Home › Mineral deficiency › Fluoride › Fluoride deficiency symptoms. What is fluoride?
Fluorine (F) is a widely distributed element in nature. It is a trace mineral existing in our body as fluoride (F-) salts.
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Fluoride deficiency can lead to symptoms like dental caries and also possibly osteoporosis. Most of the fluoride in our body is found bound to bones and teeth. Excess of F- can be toxic causing fluorosis, liver damage and hip fractures.
Fluoride function and health benefits
The well known function of fluoride is its role in reducing tooth decay and strengthening tooth enamel against attack by acid producing bacteria. F- is also found to increase the bone density and is important for maintaining strong bones and lowering risk of osteoporosis and bone fractures. F- reduces the ability of the plaque bacteria to produce acid.
Sources of fluoride in foods
Fluoride is found in soil, groundwater and seawater. Most of the seafood is found to have fairly good amounts of F-.
Vegetables grown in soil rich in F- are great dietary sources. The bones, meat and meat products of animals grazing or feeding on fodder from F- rich soils are good food sources. Fluoridated drinking water, fluoride toothpastes and fluoridated salt and milk are other sources of F-.
Causes of fluoride deficiency
Poor intake of fluoride foods, especially seafood, can cause its inadequacy in the body. In certain areas naturally occurring concentrations of F- in water and soil may be low. The changing lifestyle and dietary habits, inadequate exposure to fluorides and the use of demineralized bottled drinking water has lead to reduced availability of F- for dental health. The increased use of sugar and sugar products has increased the incidence of dental caries, compounding the need for fluoride.
Symptoms of fluoride deficiency
The early symptoms of fluoride deficiency manifest as dental carries and tooth decay. Low F- levels can lead to symptoms of brittle and weak bones in elderly. Fractured hip may be a possible symptom of F- deficiency.
Treatment of fluoride deficiency
Fluoridation of water, salt, milk and toothpaste are the proven methods to counter symptoms of dental carries.
Fluoridated water
In certain countries tap water is fluoridated by adding small amounts of fluoride (about 1 mg/liter) to the water. World Health Organization considers water fluoridation substantially reduce the prevalence and incidence of dental caries. Several community water fluoridation programs were introduced in the USA. Worldwide, extensive fluoridation programs have also been introduced in several countries.
Salt fluoridation
Salt fluoridation has been introduced in some countries in Latin America as well as in certain European countries. In Jamaica, salt fluoridation was introduced in 1987. Potassium fluoride at a concentration of 250 mg/kg was added to the common salt. A national oral health survey conducted in 1995 confirmed a remarkable fall in the incidence of dental caries.
Milk fluoridation
Milk fluoridation programs conducted in Switzerland, Scotland, Hungary, Chile and Beijing (China) targeting kindergarten and school going children have successfully demonstrated the striking reductions in the symptoms of dental caries.
Fluoride toothpastes
WHO conducted a school-based intervention study to assess the efficacy of a toothpaste specifically manufactured as an “affordable fluoride-containing toothpaste" in the province of West Kalimantan, Indonesia. One daily supervised tooth-brushing activity was conducted with this toothpaste. The study was evaluated after 3 years and there was significant reductions in the incidence of dental caries.
References:
1.Petersen PE, Lennon MA. Effective use of fluorides for the prevention of dental caries in the 21st century: the WHO approach. Community Dent Oral Epidemiol. 2004 Oct;32(5):319-21.
2.Pizzo G, Piscopo MR, Pizzo I, Giuliana G. Community water fluoridation and caries prevention: a critical review. Clin Oral Investig. 2007 Sep;11(3):189-93.
3.Stephen Peckham, Niyi Awofeso. Water Fluoridation: A Critical Review of the Physiological Effects of Ingested Fluoride as a Public Health Intervention. ScientificWorldJournal. 2014; 2014: 293019.
4.Sheila Jones, Brian A. Burt, Poul Erik Petersen, Michael A. Lennon. The effective use of fluorides in public health. Bull World Health Organ. 2005 Sep; 83(9): 670–676.
Home › Mineral deficiency › Cobalt › Cobalt deficiency symptoms and diseases. What is cobalt? Cobalt is an essential trace element. Cobalt is a constituent of vitamin B12 (cobalamin).
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Its deficiency, essentially the insufficiency of vitamin B12, can cause several disease symptoms, including pernicious anemia, hyperhomocysteinemia, neuropsychiatric manifestations and goiter. The Co atom in cobalamin is attached and surrounded to a deoxyadenosyl group, methyl group, and a cyano group or hydroxyl group.
Cobalt in food
Cobalt as cobalamin is essential for several body functions. Co in its salt forms as Cobalt chloride (CoCl2), nitrate (Co(NO3)2), carbonate (CoCO3) or sulfate (CoSO4) is required for vitamin B12 (cobalamin) synthesis by bacteria. The cobalamin synthesis by bacteria actively takes place in the rumen of ruminants. In other non-ruminant herbivores and humans, cobalamin is synthesized by bacteria in the colon.
Very small quantities of vitamin B12 is absorbed in the colon and some animals resort to ingesting feces to obtain the nutrient. Carnivores and humans have to obtain the vitamin pre-made in ruminants by eating animal products. Just ingesting the mineral salts will not cure the cobalamin insufficiency. Most of the animal sources of food, including shellfish, organ meat, yeast, fish, poultry and milk products are rich in vitamin B12.
Cobalt benefits and functions
Cobalt is essential for normal thyroid function.
It is found to be essential for the normal development of child's body and the function of the cardiovascular system.
It influences DNA synthesis.
Co stimulates erythrocytes production.
Co influences maturation of erythroid stem cells and haemoglobin synthesis.
It helps with repair of the myelin sheath.
Cobalt and physical development
Analysis of hair cobalt content, pointed towards high incidence of its deficiency (89%) in elementary school children of the Republic of Tatarstan. Svyatova NV et al. in their 2013 study found that there was significant correlations between physical development and cardiovascular system with hair Co content. They concluded that, "positive balance of cobalt is essential for normal growth and development of child's body and function of the cardiovascular system."
The role of cobalt in iron-deficiency anemia
Maria Georgieva Angelova et al. on their study on iron-deficiency anemia (IDA) found that the cobalt mean serum concentration were significantly lower in children with IDA than healthy controls. Co plays an important role in the processes of erythropoiesis by stimulating erythrocytes production by activation of the transcription factor hypoxia-inducible factor 1α (HIF-1α).
Cobalt deficiency causes
A cobalt insufficiency is ultimately also a vitamin B12 insufficiency. Co inadequacy arises due to several causes. Poor dietary intake of vitamin B12, malabsorption, severe malnutrition, protein energy malnutrition, vegan lifestyle, certain intestinal disorders and certain medications can cause the inadequacy of this nutrient.
Cobalt deficiency symptoms
Cobalamin insufficiency can give rise to severe symptoms and cause irreversible damage to the brain and nervous system. Low levels of vitamin B12 in the blood serum can give rise to symptoms like glossitis, fatigue, depression and poor memory. As the conditions progresses, symptoms like polyneuropathy, cognitive deficits, reduced immune function, pernicious anemia and hyperhomocisteinemia will appear.
Cobalt deficiency and goiter
The study conducted by Mojgan Sanjari et al. in 2014 on endemic goiter in the city of Herman (Iran), established that apart from iodine, the endemic Cobalt deficiency had lead to symptoms of goiter in school-aged children. Even decades after iodine deficiency control program was initiated in 1989 by iodizing salt, the incidence of goiter has remained an endemic condition in most parts of Iran. Studies revealed that goitrous children when compared to non-goitrous children, had lower serum Co levels. The authors concluded that, "Cobalt deficiency may be an important independent predictor for goiter in endemic regions, especially areas in which goiters persist despite salt iodization programs." The cobalt deficiency and its symptoms are treated by vitamin B12 replacement therapy.
References:
1.Sanjari M, Gholamhoseinian A, Nakhaee A. The Association between Cobalt Deficiency and Endemic Goiter in School-Aged Children. Endocrinol Metab (Seoul). 2014 Sep;29(3):307-11.
2.Svyatova NV, Sitdikov FG, Egerev ES. Effect of cobalt on parameters of the cardiovascular system in elementary school children. Bull Exp Biol Med. 2013 Jul;155(3):312-3.
3.Maria Georgieva Angelova, Tsvetelina Valentinova Petkova-Marinova, Maksym Vladimirovich Pogorielov, Andrii Nikolaevich Loboda, Vania Nedkova Nedkova-Kolarova, Atanaska Naumova Bozhinova. Trace Element Status (Iron, Zinc, Copper, Chromium, Cobalt, and Nickel) in Iron-Deficiency Anaemia of Children under 3 Years. Anemia. 2014; 2014: 718089.
Home › Mineral deficiency › Chloride deficiency symptoms - Chloride in blood - Low serum chloride levels. What is chloride?
The chloride (Cl-) is the major anion (negatively charged ion) and electrolyte present in the blood serum and the extracellular fluid.
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It is an essential nutrient required along with sodium and potassium for maintaining fluid and electrolyte balance in the human body. Deficiency of chloride is rare.
The normal chloride levels in blood serum range from 97 to 107 mEq/L. Cl- deficiency (hypochloremia) occurs when the levels drop below 97 mEq/L. Low serum chloride levels disturb the acid and base balance in the body. Chronic low Cl- levels can leading to metabolic alkalosis, low fluid volume in the blood serum and urinary potassium loss.
Chloride food sources
The primary source of Cl- is the sodium chloride, the common table salt. It is also present in seaweeds such as dulse (Palmaria palmata) and kelp. Pickled and processed foods are good sources of chloride and sodium.
It is also present in various seasonings, meat products, fish, poultry and dairy products. Most of the vegetables have low levels of Cl- in them. Lettuce, tomatoes and celery are some of the vegetables containing fair amounts of this nutrient. Cl- is both actively and passively absorbed by the body.
The Food & Nutrition Board of the Institute of Medicine, has set the daily Adequate Intake (AI) of chloride for adults (19 to 50 years) as 2.3 grams per day. Individuals in the older age group (50+ years) may need 2.0 grams/day. Intake levels lower than the AI can cause deficiency. The Tolerable Upper Intake Levels (UL) for Cl- for adults is 3.6 grams/day.
Chloride benefits and functions
Chloride is a component of all body secretions and excretions.
Cl- is an essential component of digestive juices, occurring as stomach hydrochloric acid.
It is involved in the regulation of pH of the body fluids and blood serum.
A constant exchange of chloride and bicarbonate, between red blood cells and the serum helps to govern the pH balance.
Chloride shift (also known as the Hamburger shift) brings about the transport and expiration of carbon dioxide.
The Cl- shift may also regulate the affinity of hemoglobin for oxygen.
Low levels of Cl- in the blood serum leads to increase in pH, metabolic alkalosis and contraction of the extracellular volume with serious symptoms.
Cl- ions channels render nerve cells more excitable and have a pivotal role in neurotransmission.
Chloride deficiency causes
Low Cl- levels may occur for a variety of reasons including,
severe dietary insufficiency,
acute severe malnutrition,
eating disorders (anorexia nervosa and bulimia),
malabsorption disorders,
excessive perspiration,
persistent vomiting,
severe chronic diarrhoea,
fluid loss due to burns and injuries,
overuse of diuretics or laxatives,
drinking too much water,
congenital chloride diarrhea,
renal disease,
salt-wasting nephropathy,
congestive heart failure,
cystic fibrosis,
Bartter’s syndrome and
genetic diseases.
Symptoms of low levels of chloride in blood
In mild low levels of Cl- in blood, the symptoms may not be apparent. Milder symptoms include loss of appetite, muscle weakness, dehydration, fever and restlessness. Marked low serum levels of the nutrient can manifest with symptoms like loss of control of muscle function, difficulty in breathing and swallowing. Very low Cl- in blood serum shows symptoms of alkaline blood, very high serum pH, massive loss of potassium in urine and hypokalemic metabolic alkalosis.
Diagnosis of low serum chloride levels
Low blood Cl- levels (less than 97 mEq/L) confirm the diagnosis. Simultaneously, pH and carbon dioxide levels are tested. Blood pH rises beyond 7.45. Serum carbon dioxide levels rises above 32 mEq/L.
Chloride deficiency diseases
This condition is medically termed as hypochloremia. It is usually the result of low sodium levels or elevated bicarbonate concentration in the blood serum due to volume depletions. Low blood serum concentration of Cl- ion is a rare condition. However, when it does occur, it results in a life threatening metabolic alkalosis, low fluid in the blood serum, contraction of the extracellular volume and urinary potassium loss. Certain genetic diseases like congenital chloride diarrhea can contribute to low blood serum concentration of this electrolyte.
Congenital chloride diarrhea
Congenital chloride diarrhea is due to mutations in the SLC26A3 gene. These mutations impair the synthesis of intestinal SLC26A3 protein, resulting in impaired exchange of Cl-/HCO3- ions. The mutation results in diarrhea-related Na+, Cl- and fluid depletion resulting in decreased blood serum concentration of these ions.
Treatment of low serum chloride levels
IV administration of saline is the best treatment option for correcting the electrolyte imbalance. Ammonium chloride may be administered for treating the metabolic alkalosis. The causative factors are treated for complete resolution of the condition. Hypochloremia can be prevented by consuming food moderately high in this electrolyte.
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Home › Mineral deficiency › Boron › Boron deficiency symptoms in humans. What is Boron?
Boron (B) is a trace element and an essential nutrient. Boron deficiency in humans may affect bone metabolism, brain function and plasma levels of steroid hormones.
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Boron deficiency symptoms include loss of bone mass (osteoporosis), decreased brain electrical activity, impaired reproductive function and increased oxidative stress.
Boron is essential for the optimum function of metabolic activities related to bone, mineral and lipid metabolism, energy production and utilization, antioxidant activity and immune function in humans. Several research studies suggest the regulatory role of boron in the metabolism of several other nutrients including calcium, magnesium, copper and nitrogen. Research studies reveal its mediation in production of hormones, especially of steroid hormones and in the promotion of immune function with its antioxidant activities.
Dietary increase in boron increases its concentration in human body tissues, as well as blood plasma. Diets rich in fruits, vegetables, nuts and legumes fulfill the dietary requirements of this nutrient.
The richness of boron in the plants is directly depends upon the availability of this element in the water and the soil wherein they are grown. Treatment of B deficiency is by consuming food rich in this nutrient as well as taking its supplements.
Boron rich foods
Several fruits, including apples, grapes, pears, plums, dates and kiwis are rich sources of this nutrient. Among the vegetables, beans, tomato, onions, lentils, leafy vegetables, carrots and chickpeas are rich in this element. Seeds, soybeans and nuts are also good sources. As its requirement has not yet been quantified, there is no Recommended Dietary Allowance (RDA).
Boron deficiency causes
In normal situations boron deficiency does not occur in humans, as most of the dietary sources are rich in this nutrient. People dependent on food produced from soils poor in the element may develop symptoms of low levels in the plasma. The deficiency symptoms may develop in humans in the certain situations. Some of causative situations are:
acute dietary insufficiency,
acute severe malnutrition,
persistent vomiting,
severe diarrhoea,
disturbed calcium-magnesium balance,
eating disorders (anorexia nervosa and bulimia),
malabsorption disorders and
renal disease.
Boron deficiency symptoms in humans
The symptoms and consequences of low levels of boron in humans are still being researched. The deficiency symptoms of this element can manifest as abnormal metabolism of calcium and magnesium. Hyperthyroidism is another possible symptom of insufficiency of this nutrient in humans. The imbalances in the steroid hormones like testosterone or estrogen may be a symptom of low serum levels of this nutrient.
The loss calcium and/or magnesium from the bones, osteoporosis and arthritis are well documented symptoms of low serum levels of this nutrient in animals and human beings. The decline in function of the brain and the psychological consequences are well known symptoms of boron insufficiency in humans.
Boron and bones
Boron is found to regulate the utilization of calcium by the bones in humans. Working in unison with calcium, it strengthen the bones by increasing the osteoblast activity. It also increases the production of bone strengthening hormones, estrogen and testosterone, and minimizes the risks of osteoporosis and arthritis. B reduces the need for hormone replacement therapy in postmenopausal women.
Supplementation with boron has been found to show significant improvement in arthritis and promote calcium integration into the cartilage and bone in humans. Sufficient B in the human system stems the old-age related loss of bone mass and weakening of bones. The antioxidant and anti inflammatory properties brings great relief to persons suffering from symptoms of rheumatoid arthritis.
Brain and psychological function
Low boron plasma levels in humans are observed to cause decreased brain electrical activity and resulted in poor cognitive and psychomotor function, reduced eye-hand coordination, poor dexterity, attention deficit and short and long term memory loss.
Penland JG et al. in their study 'The importance of boron nutrition for brain and psychological function (Biol Trace Elem Res. 1998 Winter;66(1-3):299-317)', supported "the hypothesis that B nutriture is important for brain and psychological function in humans."
Nielsen FH in the research study 'Is boron nutritionally relevant? (Nutr Rev. 2008 Apr;66(4):183-91.)' concluded that realistic low B intakes result in impaired bone health, brain function, and immune response in higher animals, including humans.
Boron and estrogen
Boron deprivation in humans had been reported to elevate urinary excretion of calcium and magnesium in postmenopausal women. Plasma concentrations of 17fl-estradiol and ionized calcium were depressed by a low boron diet. The conditions and symptoms that might be made worse by exposure to estrogen in humans (such as breast cancer, uterine cancer, ovarian cancer), get exasperated by B supplementation.
Boron and testosterone
Boron supplementation can increase the level of free plasma testosterone in humans. Naghii MR et al. in their study 'Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokines (J Trace Elem Med Biol. 2011 Jan;25(1):54-8.)', reported that after its intake, "the mean plasma free testosterone increased and the mean plasma estradiol decreased significantly."
The first human study report, showed that supplementation with boron resulted in a significant increase in its plasma concentration and subsequent increase in level of free testosterone in blood. Hence, boron deficiency in humans may lead to reduced free plasma testosterone levels with the consequent symptoms.
References:
1.Naghii MR, Mofid M, Asgari AR, Hedayati M, Daneshpour MS. Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokines. J Trace Elem Med Biol. 2011 Jan;25(1):54-8.
2.Sutherland B, Strong P, King JC. Determining human dietary requirements for boron. Biol Trace Elem Res. 1998 Winter;66(1-3):193-204.
3.Penland JG. The importance of boron nutrition for brain and psychological function. Biol Trace Elem Res. 1998 Winter;66(1-3):299-317.
Home › Mineral deficiency › Phosphorus › Phosphorus deficiency diseases. What is phosphorus?
Phosphorus (P) is an essential macronutrient and intracellular anion, required for the cellular processes of growth, maintenance and repair.
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Phosphorus deficiency disease (hypophosphatemia) is a condition wherein serum phosphorus (phosphate) levels drops below 2.5 mg/dL (0.8 mmol/L). Severe phosphorus deficiency can manifest as widespread organ dysfunction. Phosphorus deficiency diseases have multifactorial aetiologies and may present multiple causes in the same patient.
Phosphorus deficiency is primarily caused by inadequate intake, increased excretion or by shift from extracellular to intracellular space. Certain hereditary diseases, blood cancers, hepatic failure, presence of certain tumors, antacid abuse, alcoholism and certain medications can also promote hypophosphatemia. Severe Phosphorus deficiency disease can result in multiorgan dysfunction and death.
Hypophosphatemia is treated by oral or intravenous phosphate replacement therapy.
Phosphorus deficiency signs and symptoms
Common signs of phosphorus deficiency include general weakness, anxiety, lack of appetite and body pains. The major symptoms are, low cardiac output, respiratory depression, fragile bones, stiff joints, mental status changes and double vision. Acute hypophosphatemia (less than 1 mg/dL) can lead to damage of skeletal muscle tissue, white cell dysfunction, the abnormal breakdown of red blood cells, delirium and coma, which may culminate in death. In children there is decreased growth rate, poor bone and tooth development and their malformation.
Phosphorus food sources
Nutritional deficiency of phosphorus does not normally occurs. All protein-rich foods are good source of phosphorus. These include, milk and dairy products, meat products, poultry products, eggs, soya products, seeds, nuts, legumes, carbonated cola beverages and whole grains.
Serum phosphorus as phosphate normally ranges from 2.5 to 4.5 mg/dL in adults. The Food & Nutrition Board of the Institute of Medicine, has set the daily Adequate Intake (AI) of phosphorus for adults as 700 mg per day. Considering the harmful effects of too much phosphorus, a Tolerable Upper Intake Level (UL) per day is set at 4 grams.
Phosphorus functions in the human body
Next to calcium, phosphorus is the most abundant mineral in the human body. Along with calcium, phosphorus is required for building strong bones and teeth. Nearly 85% of P in the body is found in the bone and teeth. The rest is found in the cells and tissues and extracellular fluids.
The main component of bone and tooth enamel is hydroxyapatite, with the formula Ca5(PO4)3(OH) formed from calcium and phosphorus.
Adenosine triphosphate (ATP) is a nucleoside triphosphate. Phosphorus is an essential component of ATP and it transports chemical energy within cells for metabolism.
P is needed for the metabolism of carbohydrates and fats to produce energy.
It has a important role in the synthesis of protein, amino acids and nucleic acids.
It is a component of phospholipids which are structural components of cell membranes.
Phosphorus deficiency disease causes
Hypophosphatemia is primarily caused by inadequate intake, increased excretion or by shift from extracellular to intracellular space.
Inadequate intake and malnutrition
Severe acute malnutrition and protein energy malnutrition can lead to very low serum levels of this mineral. Other related causes are:
Malabsorption due to gastrointestinal injury,
bariatric surgery,
alcohol induced impaired phosphate absorption,
alcoholism related malnutrition,
alcohol withdrawal related respiratory alkalosis,
excessive intake of antacids,
lack of vitamin D and
chronic use of phosphate binders such as sucralfate and aluminum-containing antacids.
Increased excretion
Anticonvulsants like phenobarbital and carbamazepine may increase levels of alkaline phosphatase and remove phosphate from the body.
Corticosteroids may increase phosphorus excretion in the urine.
The treatment of diabetic ketoacidosis with high doses of insulin and IV fluids may lower serum levels of phosphates by increased cell uptake and also renal excretion.
The use of loop diuretics like acetazolamide and bisphosphonates can increase the loss of phosphorus in renal excretion.
Oncogenic osteomalacia, characterized by acquired hypophosphatemic rickets and the hereditary forms of hypophosphatemic rickets may increase renal phosphate wasting. Mutation in the FGF23 gene and its overexpression causes the renal loss of phosphorus.
In hyperparathyroidism proximal renal tubule phosphate transport is inhibited leading to hypophosphatemia.
Phosphate may be lost from the gut due to chronic diarrhea and severe vomiting.
Shift from extracellular to intracellular space
Refeeding syndrome occurs as a result of restitution of nutrition to patients who are starved or severely malnourished. Refeeding increases the basal metabolic rate and with the increase in the nutrients, there is increased glycogen, fat and protein synthesis. As this process requires phosphorus and other electrolytes, there is drastic shift of these electrolytes from serum to intracellular space. The drop in serum phosphorus can lead to cardiac arrhythmias, confusion, coma, convulsions, cardiac failure and death.
Respiratory alkalosis is a higher than normal blood serum pH from low carbon dioxide levels in the plasma. Low carbon dioxide levels in the serum causes intracellular carbon dioxide to freely diffuse out of the cell. The drop in intracellular carbon dioxide levels and subsequent increase in cellular pH triggers glycolysis resulting in massive uptake of phosphate into the cells, especially muscle cells. This shift leads to very low serum phosphorus levels and the consequences.
The incidence of low phosphorus levels in high in hospitalized patients, those undergoing intensive care, those suffering from sepsis, chronic alcoholics, patients passing through major trauma, patients with chronic obstructive pulmonary disease and in patients with advanced kidney disease.
Phosphorus deficiency diseases
Chronic low levels of serum phosphorus can lead to osteoporosis, osteomalacia, increased susceptibility to infection, muscle weakness, muscle loss and muscle damage, respiratory difficulties and neurological impairments.
A healthy bone has a normal balance of calcium and phosphorus in required proportions. Having low levels of phosphorus can lead to loss of calcium from the bones. The loss results in the disease of porous bones, known as osteoporosis. The bone loses its mass and becomes weak and brittle.
Low levels of phosphorus, calcium and vitamin D causes osteomalacia. A disease of bones, making bones soft and prone to fractures, malformation and deformation.
Phosphorus deficiency disease is reported in patients with acute hepatic failure and those undergone partial hepatectomy for transplantation. Low phosphorus level is also observed in cases of hematopoietic cell transplantation. Kidney transplant recipients are also prone to develop hypophosphatemia.
Several genetic phosphate wasting diseases like X-linked hypophosphatemic rickets, vitamin D resistant rickets and autosomal dominant hypophosphatemic rickets may manifest in childhood. Hereditary hypophosphatemic rickets with hypercalciuria is a rare disease manifesting as hypophosphatemia and hypercalciuria. Vitamin D–resistant rickets is an autosomal recessive disease characterized by hypocalcemia, hypophosphatemia and hyperparathyroidism.
Phosphorus deficiency disease treatment
Phosphate deficiency can be corrected by oral or intravenous fluid replacement therapy. A typical regimen is 15 mg/kg oral phosphate, given in three to four divided doses to minimize gastric irritation. During IV administration care must be taken monitor phosphorus levels every two hours for effecting replacement.
References:
1.Sherman RA, Mehta O. Dietary phosphorus restriction in dialysis patients: potential impact of processed meat, poultry, and fish products as protein sources. Am J Kidney Dis. 2009;54(1):18-23.
2.Steven M. Brunelli, Stanley Goldfarb. Hypophosphatemia: Clinical Consequences and Management. JASN July 2007 vol. 18 no. 7 1999-2003.
3.Shuto E, Taketani Y, Tanaka R, Harada N, Isshiki M, Sato M, Nashiki K, Amo K, Yamamoto H, Higashi Y, Nakaya Y, Takeda E. Dietary phosphorus acutely impairs endothelial function. J Am Soc Nephrol. 2009;20(7):1504-12
Home › Mineral deficiency › Potassium › Potassium deficiency diseases. What is potassium?
Potassium is an essential nutrient and electrolyte required for maintaining fluid and electrolyte balance in the human body.
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Potassium deficiency disease (hypokalemia) is a condition wherein serum potassium (K+) concentration drops below 3.5 mmol/L. Severe deficiency of potassium in the plasma can be fatal.
Potassium deficiency diseases have multifactorial aetiologies and may present multiple causes in the same patient. Apart from poor intake, loss of the mineral through diarrhea, diuresis or vomiting are the primary causes for subnormal potassium levels. Some medications, treatments and genetic mutations are also causative factors for drop in serum K+ levels.
Though potassium homeostasis depends on potassium excretion by kidneys, the skeletal muscles, possessing a huge capacity for potassium exchange, play an important role in short-term potassium homeostasis. The common hypokalemia symptoms include muscle weakness and cramps.
Severe K+ depletion from serum can lead to serious arrhythmia, which may culminate in death. Hypokalemia is treated by oral or intravenous K+ electrolyte replacement therapy.
Potassium food sources
Several food source of both animal and plant origins have considerable amounts of potassium. Bananas, avocados, oranges, cantaloupe melons, peaches, baked potatoes, tomatoes, spinach, peas and nuts are good plant sources. Meat products and dairy products also have considerable amounts of potassium. The normal K+ serum level is 3.5-5.0 mmol/L. The recommended dietary allowance for adults is 4700 mg of potassium.
Functions of Potassium
Potassium (K+) is the major cation (positive ion) inside human cells whereas the sodium (Na+) is the major cation outside the cells. A difference in the cell membrane electric potential is caused by the concentration differences of these charged particles. The electric potential created by these ions causes the cell to generate an electrical discharge critical for body functions such as neurotransmission, muscle contraction, and heart beat.
Potassium deficiency disease causes
The causes of low potassium levels are:
insufficient dietary potassium intake,
eating disorders (anorexia nervosa and bulimia),
excessive sweating and dehydration,
persistent vomiting,
severe diarrhoea,
laxative abuse,
fluid loss due to burns,
low magnesium levels,
chronic kidney disease,
diabetic ketoacidosis,
oral glucose overload,
increase in plasma insulin,
increase in catecholamines levels,
abnormally high aldosterone levels,
rare hereditary defects of renal salt transporters,
renal loss of potassium due to diuretic therapy,
sudden shift of K+ from plasma to skeletal muscles pool,
treatment of asthma with injection or inhalation of a beta-adrenoceptor agonist,
use of certain antibiotics,
affliction by AIDS,
alcoholism and
bariatric surgery.
Potassium deficiency signs and symptoms
Mild deficiency may be asymptomatic or cause mild symptoms like, muscle weakness and pain, constipation, abdominal bloating, nausea or vomiting, tingling or numb sensation, fatigue and feeling of skipped heart beats or palpitations. A serious drop in serum K+ levels can cause cramp, abnormal heart rhythms (arrhythmia), spasms, fainting, psychosis, delirium, confusion, muscle damage, heart smooth muscle damage, reduced heartbeat, flaccid paralysis, hyporeflexia and cardiac arrest.
Potassium deficiency diagnosis
Diagnosis of low K+ serum levels by testing its blood plasma levels. The serum levels of the other electrolytes may also be checked due to their inter-relationship. The status of heart may be checked by an electrocardiogram (ECG) to understand the severity of cardiac involvement. Differential diagnosis may be done to rule out renal tubular acidosis, Cushing's syndrome, and hypocalcemia.
Potassium deficiency diseases
Hypokalemia, hypokalemic periodic paralysis and sudden cardiac death are some of the effects of low serum K+ levels. Low dietary intake, severe loss from the body as gastrointestinal loss, skin loss and urinary loss and certain genetic conditions contribute to these electrolyte anomalies.
Hypokalemia
Hypokalemia, also known as hypopotassemia, is inadequate potassium levels in the blood serum. 98% of the K+ is found inside the cells and the rest 2% is found in the extracellular fluids. The concentration gradient between intracellular and extracellular K+ is maintained principally by the Na+/K+ pump. The normal serum level is 3.5-5.0 mmol/L and the drop below 3.5 mmol/L is hypokalemia. Serum levels falling below 2.5 mmol/L is severe hypokalemia and a serious situation.
Hypokalemic periodic paralysis
Hypokalemic periodic paralysis is a rare, autosomal dominant genetic disease with disturbed function of ion channel subunits or the proteins that regulate them. The patients have mutations in SCN4A or CACNA1S genes. The patient suffers from fall in serum potassium levels and associated muscle weakness or paralysis. In patients with this genetic mutation, strenuous exercise, high carbohydrate intake, high sodium intake, sudden changes in temperature, noise and flashing lights can induce an attack. Oral potassium supplements may relieve the attack and maintain muscle strength and function.
Sudden cardiac death
Sudden cardiac death is death from heart disease within one hour. Electrolyte disturbance, especially disturbed potassium homeostasis, is one among the several triggers promoting arrhythmia (irregular heartbeat), which may lead to death. Patients with cardiovascular diseases such as hypertension, coronary artery disease, heart failure and arrhythmia while being treated with diuretics, beta-adrenoceptor agonists or insulin are at risk of severe hypokalemia or transient reductions in plasma potassium concentration. Keld Kjeldsen concluded in the study 'Hypokalemia and sudden cardiac death' that,
"the more at risk of fatal arrhythmia and sudden cardiac death a patient is, the more attention should be given to the potassium homeostasis."
Potassium deficiency disease treatment
Considering the severity of symptoms and the level of drop in K+ in serum, the treatment option is selected. Those with mild or moderately low K+ levels (2.5-3.5 mmol/L) are treated with oral replacement. Those with cardiac arrhythmias and other heart ailments with significantly low K+ serum levels (less than 2.5 mmol/L) may require hospital care and IV administration.
The intravenous potassium replacement is done very slowly to stall cardiac problems and the procedure may take several hours. After restoring the K+ serum levels, the causative factor may have to be treated to avoid recurrence of the potassium deficiency disease.
References:
1.Ali Ahmed, Faiez Zannad, Thomas E Love, Jose Tallaj, Mihai Gheorghiade, Olaniyi James Ekundayo, Bertram Pitt. A propensity matched study of the association of low serum potassium levels and mortality in chronic heart failure. Eur Heart J. 2007 Jun; 28(11): 1334–1343.
2.Keld Kjeldsen. Hypokalemia and sudden cardiac death. Exp Clin Cardiol. 2010 Winter; 15(4): e96–e99.
