and then get dengue have a higher chance of developing severe dengue. In 2019, Dengvaxia was FDA approved for use in children 9-16 years old, with laboratory confirmed prior dengue virus infection, living in an endemic area such as the U.S. territories of American Samoa, Guam, Puerto Rico or the U.S. Virgin Islands.[28] Chikungunya Virus Chikungunya is a mosquito-borne viral disease first described during an outbreak in southern Tanzania in 1952. The name chikungunya comes from the Tanzanian Kimakonde language, and means to become contorted, due to the stooped appearance of sufferers with severe joint pains.[29] It is an RNA virus that belongs to the alphavirus genus of the family Togaviridae. It is most commonly spread by Aedes aegypti and Aedes albopictus mosquitos, although blood-borne transmission is possible. Rare in utero transmission has been documented, but it is not transmitted by breast milk.[30] Chikungunya virus cases and outbreaks have been identified in countries in Africa, Asia, Europe, and the Indian and Pacific Oceans. In late 2013, the first local transmission of Chikungunya in the Americas was identified in the Caribbean, and the virus then spread throughout much of the Americas. During epidemics around the world, hundreds of thousands of cases can occur.[29,31] In 2019, there were 192 reported cases of Chikungunya in the U.S., all from travel, and 2 cases in U.S. territories thought to be from local spread.[32] Geographic Distribution of Chikungunya Virus[33] Clinical Course and Symptoms[34] Chikungunya virus infection should be considered in patients with acute onset of fever and polyarthralgia, especially travelers who recently returned from endemic areas.[26] The majority of people infected with chikungunya virus become symptomatic. The incubation period is typically three to seven days with a range of one to twelve days. Symptoms include acute onset of fever (typically >39°C) and polyarthralgia. Joint symptoms are usually bilateral, symmetric, and can be severe and debilitating. Other symptoms can include headache, myalgia, arthritis, conjunctivitis, nausea/vomiting, or maculopapular rash. Clinical laboratory findings can include lymphopenia, thrombocytopenia, elevated creatinine, and elevated hepatic transaminases. Acute symptoms typically resolve within seven to ten days. Rare complications include uveitis, retinitis, myocarditis, hepatitis, nephritis, bullous skin lesions, hemorrhage, meningoencephalitis, myelitis, Guillain-Barré syndrome, and cranial nerve palsies. People at risk for severe disease include neonates exposed intrapartum, the elderly, and people with previous underlying medical conditions. Patients may have a relapse of rheumatologic symptoms such as polyarthralgia, polyarthritis, or tenosynovitis in the months following an acute illness. Persistent joint pains for some can last from months to years. Mortality is rare, and occurs mostly in the elderly. Chikungunya Rash[35] Diagnostic Testing Viral culture may detect the virus in the first three days of illness. During the first eight days of illness, chikungunya viral RNA by RT-PCR will often be positive. Chikungunya virus antibodies normally start to develop toward the end of the first week of illness. Acute phase samples may be positive for IgM, although IgG should also be tested for. Convalescent samples should be obtained from patients whose acute-phase samples are negative, with both IgG and IgM antibodies tested.[36,37] Treatment[34,37,38] There is no vaccine to prevent chikungunya virus, and treatment is symptomatic. It is recommended that for the first week of infection the patient avoid mosquito bites, as it may be passed on to another person that way. It is difficult to distinguish chikungunya and dengue based on clinical findings alone due to the fact that chikungunya and dengue viruses are transmitted by the same mosquitoes, can circulate in the same area, and occasionally cause co-infections in the same patient. Patients with suspected chikungunya should be managed as dengue until dengue has been ruled out, as proper clinical management of dengue reduces the risk of medical complications and death. It is recommended not to administer aspirin and other NSAIDS until dengue is ruled out, the patient has been afebrile ≥48 hours, and has no warning signs of severe dengue, to reduce the risk of bleeding. Warning signs for severe dengue include severe abdominal pain, persistent vomiting, mucosal bleeding, pleural effusion, ascites, lethargy, enlarged liver, and increased hematocrit with thrombocytopenia. Persistent joint pain from a chikungunya infection, after dengue has been ruled out, may benefit from use of NSAIDs, corticosteroids, or physiotherapy. Differentiation between Chikungunya and Dengue[38] Chikungunya is more likely to cause high fever, severe polyarthralgia, arthritis, rash, and lymphopenia, and dengue virus is more likely to cause neutropenia, thrombocytopenia, hemorrhage, shock, and death. The table below highlights the differences between these two disease entities. West Nile Virus West Nile virus (WNV), is a Flavivirus, and the leading cause of mosquito-borne disease in the continental U.S.[39] WNV was first isolated in a woman in the West Nile district of Uganda in 1937, which is how it got its name.[40] It is most often spread in the summer and fall by the bite of an infected mosquito. Infections have rarely occurred through organ transplant, blood transfusions and breast milk.[38] Most people infected with WNV are asymptomatic, but about 20% of those who are infected develop a fever and/or other symptoms. Only about 0.7% of infections lead to a serious and sometimes fatal illness.[39] Mosquitoes of the genus Culex are generally considered the principal vectors of WNV, in particular Culex Pipiens. Birds are the reservoir hosts of WNV. Interestingly, in Europe, Africa, Middle East and Asia, mortality in birds with WNV infection is rare. However, the virus is highly toxic to birds in the Americas.[40] Dying birds may be an indication of a WNV epidemic in an area. Horses may also become infected. In 2020, 44 states reported WNV infections in people, birds, or mosquitoes. There were 422 reported human cases of neuroinvasive disease(such as meningitis or encephalitis) and 135 cases of non-neuroinvasive disease.[41] In some previous years there were many more reported cases, with 2,647 cases reported in 2018, and 5,674 cases in 2012.[42] West Nile Virus Activity by State 2020[43] Clinical Presentation and Symptoms[44] WNV should be considered in anyone in an endemic area presenting with a febrile, or acute neurologic illness, who has had recent exposure to mosquitoes, blood transfusion, or organ transplantation, especially during the summer months. The diagnosis should also be considered in infants whose mother was infected with WNV during pregnancy or while breastfeeding. The incubation period for WNV disease is typically two to six days but ranges from two to 14 days, and can be longer, up to several weeks, in immunocompromised people. It is estimated that 70-80% of human WNV infections are subclinical or asymptomatic. Symptomatic WNV presents with an acute, non-specific febrile illness that typically includes headache, weakness, myalgia, arthralgia, gastrointestinal symptoms, and a transient maculopapular rash. About 0.7% of infected persons develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or acute flaccid paralysis. WNV meningitis is indistinguishable from viral meningitis due to other etiologies, and typically presents with fever, headache, and nuchal rigidity. WNV encephalitis is more severe and presents with fever, altered mental status, seizures, focal neurologic deficits, or movement disorders such as tremor or parkinsonism. WNV acute flaccid paralysis, also known as WNV poliomyelitis, is clinically and pathologically identical to poliomyelitis, with damage to spinal anterior horn cells that may progress to respiratory paralysis requiring mechanical ventilation. WNV flaccid paralysis often presents as an isolated limb paresis or paralysis, and can occur without fever or viral prodrome. WNV-associated Guillain-Barré syndrome and WNV radiculopathy have also been reported, and can be distinguished from WNV poliomyelitis by clinical manifestations, and electrophysiologic testing. Rarely, cardiac dysrhythmias, myocarditis, rhabdomyolysis, optic neuritis, uveitis, chorioretinitis, orchitis, pancreatitis, and hepatitis have been described in patients with WNV disease. Most patients with non-neuroinvasive WNV disease or WNV meningitis recover completely, but fatigue, malaise, and weakness can linger for weeks or months. Patients who recover from WNV encephalitis or poliomyelitis often have residual neurologic deficits. The mortality rate for neuroinvasive disease is approximately 10%, but is higher for patients with WNV encephalitis and poliomyelitis than with WNV meningitis. One study found that five of 25 patients who had WNV infections diagnosed 1.6 to 6.7 years previously continued to have WNV RNA in their urine, suggesting chronic infection. But, according to the CDC, the implications of this are still unknown.[45,46] Diagnostic Testing[47] Routine clinical laboratory studies for WNV are generally nonspecific. In patients with neuroinvasive disease, cerebrospinal fluid(CSF) examination generally shows lymphocytic pleocytosis, but neutrophils may predominate early in the course of the illness. Brain MRI is frequently normal, but signal abnormalities in the basal ganglia, thalamus, and brainstem may be seen in patients with encephalitis, and in the anterior spinal cord in patients with WNV poliomyelitis.[44] Laboratory diagnosis is typically made by testing of serum or CSF for WNV-specific IgM antibodies which are usually detectable three to eight days after the onset of illness, and can persist for 30 to 90 days. The absence of WNV IgM antibodies on an initial sample does not rule out the diagnosis of WNV infection, and a convalescent sample may need to be drawn. Unfortunately, cross-reactive antibodies from other flaviviruses are common, and all positive IgM results should be confirmed with a plaque-reduction neutralization test (PRNT), which requires acute and convalescent serum, and can differentiate which Flavivirus species is causing the infection. Viral cultures and RT-PCR testing can be performed on serum, CSF, and tissue specimens that are collected early in the course of illness, and can confirm an infection. Immunohistochemistry can detect WNV antigen in formalin-fixed tissue. Initial negative results of these tests do not rule out a WNV infection. Treatment[48] There are no specific treatments for WNV disease, other than supportive management. Patients with meningitis may require pain control for headaches, antiemetics and IV rehydration as needed for nausea and vomiting. Patients with encephalitis require ICU monitoring for the development of elevated intracranial pressure and seizures. WNV encephalitis or poliomyelitis patients should be monitored for the ability to protect their airway from aspiration. Acute neuromuscular respiratory failure may develop in WNV poliomyelitis requiring prolonged ventilatory support. No WNV vaccines are currently available. Prevention of WNV disease depends on community mosquito control programs, personal protective measures to decrease exposure to infected mosquitoes, and screening of blood and organ donors. Conclusion All four of these mosquito-borne viral diseases can present initially as a non-specific illness, making diagnosis difficult. Laboratory testing may help, but initially can be negative, requiring convalescent testing to make a firm diagnosis. Dengue is the deadliest, and in endemic areas initially treating for dengue is recommended until an alternate diagnosis is confirmed. West Nile virus is the only one of the four infections discussed in this article which is currently endemic in the continental U.S., the others are typically seen in travelers who are either from, or who have visited endemic areas. Fortunately, with its threat of fetal abnormalities, Zika virus spread has significantly declined, but around the world dengue and chikungunya infections remain significant health issues. The infections discussed in this article are just a small portion of the infections that mosquitos can transmit, which include both viruses and parasites, and are listed below. Mosquito-borne Viruses [49] · Cache Valley · Chikungunya · Dengue · Eastern equine encephalitis · Jamestown Canyon · Japanese encephalitis · La Crosse encephalitis · Rift Valley fever · Ross River virus disease · St. Louis encephalitis · West Nile · Yellow fever · Zika Mosquito Borne-Parasites · Dirofilariasis (dog heartworm) · Lymphatic filariasis · Malaria 🎓  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.  😇 References

Do you need more protein? Most Americans get enough, but some groups may benefit from more. Learn about protein, recommended intakes, and healthy sources. Culinary Medicine by Lori A Smolin, PhD    and Mary B Grosvenor, MS, RD More than 70% of Americans are actively trying to eat more protein.[1]  Grocery store shelves are filled with protein-fortified products – yogurts, breakfast cereals, pasta, ice cream, candy bars, and even water.  High-protein eating plans such as the carnivore and paleo diets are more popular than ever  and sales of protein supplements continue to rise.[2,3] While influencers claim most of us are deficient in protein and push us to eat more, surveys show that typical protein intake in the U.S. meets or exceeds recommendations.[4,5] Should we be loading up on protein or is our obsession just due to media hype? What is Protein? We think of protein as something we get by eating meat and use to build muscle in our bodies. But protein is much more than that. Protein, along with carbohydrates and fat, provides energy in our diet.  We do consume it in meat, but dairy products, beans, nuts, seeds, and grains are also good sources, and most other foods provide small amounts. In our bodies, protein is needed for the structure and function of our muscles, but it is also essential for building other body structures, maintaining immune function, transporting molecules, and regulating cellular and overall body processes. Protein is not a single substance. There are many different proteins, and each is made of one or more chains of amino acids that fold to form complex three-dimensional shapes. The shape of the protein is determined by which amino acids are in the chain and the order in which they appear, and the shape contributes to the protein’s function. When we eat protein, whether it is from a steak or a chickpea, the protein molecules are broken down and absorbed into our bodies as individual amino acids. Once in the body amino acids can be used for energy or assembled to form human proteins. The amount of protein we need depends on how big we are, how much lean vs. fat tissue we have, and what is happening in our bodies. Larger adults need more protein than smaller adults; men need more than women; those who are growing, such as small children and pregnant women, need more protein; and those who are recovering from an injury or surgery need more protein to replace damaged tissues. How Much Protein is Recommended? There are two ways in which protein recommendations are expressed. The Recommended Dietary Allowance (RDA) makes recommendations based on body weight; the RDA for a healthy adult is 0.8 g protein/kg body weight/day, which calculates to about  55 g/day for a 150-pound person.  This amount is the equivalent of a day’s intake of a bowl of cereal with a banana and milk for breakfast, a peanut butter sandwich, apple, and glass of milk for lunch, and a small chicken breast with a potato and broccoli for dinner. The other recommendation expresses protein requirements as a percentage of calories consumed; the acceptable range of protein intake in a healthy diet is 10 to 35% of calories. Using this guideline, a healthy diet for the 150-pound person could include 50 to 175 grams of protein per day.[6]     Based on either of these recommendations, national intake surveys find that, as a population, we are consuming adequate amounts of protein. On average American adults consume about 77 grams per day or about 1 g/kg body weight; this is 15% of calories as protein.[7]  In general meat-eaters consume more protein (17.2%) than vegetarians (14%) and vegetarians consume more than vegans (13.1%), but in all diets the percentage is above the 10% of calories, which is the low end of recommendations.[8] Is the Recommended Amount Enough for All Adults? There is growing evidence that the methodology used to determine the RDA for protein underestimates needs during metabolic stress, such as when muscle is broken down or synthesized. Based on this information, it has been suggested that requirements should be set higher for older adults (≥65 years), strength and endurance athletes, and those restricting calories to lose weight.[9,10] Older adults may need more than the current RDA for protein because adults lose muscle mass as they age. Higher protein intakes in combination with exercise help lessen this decline in muscle mass and strength and reduce early mortality.[11] Protein intakes of at least 1.0 to 1.2 g/kg/d have been proposed for healthy older adults, with higher intakes of 1.2 to 1.5 g/kg/d in those who are stressed by illness, injury, or vigorous physical activity [9]. One study found that women aged 65 to 79 who consumed more protein than recommended were less frail.[12] Another study found that  protein intake higher than the RDA is associated with better physical performance and greater muscle strength in older adults.[13] Endurance and strength athletes need additional protein to support muscle building, repair, and recovery . The amount of dietary protein needed for athletes to maintain and repair lean tissues and support changes in metabolism ranges from 1.2 to 2.0 g/kg/day.[14] A recent study found that consuming a daily protein intake toward the upper end of this range will maximize whole-body protein synthesis during postexercise recovery in endurance athletes.[15] Individuals who are limiting their calorie intake may have higher protein needs because weight loss often leads to loss of muscle. Higher protein intake helps maintain muscle mass. A review and meta-analysis found that consuming at least 25% more protein than recommended helped adults with overweight or obesity preserve muscle during weight loss . [ 10]   Weight loss drugs such as Ozempic and Wegovy have intensified the allure of protein as people try to retain muscle while they lose weight. Improvements in weight management and preservation of lean tissue are observed in diets that contain between 1.2 and 1.6 g/kg/day of protein.[16] Healthy Protein Choices Protein bars, shakes, and powders are a tempting way to boost intake. But these convenient, highly processed, fortified foods may not be the healthiest choice. While they are high in protein, they may also be high in sugars, sodium, and fats and lower in vitamins, and minerals than foods that are naturally high in protein. Different  high protein foods provide different combinations of nutrients. Natural a nimal products such as meat, chicken, fish, eggs, and dairy provide B vitamins, iron, zinc, and calcium along with plenty of protein.   Legumes, grains, nuts, and seeds are good plant protein sources and provide fiber, phytochemicals, and unsaturated fats along with most of the B vitamins, iron, zinc, and calcium.  But even whole foods sources of protein have their downsides. Animal products often contain unhealthy saturated fat, and they are low in fiber, a combination that increases the risk of heart disease and diabetes.[17]  Red and processed meats are associated with a higher risk of cardiovascular disease and cancer than plant proteins. [18,19]  But plant protein sources lack vitamin B12 and the minerals they contain are not readily absorbed. A healthy diet should provide adequate protein, include a variety of protein sources, and emphasize plant proteins. To ensure you are getting adequate protein, you can use a phone app to compare your protein intake to recommendations.  Alternatively, you can calculate your intake from the Nutrition Facts label on packaged foods and estimate the amounts you consume in fresh foods by assuming that meat, fish, and poultry have 7 g per ounce and fresh vegetables have about 1 g per cup. To consume a variety of proteins, choose meals that include lean meats, poultry, fish, eggs, and low-fat dairy products along with plenty of beans, soy products, quinoa, whole grains, and nuts. If you prefer to avoid animal products, it is crucial to choose a variety of different plant protein sources because individual plant sources do not contain the optimal mix of amino acids needed to build human proteins. A dietary pattern with a variety of plant proteins ensures you are getting plenty of all the essential amino acids. Bottom Line Despite the current protein obsession, the popularity of meat-based diets, and the increasing sales of protein-fortified foods and supplements, most healthy American adults already consume enough protein. Some groups, including older adults, athletes, and dieters may need to increase their protein intake. While protein fortified snacks and powders are an easy way to add protein, just including foods naturally high in protein throughout the day can help ensure that protein needs are met. To maximize the nutritional benefits of your dietary pattern, include a mixture of protein sources with an emphasis on plant sources. Aim to get most of your protein from whole foods, not out of a package. Reserve those protein-fortified snacks for special treats or when convenience is essential. References [1] International Food Information Council. 2024 IFIC Food & Health Survey. June 20, 2024. Published 2018. https://foodinsight.org/2024-foodhealth-survey/ . [2] High-Protein Diets Are Popular — but They Certainly Aren’t Sustainable. Sentient. Published March 19, 2025. Accessed April 8, 2025. https://sentientmedia.org/high-protein-diets/ [3] U.S. Protein Supplements Market Size, Share & Analysis [2029]. www.fortunebusinessinsights.com . https://www.fortunebusinessinsights.com/u-s-protein-supplements-market-107171 [4] Food Consumption, Nutrient Intakes, and Diet Quality | Economic Research Service. Usda.gov . Published August 21, 2024. https://www.ers.usda.gov/data-products/food-consumption-nutrient-intakes-and-diet-quality [5] Pendick D. How much protein do you need every day? Harvard Health Blog. Published June 22, 2023. https://www.health.harvard.edu/blog/how-much-protein-do-you-need-every-day-201506188096 [6] Wolfe RR, Cifelli AM, Kostas G, Kim IY. Optimizing Protein Intake in Adults: Interpretation and Application of the Recommended Dietary Allowance Compared with the Acceptable Macronutrient Distribution Range. Advances in Nutrition: An International Review Journal. 2017;8(2):266-275. doi: https://doi.org/10.3945/an.116.013821 [7] What We Eat in America, NHANES August 2021–August 2023. Table 1. Nutrient Intakes from Food and Beverages: Mean Amounts Consumed per Individual, by Male/Female and Age, in the United States, August 2021–August 2023. https://www.ars.usda.gov/ARSUserFiles/80400530/pdf/2123/Table_1_NIN_MaleFemale_2123.pdf . [8] Mariotti F, Gardner CD. Dietary protein and amino acids in vegetarian diets-a review. Nutrients. 2019;11(11):E2661. doi: https://doi.org/10.3390/nu11112661 [9] Weiler M, Hertzler SR, Dvoretskiy S. Is It Time to Reconsider the U.S. Recommendations for Dietary Protein and Amino Acid Intake? Nutrients. 2023;15(4):838. doi: https://doi.org/10.3390/nu15040838 [10] Kokura Y, Ueshima J, Saino Y, Maeda K. Enhanced protein intake on maintaining muscle mass, strength, and physical function in adults with overweight/obesity: A systematic review and meta-analysis. Clinical Nutrition ESPEN. 2024;63:417-426. doi: https://doi.org/10.1016/j.clnesp.2024.06.030 [11] Bauer J, Biolo G, Cederholm T, et al. Evidence-Based Recommendations for Optimal Dietary Protein Intake in Older People: A Position Paper from the PROT-AGE Study Group. Journal of the American Medical Directors Association. 2013;14(8):542-559. doi: https://doi.org/10.1016/j.jamda.2013.05.021 [12] Beasley JM, LaCroix AZ, Neuhouser ML, et al. Protein Intake and Incident Frailty in the Women’s Health Initiative Observational Study. Journal of the American Geriatrics Society. 2010;58(6):1063-1071. doi: https://doi.org/10.1111/j.1532-5415.2010.02866.x [13] Coelho-Júnior HJ, Calvani R, Tosato M, Landi F, Picca A, Marzetti E. Protein intake and physical function in older adults: A systematic review and meta-analysis. Ageing Research Reviews. 2022;81:101731. doi: https://doi.org/10.1016/j.arr.2022.101731 [14] Thomas, D. T., Erdman, K. A., and Burke, L. M. Position of the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and athletic performance. J Acad Nutr Diet 116:501–528, 2016. [15] Williamson E, Fung HJW, Adams C, West DWD, Moore DR. Protein Requirements Are Increased in Endurance-Trained Athletes but Similar between Females and Males during Postexercise Recovery. Medicine and Science in Sports and Exercise. 2023;55(10):1866-1875. doi: https://doi.org/10.1249/MSS.0000000000003219 [16] Leidy HJ. The role of protein in weight loss and maintenance. The American Journal of Clinical Nutrition. 2015;101(6):1320S1329S. doi: https://doi.org/10.3945/ajcn.114.084038 [17] Shi W, Huang X, Schooling CM, Zhao JV. Red meat consumption, cardiovascular diseases, and diabetes: a systematic review and meta-analysis. Eur Heart J. 2023 Jul 21;44(28):2626-2635. doi: 10.1093/eurheartj/ehad336 [18] Guasch-Ferré M, Satija A, Blondin SA, et al. Meta-Analysis of Randomized Controlled Trials of Red Meat Consumption in Comparison with Various Comparison Diets on Cardiovascular Risk Factors. Circulation. 2019;139(15):1828-1845. doi:10.1161/CIRCULATIONAHA.118.035225 [19] National Cancer Institute, NIH, Cancer Trends Report. Red Meat and Processed Meat Consumption. https://progressreport.cancer.gov/prevention/diet_alcohol/red_meat

The Fascinating Science Behind Sperm Motility and Testicular Location Ever wondered why testicles are outside the body? Recent research sheds light on these intriguing biological questions and how the body works in concert to ensure successful fertilization. In a study published April 2025, researchers examined mouse sperm to try to determine the biochemical makeup and process that makes spermatozoa move or swim. (Sperm and spermatozoa are generally interchangeable in meaning, but sometimes the word sperm may refer to both seminal fluid and spermatozoa.) Spermatozoa are activated by heat and in most mammals, the testes are outside of the body to keep the temperature 2 to 4 degrees C less than core body temperature.  Some animals have internal testes but have adapted to either keeping their body temperature or the area around the testes lower.  Some birds have internal testes and high core temperatures, but birds do not carry the CatSper gene. Spermatozoa need to move to come in contact with the ovum in the oviduct to start fertilization.  CatSper is the name of a calcium ion channel that controls the level of intracellular calcium.  When CatSper is activated, calcium enters the spermatozoa flagella (tail on the spermatozoa that moves), and it starts to gyrate, allowing the spermatozoa to move or swim.  The researchers in this study found that as the temperature surrounding the spermatozoa increased, the CatSper ion channel was activated resulting in more flagellar movement.  However, above 38 degrees C (100.4 degrees F) flagellar activity diminished.    They also found that the acidity of the spermatozoa’s environment affects CatSper activation.  Spermatozoa are stored in the testes at a pH of 6.9 (acidic).  They reported that an acid environment suppresses heat activation of the CatSper channel. Thus, when spermatozoa enter the vagina with its 37 degree C temperature (98.6 degrees F) and neutral pH of 7.4, much warmer and less acidic environment than the testes, there are ideal conditions for CatSper to activate and help start the spermatozoa’s movement to the egg.  However, there is one more system in place to prevent the spermatozoa from being activated too quickly.  In seminal fluid, which surrounds spermatozoa, there is a substance called spermine.  Spermine appears to blunt the temperature increase response of CatSper, which allows the spermatozoa to get closer to the egg target, before it activates (called capacitation).   Spermatozoa, once activated by CatSper, have a limited lifespan, so it is best if activation occurs in the oviducts.  The spermine gradually dissipates and is also removed by chemical reactions in the oviducts. This allows the spermatozoa to fully activate when the spermatozoa are closer to the ovum, increasing the odds of successful fertilization. Comments: Fertilization is an amazingly complex process with adaptations such as temperature, acidity of the environment, and biochemical reactions appearing to be part of the way it is controlled.  Other research has shown CatSper channel activation also occurs after exposure to female progesterone and prostaglandins (hormone-like substances), and certain odorants (chemical compounds that have a smell or odor).  It seems that CatSper activation is probably due to multiple factors. Moving the flagella, or tail rapidly allowing travel of the sperm to the ovum is only a part of the process of fertilization, and this particular study determined that body temperature and pH are critical parts of CatSper activation.  In both mice and humans, non-functioning CatSper channels, due to mutations, can cause male infertility. One of the reasons human testicles are outside the body appears to be an adaptation designed to decrease the temperature stored spermatozoa are exposed to and prevent premature activation. updated 6/23/2025 To read an article about the effects of exposure to plastic on human health, click here. References Swain DK et al. The essential calcium channel of sperm CatSper is temperature-gated. Nat Commun 16, 3657 (2025). Retrieved from: https://www.nature.com/articles/s41467-025-58824-0#citeas Brenker C, Goodwin N, Weyand I, et al. The CatSper channel: a polymodal chemosensor in human sperm. EMBO J . 2012;31(7):1654-1665. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3321208/

The Chilling Truth About Cold-Stimulus Headaches Ever wonder why a scoop of ice cream can sometimes lead to a sudden, sharp pain in your head? Learn about the common phenomenon of " brain freeze ," what causes it, and simple ways to enjoy your cold treats without the headache. Cold-stimulus headaches, otherwise known as ice cream headaches or brain freeze, are a common phenomenon after eating or drinking something cold, especially having the cold food or beverage come into contact with the palate (upper part of the mouth) and/or posterior pharyngeal wall (back of the throat).  It is estimated to occur in about 15-40% of people.  The pain typically peaks in about 30 to 60 seconds after ingesting a cold food or beverage.  It can be a stabbing or aching type of pain, usually in the mid-frontal forehead area, but can also be behind the eye, or the side of the head near the front (temporal region).  Occasionally the pain can be in the back of the head or like a toothache. The pain typically starts resolving within 20 seconds but can last for up to a few minutes. One experimenter found that crushed ice applied to the palate caused pain near the eye and temporal region (side of the head near the front) within 20-30 seconds.  If the ice was placed on one side of the palate, it was felt on that side of the head.  If the ice was placed on the midline of the palate, the pain was felt on both sides.  Interestingly, the pain could only be produced in hot weather, and he was not able to induce the pain in the wintertime.  In another study, it was reported that ice water was much more likely to cause a headache than an ice cube, possibly due to the fact that the ice cube stimulates a smaller area of the mouth than iced water.    It is not clear whether patients with a history of migraine headaches have an increased or decreased incidence of ice cream headaches, as there have been conflicting studies with both findings.  It is thought that cold food and beverages may stimulate branches of the trigeminal nerve (facial nerve) which can lead first to a constriction of arteries, then followed by rapid arterial dilation leading to pain. This is similar to how a migraine headache causes pain. Ways to Decrease Ice Cream Headaches The posterior or back part of the palate is thought to be more sensitive to cold, and it is advised that if one suffers from this condition, to try to avoid contact with this area when eating ice cream or ingesting cold liquids.  Eating ice cream slowly may also help, as one study found that very rapidly eating ice cream more than doubled the number of ice cream headaches compared to eating it more slowly. Another cause of headaches   is nitroglycerin, which is an explosive used both in dynamite and as a cardiac medication.   Click here to read about  The History of Nitroglycerin, an Explosive with Medical Benefits. References Hulihan J. Ice cream headache No need for abstinence. BMJ. Volume 314. 10 May 1997. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/instance/2126629/pdf/9161304.pdf Fuh JL et al. Ice-Cream Headache - A Large Survey of 8359 Adolescents. Cephalalgia . 2003;23(10):977-981. Retrieved from: https://journals.sagepub.com/doi/full/10.1046/j.1468-2982.2003.00620.x Selekler HM & Faik Budak F; Idiopathic Stabbing Headache and Experimental Ice Cream Headache (Short-Lived Headaches). Eur Neurol  1 January 2004; 51 (1): 6–9. Retrieved from: https://karger.com/ene/article-abstract/51/1/6/123900/Idiopathic-Stabbing-Headache-and-Experimental-Ice Kaczorowski M, Kaczorowski J. Ice cream evoked headaches. Ice cream evoked headaches (ICE-H) study: randomized trial of accelerated versus cautious ice cream eating regimen. BMJ. 2002;325(7378):1445-1446. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC139031/ Sleigh JW. Ice cream headache - Cerebral vasoconstriction causing decrease in arterial flow may have a role. BMJ Volume 315. 6 September 1997. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/instance/2127417/pdf/9302986.pdf Mages S etal. Experimental provocation of ‘ice-cream headache’ by ice cubes and ice water. Cephalalgia. 2017, Vol. 37(5) 464–469. Retrieved from: https://journals.sagepub.com/doi/pdf/10.1177/0333102416650704

A study released in March 2025, in pre-publication (not yet peer-reviewed), looked at 93,267 adult subjects under the age of 50 with a diagnosis of cannabis use compared to 4,543,361 subjects with no cannabis use diagnoses.  ICD-10 (International classification of diseases, 10th version) diagnoses were used to separate cannabis users from non-users as well as the incidence of myocardial infarction, major adverse cardiovascular events, mortality, heart failure and ischemic stroke in the subjects.  The study was a retrospective review of data from U.S. patients in a large database.   After propensity matching the groups to assure equal baseline health characteristics there were then 89,776 subjects in each group for the actual study.  Both groups were free of some known risk factors including hypertension, diabetes, hyperlipemia and heart disease and tobacco use.  Over a 5-year period of data review, there was a 6.2 times higher risk of myocardial infarction, a 4.3 times higher risk of stroke, a 3.3 times higher risk of a major adverse cardiovascular event, a 2 times higher risk of heart failure and a 1.5 times higher risk of death in the cannabis users group compared to the non-users.  Even though there was a major increase in risk, the absolute numbers were small.  There was a 0.558% incidence of myocardial infarction in cannabis-users vs. 0.09% in non-users.  For stroke there was 0.405% incidence in cannabis-users vs. 0.094% in non-users. For heart failure a 0.861% incidence in cannabis users vs. 0.424% incidence in non-users. All-cause mortality was 1.262% in cannabis users vs. 0.841% in non-users. Limitations of the study include the use of retrospective diagnoses of cannabis use and adverse events which may not be correct and there may have been confounding variables not taken into account which could have affected results.  Comments:  This study found a significant increase in risk in cannabis using subjects under 50 years of age compared to non-users, for a number of adverse cardiovascular events including myocardial infarction, ischemic stroke, heart failure, and mortality.  Although the risk of an adverse event was much higher in the cannabis group, this affected only a small percentage of total users, as the actual percentages of adverse events were small.  This is consistent with a number of other studies on cannabis use that have shown it can cause increased cardiovascular risk.  In one study, the risk of having a myocardial infarction after smoking cannabis was almost 5 times higher in the first hour after use, compared to controls.  Cannabis is thought to increase cardiovascular risk due to its effects of increasing heart rate, blood pressure, and arterial wall inflammation which can increase cardiovascular stress and also lead to worsening atherosclerosis.   For a more in-depth look at the health risks and benefits of cannabis use click here for the article, The Pharmacology, Medical Uses, and Adverse Effects of Cannabis .   References Kame I et al. Myocardial Infarction and Cardiovascular Risks Associated with Cannabis Use: A Multicenter Retrospective Study.  JACC: Advances, 2025. Retrieved from: https://www.sciencedirect.com/science/article/pii/S2772963X25001152?via%3Dihub Caplen S. The Pharmacology, Medical Uses, and Adverse Effects of Cannabis. FibonacciMedicine.  Jan 20, 2022. Retrieved from: https://www.fibonaccimd.com/post/a-look-at-cannabis-pharmacology-medical-uses-and-adverse-effects Mittlean MM et al. Triggering Myocardial Infarction by Marijuana. Circulation. Vol 103, Issue 23. June 12, 2001. Retrieved from: https://www.ahajournals.org/doi/full/10.1161/01.CIR.103.23.2805

A recent study reveals that prescribing opiates for headache in the emergency department significantly increases the risk of long-term opioid use and related adverse events. In a study published April 2025, but released on the internet before that, investigators looked at the use of opioids in the treatment of headache and the risk of opiate-related  adverse events over a 1-year period. They reviewed over 234,308 visits for headache over 10 years. Approximately 5.7% of those patients (13,375 patients) received opiate prescriptions and they were propensity matched* to a similar number of patients who did not get opiate prescriptions. Subjects with a history of previous opiate use disorder or cancer were excluded. *(Researchers construct an artificial control group by matching each treated subject with a non-treated subject with similar baseline characteristics.) The 1-year primary outcome of the experiment was a combination of three measures after the emergency department visits, long-term prescription opioid use, an opioid-related ED visit or hospitalization, or starting on new opioid agonist therapy (such as methadone or buprenorphine). Results There was a 65% increased risk of having the 1-year primary outcome in the opiate prescription group compared to the non-opiate treated group (8.6% compared to 5.8%). There was a 77% increased risk of long-term opiate prescription use in in the opiate group over the controls (7.7% compared to 4.8%). Of even more of a concern was that subjects who were classified as opiate naïve (no opiate prescriptions in the previous year), had a 216% increased risk of meeting the primary outcome of long-term prescription opioid use, an opioid-related ED visit or hospitalization, or starting on new opioid agonist therapy compared to those not given an opiate prescription. They also reported that short-term opiate prescriptions were found not to be a problem. The issue was in opiate prescriptions of more than 7 days duration which increased the risk of meeting the primary outcome by 284% over controls.  As the daily dosage of opiate in the prescription increased, the risk of meeting the primary outcome also increased incrementally. The authors stated that in their data set for every twenty-nine patients treated with opiates, one would go on to have an opiate problem, as defined by the primary outcome. They also noted that 13.7% of patients given an opiate prescription returned to the emergency department with headache complaints within 7 days compared to only 9% of non-opiate treated patients, which may indicate opiates are not as effective as other medications and might be more likely to result in rebound headaches. Comments: This article is reinforcement of the concept that opiates for certain people, even one prescription, can be problematic. It is also a reminder to health care providers that when treating headaches, other available medications should be tried first and if a prescription for opiates is required it should be of short duration and the lowest effective dosage. For an historical look at an addictive drug, click here to read an article about The History of Heroin, the “Nonaddictive” Substitute for Morphine. Reference Hayward J et al. Risks associated with opioid prescriptions for headache in the emergency department. The American Journal of Emergency Medicine. Volume 90, 2025, Pages 109-114. Retrieved from: https://www.sciencedirect.com/science/article/pii/S0735675725000361

Enlarged ventricles damage the brain despite normal pressure! Learn how in our free CME 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.  😇 Normal Pressure Hydrocephalus in Adults. How Does It Cause Damage if the Pressure is Normal? By Stuart M. Caplen, MD  What is now known as normal-pressure hydrocephalus (NPH) was first discovered in the 1700s in autopsies of patients with enlarged cerebral ventricles.  It then disappeared from the medical literature until it was “rediscovered” by Salomón Hakim in the mid-1960s.[1] NPH consists of a syndrome of enlarged cerebral ventricles (ventriculomegaly), cognitive impairment, urinary incontinence and a gait disorder (gait apraxia - an inability to lift the feet off the floor when walking as well as disequilibrium).  NPH can be idiopathic, which typically makes up about half of the cases.  Other etiologies may include subarachnoid hemorrhage, meningitis, intracerebral hemorrhage, brain tumor, or head trauma.[2] The mechanism of NPH is typically cerebrospinal fluid (CSF) flow obstruction.  One might expect that if there is outflow obstruction, the cerebrospinal fluid pressure would increase.  But that does not occur in this disorder.  Instead, the brain gets compressed as the pressure increases which normalizes the intracranial pressure at the cost of increasing force on the brain and decreased brain arterial perfusion.  It is explained by Pascal’s law of hydrodynamics, where Force = Area x Pressure.  As fluid accumulates, the pressure in the ventricles would normally increase, but instead normalizes due to increasing brain compression.  As the ventricles enlarge, their area increases.  As per Pascal’s law, if the cerebrospinal fluid pressure remains the same, as the surface area of the ventricles increases, the compressive forces exerted on the brain will also increase.  Using Pascal’s law, ventricles that have increased their surface area by a factor of two will exert twice the force against the brain given the same normal cerebrospinal fluid pressure.[1,2]  Increased force in the ventricles compresses the brain and increases the transmantle pressure (the difference between the ventricular pressure and the pressure over the brain surface), which produces a global decrease in cerebral perfusion.  The most affected areas are the frontal cortex, periventricular white matter, basal ganglia, and the thalami.[2] Imaging for NPH MRI is considered the best imaging test for NPH.  Evans index and Callosal angle on MRI [2] Criteria for NPH include an Evan’s index more than 0.3.  The Evan’s index is the ratio of maximal width of the frontal horns of the lateral ventricles and maximal internal diameter of the skull at the same level on axial CT or MRI images.  In the image above on the left, Evan’s index is 50.8/129.4= 0.39. Another measurement of NPH severity is a callosal angle of greater than 40 degrees. As the ventricles enlarge, the callosal angle also increases.  In the image above on the right, the callosal angle is 86 degrees.[2]  MRI Images of NPH [2] Image C above is an axial FLAIR MRI scan with enlarged lateral ventricles and brightening in the surrounding white matter, suggestive of transependymal edema.  Image D above illustrates Narrowing of the brain sulci and subarachnoid spaces in the frontoparietal regions seen in NPH.[2] Differential Diagnosis  When considering a diagnosis of NPH, other diseases that can cause dementia should be ruled out, such as Alzheimer’s disease, atypical Parkinsonism, dementia with Lewy bodies, progressive supranuclear palsy, and vascular dementia.[2]  Other brain pathology such as tumor or stroke should also be considered. Gait in Hydrocephalus  An analysis comparing subjects with NPH versus normal controls reported that NPH patients had slower walking velocity due to shorter stride length, had outward rotation of the feet, wider step width, and were not able to lift their feet to a normal height during the swing phase of walking.  While walking, the feet of patients with NPH struck the ground flat and not with the normal heel strike as seen in the controls.  There was also a decrease in the normal step-to-step variability of the walking pattern which led to poor compensation for body sway, which can cause problems with obstacle avoidance or on uneven walkways.[3] The typical gait of NPH is also known as magnetic gait, as the patients walk as if their feet are glued to the floor.[4]  Predictive Tests of Treatment Response  The definitive treatment for NPH is placement of a ventriculoperitoneal shunt (VP shunt).  There are several tests that can be performed to assess whether inserting a VP shunt may help a patient with NPH.  The first test is a large volume lumbar puncture  ( LVLP ) where 30 to 50 milliliters of CSF are removed.  There is a pre-and post-procedure objective evaluation of gait, cognition, and urinary incontinence.  A non-enhanced brain MRI with CBF-ASL (cerebral blood flow, arterial spin labeling) can be done pre- and post-procedure to evaluate if perfusion has also improved.  A VP shunt is recommended if post-procedure improvement is documented, although it is known that the test is not 100% accurate and in some cases there may be improvement even with a negative test.[2] Arterial spin-labeling perfusion MRI demonstrating increased brain arterial perfusion after a large volume spinal tap in a patient with NPH. [2] A study of 35 patients who had a positive LVLP test reported that 72% of the subjects had gait improvement, however there was no significant improvement in cognitive function.[5] In the medical literature, the sensitivity of the LVLP test is 26% to 62%, which means that some people who had negative tests will still improve with shunt placement.  After a successful large volume lumbar puncture test, the positive predictive value of a VP shunt improving a patient’s clinical status is 73% to 100%.[6] External lumbar drainage  (ELD) is another test that can be used when patients do not demonstrate any response to an LVLP.  A lumbar spinal catheter is inserted and CSF is slowly drained over 72 hours.[7]  A study of 151 patients found that 100 patients, or 66%, had improved clinical status after the ELD procedure and 84 of them then went on to have VP shunt placement.  76 patients, or 90.5%, had a positive outcome after shunt placement.  Eighteen patients who had a negative ELD test still decided to undergo shunt placement and four of them, or 22%, experienced clinical improvement after the shunt was placed.[6] In a lumbar infusion test (LIT ), fluid is infused into a lumbar spinal catheter, and the intracerebral pressure monitored via another lumbar catheter.  A rise in the pressure can indicate decreased fluid reabsorption from the CSF (also described as resistance to CSF outflow or Rout) and may have positive prognostic value in determining which patients with NPH may benefit from a VP shunt.[8,9]  One advantage of using the lumbar infusion test over ELD as a secondary test after a negative LVLP is that it is a 45-minute test rather than a 3-day test.   In one study the LIT  was compared to LVLP . The LIT was found to have a positive predictive value of 80% for VP shunt success, while the   LVLP had a higher positive predictive value of 94%.  However, the LIT missed 16% of patients who improved after shunt surgery, while the LVLP missed 58%.  The authors concluded that the LIT is more sensitive, while the LVLP was more specific, and both tests were complementary to each other.[8]  Another study comparing the two procedures concluded that routinely performing LIT and LVLP in patients with MRI findings and a clinical picture of NPH is not necessary, given that both tests will have significant numbers of false negatives.  However, where there is some doubt about the NPH diagnosis, they may be helpful in deciding if a VP shunting procedure should be performed.[10] Ventriculoperitoneal Shunt  A VP shunt procedure involves making a hole in the skull and inserting a catheter into one of the cerebral ventricles.  The catheter is then subcutaneously threaded down the neck and thorax and inserted in the peritoneum.  There is a one-way valve to prevent reflux of CSF back from the catheter into the ventricles.   In one study of 17,035 patients who received a VP shunt, with a mean follow-up of 3.9 years, 23.8% had a complication, 6.1% suffered an infection, and 22% needed a VP shunt revision.  If non-traumatic subdural hematoma was included as a complication, the complication rate was 33.4%. (Nontraumatic subdural hematoma is a known potential complication of overdrainage from a VP shunt.)[11] In the medical literature, VP shunts have an estimated 98% failure rate over 10 years. Some causes of shunt failure include tissue, clots or infection causing obstruction, kinking, catheter migration, fracture of the catheter, valve malfunction, and pseudocyst formation either in the brain or in the abdomen.[12] Endovascular Implantable Shunts An alternative method of draining CSF fluid is now in initial trials.  It is an endovascular implantable shunt that is placed via cannulation of the femoral vein and then threaded to the internal jugular vein.  A needle is then advanced through the catheter into the vein wall and pushed into the cerebellopontine angle cistern.  A small device with a one-way pressure valve and a tube is inserted and anchored, which can then drain CSF directly into the internal jugular vein.  An advantage of this method is that there is no need to open the cranium and pass a catheter through brain tissue, as in a VP shunt.[13]  In April 2024, after 19 patients had received the shunt, an abstract about the study was presented at a scientific meeting. The subjects all had idiopathic NPH and percutaneous transdural implant placement with this new device.  The abstract reported that there was a 32% to 39% significant gait improvement up to 180 days post-procedure, although there appeared to be a decrease in patients returning for follow-up exams over time. There was no discussion in the abstract of long-term complications or if cognitive ability or incontinence had specifically improved with the procedure.  The abstract did report there were no technical complications during placement.[14]  Clinical trials of this device are still ongoing, and more details of this specific trial should be forthcoming if and when it is formally published. Endoscopic Third Ventriculostomy Endoscopic third ventriculostomy (ETV) is a procedure where an endoscope is placed though a skull burr hole, and under direct vision a hole is made in the 3rd ventricle.  It has typically been used for obstructive hydrocephalus, but some researchers have tried it for idiopathic NPH.  Some small studies have had good results with ETV, but there is apparently only one randomized controlled trial comparing VP shunt to ETV.  In that study, 50% of the ETV group had improved after 12 months of follow-up compared to 76.9% of the VP shunt group. 19% of the VP Shunt group had overdrainage and developed a subdural hematoma and needed corrective surgery.[15]  A Cochrane review in 2015 reviewed that study and felt the data was inconclusive, and the researchers had used a non-programmable valve in the VP shunt, which was not standard practice.  They concluded the evidence was low quality, and more research was needed.[16] A meta-analysis in 2022 also concluded that current data regarding this procedure for idiopathic NPH is minimal.[17] Intracranial Shunt Draining Into the Internal Jugular Vein  Another experimental approach being evaluated is to insert an intracranial shunt similar to a VP shunt, but only brought down to the neck to drain into the internal jugular vein instead of into the peritoneal cavity.[18] Conclusion: NPH is a progressive disease that can lead to urinary incontinence, dementia, and gait disturbances, due to brain compression.  It is most commonly idiopathic in adults but can occur after other brain disorders.  Diagnosis is based on clinical suspicion and confirmed with MRI.  Predictive tests for VP shunt placement effectiveness have good positive predictive value, but some patients with negative tests may still show improvement with the placement of a VP shunt.  VP shunts can be curative, but the degree of improvement may depend on how advanced the disease is, as well as the age of the patient and the presence of other concurrent disease processes. VP shunts are not risk-free, and there is a significant complication rate.   More research is needed to see if the less invasive ETV is an acceptable modality for certain patients with idiopathic NPH. Some newer procedures that drain CSF into the internal jugular vein are being trialed, including one that is inserted percutaneously and does not require opening of the skull to place the shunt.  If that procedure turns out to be successful, without major complications, it would make inserting or replacing a shunt less invasive and be a major advance in the treatment of NPH.  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 PDF 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.  😇

Craving something special for breakfast or brunch? This Oven Pancake (aka Dutch baby!) with Roasted Cherries is light, fluffy, and incredibly easy to make. Creative Cooking for the Health-Conscious Gourmet FibonacciRECIPES  | Culinary Medicine   Recipe This fun, easy to make, puffy pancake, also called a Dutch baby or German pancake, is similar to a popover. Top it with roasted cherries for breakfast or brunch.  Add a scoop of ice cream to serve it as a dessert treat. Ingredients: Roasted Cherries 1 cup cherries 1 tsp raw sugar Pancake 2 large eggs 1/3 cup skim milk 1/3 c flour ¼ tsp salt ¼ tsp nutmeg Cooking spray 1 Tbsp butter 1 Tbsp powdered sugar Instructions Preheat oven to 400 degrees. Cut cherries in half and remove the pits. Place cherries on a parchment paper-lined cookie sheet and sprinkle with raw sugar. Roast for 10 -15 minutes until cherries start to release their juices. Cool on pan. While cherries are cooling, increase oven temperature to 450 degrees and heat a 9 or 10-inch oven-safe skillet in the oven. Beat together eggs and milk. Continue beating while adding flour a spoonful at a time. Mix in salt and nutmeg. Carefully remove the hot pan from oven, then add the butter and swirl the pan so the butter covers the bottom and sides. If the sides aren’t coated with butter,  apply cooking spray to assure the batter won’t stick Pour batter into the hot pan and return it to oven. Reduce heat to 400 degrees. Bake for 10-12 minutes until puffy and slightly browned. Immediately top with cherries and sprinkle with powdered sugar. Serve warm Store any leftover cherries in the refrigerator for up to 5 days. They are a delicious quick snack. Makes 4 servings Nutrition information per serving Calories  90, Total Fat 2.5 g, Saturated Fat 0.8 g, Cholesterol 94mg, Total Carbohydrate 12g, Dietary fiber 1g, Protein 5g, Potassium 109mg, Sodium 180mg Nutrition Chef Authors: Mary B Grosvenor, MS, RD Lori A Smolin, PhD Medically Reviewed by FibonacciMD editors. Editor’s Note- appropriate for a low-calorie, low-fat, low carb, lacto-ovo vegetarian dietary regimen. Learn about some of the health benefits of cherries in our culinary medicine article "Cherries: Sweet & Tart"

This CME article explores how communication in healthcare can impact errors, care quality, and malpractice risk, and offers strategies to improve communication skills. 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.  😇 Communication Issues in Healthcare: Its Relation to Malpractice Risk, and How to Communicate More Effectively by Stuart M. Caplen, MD Last updated 6/17/2025 Malpractice and Communication  It has been reported that communication issues were a factor in 30% of malpractice cases filed from 2009–2013.  Those 7,149 cases resulted in a reported $1.7 billion of malpractice costs.  Eight percent of communication failures that led to litigation were in the emergency department, 44% were from inpatient settings, and 48% from outpatient settings.  There was some overlap of communication issues leading to malpractice cases, but 57% involved provider-to-provider issues, and 55% were provider-to-patient communication problems.[1,2]  The Problematic Patient Handoff and Change of Shift  Joint Commission data indicate that inadequate patient handoffs are a factor in 80% of all adverse events.[2]   A survey of medical schools found only 8% taught students how to properly handoff patients.[3]  In one study, 59% of residents at Massachusetts General Hospital reported that one or more patients had been harmed during their most recent clinical rotation because of problematic handoffs, and 12% reported that the harm had been major.[4] The Joint Commission, in order to try to reduce errors in patient handoffs, requires the use of standardized methods, forms, or tools to facilitate the process.  One such method, a handoff checklist of critical information, is called “I PASS the BATON” was developed by the U.S. Agency for Healthcare Research and Quality.[2]   I PASS the BATON [2] I = Introduction —Introduce yourself and your role/job (include patient). P = Patient —Name, identifiers, age, gender, and location A = Assessment —Presenting chief complaint, vital signs, symptoms, and diagnosis S = Situation —Current status/circumstances, including code status, level of uncertainty, recent changes, and response to treatment S = Safety Concerns —Critical lab values/reports, socioeconomic factors, allergies, and alerts (falls, isolation, and so on) [the] B = Background —Comorbidities, previous episodes, current medications, and family history A = Actions —What actions were taken or are required? Provide brief rationale. T = Timing —Level of urgency and explicit timing and prioritization of actions O = Ownership —Who is responsible (nurse/doctor/team)? Include patient/family responsibilities. N = Next —What will happen next? Anticipated changes? What is the plan? Are there contingency plans? Physician Communication Behaviors and Malpractice  An experiment was performed to determine how communication behaviors might influence a patient's decision to pursue a malpractice case.  Participants were shown different videos: one of a patient being examined by a physician with good communication behaviors such as good eye contact, friendly tone of voice, and requesting information.  The other video was a physician using negative communication behaviors such as poor eye contact, harsh and clipped tones of voice, non-smiling expressions, and minimal requests for information.  The participants were then told several different possible outcomes of the patient’s disease process.  If the outcome was negative, it was reported that the participants were significantly more likely to blame the physician with negative communication behaviors, thought that the physician had been negligent, and wished to sue that physician, as compared to the physician with good communication behaviors.  Even if the outcome of the patient’s disease process was a favorable one, the subjects felt the poor communication physicians were more negligent.  They also rated the poor communicators as less professional, less caring, less friendly, less trustworthy, less competent, and significantly more negligent and liable for a poor result.  Interestingly, the authors were concerned about whether the negative behaviors the physician actors used in the simulations were unrealistic and overly excessive.  They asked the participants about that issue, and in some cases were told “Well, that's just the way they are.”[5]   Interruptions and the High Control Interview Style In a 1984 study, it was reported that 77% of patients were not able to complete their opening statements of concern or chief complaint.  Most interruptions (54%) occurred after the first expressed concern and occurred on average 18 seconds after the patient began to speak.  In 69% of the visits, the physician interrupted and started directing questions toward the chief complaint, and only one of 51 patients was given the opportunity to complete their opening statement by the physician after interrupting.[6]   One might hope physician communication behaviors had improved over time, but in 2004, an emergency department study of residents reported that only 20% of patients completed their presenting complaint without interruption.  The average time to interruption was 12 seconds.  On discharge, only 16% of patients were asked whether they had questions, and there were zero cases in which the provider confirmed patient understanding of the information.  About one-third of the residents never introduced themselves to the patient.[7] This process, whereby the physician takes control of the interaction by asking questions, and in many cases not allowing the patient to even complete their opening statement, is known as the high control interview style.  This can be problematic, as one study found that 24% of the time for somatic problems and 94% of the time for psychosocial problems, the chief complaint was not actually the patient’s most significant problem and potentially a cause of diagnostic error.[8]  An example of this might be where a patient’s first complaint is of vomiting, at which time the physician interrupts and starts asking abdominal-specific questions.  By not allowing the patient to expound further, the clinician might not discover that the vomiting was secondary to a subarachnoid hemorrhage or an acute glaucoma attack.  Other Physician Communication Issues   A study from the 1980s clearly demonstrated some physician communication issues.  It reported that doctors spent an average time of slightly more than 1 minute out of a 20-minute encounter giving information to their patients.  However, on asking the doctors how much time they spent giving their patients information, the doctors overestimated that time by about a factor of nine.  They thought they had spent much more time informing their patients than they actually did.[9] Nonverbal Communication and Vocal Tone Nonverbal communication using body language and vocal tone may be as important, or even more important, than the words that are actually spoken.  Early research in the subject determined that when there are inconsistencies between verbal and nonverbal messaging, perception of that messaging by the recipient will be 55% from nonverbal cues, 38% from the tone of voice, and only 7% from the actual words spoken.[10]  Actors are experts in nonverbal communication and clearly demonstrate that the same words delivered with different facial expressions or intonations can convey different meanings.  For example, a clinician saying that they are very interested in a patient’s problem while looking at their watch, is conveying two very different messages. In one study, medical residents who were more skilled at decoding nonverbal cues or were more effective in the use of nonverbal communication had more satisfied patients.[11]  Another study found physicians who were good at reading and correctly interpreting other people's nonverbal cues had more satisfied patients who were more likely to return for their next appointment than physicians who were less able to interpret nonverbal communication.[12] An interesting study of 57 general and orthopedic surgeons reported that when talking to patients, the surgeons whose voice tones reflected dominance and expressed less concern or anxiety in their voices were found to have significantly more malpractice cases filed against them than those surgeons that did not have those vocal behaviors.[13] In another study of nonverbal communication, greater patient satisfaction was found to be correlated to greater physician nonverbal interest, less time reading the patient's chart, more physician immediacy (such as a forward lean), more nods and gestures by physicians, and closer interpersonal distance with the physician.  Physicians who directly faced their patients, engaged in a moderate level of eye contact, and maintained an arm posture indicative of a readiness to act were rated as more empathic, interested, and warm.[14] Communication and Health Outcomes  A review of 21 studies that looked at the effect of communication behaviors on patient health outcomes found that 76% of the studies reported that effective communication had a beneficial effect on measured outcomes such as emotional health, pain control, glucose levels in diabetics, and management of hypertension.[15] In another study, one group of patients was given training on how to increase their participation in care by teaching them techniques for improving question asking,  negotiating skills, and reducing feelings of intimidation.  Compared to a control group, the intervention group had significant improvement in diabetes control, and the authors stated (without presenting the data) that there were similar favorable changes in control of hypertension in the intervention group.[16] Ways to Improve Communication  A study reported that only 49% of patients could recall decisions and recommendations made at ambulatory care visits; 36% could recall the information only if prompts were given, and 15% could not recall the information at all.[17] The teach-back technique is a method of assessing the patient’s understanding of what the clinician has tried to communicate by having the patient explain in their own words what the clinician has just told them.  A systematic review of teach-back studies reported that 95% of the studies found it to be effective.  Other studies found health literacy was increased, as was comprehension of post-visit care.[18]  Additional studies have found that the teach-back technique resulted in less rehospitalizations.[19]  In one study, participants indicated teach-back helped them to remember what they had learned from their providers and had improved patient-physician communication, although some participants felt the process was a waste of time or unnecessary.[20] The reverse process of clinicians repeating back to patients what they have told them gives the patient an opportunity to add information that might have been forgotten or to correct a previous statement.   Medical discussions and discharge instructions should be as simple and clear as possible without lapsing into medical jargon.  In a study of patients’ understanding of common medical phrases, phrases that had less physician jargon in them were better understood.  As examples, only 79% of the subjects knew that the phrase “your tumor is progressing” was bad news, only 67% knew that “positive lymph nodes” meant the cancer had spread, and only 9% knew what “febrile” meant.[21] The E4 Communication Model One model for communication in the literature is the E4 model where the steps are: Engage  the patient Empathize  with the patient Educate  the patient Enlist  the patient (1) Engage the Patient Introduce yourself (commonly forgotten).  Let the patient talk and complete their opening statement. (2) Empathize with the Patient Make the patient the center of your universe when talking to them and indicate your awareness of their needs and concerns.  Use good verbal and nonverbal communication skills. (3) Educate the Patient Some patients may not ask many or any questions, and physicians tend to give more information to patients that ask questions.  All patients wish to have some basic information about their condition, and the information listed below should be given to all patients whether they ask for it or not.[22,23]  What has happened to me? Why has it happened to me? What is going to happen to me, in the short-term and later on? What are you doing to me with respect to examination and tests? Why are you doing this rather than something else? Will it hurt me or harm me, for how long, and how much? When and how will you know what these tests mean, and when and how will I know what these tests mean? [22] (4) Enlist the Patient Involve the patient with their care.  Discuss problems or adverse events.  If a common adverse complication can occur, warn the patient.  Negative perceptions and litigiousness decrease with a bad result if the patient is informed.[5]  If a negative result occurs and you warned the patient about it, you may be perceived as an astute clinician, whereas if not warned, the patient may view that as a sign of incompetence Consider using partnership-building remarks such as “Do you have any other concerns?” and “How do you feel about….?”  In one study, only 2% of physicians’ remarks were partnership building.[23] Conclusions Poor communication, both physician-to-physician and physician-to-patient, may be problematic.  It has been definitively shown to increase malpractice risk, whereas good communication behaviors have been shown to reduce malpractice risk, improve patients’ understanding of their disease process, follow-up care, and improve health outcomes.  Simple techniques such as good eye contact, showing that one cares about the patient, and allowing them to finish their opening statement without interrupting, all can lead to better patient rapport as well as decreasing malpractice risk if there is a bad therapeutic outcome.  Clinicians should be aware of their own nonverbal behaviors as well as observing their patients for their nonverbal cues, both of which can improve physician-patient communication.  Avoid using medical jargon and use terms a layperson would understand.  If the patient is amenable, having them use the teach-back method before discharge can help ensure understanding of your communications. In a similar process, it may sometimes be helpful for the clinician to repeat back to the patient what they have told him/her to give the patient a chance to add information that might have been forgotten or correct a previous statement.   Using a formalized method of handing off patients at the end of a shift or when changing from one service to another may assist communication and help reduce errors and malpractice risk.  This author remembers being told by a senior resident during internship that the most dangerous time in medicine was change of shift.  We live in a time when clinicians’ speed of seeing patients is a measured metric, and they are frequently typing on a computer keyboard while interviewing patients.  These processes may lead to patient alienation.  Patient satisfaction is not specifically related to the time spent with the patient but to the quality of the interaction.[24]  Using good communication behaviors and ensuring the time spent with a patient is viewed as positive and therapeutic, may benefit both the patient and the clinician.   🎓  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 ✅ 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.  😇

The Medical Origins of the Gin and Tonic Discover the surprising origins of the classic gin and tonic. From a medicinal marvel to a beloved cocktail, this drink's journey is as fascinating as its taste. MEDICAL HISTORY by Stuart M. Caplen, MD   Legend has it that a Native American accidentally discovered that the bark of the cinchona tree ( Cinchona officinalis )   was a treatment for malaria. When ill with a fever, he drank from a pool of bitter, stagnant water with cinchona trees around it and got better.  The bark contains quinine and other alkaloids, which can treat malaria.  The Journey of Quinine from Peru to Europe The Spanish discovered that indigenous inhabitants of Peru were using cinchona bark in the 1600s.  It then also became known as “Jesuit’s bark” and became a European favorite medicine for treating malaria.  The bark was dried and ground down to a powder to produce quinine. Quinine’s Vital Role in the British Empire In the late 1700s, the British East India Company controlled trade and governed India.  More soldiers were lost to malaria than to battle, and by the 1800s, quinine powder was considered vital to the health of Englishmen in this tropical climate.  By 1840, they were using 700 tons of cinchona bark in India annually.  While quinine could be used to treat malaria, using it to prevent malaria was intermittently done until 1854, when an army physician ordered his men to take it while exploring the Niger River region.  None of them contracted malaria, and at that point, quinine prophylaxis started being used regularly. The Birth of Tonic Water The taste of quinine is very bitter and unpleasant, so the question was how to get people to drink it regularly.  In India, members of the British army were trying to find a way to make quinine more palatable so their soldiers would actually drink it every day.  They devised a homebrewed tonic water drink with some sugar, soda, and quinine. Dutch Courage and the British Gin Craze Gin was initially produced in the Netherlands, and during the Thirty Years' War (1618 -1648), was provided to soldiers for its calming effects before battle and became known as “Dutch Courage”.  When gin was brought back to Britain, it became so popular that it set off an era, from the late 1690s to early 1700s, known as the “Gin Craze”, with hundreds of distilleries, inexpensive gin, and a large amount of people drinking it.  It was associated with vice and social decay of the lower classes in Britain, but by the mid-1800s, gin was regaining respectability. How Gin and Tonic Became a Health Habit Someone, probably an army officer in India, decided to combine his tonic water with gin, and thus was born the gin and tonic, a popular drink, that came from a need to encourage people to take malaria prophylaxis.  The British army and the British East India Company allowed and encouraged members to drink the gin and tonic for their health and even recommended adding lime to it to prevent scurvy. The Bottled Legacy of Tonic Water Carbonated tonic waters containing quinine for malaria prophylaxis started to be produced in 1858, and by 1870, “Indian Quinine Tonic” created by Johann Jacob Schweppe of the Schweppes company, was the leading brand.  Tonic water sold today contains much less quinine than it did back then. If you enjoyed this article, read: The History of Heroin, the “Nonaddictive” Substitute for Morphine. More Medical News & Trivia References AZ quotes. Retrieved from:   https://www.azquotes.com/quote/863740 Simonetti O, Contini C, Martini M. The history of Gin and Tonic; the infectious disease specialist long drink. When gin and tonic was not ordered but prescribed. Infez Med. 2022;30(4):619-626. Published 2022 Dec 1. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9714995/ Raustiala K. The Imperial Cocktail, How the gin and tonic became the British Empire’s secret weapon. Slate. Aug 28, 2013. Retrieved from: https://slate.com/technology/2013/08/gin-and-tonic-kept-the-british-empire-healthy-the-drinks-quinine-powder-was-vital-for-stopping-the-spread-of-malaria.html