Nutritional Therapy For Hashimoto’s

Nutritional Therapy For Hashimoto’s

Hashimoto thyroiditis is a chronic autoimmune disorder caused by an interaction between genetic factors and environmental triggers. The integrative approach to autoimmune thyroiditis is a multifaceted approach that focuses on diet, lifestyle, and individualized supplementation. The practitioner should also aim at discovering and dealing with the environmental triggers that started the autoantibody attack against the thyroid (Liontiris et al., 2017).

A clinical trial on 34 women showed that a strict gluten-free diet followed for 6 months lowered thyroid antibodies, improved vitamin D levels, and improved the quality of thyroid tissue (Krysiak et al., 2019).

A review published in 2020 in the Annals of Agriculture and Environmental Medicine (AAEM) shows that scientists agree that there are numerous environmental, dietary, and lifestyle factors that exacerbate Hashimoto thyroiditis: including stress, environmental toxins, poor detoxification, gut dysbiosis, leaky gut (Cayres et al., 2021), undernutrition and malnutrition (Ihnatowicz et al., 2020). 

Can Inflammation Reduction Help Ease the Symptom’s of Hashimoto’s Disease?

The dietary intervention aims at reducing inflammation and modulating the immune response, and it focuses on a nutrient-dense diet that is gluten and dairy-free. Research shows that consumption of dairy foods negatively interacts with the thyroid medication levothyroxine (Ihnatowicz et al., 2020). Regarding gluten, research shows the negative effects that gliadin has on thyroid antibodies as well as the high prevalence of undiagnosed celiac disease in patients suffering from autoimmune thyroiditis. A study published in 2017 concluded that in patients with Hashimoto’s high levels of anti-tissue transglutaminase and IgA anti-gliadin antibodies are related to antithyroid antibodies. These findings show that dietary intervention in Hashimoto’s patients is crucial in reducing the autoimmune load and preventing the occurrence of celiac disease (Riseh et al., 2017).

Research shows that Hashimoto’s patients share frequent nutrition deficiencies: zinc, selenium, magnesium, potassium, iodine, copper, vitamin A, vitamin C, vitamin D, and B vitamins. Patients suffering from Hashimoto’s also benefit from adequate levels of high-quality protein and omega-3 fatty acids (Ihnatowicz et al., 2020).

Diet and Infflamation Reduction

 In my practice, I recommend the paleo autoimmune diet (AIP) to my clients suffering from Hashimoto’s thyroiditis (Abbott et al., 2019). This dietary intervention focuses on nutrient-dense foods; it removes foods that cause inflammation (for example, grains, soy, and peanuts), but it also removes otherwise healthy foods, like tomatoes, that contain compounds known to stimulate the immune system.

Paleo Autoimmune Diet Food List

  • Grass-fed meals, organic poultry, wild-caught fish, pastured pork, and wild game
  • Vegetables: all except nightshades
  • Sweet potatoes
  • Fruit (limit to 1-2 servings a day to keep fructose consumption to no more than 25gr daily)
  • Honey and maple syrup in small quantity 
  • Fermented foods: sauerkraut, kombucha, coconut water kefir
  • Fresh non-seed herbs
  • Green tea and non-seed herbal teas
  • Vinegar
  • Olive, coconut, and avocado oil (plus fats naturally occurring on meat and fish)
  • Bone broths

Foods not allowed on AIP

  • Grains
  • Dairy
  • Eggs
  • Nuts
  • Nightshades 
  • All sugars and non-nutritive sweeteners, except for honey and maple syrup
  • Processed oils 
  • Alcohol
  • Coffee
  • Chocolate
  • Processed foods
  • Foods the patient is sensitive or allergic to

Lifestyle Intervention For Hashimoto’s

 Smoking is a common risk factor in the development of autoimmune thyroiditis, therefore, smoking cessation is recommended (Köhling et al., 2017).  Stress is another common risk factor (Köhling et al., 2017). Stress-management techniques like guided meditation, breathing exercises, yoga, massage, and cognitive-behavioral strategies can help lower stress response (Carlson et al., 2019).

 While there are no studies regarding the impact of sleep quality on autoimmune thyroiditis, we know that poor sleep quality negatively influences stress response (Blaxton et al., 2017). For this reason, sleep hygiene is part of my autoimmune thyroiditis recovery program.

In recent years, research has investigated the role of the microbiota in autoimmune disease. H. Pylori and gut dysbiosis have been linked to autoimmune thyroiditis (Köhling et al., 2017). Therefore, a holistic approach to Hashimoto’s must include diagnosis and treatment of gut ecology imbalance. 


Abbott, R. D., Sadowski, A., & Alt, A. G. (2019). Efficacy of the Autoimmune Protocol Diet as Part of a Multi-disciplinary, Supported Lifestyle Intervention for Hashimoto’s Thyroiditis. Cureus, 11(4), e4556.

Blaxton, J. M., Bergeman, C. S., Whitehead, B. R., Braun, M. E., & Payne, J. D. (2017). Relationships Among Nightly Sleep Quality, Daily Stress, and Daily Affect. The journals of gerontology. Series B, Psychological sciences and social sciences, 72(3), 363–372.

Carlson, L. E., Toivonen, K., & Subnis, U. (2019). Integrative Approaches to Stress Management. Cancer journal (Sudbury, Mass.), 25(5), 329–336.

Cayres, L., de Salis, L., Rodrigues, G., Lengert, A., Biondi, A., Sargentini, L., Brisotti, J. L., Gomes, E., & de Oliveira, G. (2021). Detection of Alterations in the Gut Microbiota and Intestinal Permeability in Patients With Hashimoto Thyroiditis. Frontiers in immunology, 12, 579140.

Hadizadeh Riseh, S., Abbasalizad Farhang, M., Mobasseri, M., & Asghari Jafarabadi, M. (2017). THE RELATIONSHIP BETWEEN THYROID HORMONES, ANTITHYROID ANTIBODIES, ANTI-TISSUE TRANSGLUTAMINASE AND ANTI-GLIADIN ANTIBODIES IN PATIENTS WITH HASHIMOTO’S THYROIDITIS. Acta endocrinologica (Bucharest, Romania : 2005), 13(2), 174–179.

Ihnatowicz, P., Drywień, M., Wątor, P., & Wojsiat, J. (2020). The importance of nutritional factors and dietary management of Hashimoto’s thyroiditis. Annals of agricultural and environmental medicine : AAEM, 27(2), 184–193.

Köhling, H. L., Plummer, S. F., Marchesi, J. R., Davidge, K. S., & Ludgate, M. (2017). The microbiota and autoimmunity: Their role in thyroid autoimmune diseases. Clinical immunology (Orlando, Fla.), 183, 63–74.

Krysiak, R., Szkróbka, W., & Okopień, B. (2019). The Effect of Gluten-Free Diet on Thyroid Autoimmunity in Drug-Naïve Women with Hashimoto’s Thyroiditis: A Pilot Study. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, 127(7), 417–422.

Liontiris, M. I., & Mazokopakis, E. E. (2017). A concise review of Hashimoto thyroiditis (HT) and the importance of iodine, selenium, vitamin D and gluten on the autoimmunity and dietary management of HT patients.Points that need more investigation. Hellenic journal of nuclear medicine, 20(1), 51–56.

The Integrative Treatment of Thyroid Conditions. (2021). Natural Medicine Journal.

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. 


Barker, J. M., & Liu, E. (2008). Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Advances in pediatrics, 55, 349–365.

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.

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.

Hadjivassiliou, M., Williamson, C. A., & Woodroofe, N. (2004). The immunology of gluten sensitivity: beyond the gut. Trends in Immunology, 25(11), 578–582.

Lebwohl, B., Sanders, D. S., & Green, P. (2018). Coeliac disease. Lancet (London, England), 391(10115), 70–81.

Leopold, C. (2018, August 31). Everything you need to know about the cerebellum. Medical News. 

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

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.

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.

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.

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).

Life Withe Crohn’s Disease: What To Do After The Removal Of The Ileum

Life Withe Crohn’s Disease: What To Do After The Removal Of The Ileum

Crohn’s disease is genetic chronic inflammatory disorder of the digestive system that affects any part of the digestive tract, with the ileum and proximal colon being affected the most.  Crohn’s disease causes gastrointestinal symptoms ranging from diarrhea, blood in the stool, abdominal pain, loss of appetite, weight loss, and malnutrition.  Liver disorder can also occur.

In some cases, parts of the digestive tract need removal.  This client has had a small bowel resection, and it important to provide nutritional therapy to prevent malnutrition. 

The small intestine is the site of absorption of carbohydrates, fats, proteins, calcium, magnesium, trace elements and vitamins.  It is also in the small intestine that bile salts are recycled.   

Removal of the ileum reduces the absorptive surface area of the small intestine.  Bile acids cannot be absorbed. This causes fat maldigestion and malabsorption of fat-soluble vitamins.  Bile acids also spill in the colon causing watery diarrhea.  The watery diarrhea is usually present in the post-operative period, and oftentimes medications are prescribed to manage the symptoms.  The watery diarrhea causes dehydration; therefore, it is important to support electrolyte and fluid balance. 

If this patient is not a renal patient, I recommend liberal use of unrefined salt.  I cannot stress enough the importance of hydration: this client should drink filtered or spring water, away from meals, as well as nourishing bone broths.  He should also reduce caffeine, soda, and alcohol to a minimum, as these beverages are dehydrating as well as irritating to the digestive tract.  Should this client also be a renal patient, I would work collaboratively with his renal nurse specialist to find the right sodium and water requirements.

The Importance Of Vitamin B 12 When the Ileum Is Removed

Vitamin B 12 is absorbed in the lower ileum; it is necessary for red blood cell formation, DNA synthesis, and nerve function.  Removal of the ileum causes vitamin B12 deficiencies; therefore, it is necessary for this client to start supplementing vitamin B12 immediately. I would recommend vitamin B12 injections, which are more bioavailable as they bypass the digestive tract.  It is important to monitor vitamin B 12 levels yearly and adjust supplement dosage accordingly. 

Altered anatomy also leads to fat maldigestion and deficiencies of fat-soluble vitamins.  Vitamin D is necessary for healthy bones, calcium metabolism and immune system function, and deficiency can cause bone disease and osteoporosis.  Supplementation of vitamin D as well as sun therapy are very important.  Vitamin K is important for blood clotting and bone structure; deficiency can cause bleeding and bruising.  Vitamin K deficiency is rare because the flora of the large intestine manufactures most of the vitamin K our bodies need.  Vitamin A deficiency can be present.  This fat-soluble vitamin is important for eyesight as well as tissue growth and healing, and deficiencies can cause night blindness and infections.  Vitamin A is stored exclusively in the liver, and serum levels may not be a good indicator of body reserves. Ancient Egyptians treated vitamin A deficiency with liver. 

What Happens During The Post-Operative Period?

In the immediate post-operative period a low-residue diet is indicated to control diarrhea.  In some cases, enteral nutrition is necessary.

I recommend for this client a nutrient-dense diet, high in protein diet but moderate in fats.  Carbohydrates should be easy to digest and void of fibers (no whole grains for now, focus on potatoes without the skin, bananas, white rice).  The diet will be low in oxalates and low-residue, as fiber, and especially insoluble fiber, is hard to digest in the post-operative period.  Small amounts of well cooked vegetables can be added if tolerated (starting with ½ cup).  Raw vegetables need to be avoided at this time.  I recommend excluding vegetables that cause intestinal gas and discomfort: onions and garlic, vegetables of the brassica family, and legumes.3  


1 Costantini A, Pala MI. Thiamine and fatigue in inflammatory bowel diseases: an open-label pilot study. Journal of Alternative and Complementary Medicine (New York, NY). 2013 Aug;19(8):704–8.

2 Boelens PG, Heesakkers FFBM, Luyer MDP, van Barneveld KWY, de Hingh IHJT, Nieuwenhuijzen GAP, et al. Reduction of Postoperative Ileus by Early Enteral Nutrition in Patients Undergoing Major Rectal Surgery: Prospective, Randomized, Controlled Trial. Annals of Surgery. 2014 Apr;259(4):649–655.

3 Nutrition Guidelines for People With Short Bowel Syndrome | Memorial Sloan Kettering Cancer Center [Internet]. [cited 2020 Oct 10]. Available from:

Celiac Disease & Gluten Filled Food Products

Celiac Disease & Gluten Filled Food Products

Celiac disease is an autoimmune gastrointestinal condition that causes a variety of health issues including nutrient malabsorption and deficiencies, changes in bowel habits, anemia, bone diseases, and eczema.  It is more prevalent in females, and it usually occurs early in life.

Celiac disease is caused by an immune response to gluten in genetically sensitive individuals.  One of the main culprits is gliadin, a protein component of gluten found in wheat, barley, rye, oats, malt, spelt, triticale, semolina, and bulgur.

Celiac disease causes an immune-system mediated damage of the digestive tract.  This is carried out mostly by T-cells that become activated when sensitive individuals are exposed to gluten.  Ingestion of gluten causes the body to produce antibodies against it; the presence of antibodies causes a mucosal inflammatory response, which triggers the T-cells to come to the site of inflammation and infiltrate the intestinal mucosa.  Over time, repetitive exposure to gluten, and consequent autoimmune response, causes intestinal damage.  The duodenum is the part of the small intestine that is affected the most.  The autoimmune response causes hyperplasia of the crypts of Lieberkuhn, and atrophy of the villi and microvilli.  This greatly decreases the absorptive surface area of the lumen, causing the small intestine to lose its ability to absorb nutrients, which leads to a myriad of nutrient deficiencies and symptoms.

How Genetic Make-Up Plays A Role In Determining Who Expresses Celiac Disease

Genetics play a big role in the development of celiac disease. There is a 10-15% chance of suffering from this autoimmune condition if a first degree relative suffers from it; rates are considerably higher in identical twins.  People suffering from other autoimmune conditions (Type-1 diabetes, Sjogren’s Syndrome, juvenile chronic arthritis) have increased risk of developing celiac disease.  Among other genetic conditions that can increase risk of developing celiac disease are Down’s Syndrome, Turner Syndrome and William Syndrome.

Gastrointestinal symptoms include abdominal pain, diarrhea (chronic or recurrent), weight loss, and malabsorption.  Distention, bloating and steatorrhea can also be present. Celiac disease is accompanied in 10-15% of cases by a painful skin condition called dermatitis herpetiformis.  Dermatitis herpetiformis, also called celiac rash, causes intense pruritus and painful vesicles and papules, most often on forearms, buttocks, knees, and scalp. Other features of celiac disease include failure to thrive, osteoporosis and metabolic bone disease, anemia, idiopathic peripheral neuropathy, fatigue, headaches, infertility, dental enamel hypoplasia, and stomatitis. 

Diagnosis involves testing to serum autoantibodies while the patient is on a gluten-containing diet, and small intestine biopsy that requires 4 to 6 samples.  The biopsy looks for increased intraepithelial lymphocytes, villous atrophy, and crypt hyperplasia, all of which must be present to distinguish celiac disease from non-celiac gluten sensitivity. 

Treatments For Celiac Disease

Treatment for celiac disease is a strict celiac disease diet: all foods containing gliadin and gluten must be removed and completely avoided.  Even traces amounts can be deleterious, and, unfortunately, gluten is hidden in foods, medications, and even non-food stuff, from make-up to stamps, to play dough.  People with celiac disease need be careful when eating out, as cross-contamination is unfortunately widespread even in restaurants with gluten free menus. 

The good news is that when followed strictly, the diet reduces inflammation to the small intestine and individuals can see improvement of symptoms within 3 months.  In the presence of severe nutritional deficiencies and anemia, it is important to supplement with multi vitamins and minerals as well with targeted nutrients.  When the digestive system can’t handle vitamin pills, injections may be prescribed.  In some cases, steroid medications can be prescribed to keep inflammation under control while the small intestine regenerates.  Unfortunately, about 1 in 50 people affected by celiac disease suffer from refractory celiac disease.  People affected by refractory disease show no improvement in malabsorption and villi atrophy 6 to 12 months after strict gluten free diet.  There is currently no treatment for refractory celiac disease. 


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The Myth Of Carbohydrates Debunked

The Myth Of Carbohydrates Debunked

Carbohydrates are an important class of organic molecules found in all organisms.  They are synthesized from carbon, oxygen, and hydrogen atoms.  They are a source of energy, a form of stored energy, and they can have structural roles.  

Monosaccharides, also called sugars, are the simplest form of carbohydrates.  They are soluble and sweet tasting.  They have between 3 and 6 carbon atoms, and their general formula is (CH2O)n,  They are named according to the number of carbon atoms (triose C3H6O3, tetros C4H8O4, pentose C5H10O5, hexose C6H12O6).  Glucose, fructose and galactose are all hexoses; while they all have the same chemical formula, they are structurally and chemically different.

Understanding The Importance of Glucose

Glucose is the main source of energy in respiration, and it is the building block for larger carbohydrates.  It is a small, soluble monosaccharide that is easily transported in and out of cells through carrier proteins.  It is less reactive than other monosaccharides; therefore, its breakdown must be catalyzed by enzymes.  There are two forms of glucose: alpha-glucose and ß-glucose, which differ by the position of the hydroxyl group.  The presence of either one yields very different polysaccharides. 

Monosaccharides are joined together via a condensation reaction to form disaccharides and polysaccharides. During a condensation reaction one oxygen and two hydrogen atoms are removed from monosaccharides forming water.  The removal of water bonds the monosaccharides together by a covalent bond known as a glycosidic bond.  The names of glycosidic bonds depend on the location of the carbon atoms between which they are formed.  For example, a bond formed between carbon 1 and carbon 4 is called a 1,4 glycosidic bond (i.e. maltose).  Conversely, disaccharides and polysaccharides can be broken down into monosaccharides through hydrolysis. Being the opposite of condensation, a hydrolysis reaction requires water.

Disaccharides, also called sugars, are sweet-tasting and soluble. Different combinations of monosaccharides will form different disaccharides. For example, two molecules of alpha-glucose form maltose; alpha-glucose and fructose combine to form sucrose; ß-glucose and galactose combine to form lactose. Sucrose is formed by alpha glucose and beta fructose.

The Structure Of Sugar

Polysaccharides are polymers of simple sugars bonded via condensation reactions.  Unlike monosaccharides and disaccharides, polysaccharides are not sweet-tasting nor easily soluble; they are not sugars.  There is a variety of polysaccharides, depending on which monomers bond together to form the polysaccharide and where the bond takes place.  For example: a polymer of alpha-glucose monosaccharides creates amylose.  A polymer of ß-glucose gives us cellulose.  A 1,4 glycosidic bonding gives us amylose, while a 1,4 and 1,6 glycosidic bonding gives us amylopectin.

Polysaccharides are the main source of stored energy for both plants and animals; they can also have structural roles.  They are very compact, allowing storage of a lot of energy in a small space.  They are insoluble in water; therefore, they do not affect the osmotic balance of the cell.  They are large molecules that do not diffuse in and out of the cells.  Finally, they can be easily hydrolyzed in alpha-glucose when energy is needed.  Cellulose, chitin, starch, and glycogen are all examples of important polysaccharides.

 Cellulose consists in beta glucose units connected via 1,4 glycosidic bonds and is important for the overall structure of plants.  Chitin is made of N-acetyl-D-glucosamine polymers and it has a similar structure to cellulose.  It is present in some fungi and in the exoskeleton of arthropods providing structure and strength that protect these organisms from the outside world.  Starch is made from alpha-glucose, and it is found in photosynthesizing cells in leaves and storage cells in seeds.  Glycogen is an important form of energy storage in animals.  It is made of alpha-glucose molecules joined together by 1,4 and 1,6 glycosidic bonds.  In times of strenuous activities or in between meals enzymes break down some of this glycogen in individual glucose molecules.  When in excess, other enzymes add glucose units back to the chain to store them for later use.

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