Is Obesity a Disease?

Is Obesity a Disease?

The scientific community is still in disagreement as to whether or not obesity is a disease. While some still consider obesity a self-inflicted disease caused by poor eating habits and lack of exercise, there is growing evidence to support the claim that obesity is a disease. 

According to Pi-Sunyer (2002), not only is obesity a disease but within the United States it is considered to be a condition of epidemic proportions. Statistics show that, in our country, over 20% of adults are diagnosed as clinically obese (Pi-Sunyer, 2002).  The rationale that obesity is a disease is due to the fact that it causes many different comorbidities such as high blood pressure, diabetes, heart disease, etc. 

Has Obseity Reached Epidemic Proportions In Western Countries?

I agree with Conway and Rene (2004) who believe that obesity is not only a condition that has reached epidemic proportions, but it is a disabling, multifaceted disease that causes changes in organ function and can come with a host of comorbidities. The excess body weight puts a strain on the heart, leading to changes in anatomical structure and the function of the organ. Obesity has also repercussions on the immune system (de Heredia et al., 2012), endocrine system (Poddar et al., 2017), and pulmonary system (Dixon & Peters, 2018). These repercussions are caused by both mechanical and functional alteration of tissues and organs. 

Data Suggests That Obseity Is Associated With Several Very Serious Health Concerns

Research studies show that obesity is associated with an increased risk of developing cancer in at least 13 different organs (Avgerinos et al., 2019). Obesity is also linked to type-2 diabetes (Maggio & Pi-Sunyer, 2003), arthritis (Moroni et al., 2020). At the same time, a systematic review of scientific data that was published in 2017 shows that weight-loss interventions in the obese adult population decrease all-cause mortality (Ma et al., 2017). The same review shows that weight loss has a positive impact on cardiovascular mortality and cancer mortality (Ma et al., 2017). 

Lastly, obesity’s status and acceptance as a disease are pivotal in determining its treatment, reimbursement for treatment, and the development of widespread interventions. For these reasons, I believe that obesity should be recognized as a disease.

References

Avgerinos, K. I., Spyrou, N., Mantzoros, C. S., & Dalamaga, M. (2019). Obesity and cancer risk: Emerging biological mechanisms and perspectives. Metabolism: clinical and experimental, 92, 121–135. https://doi.org/10.1016/j.metabol.2018.11.001

Conway, B., & Rene, A. (2004). Obesity as a disease: no lightweight matter. Obesity Reviews, 5(3), 145–151. https://doi.org/10.1111/j.1467-789x.2004.00144.x 

de Heredia, F. P., Gómez-Martínez, S., & Marcos, A. (2012). Obesity, inflammation and the immune system. The Proceedings of the Nutrition Society, 71(2), 332–338. https://doi.org/10.1017/S0029665112000092

Dixon, A. E., & Peters, U. (2018). The effect of obesity on lung function. Expert review of respiratory medicine, 12(9), 755–767. https://doi.org/10.1080/17476348.2018.1506331

Ma, C., Avenell, A., Bolland, M., Hudson, J., Stewart, F., Robertson, C., Sharma, P., Fraser, C., & MacLennan, G. (2017). Effects of weight loss interventions for adults who are obese on mortality, cardiovascular disease, and cancer: systematic review and meta-analysis. BMJ (Clinical research ed.), 359, j4849. https://doi.org/10.1136/bmj.j4849

Maggio, C. A., & Pi-Sunyer, F. X. (2003). Obesity and type 2 diabetes. Endocrinology and metabolism clinics of North America, 32(4), 805–viii. https://doi.org/10.1016/s0889-8529(03)00071-9

Moroni, L., Farina, N., & Dagna, L. (2020). Obesity and its role in the management of rheumatoid and psoriatic arthritis. Clinical rheumatology, 39(4), 1039–1047. https://doi.org/10.1007/s10067-020-04963-2

Pi-Sunyer, F. X. (2002). The obesity epidemic: Pathophysiology and consequences of obesity. Obesity Research, 10(S12), 97S-104S. https://doi.org/10.1038/oby.2002.202

Poddar, M., Chetty, Y., & Chetty, V. T. (2017). How does obesity affect the endocrine system? A narrative review. Clinical obesity, 7(3), 136–144. https://doi.org/10.1111/cob.12184

The Four Primary Types Of Gluten Related Disorders

The Four Primary Types Of Gluten Related Disorders

Gluten is a family of storage proteins found in wheat, rye, triticale, and barley. In predisposed individuals, ingestion of gluten causes disease reactions that are grouped under the term gluten-related disorders (GRD). Only a decade ago, GRD were rare in the United States, but the rate of gluten-related disorders has greatly increased since then. It is now estimated that GRD affect close to 10% of the population (Sapone et al., 2012). 

There are five kinds of gluten-related disorders recognized by the medical community. Each disorder presents with unique pathophysiology and etiology. Celiac disease, dermatitis herpetiformis, and gluten ataxia are autoimmune conditions; wheat allergy is an allergic disease (Taraghikhah et al., 2020), and non-celiac gluten sensitivity is a non-autoimmune-allergic disease (Sharma et al, 2020).   

Celiac Disease and Gluten

Celiac disease (CD) is a chronic, auto-immune condition that affects genetically predisposed individuals. It is thought that genetically predisposed individuals develop an immune response to unknown environmental factors which is then triggered by the ingestion of gluten (Lebwohl et al., 2018). CD can cause atrophy of the small intestinal villi, which leads to malabsorption, diarrhea, and failure to thrive. But manifestations of CD can also be minimal, like negligible mucosal lesions, or it can have an asymptomatic presentation, which often causes delayed diagnosis. Celiac disease can also present with extraintestinal manifestations ranging from neurologic disorders, psychiatric disorders, infertility, recurrent miscarriages, osteoporosis and osteopenia, arthritis, aphthous stomatitis (a disease my mother suffers from), dental enamel hypoplasia, and elevations in transaminases (Barker & Liu, 2008). 

Dermatitis Herpetiformis and Gluten

Dermatitis Herpetiformis (DH), also known as Duhring-Brocq disease, is an auto-immune condition that affects the skin and causes chronic blistering and lesions. The lesions and blisters generally cover the areas of the scalp, knees, elbows, ankles, and buttocks, producing intense burning and itching. The skin of people affected by DH presents with the same protein IgA1 with J chain and secretory component found in the small intestinal mucosa in adult celiac disease, suggesting a strong correlation between the two conditions (Cohen et al., 1997). For this reason, DH is also called the “celiac disease of the skin”, and the European Society for Pediatric Gastroenterology, Hepatology and Nutrition now states that a dermatitis herpetiformis diagnosis confirms the celiac disease diagnosis without the need for intestinal biopsy. People affected by DH can suffer from various degrees of gastrointestinal issues that vary from milk lesions of the mucosal lining of the small intestine to villous atrophy (Mendez et al., 2013).

Gluten Ataxia as an Autoimmune

Gluten ataxia (GA) is an autoimmune disease triggered by the ingestion of gluten that affects primarily the cerebellum, the part of the brain responsible for coordination and movement. The cerebellum is also responsible for balance, eye movement, and the kind of motor learning abilities involved in learning movements that require practice and fine-tuning, for example, riding a bike or playing an instrument (Leopold, 2018). In GA, the immune system creates antibodies that attack and destroy the Purkinje cells, causing problems with vision and fine motor skills, gait abnormalities, and balance issues. It can also cause peripheral neuropathy, also known as gluten neuropathy (Hadjivassiliou et al., 2004). The damage to the Purkinje cells is irreversible, and studies involving brain MRIs show that up to 60% of subjects affected by GA suffer from permanent shrinkage of the cerebellum (Sapone et al., 2012).

Wheat Allergies and Gluten

Wheat allergy (WA) is an allergic reaction to gluten in which the immune system produces immunoglobulin E antibodies in response to wheat proteins. It can present with gastrointestinal symptoms similar to celiac disease, but unlike CD, WA has a fast onset. When inhaled (baker’s asthma), WA can cause asthma and rhinitis. When someone affected by WA touches wheat, skin reactions occur. When ingested, wheat causes gastrointestinal pain, diarrhea, malabsorption, and, if untreated, it can lead to failure to thrive. WA can also cause anaphylactic shock, but it does not cause villi atrophy (Elli et al., 2015).

Gluten Sensitivity

Non-celiac gluten sensitivity (NCGS) is a non-autoimmune-allergic disease that presents with gastrointestinal and/or extraintestinal symptoms similar to the ones seen in CD (altered bowel habits, skin rashes, bone pain, headaches, fatigue, and depression). Laboratory testing shows no serum antibodies, and intestinal biopsies do not show villous atrophy. This lack of biomarkers makes NCGS difficult to diagnose, and it also can lead to misdiagnosis. NCGS can be misdiagnosed as IBS, and oftentimes only a strict elimination diet allows for a conclusive diagnosis (Biesiekierski et al., 2011). Molina-Infante et al. (2014) estimate that the prevalence of NCGS is 6 to 10 times higher than CD and WA and that it is more prevalent in family members of CD sufferers. 

References

Barker, J. M., & Liu, E. (2008). Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Advances in pediatrics, 55, 349–365. https://doi.org/10.1016/j.yapd.2008.07.001

Biesiekierski, J. R., Newnham, E. D., Irving, P. M., Barrett, J. S., Haines, M., Doecke, J. D., Shepherd, S. J., Muir, J. G., & Gibson, P. R. (2011). Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. The American journal of gastroenterology, 106(3), 508–515. https://doi.org/10.1038/ajg.2010.487

Cohen LM, Skopicki DK, Harrist TJ, Clark WHJ. Elder D, Elenitsas R, Jarsorsky C, Johnson BJ. Lever’s Histopathology of the Skin. 8. Raven: Lippincott; 1997. Noninfectious Vesiculobullous and Vesiculopustular Diseases; pp. 209–252.

Elli, L., Branchi, F., Tomba, C., Villalta, D., Norsa, L., Ferretti, F., Roncoroni, L., & Bardella, M. T. (2015). Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity. World journal of gastroenterology, 21(23), 7110–7119. https://doi.org/10.3748/wjg.v21.i23.7110

Hadjivassiliou, M., Williamson, C. A., & Woodroofe, N. (2004). The immunology of gluten sensitivity: beyond the gut. Trends in Immunology, 25(11), 578–582. https://doi.org/10.1016/j.it.2004.08.011

Lebwohl, B., Sanders, D. S., & Green, P. (2018). Coeliac disease. Lancet (London, England), 391(10115), 70–81. https://doi.org/10.1016/S0140-6736(17)31796-8

Leopold, C. (2018, August 31). Everything you need to know about the cerebellum. Medical News. https://www.medicalnewstoday.com/articles/313265#function 

Mendes, F. B., Hissa-Elian, A., Abreu, M. A., & Gonçalves, V. S. (2013). Review: dermatitis herpetiformis. Anais brasileiros de dermatologia, 88(4), 594–599. https://doi.org/10.1590/abd1806-4841.20131775

Molina-Infante, J., Santolaria, S., Montoro, M., Esteve, M., & Fernández-Bañares, F. (2014). Sensibilidad al gluten no celiaca: una revisión crítica de la evidencia actual [Non-celiac gluten sensitivity: a critical review of current evidence]. Gastroenterologia y hepatologia, 37(6), 362–371. https://doi.org/10.1016/j.gastrohep.2014.01.005

Sapone, A., Bai, J. C., Ciacci, C., Dolinsek, J., Green, P. H., Hadjivassiliou, M., Kaukinen, K., Rostami, K., Sanders, D. S., Schumann, M., Ullrich, R., Villalta, D., Volta, U., Catassi, C., & Fasano, A. (2012). Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC medicine, 10, 13. https://doi.org/10.1186/1741-7015-10-13

Sharma, N., Bhatia, S., Chunduri, V., Kaur, S., Sharma, S., Kapoor, P., Kumari, A., & Garg, M. (2020). Pathogenesis of Celiac Disease and Other Gluten Related Disorders in Wheat and Strategies for Mitigating Them. Frontiers in Nutrition, 7. https://doi.org/10.3389/fnut.2020.00006

Taraghikhah, N., Ashtari, S., Asri, N., Shahbazkhani, B., Al-Dulaimi, D., Rostami-Nejad, M., Rezaei-Tavirani, M., Razzaghi, M. R., & Zali, M. R. (2020). An updated overview of spectrum of gluten-related disorders: clinical and diagnostic aspects. BMC Gastroenterology, 20(1). https://doi.org/10.1186/s12876-020-01390-0

Digestive Fuction and Testing

Digestive Fuction and Testing

Over 2,000 years ago Hippocrates, the father of medicine said: “All disease begins in the gut”. Healthy digestion and a healthy microbiome are fundamental to health. The digestive tract is a long tube that goes from the mouth to the anus. It is composed of several organs and accessory organs that work together to intake, break down and absorb food as well as excrete waste material. Each organ of the digestive tract can be affected by dysfunction from gastroesophageal reflux to H. Pylori infections, leaky gut, malabsorption syndrome, maldigestion, food allergies, celiac disease, irritable bowel syndrome, inflammatory bowel disease, etc. It is important to know that digestive issues are not confined to the affected organ, but that they have repercussions for the entire system. Moreover, digestive dysfunction causes maladies that are not exclusively relegated to the organs of digestion. Research shows that several conditions are caused by or correlated with unhealthy microbiome and digestive dysfunction: obesity, type-2 diabetes (Fan & Pedersen, 2021), connective tissue disease (CTD) (Bizzaro et al., 2003), systemic lupus erythematosus (SLE), Grave’s disease (Shor et al., 2012), just to name a few.

What Laboratory Tests Are Available Today?

There are several laboratory tests available to test gastrointestinal function. Stomach acid can be measured with a Heidelberg capsule (Lord & Bralley, 2012). Pepsin can be tested via a saliva test (Strugala et al., 2015). Fecal and plasma tests can be used to measure pancreatic output of protease and lipase. A fecal fat test can reveal impaired liver or gallbladder function. Stool cultures, DNA stool test, comprehensive stool digestive analysis (CSDA), fecal butyrate testing are tools used to assess colon function (Lord & Bralley, 2012). Colonoscopy, barium enema, magnetic resonance imaging (MRI), computed cosmography scan (CT scan), defecography, ultrasounds and other imaging tests are also available to assess colon health (Digestive Diagnostic Procedures). A hydrogen-methane breath test is used to diagnose small intestinal bacterial overgrowth (SIBO). 

Several tests are available to test for food allergies and intolerances: increased levels of IgA can be measured through feces, urine and serum analysis and can reveal the presence of gut inflammation, celiac disease, mucosal infection, food allergies, and other inflammatory conditions (Breedveld & van Egmond, 2019). Serum IgE and IgG levels can be checked to test for food allergies, infections and inflammatory diseases (Mayo Clinic Labs). According to the Genova Diagnostics website, high levels of IgG antibodies can also indicate the presence of leaky gut syndrome. 

What Is The Helicobacter Test?

The test I chose for this essay is the Helicobacter Pylori Stool Antigen EIA. The American Gastroenterological Association (AGA) (Talley et al., 2005) and the American College of Gastroenterologists (ACG) (Chey et al., 2007) consider the H. Pylori stool antigen to be superior to the serum testing. 

H. Pylori is a bacterium that inhabits the stomach, usually without causing any disease. According to Iisashi et al. (2015) H. Pylori can suppress inflammatory bowel disease (IBD), and it is linked to a reduced incidence of asthma. A study from Talebi Bezmin Abadi (2014) even suggested that an eradication of H. Pylori contributes to an increase of GERD. It is still unknown why, in certain people, H. Pylori colonies wreaks havoc in the stomach, causing stomach ulcers, gastric inflammation, stomach cancer and gastric mucosa-associated lymphoid-tissue lymphoma (Yang it al., 2014). Symptoms associated with H. Pylori infections are burping, bloating, nausea, gastritis presenting with pain and a burning sensation, loss of appetite and weight loss (Mayo clinic, 2017).  A patient that presents with these symptoms should be tested for H. Pylori infection. The stool antigen EIA test looks for the present of antigens that reveal the presence of H. Pylori. Certain medications like antibiotics and acid blockers can interfere with the test results; therefore, patients are asked to discontinue the use to these medications for one to two weeks prior to testing. 

References 

Bizzaro, N., Villalta, D., Tonutti, E., Tampoia, M., Bassetti, D., & Tozzoli, R. (2003). Association of celiac disease with connective tissue diseases and autoimmune diseases of the digestive tract. Autoimmunity reviews, 2(6), 358–363. https://doi.org/10.1016/s1568-9972(03)00055-7

Bravo, D., Hoare, A., Soto, C., Valenzuela, M. A., & Quest, A. F. (2018). Helicobacter pylori in human health and disease: Mechanisms for local gastric and systemic effects. World journal of gastroenterology, 24(28), 3071–3089. https://doi.org/10.3748/wjg.v24.i28.3071

Breedveld, A., & van Egmond, M. (2019). IgA and FcαRI: Pathological Roles and Therapeutic Opportunities. Frontiers in Immunology, 10. https://doi.org/10.3389/fimmu.2019.00553

Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-1825.

Digestive Diagnostic Procedures. (n.d.). Www.hopkinsmedicine.org. https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/digestive-diagnostic-procedures

Fan, Y., & Pedersen, O. (2021). Gut microbiota in human metabolic health and disease. Nature reviews. Microbiology, 19(1), 55–71. https://doi.org/10.1038/s41579-020-0433-9

Gastrointestinal Test | helicobacter pylori Stool Antigen EIA. (n.d.). Www.gdx.net. Retrieved July 16, 2021, from https://www.gdx.net/product/helicobacter-pylori-stool-antigen-eia-test

www.gdx.net. (2010). Food Sensitivity Test | IgG Food Antibody Assesment. Gdx.net. https://www.gdx.net/product/igg-food-antibodies-food-sensitivity-test-blood

IGE – Clinical: Immunoglobulin E (IgE), Serum. (n.d.). Www.mayocliniclabs.com. https://www.mayocliniclabs.com/test-catalog/Clinical+and+Interpretive/8159

Iizasa, H., Ishihara, S., Richardo, T., Kanehiro, Y., & Yoshiyama, H. (2015). Dysbiotic infection in the stomach. World journal of gastroenterology, 21(40), 11450–11457. https://doi.org/10.3748/wjg.v21.i40.11450

Lord, R. and Bralley, J., n.d. Laboratory evaluations for integrative and functional medicine. 2nd ed. (2012), Metametrix institute.

Lu, P. J., Hsu, P. I., Chen, C. H., Hsiao, M., Chang, W. C., Tseng, H. H., Lin, K. H., Chuah, S. K., & Chen, H. C. (2010). Gastric juice acidity in upper gastrointestinal diseases. World journal of gastroenterology, 16(43), 5496–5501. https://doi.org/10.3748/wjg.v16.i43.5496

Mayo Clinic. (2017). Helicobacter pylori (H. pylori) infection – Symptoms and causes. Mayo Clinic; https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171

Shor, D. B., Orbach, H., Boaz, M., Altman, A., Anaya, J. M., Bizzaro, N., Tincani, A., Cervera, R., Espinosa, G., Stojanovich, L., Rozman, B., Bombardieri, S., Vita, S. D., Damoiseaux, J., Villalta, D., Tonutti, E., Tozzoli, R., Barzilai, O., Ram, M., Blank, M., … Shoenfeld, Y. (2012). Gastrointestinal-associated autoantibodies in different autoimmune diseases. American journal of clinical and experimental immunology, 1(1), 49–55. 

Strugala, V., Woodcock, A. D., Dettmar, P. W., Faruqi, S., & Morice, A. H. (2015). Detection of pepsin in sputum: a rapid and objective measure of airways reflux. European Respiratory Journal, 47(1), 339–341. https://doi.org/10.1183/13993003.00827-2015

Talebi Bezmin Abadi A. (2014). Helicobacter pylori: A Beneficial Gastric Pathogen?. Frontiers in medicine, 1, 26. https://doi.org/10.3389/fmed.2014.00026

Talley NJ; American Gastroenterological Association. American Gastroenterological Association medical position statement: evaluation of dyspepsia. Gastroenterology. 2005;129:1753-1755.

Yang, J. C., Lu, C. W., & Lin, C. J. (2014). Treatment of Helicobacter pylori infection: current status and future concepts. World journal of gastroenterology, 20(18), 5283–5293. https://doi.org/10.3748/wjg.v20.i18.5283

Elimantion Diets: What You Need To Know

Elimantion Diets: What You Need To Know

According to Dr. O’Neil-Smith, more than 20% of the population suffers from food allergies and intolerances. Elimination diets and IgG food antibody testing can be successfully used in clinical practice to address symptoms like bloating, constipation and diarrhea, fatigue, anxiety, asthma, joint pain, sleep disturbance, and headaches. As practitioners, we must relate this information to clients and patients in an easy-to-understand manner. When I introduce an elimination diet to my clients, I explain that eliminations diets are a great tool to identify food allergies and sensitivities. I would like the client to keep a food/symptom log for five days to see if there are patterns that can point to specific foods causing symptoms. The only downside is that not all reactions are immediate. Some foods can cause delayed reactions, meaning that an offending food can cause a reaction from several hours to several days after it has been ingested. This can make keeping a food/symptom log frustrating and confusing.

What Is The Difference Between An Allergy and A Sensitivity

I think that when we discuss elimination diets, it is important to understand the difference between a true allergy and a sensitivity. Food allergies can be life-threatening due to anaphylaxis. Food sensitivities can be caused by physiological and psychological issues. For example, leaky gut causes maldigested food particles to diffuse in the bloodstream, which causesimmune cells to mount an attack. Overgrowth of bacteria in the small intestine (SIBO) can cause severe reactions to fermentable foods, and it needs to be addressed with a very specific elimination diet called low-FODMAP. Enzyme deficiency and irritable bowel can also cause food intolerances. Stress and psychological factors can also be responsible for food reactions. To this day, there are foods I was forced to eat as a child that will literally make me sick, even though I do not have a true immune reaction to them. We can also be sensitive to “added” substances like food coloring, preservatives, and sulphites (Li, J. 2019).

Elimination Diets Need To Be Tailored To Individual Needs

For these reasons, the elimination diet needs to be tailored to the individual and their specific symptom burden. We must understand that an elimination diet does not merely remove foods, but it also prescribes that the client eats specific foods. For example, if leaky gut is the cause of food intolerances, we need to make sure that their diet includes plenty of gut healing foods. The same applies when we are dealing with food intolerances caused by imbalanced gut flora or irritable bowel. We can’t just refrain from eating offending foods; we must ensure that our diet is nutrient dense and health-promoting (Rinninella et al., 2019).

The good news is that food intolerances usually resolve themselves in a matter of 3 to 6 months, when the client avoids offending foods completely, and we address the root causes of the intolerances. While implementing an elimination diet, we monitor progress closely. This allows us to fine-tune the diet, and it also helps us to decide when the client is ready to reintroduce and to test the foods that were triggering a reaction. The reintroduction phase of the diet is as important as the elimination phase. We must not rush through the process. When symptoms have resolved, we will decide together which foods to reintroduce in the diet and in 

which order. It is important that the client tests one food at a time every 4 to 5 days. This allows us to see if there are any delayed reactions to the food that we reintroduce. Keeping a detailed food/symptom log is going to be very useful during the reintroduction phase. 

Reference

Li, J. (2019). Food allergy vs. food intolerance: What’s the difference? Mayo Clinic; https://www.mayoclinic.org/diseases-conditions/food-allergy/expert-answers/food-allergy/faq-20058538

O’Neil-Smith, K. (n.d.). Using the elimination diet in clinical practice: Explanations and case studies [Video]. Genova Diagnostics. https://www.gdx.net/clinicians/medical-education/previous-webinars/using-the-elimination-diet-in-clinical-practice

Rinninella, E., Cintoni, M., Raoul, P., Lopetuso, L. R., Scaldaferri, F., Pulcini, G., Miggiano, G., Gasbarrini, A., & Mele, M. C. (2019). Food Components and Dietary Habits: Keys for a Healthy Gut Microbiota Composition. Nutrients, 11(10), 2393. https://doi.org/10.3390/nu11102393

Everything You Need To Know About the Magic Four Minerals

Everything You Need To Know About the Magic Four Minerals

Iodine, selenium, zinc, and manganese

Minerals are a vital component of our diet as they facilitate proper growth and development, and they are crucial cofactors in metabolism.  Like vitamins, minerals have recommended daily allowance (RDA), and both deficiency in mineral intake and toxicity can cause problems. 

 This essay looks at iodine, selenium, zinc, and manganese.  It will focus on their role in the body and the systems that they affect. 

Iodine & Thyroid Function

Iodine is necessary to produce the thyroid hormones thyroxine (T4) and triiodothyronine (T3).  T3 and T4 regulate metabolism and body temperature; they affect growth and development, the nervous system, and even our mood.  The thyroid is also responsible for the production of another hormone, calcitonin., which works with parathyroid hormone to regulate calcium level in the body.  During pregnancy, iodine is crucial for fetal brain and bone development, and in the postnatal period it is necessary for proper growth of the infant.  Iodine is found in fish, seaweed, and shellfish.  In the American diet, iodized salt and dairy products are the major dietary source of iodine.  Iodine is also found as a dietary supplement in the form of sodium iodide or potassium iodide. 

Selenium: A Critical Trace Mineral

Selenium is an essential trace mineral needed in small quantities; without it we cannot live.  Selenium is an antioxidant that helps protect cells from damage caused by oxidative stress.  In addition to reducing oxidative stress, selenium supports proper immune function, and it seems to lower the risk of certain cancers.  It is also necessary to produce enzymes.  Brazil nuts are the best source of selenium.  Other sources are fish, pork, beef, turkey and chicken, cottage cheese, eggs, brown rice, and sunflower seeds.  Some processed foods are also enriched with synthetic selenium. 

 Zinc is a mineral found in cells throughout the body and is involved in cell division, cell growth, and wound healing.  Zinc is necessary for immune system function, sperm production, and carbohydrate metabolism.  It is also needed for our sense of taste and smell, and it plays an important role in insulin use.  Zinc is essential for fetal development.  It is also essential for growth and development of infants and children. 

The Importance Of Magnesium

Lastly, manganese is a precursor to many enzymes, and it is needed for protein digestion and absorption as well as cholesterol metabolism.  It is important for bone health, and, when taken with calcium, zinc and copper, it helps reduce spinal bone loss in older women.  Manganese is necessary for blood sugar regulation, and it functions as an antioxidant.  It is a key element for wound healing, and it does so by aiding in the production of proline, an amino acid necessary for collagen production.  Manganese is found in a variety of foods including oysters, clams and mussels, nuts, legumes and unrefined grains, coffee, tea, and many spices.  Our body stores up to 20 mg of manganese in the kidneys, liver, pancreas and bones. 

What is the RDA level for each of the minerals? What is the upper limit for each of the vitamins? What are the signs or symptoms of deficiency and toxicity for each of the minerals? (300 words)

The recommended dietary amount for iodine is age dependent.  A newborn requires 110 mcg of iodine daily.  An infant between 7 to 12 months requires 130 mcg.  Children between 1 and 8 years require 90 mcg, and children between 9 and 13 require 120 mcg.  Teenagers between 14 and 18 require 150 mcg daily, which is the same for adult males and females.  Pregnant women require at least 220 mcg daily, and lactating women require 290 mcg.  Excess iodine intake causes fever, nausea, vomiting, weak pulse, stomach pain, and a burning sensation in the throat, mouth, and stomach, and coma.  Chronic iodine toxicity is rare but can result in thyroid gland inflammation and even thyroid cancer.  Iodine deficiency causes inadequate production of thyroid hormones which leads to hypothyroidism.  Iodine deficiency can also cause the thyroid gland to enlarge, causing goiter.  Iodine deficiency increases risk of miscarriage, stillbirth, and congenital abnormalities in babies.  Tolerable upper limit intake level (UL) has also been established for iodine.  This is the maximum amount of iodine that can be safely ingested without risking toxicity/overdose.  The UL for iodine intake is as follows: children between 1 and 3 have a UL of 200mcg; for children between 9 and 13 UL is 600mcg; UL is 900mcg for teenagers between 14 and 18 years, and it is 1100mcg for adults.

Selenium Deficiency

Selenium deficiency is rare in the general population, but cases of selenium deficiency are often reported in patients who receive intravenous feeding therapy for extended periods of time.  As a result, patients are likely to develop Keshan disease, a cardiomyopathy that presents with enlargement of the heart muscle resulting in congestive cardiac failure, cardiogenic shock and death.  Another condition caused by selenium and iodine deficiency is Kashin-Beck disease.  Kashin-Beck is prevalent mostly in China, Siberia, Korea and Tibet and is caused by mineral deficiencies associated with depleted soil. 

It affects joints and bones to the point that limbs’ growth are stunted, joints are deformed, and the individual experiences loss of stature caused by necrosis of growth plates of the bones and of the cartilage in the joints.  Cognitive function is also affected and mental retardation can be present.  Excess selenium in the body results in selenosis, which causes fatigue, nausea, mild nerve damage, disrupted vision, nail problems, and hair loss. The RDA for selenium vary based on age, gender, illnesses, pregnancy, and they are as follows:

CategoryAgeUnits in mcg/day
InfantsUp to six months15
7 – 12 months20
Children1 – 3 years20
4 – 8 years30
9 – 13 years40
Adolescents and adultsAbove 14 years55
Pregnant women60
Lactating women70

Signs and Symptoms Of Zinc Deficiency

The signs and symptoms of zinc deficiency include poor appetite, stunted growth, alopecia, skin sores, wounds that do not heal easily, hypogonadism, poor olfactory and taste senses, and poor vision.  Similarly, a high zinc intake (usually through supplements) causes vomiting, diarrhea, and abdominal cramps within three to ten hours.  These symptoms generally stop once supplementation ends.  Zinc toxicity has antagonistic effects on copper and iron.  The RDA for zinc are established to prevent deficiency or toxicity and are as follows: infants between 0 and 6 months should take 2mg/day; infants and children 7 months to 3 years should take 3mg/day; RDA for children between 4 and 8 years is 5mg/day, and 8mg/day is recommended for children between 9 and 13 years. Males over 14 years should take 11mg/day, while females between 14 and 18 years should take 9mg/day. Females over 19 years of age require 8mg/day, 11mg/day during pregnancy and 12mg/day when lactating.  Pregnant teenagers require 12mg/day, whereas those lactating require 13mg/day.

Manganese Deficiency Is Rare, But Its Absence Can Disrupt Healthful Living

Although rare, manganese deficiency is possible and manifests with retarded growth, infertility, skeletal abnormalities, low sugar tolerance, and altered fat and carbohydrate metabolism.  Manganism or manganese poisoning results from chronic exposure to manganese and can manifest neurological disorders including tremors, facial muscle spasms or difficulty walking; these neurological symptoms are usually proceeded by hallucinations, reduced lung activities, and aggression.  There is no RDA for manganese; however, the adequate intake (AI) is 1.8-2.3 mg/day, and the upper limit is 11mg/day for adults above 19 years.

What impact does the quality of the soil play in the role of the available minerals in our food supply? What types of chemicals in our environment impede mineral absorption?

Soil is an essential factor in healthy food and human and animal nutrition.  While most of us are familiar with malnutrition that comes from lack or poor quality macronutrients, not everyone knows about another form of malnutrition called “hidden hunger”.  Hidden hunger occurs when our diet is void of micronutrients, such as B vitamins, vitamin A, iodine, selenium, and zinc.  Micronutrients are essential to health, being cofactors in metabolic functions, digestion, neurotransmitter production, eyesight, energy, and more.  The Food and Agriculture Organization estimates that around 2 billion people worldwide suffer from hidden hunger; that is almost 1/3 of the world population.  The quality of our soil is a key factor affecting micronutrient availability in food and nutrient quality. 

Most the foods that we eat come from the soil: vegetables, fruits, grains and grains products.  Hidden hunger is caused by lack of variety, consumption of crops that are not nutrient-rich, and soil depletion.  Plants need 18 essential elements for proper growth and nutrient-density.  Three of them (carbon, hydrogen and oxygen) are obtained through photosynthesis; the rest need to be present in the soil.  Unsustainable soil management strips the soil of nutrients, causing the foods grown in it to have suboptimal nutrient profiles.  We need to get away from mass farming procedures that encourage unsustainable soil management, and we need to embrace agricultural practices that are based on crop rotation and diversification which promote soil fertility; healthy soil leads to healthy food.  

Healthy Soil Means A Healthy You

Another factor that plays an important role in soil health, and therefore the health of our crops, is exposure to chemicals, heavy metal pollution, and man-made fertilizers.  Studies show that long-term use of man-made fertilizers causes a decline in soil quality and productivity.  Particularly hazardous is long term exposure to heavy metals, insecticides and aromatic hydrocarbons.  These substances have toxic effects on plants and humans; they prevent mineral absorption, disrupt vital enzymatic processes, change the microbiota, and compete with minerals for absorption.  Cadmium, mercury, lead, arsenic and copper are the heavy metals most commonly found in the soil.  They accumulate through disposal of high metal wastes, sewage sludge, wastewater irrigation, emissions from industrial areas, and spillage of petrochemicals.  

How Cadmium Can Be Destructive For Healthy Living

Cadmium interferes with copper, iron and zinc.  Mercury damages the nerves and interferes with cellular respiration.  Lead ingestion can lead to anemia, kidney and brain damage and even death.  Particularly problematic is exposure to lead by individuals whose diets are deficient in vitamin E, calcium, phosphorus, iron and zinc.  Arsenic is a known carcinogen, which causes skin changes, nausea and vomiting, arrhythmia, and cramps.  While there is no medication to combat arsenic poisoning, the use of vitamin E and selenium have shown to limit the symptoms and damage of arsenic poisoning. 

Heavy metals do not only pose a risk to our health, but they are also harmful to soil regeneration and biodegradation of organic contaminants.  Soil washing, immobilization, phytoremediation are all technologies available to clean up contaminated soils.

References

Stipanuk MH, Caudill MA, editors. Biochemical, physiological, and molecular aspects of human nutrition. 4th ed. St. Louis, Mo: Elsevier; 2019. 959 p.

Al-Fartusie, F. S., & Mohssan, S. N. (2017). Essential trace elements and their vital roles in human body. Indian J Adv Chem Sci5(3), 127-136. 

Kavtarashvili, A. S., Stefanova, I. L., Svitkin, V. S., & Novotorov, E. N. (2017). Finctional egg production. II. The roles of selenium, zinc, and iodine. BIOLOGY AGRICULTURAL, 700.

 Mishra, S., Bharagava, R. N., More, N., Yadav, A., Zainith, S., Mani, S., & Chowdhary, P. (2019). Heavy metal contamination: an alarming threat to environment and human health. In Environmental biotechnology: For sustainable future (pp. 103-125). Springer, Singapore.

Zimmermann, M. B., & Boelaert, K. (2015). Iodine deficiency and thyroid disorders. The Lancet Diabetes & Endocrinology3(4), 286-295.

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