Showing posts with label diseases. Show all posts
Showing posts with label diseases. Show all posts

Copper deficiency symptoms - Copper deficiency diseases

   ›      ›      ›   Copper deficiency symptoms and diseases.
What is copper?
Copper (Cu) is an essential trace mineral and an important cofactor in several enzymatic and metabolic processes.
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Copper deficiency causes myelodysplastic syndrome (myelodysplasia) and neurologic degeneration. Cu insufficiency symptoms include anemia, neutropenia, myelopathy and peripheral neuropathy. Copper supplementation in patients with acquired copper deficiency rapidly reverses myelodysplasia and also arrests further neurologic deterioration.

Copper function and health benefits

Sources of copper in foods

Seafood such as shellfish and shrimp are good dietary sources of Cu. Organ meat including liver, heart and kidney are good Cu containing foods. Whole grains, legumes, nuts, mushrooms, dark green leafy vegetables, coconuts, papaya and apples are good sources of this nutrient.

Copper absorption and excretion

Cu is absorbed from the stomach and duodenum in humans. The absorption range varies from !5% to 90% depending upon the composition of the diet and form of Cu. The presence of animal proteins, citrates and phosphates in the diet enhances absorption. Elevated levels of dietary phytates, indigestible fiber, Vitamin C, simple sugars, zinc, cadmium and iron may inhibit copper absorption. The absorbed Cu is bound to albumin, glutathione and amino acids and is carried to liver. It is incorporated into copper-proteins and released into the blood. Excess Cu is excreted into the bile, a major pathway for the excretion of this trace mineral.
Image of copper rich foods
Picture of copper rich foods

Causes of copper deficiency

Cu is required by the human body in traces and several food sources contain fairly good levels of this nutrient. Hence normally dietary inadequacy of this mineral does not arise. Ingestion of excess zinc interferes with Cu absorption and utilization by the body. Acute chronic malnutrition, malabsorption, malabsorption diseases and protein energy malnutrition are causes for developing low Cu serum levels with devastating neurological symptoms.

Acquired copper deficiency

In those under prolonged parenteral nutrition and in those who have undergone bariatric surgical procedures or gastric bypass surgery, symptoms of insufficiency of Cu manifest. The symptoms manifest as myelodysplasia and neurologic deterioration when Cu is not supplemented.

B.P. Goodmana et al. reported a case of myeloneuropathy in a 53-year-old woman. She also suffered from anemia. Serum copper and ceruloplasmin levels were found to be markedly decreased. The patient did not have a history of gastric bypass surgery, malnutrition or excess zinc ingestion. However the patient had hyperzincemia. The researchers hypothesized that copper deficiency in such patients is likely due to a luminal copper transport or trafficking defect. It is possibly a case of copper binding to metallothionein (zinc stimulated) in intestinal enterocytes and subsequent loss into the intestinal lumen.

Inherited copper deficiency

Menkes disease is a disorder of copper malabsorption, which develops in infants, manifesting with neurologic and systemic symptoms. Menkes syndrome is an X-linked inherited disorder. It is characterized by sparse, kinky hair, low body weight and failure to thrive. Children with Menkes disease develop symptoms during infancy and do not live past three years of age. It is caused by mutations in the ATP7A gene. These mutations result in poor regulation of Cu levels in the body. The activity of several cuproenzymes gets reduced affecting the structure and function of organ systems.

Occipital horn syndrome is a X-linked inherited form of cutis laxa. Occipital horn syndrome is also caused by mutations in the ATP7A gene. These mutations result in poor regulation of copper levels in the body. This is considered milder form of Menkes syndrome. The symptoms are, sagging and inelastic skin, droopy appearance, extremely wrinkled skin, coarse hair, wedge-shaped calcium deposits in the occipital bone at the base of the skull and loose joints.

Symptoms of copper deficiency

The symptoms of copper inadequacy manifest on several organs, including skin and skin appendages, skeletal and soft muscles, bone and connective tissues, cardiovascular system, respiratory system and nervous system. Some of the connected symptoms and manifestations are:
  • fatigue,
  • limb numbness,
  • skin sores,
  • hair loss,
  • dermatitis,
  • proximal weakness,
  • anemia,
  • paleness,
  • leucopenia,
  • edema,
  • oxidative damages,
  • unsteady gait,
  • poor nerve conductivity,
  • absence of vibration sense,
  • myelopathy,
  • myeloneuropathy,
  • severe proprioceptive deficiency,
  • profound sensory ataxia,
  • respiratory failure,
  • bilateral optic neuropathy,
  • bone and connective tissue abnormalities and
  • cardiovascular diseases.

Diagnosis of copper deficiency

Decrease in serum copper and ceruloplasmin levels indicates the condition. A delayed diagnosis can lead to irreversible neurological disability and symptoms. The neurological symptoms may be present without the hematologic manifestations.

Copper deficiency diseases

Low serum levels of Cu can lead to several disease conditions with hematological and neurological manifestations.

Hematological manifestations

Hematological diseases such as myelodysplasia (ineffective production of all blood cells), anemia (decrease in the amount of red blood cells), leukopenia (low white blood cell count), neutropenia (low count of neutrophils) and thrombocytopenia (low blood platelets) are caused when there is deficiency of copper in the body system. All these disease symptoms totally resolve on Cu supplementation therapy.

Neurological manifestations

Neurological diseases such as myelopathy, peripheral neuropathy, and optic neuropathy with devastating symptoms and consequences are caused due to deficiency of copper in the blood serum.

Myelopathy
Myelopathy (disease of the spinal cord) linked to copper deficiency was first described by Schleper B, et al.(J Neurol. 2001 Aug; 248 (8): 705 - 6) in 2001. Patients with myelopathy have the typical symptom of severe tetraparesis (muscle weakness affecting all four limbs). The symptoms manifest as difficulty in walking caused by irregular muscle coordination due to degenerative damage of the spinal cord.

Peripheral and optic neuropathy
Peripheral neuropathy is another common symptom of copper deficiency. The initial symptoms are painful paraesthesias (a sensation of tingling, tickling, pricking, or burning of skin). The condition may progress into diminished or abnormal upper and limb reflexes. The sensation to light touch, pin prick and vibration may be gradually lost. Proprioception may get markedly reduced leading to the risk of fall and injury. In some patients low levels of copper causes optic neuropathy and nerve fiber layer loss manifesting as gradual vision loss and color vision loss.

Treatment of copper deficiency

Insufficiency of Cu in the body is treated by parenteral and oral copper replacement to achieve normal serum Cu levels. The hematologic manifestations of low Cu levels and the associated symptoms are rapidly reversible after Copper supplementation therapy. However, the neurologic deterioration may, at best, stabilize and the patient may remain with debilitating neurological symptoms. In a few cases, improvement is observed in copper deficiency related sensory symptoms with Cu supplementation.
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References:
1.Prohaska JR. Impact of copper deficiency in humans. Ann N Y Acad Sci. 2014 May;1314:1-5. doi: 10.1111/nyas.12354.
2.Imataki O, Ohnishi H, Kitanaka A, Kubota Y, Ishida T, Tanaka T. Pancytopenia complicated with peripheral neuropathy due to copper deficiency: clinical diagnostic review. Intern Med. 2008;47(23):2063-5. Epub 2008 Dec 1.
3.B.P. Goodmana, B.W. Chongb, A.C. Patelb, G.P. Fletcherb, B.E. Smitha. Copper Deficiency Myeloneuropathy Resembling B12 Deficiency: Partial Resolution of MR Imaging Findings with Copper Supplementation. AJNR Am J Neuroradiol. 2006 Nov-Dec;27(10):2112-4.
4.Spain RI1, Leist TP, De Sousa EA. When metals compete: a case of copper-deficiency myeloneuropathy and anemia. Nat Clin Pract Neurol. 2009 Feb;5(2):106-11. doi: 10.1038/ncpneuro1008.
5.Yarandi SS, Griffith DP, Sharma R, Mohan A, Zhao VM, Ziegler TR. Optic neuropathy, myelopathy, anemia, and neutropenia caused by acquired copper deficiency after gastric bypass surgery. J Clin Gastroenterol. 2014 Nov-Dec;48(10):862-5. doi: 10.1097/MCG.0000000000000092.
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Cobalt deficiency symptoms - Cobalt deficiency diseases

   ›      ›      ›   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.

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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.
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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.
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Chromium deficiency symptoms - Chromium deficiency diseases

   ›      ›      ›   Chromium deficiency symptoms and diseases.
What is Chromium? Chromium (Cr), an essential trace nutrient, is a component of metalloenzymes. Chromium functions as a coenzyme in various metabolic reactions.
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Chromium deficiency had been observed in patients on total parenteral nutrition with symptoms like glucose intolerance, altered lipid metabolism, encephalopathy and peripheral neuropathy. Supplementing the parenteral nutrition solution with this trace nutrient is found to resolve these symptoms.

Chromium benefits and functions

Chromium food sources

Trivalent Cr is found in foods and is also available as dietary supplement. Chromium is available in fruits, vegetables (green beans and broccoli), nuts, egg yolk, whole grains, cereals, brewer's yeast and meat products. The Food & Nutrition Board of the Institute of Medicine, has set the daily Adequate Intake (AI) for chromium at 35 mcg/day for adult males (19 to 50 years) and 25 mcg/day for females. Pregnant and lactating women will require 30 mcg/day and 45 mcg/day respectively.

Chromium absorption and excretion

Much of the dietary Cr is excreted in the feces. Less than 0.4% to 2.5% of dietary Cr is absorbed by the in intestines. Cr is absorbed in the small intestines and its total body concentration regulates its absorption. The absorption of this trace element is also regulated by its intake and is inversely proportional. It is primarily transported by binding to transferrin and albumin. Most of the absorbed Cr is excreted rapidly in the urine.

Chromium deficiency causes

Reported cases of Cr deficiency are very rare.
  • Chromium deficiency is observed in patients on total parenteral nutrition.
  • Serum Cr level is high in newborns and declines with age.
  • THe Chromium concentrations in hair, sweat, and urine are found to decrease significantly with age.
  • In old age there is increase in urinary excretion of this trace nutrient.
  • As dietary Cr and iron compete for the common binding sites, excess intake of iron interferes with Cr absorption.
  • In cases of severe acute malnutrition and malabsorption disorders, Cr levels may decrease below the optimum levels.

Chromium deficiency symptoms

The foremost symptom of low Cr levels is impaired glucose tolerance. It is a pre-diabetic state of hyperglycemia and is associated with symptoms of insulin resistance. Glucose intolerance may progress into type 2 diabetes mellitus.

Patients receiving total parenteral nutrition were found develop symptoms of peripheral neuropathy. The infusion of chromium resulted in clinical remission of symptoms.

Another symptom of low Cr levels is weight loss. In the absence of sufficient Cr and glucose tolerance, apart from urinary loss of sugar, the body is not able to use the sugar leading symptoms like constant hunger and continuous weight loss. Cr supplementation corrects the unnatural weight loss.

Extreme fatigue is a symptom of Cr insufficiency. As the body is not able to properly utilize sugar for energy production severe fatigue and extreme weakness is experienced.

Chromium deficiency treatment

The inadequate levels of Cr can be corrected by taking food products rich in this nutrient. Cr supplements are also available. In patients on TPN, Cr supplement is added to IV fluids.
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References:
1.Freund H, Atamian S, Fischer JE. Chromium deficiency during total parenteral nutrition. JAMA. 1979 Feb 2;241(5):496-8.
2.Cefalu WT, Hu FB. Role of chromium in human health and in diabetes. Diabetes Care. 2004 Nov;27(11):2741-51.
3.Balk EM, Tatsioni A, Lichtenstein AH, Lau J, Pittas AG. Effect of chromium supplementation on glucose metabolism and lipids: a systematic review of randomized controlled trials. Diabetes Care. 2007 Aug;30(8):2154-63.
4.Moukarzel A. Chromium in parenteral nutrition: too little or too much? Gastroenterology. 2009 Nov;137(5 Suppl):S18-28.
5.Suksomboon N1, Poolsup N, Yuwanakorn A. Systematic review and meta-analysis of the efficacy and safety of chromium supplementation in diabetes. J Clin Pharm Ther. 2014 Jun;39(3):292-306.
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Chloride deficiency symptoms - Low chloride levels in blood serum

   ›      ›   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.
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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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References on low levels of Cl- ions in blood serum:
1.Grossman H, Duggan E, McCamman S, Welchert E, Hellerstein S. The dietary chloride deficiency syndrome. Pediatrics. 1980 Sep;66(3):366-74.
2.Chipperfield AR, Harper AA. Chloride in smooth muscle. Prog Biophys Mol Biol. 2000;74(3-5):175-221.
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Boron deficiency in humans - Boron deficiency symptoms

   ›      ›      ›   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.
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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.
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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.
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Phosphorus deficiency diseases

   ›      ›      ›   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.
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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 , 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 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.
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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
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