This CME article explores subclinical hypothyroidism, focusing on diagnostic challenges, treatment decisions, and therapeutic effectiveness. Read Article, Take Test , Get FREE 🎓 CME Certificate with Valid Email We’ll send you occasional updates. Your email stays private—never sold or shared.  😇 The Conundrum of Subclinical Hypothyroidism By Stuart M. Caplen, MD   This article will discuss the entity of subclinical hypothyroidism, looking at some of the complex issues clinicians face with respect to making the diagnosis, deciding whether to initiate treatment, and how effective that treatment will be. The thyroid gland located in the anterior neck produces three hormones: T4, thyroxine which contains four iodide atoms, T3, triiodothyronine containing three iodide atoms, and calcitonin which is involved in calcium regulation in the body. T3 and T4 hormones are involved in the control of body metabolism. The release of thyroid hormones is in a feedback loop with the hypothalamus where thyrotropin releasing hormone (TRH) stimulates the pituitary gland to release thyroid stimulating hormone (TSH), also known as thyrotropin, which increases the production and release of T3 and T4 from the thyroid gland. In hypothyroidism when T3 and T4 levels are low more TRH and TSH is released and in hyperthyroidism when T3 and T4 are elevated, TRH and TSH release is reduced. About 20% of T3 is produced in the thyroid gland. T4 is metabolically inactive and is converted to T3 in a process called deiodination to produce the other 80% of needed T3.[1] The deiodination of T4 occurs mainly in the liver and kidneys but also can occur in the central nervous system, pituitary gland, brown adipose tissue and muscle.[2] A small decrease in serum T4 may result in a relatively large increase in serum TSH, which can elevate the serum TSH level while T4 levels are still within the normal range.[3] When people are floridly hypothyroid there is little debate about the need for treatment. However, in subclinical hypothyroidism where TSH levels are elevated with normal T3 and T4 levels, the decision to treat or not treat is more complex. The TSH elevation in subclinical hypothyroidism indicates a relative lack of thyroid hormone in the body which requires more TSH to be released which stimulates the thyroid gland to produce and release more hormones to maintain normal T3 and T4 levels. Even though the T3 and T4 levels may be normal, some patients with subclinical hypothyroidism will have adverse symptoms. The prevalence of subclinical hypothyroidism varies among populations and ranges from 3% to 15%.[3] There is a higher prevalence of between 8% and 18% in adults over 65 years of age.[4] The conversion from subclinical hypothyroidism to overt hypothyroidism is about 2% to 6% per year, and is more likely in the elderly, women, people with higher TSH levels, the presence of thyroid antibodies, people with a low-normal T4 level,[3] high iodine intake or who have a goiter.[5] Up to 46% of patients found to have an isolated elevated TSH level will revert back to normal within two years.[3] In asymptomatic patients with an elevated TSH, it is recommended to get a repeat TSH level in two to three months before making a diagnosis of subclinical hypothyroidism due to the high number of people who spontaneously revert back to normal.[3] Causes of subclinical hypothyroidism in the adult include; chronic autoimmune thyroiditis (Hashimoto's disease), treated hyperthyroidism (Grave’s disease), radiation to the neck, iodine deficiency, medications such as lithium, iodine, amiodarone or antithyroid drugs, infiltrative diseases, such as amyloidosis, sarcoidosis, or hemochromatosis,[5] idiopathic hypothyroidism, and hypopituitarism causing secondary hypothyroidism.[6] Hashimoto’s disease is thought to be responsible for 60% to 80% of cases.[5] Symptoms of Subclinical Hypothyroidism Up to 70% of patients with subclinical hypothyroidism feel normal without any symptoms of hypothyroidism,[5] but some do present with mild symptoms, such as fatigue, muscle weakness, weight gain, cold intolerance, constipation, dry skin, puffy eyes or some reduction in cognitive function and memory.[3] Overt hypothyroidism can cause peripheral neuropathy, but the evidence for causation in subclinical hypothyroidism is mixed.[7,8] However, there are some studies that found symptoms of diabetic neuropathy are worsened in patients with subclinical hypothyroidism.[9,10] A literature review of the cardiac effects of subclinical hypothyroidism found that as TSH levels increased so did the number of adverse cardiac events, although it did not increase mortality. Coronary events were highest in subclinical hypothyroidism patients with TSH levels between 10 and 19.9 mIU/L (milli-international units/liter).[11] In a literature review, patients with subclinical hypothyroidism were found to be at higher risk for congestive heart failure, especially those with levels over 10mIU/L.[12] Subclinical hypothyroidism is known to increase total cholesterol and low-density lipoprotein (LDL) levels.[3] An analysis of subclinical hypothyroidism and stroke found no overall increase in events in the total group but there was an increased risk of stroke in adult patients with subclinical hypothyroidism under 65 years of age.[13] Subclinical hypothyroidism may increase the risk of female infertility, spontaneous abortion, gestational hypertension and preeclampsia. Normal values for TSH and T4 are altered during pregnancy.[3] Laboratory Testing Subclinical hypothyroidism is defined as a serum TSH over the reference range with a normal T4 level. Over 99% of T3 and T4 are bound to protein in the body and inactive biologically.[14] The preferred test is free T4 to measure the biologically active levels of the hormone rather than total T4 which includes the inactive protein bound portion. Conversely, in pregnancy measurement of total T4 is recommended because alterations in serum proteins may yield lower values of free T4 based on reference ranges established with normal non-pregnant individuals.[15] There is a consensus recommendation that T3 levels are not needed for the diagnosis of hypothyroidism and do not need to be drawn.[15] The normal values may vary slightly depending on the laboratory, but the reference range for free T4 (ages 20 and older) is 0.8-1.8 ng/dL (nanograms/deciliter) used by one national laboratory.[16] Total T4 normal values in females (over 20 years of age) are 5.1-11.9 mcg/dL (micrograms/deciliter).[17] The TSH reference range for patients ages 20 and older is 0.40-4.50 mIU/L,[18] although one consensus guideline recommends 4.12 mIU/L as the upper limit of normal.[15] In pregnancy the TSH reference ranges are much lower than in nonpregnant women with the first trimester reference range being 0.26-2.66 mIU/L, second trimester 0.55-2.73 mIU/L, and third trimester 0.43-2.91 mIU/L.[18] It should be noted that some authorities have recommended lowering the upper limit of normal of TSH to 3.0 mIU/L. The arguments for doing that is that the mean and median values of approximately 1.5 mIU/L are much closer to the lower limit of the reported normal reference range than the upper limit, and the distribution of TSH values used to establish the normal reference range is skewed to the right by values over 3.0. The arguments against lowering the upper limit of a normal TSH is that it would lead to more than 10 million additional diagnoses of hypothyroidism in the United States per year, without any clear-cut benefit, and many of those patients would not actually have subclinical hypothyroidism.[15] Thyroid peroxidase antibodies are antibodies of an enzyme involved in the synthesis of thyroid hormones. Patients who have these antibodies are more likely to progress to overt hypothyroidism compared to those that don’t; 4.3% per year in the antibody positive group versus 2.6% per year in subclinical hypothyroidism patients without antibodies.[15] Thyroid peroxidase antibodies may be seen in Hashimoto’s thyroiditis as well as idiopathic myxedema and Graves’ disease (hyperthyroidism).[3,19] Thyroglobulin antibodies are antibodies to a thyroid protein used to make thyroid hormones, and a correlation between elevated levels of these antibodies and symptoms of hypothyroidism has been found.[20] This test is more commonly used in thyroid cancer screening as elevated thyroglobulin levels are used to screen for cancer reoccurrences, and the presence of antibodies may make the test inaccurate.[21] Thyroglobulin antibodies are not as sensitive as thyroid peroxidase antibodies for subclinical hypothyroidism testing.[15] High dose biotin supplementation has been found to interfere with some thyroid immunoassay testing and can falsely elevate T4 and T3 levels and falsely decrease TSH levels.[22,23] It is recommended that patients stop biotin at least two days before testing to prevent spurious values and misdiagnosis.[22,24] Biotin supplementation is not uncommon. In one study of emergency department patients, 7.7% of the subjects were taking biotin supplements and 7.4% had serum concentrations at or above the lowest known threshold for biotin interference with thyroid testing.[25] Does Treatment Help? What is the evidence that treatment will help patients with subclinical hypothyroidism? There is strong evidence that early treatment will prevent onset of more severe symptoms if the patient progresses to overt hypothyroidism. There is strong evidence that treatment of subclinical hypothyroidism will improve symptoms of hypothyroidism especially with TSH levels over 10 mIU/L. There is moderate evidence that treatment will reduce total cholesterol and LDL levels but it is not certain whether this decreases the risk of a cardiovascular event. There is only weak evidence of a benefit to prevent strokes, CHF, cognitive decline, and coronary heart disease in TSH levels less than 10 mIU/L. The evidence for reduction of congestive heart failure and coronary artery disease is stronger for TSH levels above 10 mIU/L.[3] A Cochrane systematic review of the literature concluded that there was no survival benefit, reduced cardiovascular morbidity or improvement in health‐related quality of life for subclinical hypothyroidism patients treated with levothyroxine. There was some evidence that treatment improved lipid profile parameters and left ventricular function.[26] A trial of elderly patients with subclinical hypothyroidism comparing levothyroxine versus placebo found no symptomatic benefits in the treatment group over placebo.[27] Treatment recommendations Most sources base treatment recommendations for subclinical hypothyroidism on the amount of TSH elevation, patient symptoms and age. The American Thyroid Association and the American Association of Clinical Endocrinologists guidelines for elevated TSH levels under 10mIU/L state that treatment should be individualized, and recommend treating subclinical hypothyroidism only if the patient has symptoms of hypothyroidism, is positive for thyroid peroxidase antibodies, or has evidence of atherosclerotic cardiovascular disease, heart failure, or major cardiac risk factors. The rest should be followed and treatment started as needed. For TSH levels over 10mIU/L the consensus is to start thyroid replacement treatment.[15] There are slightly different recommendations from the European Thyroid Association (ETA) based on age. With TSH levels less than or equal to 10 mIU/L, they recommend that geriatric patients, especially those over 80 years of age without specific signs of hypothyroidism can be followed with careful follow-up with a wait-and-see strategy trying to avoid hormonal treatment if possible. The ETA also recommends lower treatment target TSH levels of 0.4 to 2.5 mIU/L for adult patients less than 70 years of age, and a higher TSH target range of 1 to 5 mIU/L for patients over 70 years old.[28] In pregnancy, treatment for subclinical hypothyroidism is recommended at lower TSH levels. There are questions of whether subclinical hypothyroidism can impair intellectual and psychomotor development in the fetus and increase miscarriages.[15] A meta-analysis and systemic review of 18 studies concluded that subclinical hypothyroidism patients were at higher risk for pregnancy loss, placental abruption, premature rupture of membranes, and neonatal death compared with euthyroid pregnant women, but the effects of replacement therapy were uncertain in preventing these complications.[29] Treatment Options Levothyroxine (T4) is considered the drug of choice for subclinical hypothyroidism. Because of differences in the biologic availability of various levothyroxine products, switching between different levothyroxine products should be avoided in patients whose condition is stable. Levothyroxine should be taken on an empty stomach with water 30-60 minutes before breakfast or at bedtime at least 4 hours after the last meal.[3,15] Liothyronine is a manufactured form of the triiodothyronine (T3) and is sold individually and in a combination pill with levothyroxine, and is not generally recommended for treating subclinical hypothyroidism, as there is no evidence supporting a benefit over using levothyroxine alone.[15,28] Combination Therapy Desiccated Thyroid is made from the thyroid gland of animals and contains both T3 and T4. It was in use before levothyroxine was available and is still available today. The ratio of T4 to T3 may vary in desiccated thyroid preparations by brand and whether it is of porcine or bovine origin,[15] and T3 levels vary substantially throughout the day in those taking desiccated thyroid.[30] The American Association of Clinical Endocrinologists and the American Thyroid Association guideline, based on expert opinion, states that “There is no evidence to support using desiccated thyroid hormone in preference to L-thyroxine monotherapy in the treatment of hypothyroidism and therefore desiccated thyroid hormone should not be used for the treatment of hypothyroidism”.[15] However, a small study of 70 patients comparing desiccated thyroid to levothyroxine found 48.6% of patients preferred the desiccated preparation compared to 19% who preferred T4 monotherapy. Subjects reported subjective increases of concentration, memory, sleep, decision-making capability, happiness, and energy levels while on the desiccated preparation. While more study is needed, and there was no difference in thyroid blood levels, the paper presents the possibility that there may be subgroups of hypothyroid patients that may benefit from combined T4/T3 therapy in ways that may not be easily clinically discernable.[31] While monotherapy with levothyroxine is currently recommended for most patients with hypothyroidism one study found that people with certain genetic variants in the deiodinase 2 gene (DIO2) which helps convert T4 to T3 in the body were found to have decreased psychological well-being while on T4 monotherapy which improved when combination T4/T3 therapy was used. In that study the DIO2 variant was present in 16% of the study population. This polymorphism (variant form of a DNA sequence) had no effect on circulating thyroid hormone levels.[32] Another small study with 45 subjects found that 63% patients with one variant gene, DIO2 or MCT10 (which may affect the transport of thyroid hormones into the brain) preferred thyroid combination therapy to T4 monotherapy. 100% of the patients that had both polymorphisms preferred the combined therapy.[33] A third study of 141 patients had different findings and concluded that any preference for combination T4/T3 therapy over T4 monotherapy could not be explained by DIO2 polymorphisms.[34] While the data on combined T4/T3 therapy’s advantage for certain individuals over monotherapy is subjective, based on small studies, and uses psychological profiles and patient preferences, some authors have suggested that in the future individualized hypothyroid replacement therapy based on genotype may become the standard.[35] However, much larger studies need to be done to confirm these findings, as no differences in thyroid hormone levels were found between groups. The American Association of Clinical Endocrinologists and the American Thyroid Association guideline states that the evidence does not support using L-thyroxine and L-triiodothyronine combinations to treat hypothyroidism, but there are still unresolved issues raised by studies that report that some patients prefer and some patient subgroups may benefit from a combination of L-thyroxine and L-triiodothyronine.[15] Dosage Subclinical hypothyroidism is a fairly common disease entity which increases in prevalence with age. Treatment with a TSH level over 10mIU/L is generally recommended. However, with TSH levels between 4.5 to 10 mIU/L therapy needs to be individualized for each patient, with recommendations to only treat symptomatic patients and those with cardiac risk factors, as the benefits for asymptomatic patients are uncertain. Levothyroxine is the recommended treatment and liothyronine is not recommended for most patients. Combination T4/T3 therapy is not recommended but there may be subgroups who might benefit and more research is needed. When treating subclinical hypothyroidism start with low doses of levothyroxine to avoid causing iatrogenic hyperthyroidism. There are different recommendations regarding testing and treatment of subclinical hypothyroidism in pregnancy to avoid potential complications. Conclusion Subclinical hypothyroidism is a fairly common disease entity which increases in prevalence with age. Treatment with a TSH level over 10mIU/L is generally recommended. However, with TSH levels between 4.5 to 10 mIU/L therapy needs to be individualized for each patient, with recommendations to only treat symptomatic patients and those with cardiac risk factors, as the benefits for asymptomatic patients are uncertain. Levothyroxine is the recommended treatment and liothyronine is not recommended for most patients. Combination T4/T3 therapy is not recommended but there may be subgroups who might benefit and more research is needed. When treating subclinical hypothyroidism start with low doses of levothyroxine to avoid causing iatrogenic hyperthyroidism. There are different recommendations regarding testing and treatment of subclinical hypothyroidism in pregnancy to avoid potential complications. Correction: The European Thyroid Association recommendation is that geriatric patients with TSH levels less than or equal to 10 mIU/L , especially those over 80 years of age without specific signs of hypothyroidism can be followed with careful follow-up with a wait-and-see strategy trying to avoid hormonal treatment if possible. It was incorrectly presented as “TSH levels > 10 mIU/L” in a previous version. 🎓  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 Updated post 9/14/22 ✅ 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.  😇

New study introduces a groundbreaking antiviral chewing gum made with Flt3 Receptor Interacting Lectin (FRIL), a potent compound from lablab beans. Lablab Bean Pods In an interesting study published in January 2025, scientists created a chewing gum with antiviral properties that potentially could decrease the transmission of communicable diseases such as influenza and oral herpes simplex (cold sores). Flt3 Receptor Interacting Lectin (FRIL), a substance which comes from lablab beans, has been found to have significant anti-viral properties against a wide range of pathogens.  It has binding sites that can attach and entrap viruses and neutralize them.  The theory is that by trapping viruses, the gum can reduce their spread.  The researchers made a chewing gun with FRIL in a gum made from lablab bean powder. Lablab purpureus  is commonly called hyacinth bean and is edible when immature, however the mature seeds (beans) contain toxins that need to be boiled out before eating.    In this pilot study, they reported that the FRIL in the lablab bean chewing gum was stable for at least 2.2 years.  Using masticator simulators to reproduce chewing, they reported that 95% of the FRIL was released from the gum within one hour, with most of it released in the first half-hour. The chewing gum was tested for its ability to reduce viral loads by using a plaque reduction neutralization test which is the gold standard test for antibody neutralization of viruses. The FRIL lablab bean chewing gum caused a 95% decrease in the amount of active virus for both the herpes simplex and influenza samples. Comments: Oral Herpes simplex or herbes labialis which causes cold sores are thought to be carried by 64% of the world’s population.  It is very contagious, can cause pain, be unsightly, and be recurrent.  In an immunocompromised person it sometimes may disseminate causing serious body-wide infections. The CDC estimated that in the U.S. during the 2024-2025 flu season, 46-81 million people were infected with  influenza with 600,000 to 1.3 million hospitalizations and 26,000 to 130,000 deaths.     A chewing gum that could effectively decrease the transmission of these diseases by decreasing oral viral load would be a significant step forward for public health.  This is just a pilot study, and more research is needed to assess effectiveness and safety. The authors state that investigations by other researchers are already underway to determine if oral COVID-19 viruses can be neutralized by a chewing gum containing antiviral substances. Click here to read the article, Influenza Found to Cause More Long-Term Neurological Sequalae Than COVID-19. References Daniell, H et al. Debulking influenza and herpes simplex virus strains by a wide-spectrum anti-viral protein formulated in clinical grade chewing gum. Molecular Therapy, Volume 33, Issue 1, 184 – 200. Retrieved from: https://www.cell.com/action/showPdf?pii=S1525-0016%2824%2900808-6 Missouri Botanical Garden. Lablab purpureus. Retrieved from: https://www.missouribotanicalgarden.org/PlantFinder/PlantFinderDetails.aspx?kempercode=a114#:~:text=Noteworthy%20Characteristics,color%20of%20the%20seed%20pods . Herpes simplex virus. World Health Organization. 11 December 2024. Retrieved from: https://www.who.int/news-room/fact-sheets/detail/herpes-simplex-virus Preliminary Estimated Flu Disease Burden 2024-2025 Flu Season. CDC. April 4, 2025. Retrieved from: https://www.cdc.gov/flu-burden/php/data-vis/2024-2025.html

The Edwin Smith Surgical Papyrus Medical Trivia by Stuart M. Caplen, MD   Cervical spine cases in the Edwin Smith Papyrus Written in approximately 1700 BC, the Edwin Smith surgical papyrus is the oldest written medical text. It contains 48 cases of traumatic injury and how to evaluate and treat them.  It was found in a tomb in 1862, in Thebes, Egypt and sold to Edwin Smith, an antiquities dealer.  It was later donated to the New York Historical Society and a translation was first published in 1930. The papyrus is now felt to be a copy of an even older document of an uncertain age.  The cases include injuries to the head, face, throat and neck, spine, clavicle, humerus, sternum, and shoulders.  Each case describes the problem and then suggests a treatment (an ailment I will treat) or recommends no treatment (an ailment not to be treated), if the medical issue is too severe to effectively treat.  In one example, a method is described for reducing a dislocated jaw (mandible) that is still used today.  For nasal fractures, recommendations included relocation, and insertion of linen plugs with honey and some form of lubricant and the nose was to be externally splinted. There are instructions on how to treat a fractured or dislocated clavicle as well as a fractured humerus, including setting, relocation and splinting.  In the case of a fractured humerus with a deep wound injury down to the fracture the author describes it as “An ailment not to be treated.” and it seems an open fracture in ancient Egypt was considered a lethal injury.  It also discusses catastrophic cervical spine injuries. “One having a crushed vertebra in his neck; he is unconscious of his two arms (and) his two legs (and) he is speechless. An ailment not to be treated”  For scalp lacerations, the author describes how to examine them, and the treatment recommended was to bind fresh meat on it the first day and apply two strips of fresh linen.  This was followed by application of grease, honey and lints every day until recovery.  Lints made from linen or vegetable fibers were used to absorb secretions and linen strips were used to hold wound edges together. There are many other traumatic injuries discussed in the papyrus.     Comments: It is truly amazing that one or more Egyptian physicians over 3,700 years ago had invented and documented treatment procedures that in some cases are similar to what is still practiced today.  References  van Middendorp JJ, Sanchez GM, Burridge AL. The Edwin Smith papyrus: a clinical reappraisal of the oldest known document on spinal injuries. Eur Spine J. 2010;19(11):1815-1823. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989268/ The Edwin Smith Surgical Papyrus, Volume 1: Hieroglyphic Transliteration, Translation, and Commentary.  J. H. Breasted. (Reissued 1991 with a foreword by T. A. Holland). Retrieved from: https://www.jameslindlibrary.org/edwin-smith-surgical-papyrus-c-1550-bce/ Edwin Smith Surgical Papyrus (c. 1550 BCE). The James Lind Library. Retrieved from: https://www.jameslindlibrary.org/edwin-smith-surgical-papyrus-c-1550-bce/ BREASTED JH. THE EDWIN SMITH SURGICAL PAPYRUS. THE UNIVERSITY OF CHICAGO ORIENTAL INSTITUTE PUBLICATIONS. 1930. Retrieved from: https://isac.uchicago.edu/sites/default/files/uploads/shared/docs/oip3.pdf

Transform ordinary carrots into a gourmet side dish with this recipe! Sweet, tangy, and low-calorie, vegetarian, and packed with fiber. Creative Cooking for the Health-Conscious Gourmet FibonacciRECIPES  | Culinary Medicine   Recipe These balsamic and molasses infused carrots bring cooked carrots to a gourmet level. The photo shows rainbow carrots but regular carrots work just as well. Ingredients: 1 pound fresh carrots 2 Tbsp butter 1 Tbsp +1 tsp molasses 1 Tbsp  balsamic vinegar ½ tsp dried basil ¼ tsp salt ¼ cup water 1/8 tsp pepper Instructions: Slice carrots once lengthwise, so you have a flat side and a rounded side Melt butter in fry pan and add 1Tbsp molasses, 2tsp balsamic, salt, pepper, and water, whisk together Place carrots cut side down on top of the sauce Boil mixture for 3 minutes Reduce heat and rotate pan so sauce splashes on top of the carrots Cover pan and simmer for 10-15 minutes Uncover and pour 1tsp each molasses and balsamic over carrots Continue to simmer until sauce thickens slightly and carrots can be pierced with fork Plate the carrots  and drizzle with remaining sauce. Add salt and pepper to taste Nutritional Information Makes 4 Servings Nutrients in a serving:   Calories  120, Total Fat 6g, Saturated Fat 3.5 g, Cholesterol 15mg, Total Carbohydrate 17g, Dietary fiber 3.3g, Protein 1.2g, Potassium 470mg, Sodium 250mg Nutrition Chef Authors : Mary B Grosvenor, MS, RD Medically Reviewed by FibonacciMD editors. Editor's Note: L ow calorie, low fat, low cholesterol, and natural source of fiber. Appropriate for lacto-vegetarian dietary regimen.

References for CME Article " Normal Pressure Hydrocephalus in Adults. How Does It Cause Damage if the Pressure is Normal? " References [1] Hakim S, Adams RD. The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure Observations on cerebrospinal fluid hydrodynamics. J Neurol Sci. 1965;2:307–327, Retrieved from: https://www.jns-journal.com/article/0022-510X(65)90016-X/abstract [2] Oliveira LM, Nitrini R, Román GC. Normal-pressure hydrocephalus: A critical review [published correction appears in Dement Neuropsychol. 2019 Jul-Sep;13(3):361]. Dement Neuropsychol. 2019;13(2):133-143. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601311/#B2 [3] Stolze, H et al. Gait analysis in idiopathic normal pressure hydrocephalus--which parameters respond to the CSF tap test? Clinical Neurophysiology, 111(9), 1678-1686. 2000. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/10964082/ [4] Fraser JJ, Fraser C. Gait disorder is the cardinal sign of normal pressure hydrocephalus: a case study. J Neurosci Nurs. 2007;39(3):132-192. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/17591408/ [5] Malm J, Kristensen B, Karlsson T, Fagerlund M, Elfverson J, Ekstedt J. The Predictive Value of Cerebrospinal Fluid Dynamic Tests in Patients With the Idiopathic Adult Hydrocephalus Syndrome. Arch Neurol. 1995;52(8):783–789. Retrieved from: https://jamanetwork.com/journals/jamaneurology/article-abstract/593582 [6] Marmarou A, Young HF, Aygok GA, et al. Diagnosis and management of idiopathic normal-pressure hydrocephalus: a prospective study in 151 patients. J Neurosurg. 2005;102(6):987-997. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/16028756/ [7] Shprecher D, Schwalb J, Kurlan R. Normal pressure hydrocephalus: diagnosis and treatment. Curr Neurol Neurosci Rep. 2008;8(5):371-376. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674287/ [8] Ryding E, Kahlon B, Reinstrup P. Improved lumbar infusion test analysis for normal pressure hydrocephalus diagnosis. Brain Behav. 2018;8(11):e01125. Retrieved from:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236248/ [9] Kahlon B, Sundbärg G, Rehncrona S.  Comparison between the lumbar infusion and CSF tap tests to predict outcome after shunt surgery in suspected normal pressure hydrocephalus. Journal of Neurology, Neurosurgery & Psychiatry 2002;73:721-726. Retrieved from: https://jnnp.bmj.com/content/73/6/721 [10] The European iNPH Multicentre Study on the predictive values of resistance to CSF outflow and the CSF Tap Test in patients with idiopathic normal pressure hydrocephalus    Carsten Wikkelsø  https://jnnp.bmj.com/content/84/5/562.long [11] Merkler AE, Ch'ang J, Parker WE et al. The Rate of Complications after Ventriculoperitoneal Shunt Surgery. World Neurosurgery. Volume 98, 2017, Pages 654-658. Retrieved from: https://www.sciencedirect.com/science/article/abs/pii/S1878875016311378?via%3Dihub [12] Ferras M, McCauley N, Stead T et al. Ventriculoperitoneal Shunts in the Emergency Department: A Review. Cureus. 2020;12(2):e6857. Published 2020 Feb 3. Retrieved from:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053664/ [13] Lylyk P, Lylyk I, Bleise C, et al. First-in-human endovascular treatment of hydrocephalus with a miniature biomimetic transdural shunt. J Neurointerv Surg. 2022;14(5):495-499. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9016261/ [14] Lylyk P et al. The eShunt® System: A Novel Minimally Invasive CSF Shunting System for the Treatment of Idiopathic Normal Pressure Hydrocephalus. Neurology. April 9, 2024, issue102 (17_supplement_1). Retrieved from: https://www.neurology.org/doi/10.1212/WNL.0000000000206181 [15] Pinto FC, Saad F, Oliveira MF, et al. Role of endoscopic third ventriculostomy and ventriculoperitoneal shunt in idiopathic normal pressure hydrocephalus: preliminary results of a randomized clinical trial. Neurosurgery. 2013;72(5):845-854. Retrieved from: https://pubmed-ncbi-nlm-nih-gov.elibrary.einsteinmed.edu/23313977/ [16] Tudor KI, Tudor M, McCleery J, Car J. Endoscopic third ventriculostomy (ETV) for idiopathic normal pressure hydrocephalus (iNPH). Cochrane Database Syst Rev. 2015;2015(7):CD010033. Published 2015 Jul 29. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9187909/ [17] Greuter, L., Schenker, T., Guzman, R., & Soleman, J. (2022). Endoscopic third ventriculostomy compared to ventriculoperitoneal shunt as treatment for idiopathic normal pressure hydrocephalus: a systematic review and meta-analysis. British Journal of Neurosurgery, 1–7. Retrieved from: https://www.tandfonline.com/doi/full/10.1080/02688697.2022.2149697 [18] Munthe S et al. Ventriculosinus shunt: a pilot study to investigate new technology to treat hydrocephalus and mimic physiological principles of cerebrospinal fluid drainage Journal of Neurosurgery. Volume 139: Issue 5. 21 Apr 2023. Retrieved from: https://thejns.org/view/journals/j-neurosurg/139/5/article-p1412.xml?tab_body=fulltext

References for CME Article " The Increasing Incidence of Early Onset Colorectal Cancer " References [1] Fritz CDL et al. Red-flag signs and symptoms for earlier diagnosis of early-onset colorectal cancer. J Natl Cancer Inst. 2023;115(8):909-916. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/37138415/ [2] Bailey CE et al. Increasing disparities in the age-related incidences of colon and rectal cancers in the United States, 1975-2010 [published correction appears in JAMA Surg. 2015 Mar 1;150(3):277. Retrieved from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4666003/ [3] US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation Statement. JAMA. 2021;325(19):1965–1977. Retrieved from:  https://jamanetwork.com/journals/jama/fullarticle/2779985 [4] Jin EH et al.  Sex and Tumor-Site Differences in the Association of Alcohol Intake With the Risk of Early-Onset Colorectal Cancer. JCO 41, 3816-3825(2023). 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Detection of Various Microplastics in Patients Undergoing Cardiac Surgery Environmental Science & Technology 2023 57 (30), 10911-10918. Retrieved from: https://pubs.acs.org/doi/abs/10.1021/acs.est.2c07179 [47] Jenner LC et al. Detection of microplastics in human lung tissue using μFTIR spectroscopy. Science of The Total Environment. Volume 831, 2022. Retrieved from: https://www.sciencedirect.com/science/article/pii/S0048969722020009?via%3Dihub [48] Saha SC, Saha G. Effect of microplastics deposition on human lung airways: A review with computational benefits and challenges. Heliyon. 2024;10(2):e24355. Published 2024 Jan 11. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10826726/   [49] Hu CJ et al. Microplastic presence in dog and human testis and its potential association with sperm count and weights of testis and epididymis, Toxicological Sciences, 2024. 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Urinary, circulating, and tissue biomonitoring studies indicate widespread exposure to bisphenol A. Environ Health Perspect. 2010;118(8):1055-1070. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920080/ [63] da Silva MM et al. Inhibition of Type 1 Iodothyronine Deiodinase by Bisphenol A. Horm Metab Res. 2019;51(10):671-677. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/31174228/ [64] Symeonides, C., Vacy, K., Thomson, S. et al. Male autism spectrum disorder is linked to brain aromatase disruption by prenatal BPA in multimodal investigations and 10HDA ameliorates the related mouse phenotype. Nat Commun 15, 6367 (2024). Retrieved from: https://www.nature.com/articles/s41467-024-48897-8 [65] Hafezi SA, Abdel-Rahman WM. The Endocrine Disruptor Bisphenol A (BPA) Exerts a Wide Range of Effects in Carcinogenesis and Response to Therapy. Curr Mol Pharmacol. 2019;12(3):230-238. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6864600/ [65A] Guo x et al. 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This Spring Frittata (Egg-less) is a flavorful, plant-based twist on a classic. Loaded with fresh veggies, vegan sausage, and dairy-free cheese, it’s perfect for springtime brunch or dinner. Whether you're vegan, watching cholesterol, or just love a hearty meal, this dish is a must-try! Creative Cooking for the Health-Conscious Gourmet FibonacciRECIPES  | Culinary Medicine   Recipe This frittata uses tomatoes, asparagus, potatoes and peppers along with plant-based egg, cheese, and sausage alternatives.  So whether you’re moving to a plant-based diet, trying to limit your cholesterol intake, or want to avoid the high costs of egg during the bird flu outbreak, enjoy this lovely springtime meal. It has become a family staple since it was shared with me by a vegan friend. Ingredients: Cooking spray 1 medium potato with skin, shredded 1 vegan sausage (Field Roast Italianô) ¾ cup shredded vegan cheese 20 Cherry tomatoes 14 asparagus spears ½ cup yellow onion, diced ½ cup red sweet peppers, diced 2 cups liquid egg substitute (Just Eggsô) 1Tbsp nutritional yeast ½ tsp dill ½ tsp smoked paprika ½ tsp maple syrup ½  tsp smoked paprika Instructions: Preheat oven to 350°F & coat a glass baking dish with cooking spray Cover bottom of baking dish with shredded potatoes Dice sausage and add with onion & peppers on top of the potatoes  Sprinkle cheese over the mixture Dice 10 each cherry tomatoes and asparagus, add to dish Pour in “eggs” Cut remaining cherry tomatoes in half, slice 4 asparagus lengthwise, place on top of mixture to decorate Sprinkle with nutritional yeast, paprika, and dill Bake for 50-60 minutes until center is set and top is slightly browned Remove from oven and let set for 10 minutes before slicing Nutritional Information Makes 6 Servings Nutrients in a serving:   215 Calories,  13g fat, 4g sat fat, 6mg cholesterol, 54g carbohydrate, 2g fiber, 21g protein 590mg sodium, 400 mg potassium Nutrition Chef Authors : Mary B Grosvenor, MS, RD Medically Reviewed by FibonacciMD editors. Editor's Note:  Appropriate for low-calorie, low cholesterol, low saturated fat, high protein, vegan dietary regimen. The brands used in this recipe are listed in the ingredients but you can use any variety or combination of plant-based brands and/or real eggs, cheese and sausage. If you use animal products, the dish will be higher in cholesterol and saturated fat.

The Classic Dichotomy. COPD- an attempt to differentiate the patient with moderate to severe emphysema (pink puffer) from the patient with chronic bronchitis (blue bloater). Pulmonology by Adele Shenoy, MD Edited by Charles L. Fishman, MD Contributor – Rich Strongwater, MD The pink puffer vs blue bloater distinction may be less useful given the overlap of chronic bronchitis in both groups (emphysema vs non-emphysema) and the non-distinct timeline of hypoxia in both groups.   BMI does seem to be lower in the emphysema group. While the pink puffer and blue bloater classifications offer insights into COPD presentations, a deeper understanding of each patient's unique characteristics is crucial for effective management and treatment. The Pink Puffer Although these terms may seem out of date and politically incorrect they were an attempt to differentiate the patient with moderate to severe emphysema from the patient with chronic bronchitis. The term “ pink puffer ” is colloquially used to describe the “typical” presentation of a patient with emphysema, in contrast to the “typical” patient with chronic bronchitis, who has been described as a “blue bloater.” Patients with predominant emphysema will respond to dyspnea by hyperventilating, and will for a time be able to maintain oxygenation and remain “pink.” Emphysema Causes and Risk Factors In emphysema, alveoli are lost, and the airways lose elasticity, leading to air trapping within the respiratory units, making exhalation more difficult. Oxygenation can be maintained by increasing minute volume ( by increasing their breathing rate ). Pursed lip breathing will help to increase the pressure within the airways and prevent collapse. Pink Puffer Signs and Symptoms Pink puffers often exhibit a thin body habitus, pursed lips with breathing, barrel chest, increased work of breathing, and rarely have cyanosis. They have prolonged expiration time, and may speak in short sentences. As emphysema and respiratory failure worsen, hypoxemia and loss of “pink” color can result. The Blue Bloater The term “ blue bloater ” is colloquially used to describe the “typical” presentation of a patient with chronic bronchitis, in contrast to the “typical” patient with emphysema, who has been described as a “pink puffer.” Patients with moderate chronic bronchitis are more likely to have hypoxemia compared to patients with moderate emphysema, and thus can have cyanosis and appear “blue.” Chronic Bronchitis Causes and Risk Factors In chronic bronchitis, there is increased mucous production, along with damage to airway epithelium. Gas exchange is disturbed, leading to a mismatch between ventilation and perfusion, and hypoxemia, hypercapnia and respiratory acidosis. This eventually leads to pulmonary vasoconstriction and right heart failure. It should be noted that severe emphysema can also cause respiratory failure, and that emphysema and chronic bronchitis are often found in the same patient. Blue Bloater Signs and Symptoms Blue bloaters have chronic productive cough, cyanosis, and peripheral edema (due to right heart failure). They will often appear plethoric ( with facial swelling and redness or darkening of the face ) and obese. The Classic Dichotomy Emphysema vs Chronic Bronchitis Table: Comparison between emphysema and chronic bronchitis ​ Emphysema ​ Chronic bronchitis Definition Pathological: alveolar parenchymal destruction and irreversible airspace dilatation Clinical: Productive cough on most days for > 3 months a year for > 2 years. Pathogenesis Imbalance between proteases and anti-proteases leads to destruction of lung parenchyma Airway irritation leading to mucus gland hypertrophy/hyperplasia, mucus overproduction, and small airway clogging Pathophysiology Destruction of alveolar walls causes loss of elastic recoil, leading to increased compliance, air trapping, and hyperinflation. Hypoxemia is a late feature since there is no V/Q mismatch Airway plugging leads to expiratory airflow obstruction and air trapping Obstruction impairs alveolar ventilation, causing V/Q mismatch and hypoxemia with CO2 retention Chronic hypoxemia causes pulmonary hypoxic vasoconstriction, leading to pulmonary hypertension and eventually cor pulmonale ​ Clinical features "Pink puffer" Progressive dyspnea Pursed-lip breathing, accessory muscle use "Barrel chest" configuration Cachexia ​ "Blue bloater" Productive cough, wheezing Early cyanosis Signs of cor pulmonale (peripheral edema, jugular venous distension, hepatomegaly) Associated with obesity and metabolic syndrome Adapted from Ni, A, ed. "Block B: Respiration" from "Osler Notes". McGill Medical Students Society, 2019. Conclusion: Chronic Obstructive Pulmonary Disease (COPD) The blue bloater vs pink puffer distinction may be less useful given the overlap of chronic bronchitis in both groups (emphysema vs non-emphysema) and the non-distinct timeline of hypoxia in both groups. Chest CT scan along with formal pulmonary function testing may be the best way to differentiate and characterize your COPD patient. Changes on CT scan in pulmonary emphysema results from dilatation of airspaces and destruction of airspace walls distal to terminal bronchioles. This is seen as low attenuation areas on the CT with vascular distortion and thinning. High-resolution computed tomography (HRCT) may discover abnormal findings associated with emphysema earlier and may also give a better view of pathology progression. Chronic bronchitis exists in both groups thereby explaining why patients with “asthma-overlap” exist in both groups. Nevertheless, COPD-asthma overlap is more common in non-emphysematous COPD, as is bronchodilator responsiveness. One third of patients with COPD may have eosinophilic airway inflammation and treatment directed at eosinophilia may be warranted. More studies regarding eosinophila as a potentially useful biomarker in the treatment of COPD are needed. BMI does seem to be low in the emphysema group. BMI is higher in the chronic bronchitis group. This along with chronic inflammation may explain the association with non-emphysema COPD and diabetes or metabolic syndrome. While the pink puffer and blue bloater classifications offer insights into COPD presentations, a deeper understanding of each patient's unique characteristics is crucial for effective management and treatment. #Pulmonology #PinkPuffer #BlueBloater #COPD References Petty, T. COPD: Clinical phenotypes. Pulmonary Pharmacology & Therapeutics. 2002;15(4):341-351. Mirza S, Clay RD, Koslow MA, Scanlon PD. COPD Guidelines: A Review of the 2018 GOLD Report. Mayo Clin Proc. 2018 Oct. 93 (10):1488-1502. Petty, T. COPD: Clinical phenotypes. Pulmonary Pharmacology & Therapeutics. 2002;15(4):341-351. Mirza S, Clay RD, Koslow MA, Scanlon PD. COPD Guidelines: A Review of the 2018 GOLD Report. Mayo Clin Proc. 2018 Oct. 93 (10):1488-1502. Hersh C, Make B, Lynch D, et al. Non-emphysematous chronic obstructive pulmonary disease is associated with diabetes mellitus. BMC Pulm Med. 2014; 14: 164. Published online 2014 Oct 24. doi: 10.1186/1471-2466-14-164 Balachandran, J. Chronic Obstructive Pulmonary Disease and Eosinophils. Editorial. Pulmon. 24(2):p57-58. May-Aug 2022. Doi: 10.4103/pulmon.pulmon_4_22 Ni A. An Approach To Chronic obstructive pulmonary disease (COPD) Published online: 19 October 2020 Faculty of Medicine, McGill University, Montreal, QC, Canada. Grenier P. Emphysema at CT in Smokers with Normal Spirometry: Why It Is Clinically Significant. Editorial. Radiology. Published Online:Jul 7 2020 https://doi.org/10.1148/radiol.2020202576 David B, Bafadhel M, Koenderman L, De Soyza A. Eosinophilic inflammation in COPD: from an inflammatory marker to a treatable trait. BMJ. Thorax. 2021. Volume 76, Issue 2 . https://thorax.bmj.com initially published January 2023

New Research Links Poor Air Quality to Reduced Focus and Emotion Recognition In a study published February 2025, researchers looked at the effect of air quality on cognitive function.  There were 26 subjects, mean age of 27.7 years, who performed cognitive tests and were then exposed either to air with high particulate matter concentrations or fresh air for one hour.  Four hours after exposure, the cognitive tests were repeated.  Lit candles were used to increase particulate matter in the air which was consistent with particulate matter in an urban area.  Participants in both the clear and polluted air groups did one session with nose clips just oral breathing and one session breathing both through the nose and the mouth.  It was reported that there were significant reductions in selective attention (the ability to focus on one thing while ignoring distractions) and emotion expression discrimination (the ability to recognize differences between emotions as they are expressed through facial expressions, body language, vocalizations, and other cues) after particulate matter exposure when compared to subjects in the clean air breathing group.  Air quality did not significantly impact psychomotor vigilance (a person's ability to focus and respond to visual or auditory stimuli in a timely manner) or working memory performance (the ability to actively hold and manipulate a small amount of information for a brief period, allowing completion of complex cognitive tasks like reasoning, problem-solving, and decision-making).  As there was no difference in cognitive testing between oral versus oral with nasal breathing, the authors postulated that the negative effects on cognition might be from inhalation of substances in the lung rather than through the nose and olfactory bulb (the part of the brain that processes smells).  This study was a very small one with few subjects and as such results need to be confirmed with larger studies. Comments: According to the World Health Organization (WHO), air pollution both outside and inside the home is responsible for an estimated seven million premature deaths world-wide.  99% of the world’s population are thought to reside in areas where air particulates exceed the WHO guideline limits and contain high levels of pollutants.  It is thought that pollutant particulate matter of less than 2.5 micrometers (also called microns) in diameter is responsible for most of the negative effects on human health.  (Copy paper is typically 50 to 100 micrometers thick.) In this interesting study, reducing air quality by burning candles appeared to adversely affect some cognitive functions.  Caution is advised given there were very few subjects, but there is other scientific literature that supports this concept.  Air pollution in other research has been shown to potentially increase the incidence of cognitive decline and dementia.  Animal studies have demonstrated that air pollution can increase inflammation, oxidative stress, and affect neurotransmitters in the brains of rodents.   This current study adds to other previously published studies that suggest that air pollution is harmful in many ways, including potentially having a negative effect on cognitive abilities.  Click here to read about another study which reported Decreased Alzheimer’s Disease Incidence in Taxi Cab and Ambulance Drivers. _____________________________________________________________________________________________ References Faherty, T., Raymond, J.E., McFiggans, G. et al. Acute particulate matter exposure diminishes executive cognitive functioning after four hours regardless of inhalation pathway. Nat Commun 16, 1339 (2025). Retrieved from: https://www.nature.com/articles/s41467-025-56508-3 Shehab, M. A. & Pope, F. D. Effects of short-term exposure to particulate matter air pollution on cognitive performance. Sci. Rep. 9, 8237 (2019).Retrieved from: https://doi.org/10.1038%2Fs41598-019-44561-0 Delgado-Saborit, J. M. et al. A critical review of the epidemiological evidence of effects of air pollution on dementia, cognitive function, and cognitive decline in adult population. Sci. Total Environ. 757, 143734 (2021). Retrieved from: https://doi.org/10.1016%2Fj.scitotenv.2020.143734 J.M. Delgado-Saborit JM et al. A critical review of the epidemiological evidence of effects of air pollution on dementia, cognitive function, and cognitive decline in adult population. Sci. Total Environ., 757 (2021). Retrieved from: https://www.sciencedirect.com/science/article/pii/S004896972037265X/pdfft?md5=3144ca28103349d3bcba8ecee2f82b44&pid=1-s2.0-S004896972037265X-main.pdf Saenen, N. D. et al. Recent versus chronic exposure to particulate matter air pollution in association with neurobehavioral performance in a panel study of primary schoolchildren. Environ. Int. 95, 112–119 (2016).  Retrieved from: https://doi.org/10.1016%2Fj.envint.2016.07.014 Air Pollution. World Health Organization. Retrieved from:  https://www.who.int/health-topics/air-pollution#tab=tab_1

Explore Dark Chocolate’s Health Benefits and How to Choose the Best Options Culinary Medicine / Nutrition In Brief Dark Chocolate by Stefanie Schwartz, MS, RD, CDN Dark chocolate (theobroma cacao) is made from the seed of the cacao tree. The higher the percentage of cacao solids in your chocolate, the greater the amount of antioxidants it contains. This includes the polyphenolic and methylxanthine compounds. More specifically, the polyphenolic flavonols (catechin, epicatechin, and procyanidins) may reduce the risk of cardiovascular disease by reducing blood pressure, cholesterol levels and insulin resistance. Dark chocolate may actually improve cognitive function. The flavinols in dark chocolate exert their positive health effects in several ways including increasing the production of nitric oxide which in turn may reduce endothelial dysfunction, lipoprotein oxidation, platelet aggregation and endothelial inflammation. Dark chocolate also contains fiber and minerals beneficial for vascular function. The greatest health benefits of dark chocolate are seen above a concentration of 60% cocoa solids. One ounce of dark chocolate containing 60%-69% cacao solids has 165 calories, 11 g of fat, and 15 g of total carbohydrate. As the percent of dark chocolate reaches 70%, the calories increase to 170 per ounce, but with only 7 g of sugar and about 40 mg of caffeine. Adverse effects Chocolate can be contaminated with the heavy metal cadmium, which is a renal toxin. Consumer Lab.com independently tested 42 chocolate products for purity and found that many common chocolate brands have dangerous levels of cadmium. Dark chocolate bars having the highest flavonol content and lowest levels of cadmium are Endangered Species 88% cacao, Ghiardelli Intense Dark 86% cacao, and Lindt Excellence 90% cacao Supreme Dark. Pearl to Know Dark chocolate has a greater polyphenol and flavonol content then does tea. Dark chocolate increases blood flow to the heart and brain. White chocolate offers few of these benefits, and milk chocolate contains too much sugar. The key to getting the benefits from chocolate without the weight gain is to choose a high-quality dark chocolate that contains 60%-90% cacao and to limit portion size to 1 ounce per day. References Schewe T, Steffan Y, Sies H. How do flavonols improve vascular function? A position paper. Arch Biochem Biophys . 2008;476:102-106. Baba S, Natsume M, Yasuda A, et al. Plasma LDL and HDL cholesterol and oxidized LDL concentrations are altered in normo- and hypercholesterolemic humans after intake of different levels of cocoa powder. J Nutr. 2007;137:1436-1441. Djoussé L, Hopkins PN, North KE, Pankow JS, Arnett DK, Ellison RC. Chocolate consumption is inversely associated with prevalent coronary heart disease: the National Heart, Lung, and Blood Institute Family Heart Study. Clin Nutr. 2011;30:182-187. Katz D, Doughty K, Ali A. Cocoa and Chocolate in Human Health and Disease. Antioxid Redox Signal. 2011 Nov 15; 15(10): 2779–2811. Michael J. Dark Chocolate: Does It Have Benefits? Nutrition Advance. May 27,2020. https://www.nutritionadvance.com/dark-chocolate-health-benefits/

A Quick and Healthy Stovetop Curry for a Light Meal This quick and easy stovetop curry is low in calories, carbs, cholesterol, and fat, making it a perfect light and flavorful meal. Creative Cooking for the Health Conscious Gourmet FibonacciRECIPES | Culinary Medicine Low-Calorie | Low-Carbohydrate | Low-Cholesterol | Low-Fat Healthy Chicken Curry Recipe This healthy chicken curry recipe is quick and easy to make on your stove top. Nutritional information below, i.e. appropriate for low-calorie, low-cholesterol, low-fat, low-carbohydrate diet regimens. Ingredients: 1 tbsp olive oil 1 medium onion, sliced 0.33 cup golden raisins (optional) Salt and freshly ground pepper 1.5 tsp yellow curry powder, or to taste 4 skinless, boneless, chicken breast halves (1-1.5 pounds) 1 cup sour cream Fresh cilantro or parsley, minced, for garnish Directions: Warm the oil in a large skillet over medium-high heat. Add the onions, sprinkle with some salt and pepper, and cook, stirring occasionally, until translucent (~5 min). Turn the heat down to medium, sprinkle with half of the curry powder, and continue to cook for 1-2 min. Season the chicken with salt and pepper to taste and sprinkle on remaining curry powder. Move the onion to one side of the skillet, and add the chicken in one layer. Cook for about 2 min on each side. Transfer the chicken to a plate. Add the sour cream and stir constantly over medium-low heat until the mixture thickens. Return the chicken to the skillet and cook for a couple more minutes. Serve over rice. Nutritional Information Servings: 4 Nutrition facts Per serving: Calories: 204 Total fat: 7.9g Saturated fat: 4g Cholesterol 13mg Sodium: 90mg Total carbohydrate: 7.8g Dietary fiber: 1g Total sugars: 3.9g Protein: 1.5g Recipe Author/Chef: Justin Gillette Medically Reviewed by FibonacciMD editors. #FibonacciRECIPES