Showing posts with label disease. Show all posts
Showing posts with label disease. Show all posts

Magnesium and chronic kidney disease

   ›      ›   Magnesium and kidney disease.
Magnesium homeostasis is brought about mainly by kidneys and intestines. To a moderate extent bones also contribute to magnesium balance.
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The renal reabsorption and excretion of magnesium is highly adaptable. The kidneys can eliminate excess of magnesium in the blood by increased excretion. In chronic kidney disease (CKD), with the decline of renal function the ability to regulate magnesium deteriorates.

In the initial and moderate stages of chronic kidney disease the fractional excretion of magnesium is increased to maintain its homeostasis. The increased excretion compensates for the decline in glomerular filtration rate. As the CKD progresses the increased excretion is inadequate to compensate the steadily increasing serum magnesium levels. With the creatinine clearance falling below 30 mL/min, the symptoms of hypermagnesemia set in.

Chronic kidney disease is the progressive deterioration of renal function over a period of several months. The known contributing factors of CKD are, high blood pressure, diabetes mellitus, glomerulonephritis and familial predisposition.
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The progression of CKD is categorized into five stages with relation to the decline in creatinine clearance. Stage 1 is the initial stage with few symptoms, whereas stage 5 is the end stage of CKD requiring dialysis or kidney transplant.

Initial and moderate CKD may be asymptomatic. The CKD is diagnosed by measuring creatinine clearance and serum creatine levels. High level of serum creatinine indicates decline in glomerular filtration rate. As the CKD advances the creatinine clearance declines and serum creatinine, magnesium (Mg2+), potassium (K+) and phosphate levels increase. Urinalysis will reveal red blood cells and proteins in the urine.

The increased P+, phosphate and Mg2+ and the resultant hyperkalemia, hyperphosphatemia and hypermagnesemia lead to many cascading effects causing diseases like hypocalcemia, secondary hyperparathyroidism, renal osteodystrophy, vascular calcification, metabolic acidosis, iron deficiency anemia, impaired cardiac function and atherosclerosis. The end stage chronic kidney disease, apart from causing excess Mg2+ related symptoms, causes fluid retention in the body. In certain studies, it was found that low serum levels of magnesium had lead to decline in the kidney function.
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References:
1.http://ods.od.nih.gov/factsheets/ Magnesium-HealthProfessional
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Current topic in nutritional deficiency: Magnesium and kidney disease.

Porous bones - Osteoporosis definition - What is osteoporosis?

Feb 2014  What is osteoporosis - osteoporosis definition - porous bones
What is osteoporosis?
Osteoporosis is a disease of the bones. The word osteoporosis literally means 'porous bones' and is derived from the Greek words 'ostoun' meaning bone and 'poros' meaning pore.
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It is an age-related disorder associated with progressive loss of bone mass and density. There is gradual decrease in the mineral density, deterioration of the structure into porous state and altering of the protein components in the skeletal system.

The osteoporosis disease is classified into primary type 1, primary type 2, and secondary type. Postmenopausal occurrences in women are referred as primary type 1. Primary type 2 occurs in men and women after 75 years of age. The secondary type can arise at any age and in any gender. Several predisposing factors can give rise to porous skeletal system. The consequence of all these forms is the increased risk of porous fractures which may be debilitating.

The bone density peaks by the age of 30 years and then there is a gradual loss throughout our lives. High bone density at the age of thirty years means less likelihood of developing the porous disease. Hence the density has to be built right from the childhood by taking balanced diet rich in calcium, phosphorus and vitamin D. Exercises, especially weight-bearing exercises will help in increasing the density.

Malnutrition, estrogen deficiency in women, decrease in testosterone levels in men, consumption of alcohol, genetic predisposition, tobacco smoking and sedentary lifestyle are some of the predisposing factors that can cause osteoporosis disease. The signs and symptoms of osteoporosis disease may not be very apparent in many patients. There may dull chronic pain in the lower back while the bone is becoming porous. The diagnosis of osteoporosis is by x-rays and bone density tests.
Elderly woman with osteoporosis
elderly women affected by osteoporosis
Osteoporosis treatment and management is by changing the lifestyle. The risk of porous fractures due to osteoporosis disease can be reversed and reduced by taking diet rich in calcium and vitamin D, exercising regularly and taking precautions to prevent falls.

Web definitions

1.The wordnetweb.princeton.edu defines as "abnormal loss of bony tissue resulting in fragile porous bones attributable to a lack of calcium; most common in postmenopausal women."

2.The merriam-webster.com defines as "medical : a condition in which the bones become weak and break easily."

3. The medical-dictionary.thefreedictionary.com defines as "The word osteoporosis literally means "porous bones." It occurs when bones lose an excessive amount of their protein and mineral content, particularly calcium. Over time, bone mass, and therefore bone strength, is decreased. As a result, they become fragile and break easily. Even a sneeze or a sudden movement may be enough to break a bone in someone with severe osteoporosis."


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Image source: http://en.wikipedia.org/wiki/File:OsteoCutout.png
Image author: James Heilman, MD | License: CC BY-SA 3.0
Current topic in nutritional deficiency diseases:
What is osteoporosis disease - definition - porous bones.

Zinc immune system function - Disease resistance in human body

Jan 2014  Zinc immune system function and disease resistance in human body
Zinc, an essential trace mineral, exerts its ubiquitous effects on the function of the immune system in human body and modulates its disease resistance.
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The basic cellular functions of Zinc in human body are in gene expression, deoxyribonucleic acid (DNA) replication, ribonucleic acid (RNA) transcription, cell membranes stability, and cell activation, division, proliferation and apoptosis.

Zinc and disease resistance in human body

  Many research studies have documented that zinc has a pivotal role in the function in immune system of human body. It has been found to increase the infection resistance in human body. Its deficiency has been associated with recurrent episodes of diarrhea in children. Administration of zinc lozenges has been found to decrease the severity and duration of common cold. In many incidences of infections, lower plasma concentrations of this trace mineral have been recorded.

However it is to be noted that there is a delicate zinc mediated regulation of the function of immune system in human body and any increased or decreased plasma levels of the trace mineral can disturb the function of the system. Reduction in taste acuity, growth retardation, retardation of reproductive growth, skin diseases, immune depression and slowed healing of wound are some of the clinical symptoms of marginally low plasma levels (<60 mcg/dL) of zinc on the human body systems. Very low plasma levels (<30 mcg/dL) are characterized by mental impairment, diseases, severe immune depression and alopecia.

Excess zinc and immune depression

On the negative side, excess supplementation of zinc is associated with disease resistance depression and a myriad of health issues and diseases. As the pathogens also require this mineral for their cellular functions, excess of this trace mineral may in fact increase the progression of diseases as found in some AID patients. However multifarious factors affect the availability of zinc for both the host human body as well as the pathogen and this aspect of immune system requires further research input.

Zinc and innate immune system

The nonspecific protective mechanism is affected by zinc deficiency with the effects like damages to epidermis, damages to pulmonary tract and gastrointestinal tract lining. As a consequence, diseases of skin, gastrointestinal and respiratory systems crop up. The functions of neutrophils or polymorphonuclear leukocytes (PMNs) are affected. The function of Natural killer cells and the complementary activities get compromised.

Zinc and specific immunity

Zinc deficiency causes reduction in the number of T and B lymphocytes present in the spleen tissue as well as in the peripheral blood. T and B lymphocytes function is depressed and their presence is reduced. In animal studies gestational deficiency of this trace mineral has been found to have epigenetic effects by which some immunodeficiency get passed on even to third generation offspring.
Hematopoiesis in human body
immune system development


Thymus is the organ for T lymphocyte development and zinc deficiency leads to thymic involution and thymic atrophy, causing reduction of T lymphocytes. With the reduction of T lymphocytes, many protective mechanisms in human body like antigen recognition, cell proliferation, cytolysis, delayed hypersensitivity and cytotoxic activities are suppressed. Bone marrow is the center for the development of B lymphocytes. In case of deficiency the development of B lymphocytes is blocked and results in compromise of production of antibody molecules, especially immunoglobulin G in human body. The function of macrophage in phagocytosis of disease microbes is deregulated.

The intra and extracellular reactions of zinc in human body clearly demonstrate its central role in defence from diseases and priming up immune system.
Image credit: Wikipedia

Can selenium prevent heart diseases?

Home > Selenium and heart diseases

Selenium being an antioxidant, its action in preventing heart disease is being investigated.

Most of the incidences of heart diseases are associated with lower intake of antioxidants.
Selenium is an essential component of the selenoproteins forming antioxidant enzymes like glutathione peroxidase (GPX).
During the process of metabolism in our body, free radicals are formed as by-products which have devastating effects on the body tissues, oxidizing the LDL (low density lipoproteins) and leading to plaque formation on the walls of the blood vessels.
The antioxidants reduce the free radicals and protect the tissues from their damage.
Well documented evidence is available on the preventive effects of vitamin E and vitamin C on the cardiac problems.
In the case of selenium conflicting results have been obtained towards its use for prevention of cardiac problems.

Selenium deficiency causes Keshan disease

It is well known that chronic deficiency of Selenium in diet can lead to Keshan disease, a potentially fatal form of congestive cardiomyopathy.
This condition is characterized by cardiac enlargement leading to pulmonary edema and cardiac failure.
There is a great possibility of the sub clinical form of this existing in larger population whose diet is insufficient in Se.
This section of the population which may have minor cardiac ailments is bound to benefit a lot if their low blood selenium levels are checked and proper supplementation is given.

Usefulness of selenium in heart diseases

In a meta-analysis performed on studies conducted from 1966 to 2005 it was found that the risk of cardiovascular ailments was inversely linked to the mineral concentration in the blood.
One of the risk factor for coronary problems is high plasma levels of homo-cysteine.
In a study conducted by University of Oveido Selenium has been found to reduce the homocysteine levels in blood.
Ongoing research has to prove conclusively that low blood levels of selenium increase the risk of cardiac problems.
Some investigations found that selenium does not give protection against cardiac problems.
State University of New York Analyzed the results of the Nutritional Prevention of Cancer Trial (NPC Trial) conducted in 90s.
It was found that in participants taking  supplement at 200 mcg/per day for 7½ years the incidence rate of death, stroke and heart attack had not changed and that the mineral did not prevent cardiac ailments.

Selenium supplements may increase the risk of heart problems?

In a study conducted by researchers from University of Warwick, the link between the levels of Selenium and lipids in the blood was investigated.
The study was conducted on more than 1000 participants in the age group 19-64 years.
It was found that total cholesterol levels increased by 8% with a increase of 10% in LDL cholesterol in participants having more than 1.20 mol/L of the mineral in their blood.
The study concluded that taking Se supplements without requirement may boost the cholesterol levels leading to increase in risk of cardiac problems.
Further research is required for conclusively arriving at the benefit, if any, of selenium supplements for preventing heart problems.
Related topics on selenium health benefits:
Health benefits
Selenomethionine
Antioxidant functions.
HIV/AIDS.
For prostate cancer.
Selenium overdose and side effects
Thyroid hormones.
SELECT for cancer prevention.
Treatment of Keshan disease.
Supplements and dosage.
Selenium for heart disease (current topic).

Keshan disease - Selenium for treatment of Keshan disease

Selenium and Keshan disease

Keshan disease is a deficiency condition caused by the dietary deficiency of selenium.

Keshan disease is a disease of heart muscle (congestive cardiomyopathy) which is potentially fatal.
It was first noted in the Keshan province in Heilongjiang, China.
It was later found to be prevalent in a wide belt extending from Southwest to Northeast China.
In 1960s this ailment had claimed thousands of lives.
The soils of these regions are found to be deficient in selenium.
Apart from China selenium soil deficiency is found to be prevalent in parts of Finland, Russia and New Zealand.
This ailment often found to afflict children and young women.

Causes of Keshan disease

This ailment is primarily caused by the dietary deficiency of the essential trace mineral Se.
Some medical experts believe that coxsackievirus B3 may be partly responsible for the development of this condition.
It is believed that benign Coxsackie B3 viruses may mutate to cardiotoxic strains in condition of selenium deficiency.

Symptoms

Initially there may be symptoms like diarrhea, vomiting, fever and body pains.
The initial symptoms include heart inflammation, Arrhythmia, Cardiac insufficiency and enlargement accompanied by loss of heart muscle tissues.
Advanced stage is characterized by pulmonary edema and heart failure.

Diagnosis

If an individual is having persisting symptoms a visit to medical professional is necessary to rule out the possibility of having the ailment.
Echo cardiogram is used to check for structural and functional problems of heart.
Resting ECG and stress ECG are taken to further determine the condition of heart.
Myocardium of the affected person shows mycolysis and multifocal necrosis with fibrous replacement.
Blood sample is taken and investigated for the selenium levels.

Treatment

Treatment for this condition is by supplementation of Selenium in diet.
Many initial intervention studies showed the prophylactic effect of the inorganic sodium selenite.
If treated early the effects of this ailment can be reversed.
However damage to heart muscle cannot be reversed and the supplements can only stop further progress of the condition.
Smoking and alcohol must be totally avoided as they can worsen the condition of the heart.
Healthy balanced food rich in selenium must be consumed for early repair of the damaged tissues.
The patient must rest well and refrain from stressful activities so as to give the heart a chance to recover.
If necessary and if possible, surgery is performed to correct the heart condition.

Prevention of Keshan disease

Consuming food rich in selenium can ward off the occurrence of this health problem.
People living in regions deficient in soil Selenium must take supplements to protect themselves from occurrence of this condition.
The recommended dietary allowance for selenium is 55-60 mcg per day for an adult.
Pregnant women require 60 mcg of Selenium and lactating mothers require 70 mcg of selenium per day.
Inclusion of seafood, garlic, mushroom and Brazil nut (which is the richest source of selenium) in diet can help in preventing the onset.

Scurvy - Disease of vitamin C deficiency


Scurvy is a historically documented disease and was encountered in earlier days by sailors on long voyages foregoing fresh fruits and vegetables.
Scurvy is a disease caused by the insufficiency of vitamin C (ascorbic acid).
Though many animals can synthesize it in their body and are free from scurvy, unfortunately man has to depend on his food sources for vitamin C.
Health care and nutrition guidelines recommend a daily intake of 75 to 100mg of ascorbic acid (vitamin C).
Inadequate or irregular intake of ascorbic acid can lead to clinical manifestations of this disease in two to three months.
Initial symptoms of scurvy disease include lethargy, tiredness and malaise.
With chronic deficiency scurvy progresses and is characterised by spongy gums, bleeding gums, loosened teeth, bleeding beneath the skin, bleeding from the mucous membranes, extreme weakness, myalgia, anemia, pain in the bones, easy bruising and retarded wound healing, oedema, perifolicular hemorrhage and corkscrew hairs and depression.
Scurvy disease pictures: gingivitis hemorrhage in vitamin C deficiency
Scurvy disease pictures: Hemorrhage of gums caused by vitamin C deficiency (enlarge)
In its severity and in extreme stages scurvy disease is life threatening causing extreme edema, acute bleeding, neuropathy, jaundice, haemolysis, convulsions, fever and death. Scurvy disease pictures: cork screw hair condition brought about by vitamin C deficiency
Scurvy pictures - corkscrew hair condition caused by ascorbic acid deficiency (enlarge)
As ascorbic acid is lost over storage and heating present day food habits are to be monitored to check the possibility of deficiency of vitamin C.
A relationship appears to be present between alcoholism and vitamin C.
scurvy disease pictures
Scurvy pictures - bleeding behind the fingernails (enlarge)
When blood levels of alcohol are high, vitamin C appears to be excreted in urine in greater quantities causing deficiency.
This can be treated by supplementation of ascorbic acid in high doses till recovery.
For more information on vitamin C deficiency please visit my web site http://www.thedynamicnature.com.

Rachitis disease in children

Rachitis disease in children

Rachitis is the disorder of the bones in children leading to their weakening and softening due to deficiency of vitamin D and then calcium.

Rickets is believed to be the distortion of the word 'wrickken'(meaning 'twist') used in the old English dialect. The scientific name 'rachitis' is derived from Greek meaning 'inflammation of the spine'.
It is caused primarily due to deficiency of vitamin D (Cholecalciferol) and also calcium and phosphate.
Although the deficiency of vitamin D may occur in adults it is called osteomalacia. Mostly, the incidence of this disease is found in malnourished children with deficiency in sun exposure.
Calcium is an essential mineral for the formation of bones and its absorption in intestine is dependent upon the availability of vitamin D in the system.
With sufficient sun exposure all the required vitamin D can be synthesized by the skin.
In youngsters with poor exposure to sunlight, the synthesis of this nutrient is affected causing rachitis.
This in turn affects the absorption of calcium in the intestines and rachitis disease is caused.
Moreover Cholecalciferol controls the levels of like and phosphorus in the blood.
Deformities in the skeleton like pigeon chest, bowed legs and spinal and pelvic deformities are some of the signs of rachitis.
Breast-fed infants who are not exposed to sufficient sun light may develop the condition.
Infants of mothers who are not exposed to sunlight can also develop the disease.
Children who are lactose intolerant and are with darker skin are also predisposed to develop rachitis.
rachitis disease rickets children
Children are affected by rachitis (enlarge)(courtesy: Dr. Tom and Rosie Thacher)

Children in the age group of six months to two years are among the high risk groups for this disease as their bone growth is at a faster rate.
Vitamin D supplements are advised for breastfed infants above 2 months.
Any deficiency at this age and negligence can cause bowed legs and bent backs leading to permanent disability and affliction of rachitis.
Some of the symptoms are pain and tenderness in the bones, muscular pains and predisposition for bone fractures; dental deformities like delay in the formation of teeth and defects in their structure is also seen in rachitis affected.
Distorted skull formation and retarded growth are the other effects of the disease.
Blood tests of the affected children show low levels of serum calcium and serum phosphorus rachitis affected.
This deficiency of vitamin D caused rachitis can be corrected completely, if diagnosed early and treated.
Exposure to sun light, intake of food rich in all essential nutrients and minerals and intake of supplements when required can cure rachitis.
Sufficient intake of milk, milk products, vegetables, fish,egg and fish liver oils in addition to sunlight can prevent the disease in children.
Renal disorders and hereditary factors can also become the causative factors of rachitis disease in children.

Vitamin D deficiency causes rickets in children

Home > Vitamin D deficiency causes rickets

Deficiency of vitamin D or/and calcium and phosphorus are the causes of the nutritional disorders and rickets disease in children.

A number of factors including lack of sunlight exposure and nutritional vitamin D deficiency cause rickets. Certain metabolic disorders, digestive disorders and genetic factors can also lead to rickets.

Lack of sufficient exposure to sunlight (ultraviolet B light) causes rickets

Most of the vertebrate animals including man produce vitamin D in their skin photochemically, with the exception of cats, dogs and a few other animals.
The ultraviolet B light (UVB) from the sun reacts with 7-dehydrocholesterol in the stratum basale and stratum spinosum of the epidermis layer (upper layer of skin) and by a chemical process cholecalciferol is synthesized.
The melanin pigment deposits in the skin function as UVB filter and the dark-skinned people have to be exposed to, more sunlight than the light colored people to produce the same quantity of cholecalciferol.
Children and people who always live and work indoors and are rarely exposed to sunlight are high risk group for developing deficiency of vitamin D.
The intensity of sunlight decreases with higher latitudes and in children living there deficiency of cholecalciferol arises in winter especially if they are dark skinned.

Nutritional deficiency of calcium and phosphorus causes rickets

Calcium and phosphorus are very important for the formation and growth of bone tissue and bones. Any insufficiency of these minerals lead to bone deformities and rickets disease.

Maternal deficiency of cholecalciferol, calcium and phosphorus causes rickets in the newborns

The deficiency in pregnant women reduces the availability of these to the fetus.
Bone formation in the fetus may be affected and the density of the bones is reduced and results low birth weight.
Further if the shortfall is not cured by supplements, birth deformities occur in the newborn children.
Nursing mother's nutritional deficiency causes rickets disease in the infant.
The human milk has just sufficient quantities of cholecalciferol in a healthy woman.
If the lactating mother is not having sufficient reserves of it and is poorly nourished having little exposure to sunlight, the milk becomes poor in this nutrient.

Lactose intolerance and food habits causes rickets disease

Milk and milk products which are rich in calcium are not tolerated by some people and they have problem digesting them.
Unless they eat other sources of calcium they develop vitamin D deficiency.
Vegans who do not include milk and milk products are among the high risk groups to get vitamin D deficiency.

Malabsorption of fats from intestine causes rickets disease

Vitamin D is fat-soluble and requires dietary fat in the intestine for absorption.
In various conditions and ailments like Crohn's disease, cystic fibrosis and in certain liver disorders fat and vitamin D absorption from the intestine is affected and results in its deficiency.

Certain medication causes rickets disease

Phenobarbital and phenytoin are used for preventing and controlling epileptic seizures.
These drugs convert vitamin D into inactive compounds by increasing the hepatic metabolism. This leads to reduction in calcium absorption. Orlistat (weight-loss drug) and cholestyramine (cholesterol-lowering drug) reduces absorption of fat soluble vitamin D.
Corticosteroids like prednisone can affect cholecalciferol metabolism and decrease calcium absorption and result in rickets.

Hereditary predisposition for rickets disease

Vitamin D resistant rickets is hereditary. Here the rickets disease is inherited as a sex-linked genetic disorder. In this condition kidney is impaired from retaining phosphate.
Excessive use of sunscreen and spending more time in-doors causes this ailment.
Understanding the causes and proper preventive measures and treatment can resolve rickets disease.

Related topics:
Rickets disease overview
Symptoms
Diagnosis
Treatment
Prevention
Osteomalacia (in adults)
Current topic:
Vitamin D deficiency causes rickets

pellagra disease (niacin deficiency) - diagnosis, treatment and prevention

Diagnosis, treatment and prevention of pellagra disease

Diagnosis of pellagra disease (niacin deficiency) is very difficult, whereas its treatment and prevention are simple.

Diagnosis of pellagra

For diagnosis of pellagra, earlier we had to rely on the symptoms narrated by the patient, signs observed and the nutritional deficiency status and diet of the patient.
In the early stages fewer of the niacin deficiency signs may be present and it becomes very difficult for the diagnosis of pellagra.
It will be easier for diagnosis and confirmation of the presence of pellagra disease, if all the three "D" symptoms (dermatitis, diarrhea and dementia) are present.
Nowadays the diagnosis can be confirmed by the measurement of excretion of N-methylnicotinamide per day in urine and treatment can be started.
However the facilities may not be easily available for the analysis and diagnosis in the developing and underdeveloped countries to start pellagra treatment with niacin supplements to remove deficiency.
If the patient has some of the signs and symptoms of pellagra the following steps may help in treatment and prevention.
The first step in diagnosis, treatment and prevention is to find out whether the patient is coming from pellagra prevalent region with niacin deficiency.
Next step in diagnosis and prevention is to ascertain the patient's food habits and find out whether maize is his staple food.
Persons afflicted by pellagra disease generally appear weak, underweight and poorly nourished.
It has to be ascertained whether the patient has dermatitis, diarrhea or dementia and nervous impairment.
Therapeutic doses of nicotinamide may be given for a few days to investigate for improvement in the condition.
If the disease is pellagra there will be marked improvement and the diagnosis of the disease is complete and treatment can be started.
Low serum levels of niacin and tryptophan may also confirm the disease and treatment can be started.
Low levels of pyridone and N-methylnicotinamide in urine can be due to niacin deficiency confirming the diagnosis for pellagra.
If less than 1.5mg of these organic compounds are excreted in a day, diagnosis of severe niacin deficiency is confirmed and immediate treatment is required.
The presence of three "Ds" (dermatitis, diarrhea and dementia) confirms the diagnosis of pellagra disease.
Dermatitis in pellagra patients has a characteristic appearance.
The exposed regions of the skin to sunlight get inflamed and red in appearance initially with marked margin with the unexposed skin.
This is a clear cut diagnosis of pellagra.
The swelling of tongue and mouth and oral sores also help in the diagnosis.
The chronic diarrhea and bleeding from intestine also help in diagnosis and treatment.
Symptoms like diminished sensitivity to touch, irritability, and tremor help in diagnosis.

Treatment for pellagra disease

If the patient is fairly in the advanced stage of pellagra, hospitalisation is required for of acute niacin deficiency.
Patient with milder symptoms may undergo treatment at home for niacin deficiency.
Patients with dementia are preferably given treatment at hospital for prevention of complications with niacin deficiency.
Oral administration of nicotinamide or nicotinic acid helps in the reversal of symptoms of niacin deficiency.
The exact dosage will be recommended by physician considering the stage of the disease and the age and weight of the patients.
Persons who are comatose, uncooperative or with severe swelling and blocking of the mouth may be given injections of vitamin B3 to resolve niacin deficiency.
For patients with dementia and severe pain tranquilizers may be given.
Anti-inflammatory antibiotic creams must be applied to skin conditions till the niacin deficiency resolves.
During treatment, prevention to exposure to sunlight is very important.
There can be dramatic change and healing after a few days of treatment for niacin deficiency.
With the treatment dermatitis slowly disappears, the gastrointestinal inflammation goes and the patient will be able to eat.
The neurological disorders slowly disappear and the patient becomes normal.
As the pellagra afflicted person will be malnourished, he should be given easily digestible protein rich, well followed by multivitamin supplement.
Though the primary pellagra responds well to treatment the secondary pellagra disease is harder because of the causes for its occurrence.

Prevention of pellagra disease

In the maize eating population relying on maize only as staple food has to be discouraged and addition of other cereals has to be encouraged for prevention of pellagra disease, affecting populations as a whole.
An inducement and requirement to fortify milled maize flour with niacin must be emphasised and regulated for prevention of pellagra.
For the prevention of nutritional deficiency caused diseases, it is very important to have diversity in the food consumed.
Food from animal sources like milk, egg, meat and fish is rich in vitamin B complex and tryptophan and this resource is to be included in daily consumption for prevention of deficiency.
Niacin rich plant food like nuts especially groundnuts must be included in diet for prevention deficiency and pellagra.
Prisoners, refugees and famine affected may not have and protein rich food and they are to be given nicotinamide supplements for prevention of pellagra disease.
Education on nutrition must be emphasised to spread awareness among people for prevention of Pellagra disease.
Current topic:
Diagnosis of niacin deficiency and pellagra and its treatment and prevention.

Dr Joseph Goldberger - pellagra research contribution

Home > Dr Joseph Goldberger

One of the greatest research findings for the cause of the neglected humanity was by Dr Joseph Goldberger.

Dr Joseph Goldberger was born in Giralt, Hungary on July 16, 1874. He migrated along with his parents to United States in 1883 and settled in New York City. He earned his MD Degree in 1895 from the Bellevue Hospital Medical College (New York University School of Medicine).
Dr Joseph Goldberger after a stint of private practice at Wilkes-Barre, Pennsylvania, joined United States Marine Hospital Service (later PHS) as an Assistant Surgeon.
His first place of appointment was at the Port of New York and was assigned for the health inspection of immigrants.
Epidemiological skills of Dr Joseph Goldberger were sharpened when he worked on the control of yellow fever, dengue fever and typhus during 1902 - 1906.
In the year 1906 he married Marry against the wishes of the families.
During his studies on epidemics, Dr Joseph Goldberger contracted the diseases he studied like typhus and dengue fever.
In 1909 he published his research findings on Schamberg's disease connecting its origin to acarine mite.
Dr Joseph Goldberger was asked in 1914 to investigate on pellagra disease.
Working on the project he found that the inmates of prisons, orphanages and mental asylums were developing the ailment while the employees are not getting affected.
Dr Joseph Goldberger was sure that pellagra disease is not contagious and no germ is involved with it.
He also fed the affected children of orphanages and asylums with fresh food, meat and fresh vegetables.
There was dramatic recovery in their condition. Those of them who did not have the disease did not develop the disease.
Further he experimented with health volunteer prisoners and fed them only corn based food. Many of them developed pellagra rashes in about five months.
Joseph Goldberger
Dr Joseph Goldberger
Dr Joseph Goldberger to prove his point and to silence his detractors, injected blood of pellagra affected into his body and also on his assistant.
He also took swabs of nasal and throat secretions of the patients and rubbed onto his nose and throat.
Dr Joseph Goldberger collected scabs of pellagra disease rashes and swallowed them.
He did not contract the pellagra disease. Even after these demonstrations a section of the scientific community did not accept his theory that pellagra disease is due to nutritional deficiency.
Dr Joseph Goldberger contracted renal cell carcinoma and died on January 17, 1929. His ashes were sprinkled over the river Potomac.

Related interesting topics:
Pellagra disease
Causes
Symptoms
Diagnosis-Treatment
 Niacin flush

Current topic:
Dr Joseph Goldberger contribution to pellagra research.

Vitamin C - Heart disease

Home > Vitamin C and heart disease

Vitamin C as an antioxidant and contributor in collagen synthesis, has very crucial role in prevention and treatment of heart disease.

Clinical prevention of scurvy disease can be achieved with daily intake of about 100 gm of vitamin C.
But the nutritional requirement of ascorbic acid is much higher than this for warding off adverse health conditions, especially the ischemic heart disease.
subclinical form of vitamin C deficiency exists in many people leading to diseases like cardiac disease, strokes, diabetes etc.

Vitamin C - heart disease and arterial walls

As the heart pumps blood back to the body all the blood vessels experience pressure, especially arteries.
When the blood vessels are healthy, normal blood flow is maintained.
If the arteries are weak, constricted or have deposits in the wall, there is cardiac stress and diseases like hypertension, cardiovascular disease is caused.
Collagen is found in the artery wall and is necessary for the elasticity and tenor of the artery.
Ascorbic acid is necessary for collagen synthesis.
When there is deficiency of vitamin C, the artery walls harden and develop minute cracks and blood leaks into the surrounding tissues.
A focal point inflammatory, disease and infection is formed.
This leads to production of prostaglandin thromboxane.
In order to plug these leaking cracks platelets aggregate and lipoproteins are deposited.
The LDL cholesterol in the blood forms further deposits at this point and a plaque is formed.
This leads to narrowing of the blood vessels and to keep up circulation the heart has to pump harder.
Fresh cracks get formed due to pressure and a chain reaction starts leading to further narrowed vessels.
The consumption of ascorbic acid makes the endothelial lining of the artery wall healthy and elastic by proper and sufficient deposits of collagen.
Further ascorbic acid can prevent the plaque formation. Ascorbic acid inhibits the oxidative modification of LDL (low density lipoproteins) and prevents deposits.
Ascorbic acid hinders blood platelets aggregation and the formation of clot.
Ascorbic acid increases the fibrinolytic activity and the dissolution of plaques.
Ascorbic acid restores the characteristics of atherosclerotic arteries back to normalcy by dilation and restores proper blood supply curing cardiac disease.
It is vital for the healthy heart and for protection from cardiac conditions.

Related topics:
Ascorbic acid functions
Health benefits
Vitamin C and Liver
Kidney

Current topic:
Vitamin C and heart disease

Rickets disease - Treatment and cure

Home > Rickets disease - Treatment and cure

Rickets disease treatment and cure involves ultraviolet B light (sunlight) exposure, nutritious food containing vitamin D, calcium and phosphorus and cholecalciferol supplements.
Rickets disease treatment and cure can be complete if it is started early during the growing age of the child.
The skeletal deformities usually improve and may disappear.
If the treatment is delayed the deformities and the short stature may become permanent requiring surgical intervention.
Treatment is done to relieve the symptoms of rickets disease and eliminate the causes of the rickets.
Replacement of vitamin D, calcium and phosphorus will relieve most of the signs and cure rickets.

Rickets disease treatment and cure in infants

The lactating mother of the affected infant is immediately put on cholecalciferol and mineral supplements and if necessary given vitamin D injections for treatment and cure of rickets disease.
A diet rich in vitamin D, calcium and phosphorus is given to the mother.
She is encouraged to spend about 30 minutes in the sunlight.
The infant is also exposed to ultraviolet B light (sunlight).
Supplements are also given to the infant.

Rickets disease treatment and cure with good nutrition

Diet rich in calcium, phosphorus and cholecalciferol like fish, fortified milk, liver, fish liver oils given; eggs and fortified flour are included in daily menu for cure.

Rickets cure with sunlight

The affected child is encouraged to go out in the sun for about 30 minutes for the skin to produce vitamin D.
The affected children are encouraged to play in the sunlight for a short time.

Rickets treatment with supplements

Cholecalciferol supplements are given to boost its availability for calcium absorption from the intestine and its utilisation in the body.
Depending on the condition of the patient single dose of cholecalciferol is split into 5 oral doses and given. Alternatively cholecalciferol is given gradually for about 3 months till the symptoms are resolved.
The vitamin D is stored in the body and utilised slowly.
Intramuscular injections are also given nowadays to resolve rickets early and get total cure.

Treatment and cure for the rickets deformities

Braces and other orthopedic aids are used to help in the correction of deformities and gait in children.
If necessary corrective surgery is done to remove the deformity caused by rickets disease.

National Academy of Sciences (NAS) and American Academy of Pediatrics (AAP) recommendations for rickets disease prevention

National Academy of Sciences (NAS) and American Academy of Pediatrics (AAP) have recommended a supplement of 200 IU per day of vitamin D for all breastfed infants till they are weaned to at least 500 ml per day of fortified milk or fortified formula feed.
For those non breastfed infants who are ingesting less than 500 ml per day of fortified milk or fortified formula feed, again a vitamin D supplement of 200 IU per day is recommended.
Children and adolescents who do not get regular sunlight exposure, do not ingest at least 500 mL per day of vitamin D-fortified milk, or do not take a daily multivitamin supplement containing at least 200 IU of vitamin D are recommended to take 200 IU of vitamin D supplement daily.

Prognosis

The situation usually improves within 10 days from the start of the treatment for rickets disease and deformities may take longer time to correct.

Related topics:
Rickets disease
Causes
Symptoms
Diagnosis
Prevention
Osteomalacia (in adults)

Current topic:
Treatment and cure for rickets disease.

Rickets disease -Lack of vitamin D - Prevention

Lack of vitamin D and rickets disease prevention

Prevention of rickets disease involves sufficient exposure to sunlight (ultraviolet B light) and dietary intake of sufficient human growth hormone (HGH), calcium, phosphorus and vitamin D (Cholecalciferol).
Measures for prevention of rickets disease are to be started right during pregnancy.
Pregnant woman must have adequate intake of balanced diet with additional supplements of vitamin D and minerals and lack of these can affect the growing fetus.
Human milk is just sufficient in vitamin D depending on the nutritional status of the lactating mother.

As the growing infant has great demand for calcium and Cholecalciferol the nursing mother should not lack in exposure to sunlight.
The nursing mother should consume diet rich in calcium and Cholecalciferol and also take supplements if required for the warding off lack of vitamin D.
The infant who is solely dependent on mother's milk should be given sufficient exposure to sunlight daily for prevention of low levels of vitamin D and occurrence of this disease.

rachitis disease rickets children
Children are affected by rickets disease (enlarge)(courtesy: Dr. Tom and Rosie Thacher)
Further as the daily demand of nutrients increases many fold in infants, vitamin D and other supplements may be started early for prevention of rickets arising due lack of them.
Light skinned infants may require about twenty minutes of ultraviolet light exposure per day for protection from developing rickets.
Dark skinned infants require more exposure for warding off this vitamin D deficiency, as the skin pigment interferes in the Cholecalciferol synthesis by cutting off the light.

Vegans who do not consume even milk have low levels of both calcium and vitamin D (Cholecalciferol).
Vegans and their infants are highly prone to develop rickets disease; their nutritional status regarding both calcium and Calcitriol must be monitored. They must take vitamin D supplements as protection.

Premature infants and underweight infants have greater demand for vitamin D, calcium and phosphorus and may develop rickets, if they are insufficient in them.
People living in higher latitudes are at the risk of developing rickets especially in the winter months due to lack of sufficient sun exposure in short days .

Dark skinned children living in higher latitudes are highly prone to rickets and they must be supplemented with cholecalciferol as prevention.
For prevention of rickets disease people living in higher latitudes must take food rich in Calcitriol and also take supplements.

People suffering from gastrointestinal disorders and prolonged illness may lack vitamin D must take supplements  to ward off deficiency.
Renal disease cause lack of Calcitriol absorption and calcitriol supplements must be taken for
prevention of rickets.The deficiency can be checked. For prevention of rickets disease sufficient exposure to sunlight, taking food rich in vitamin D and taking supplements is necessary.

Current topic:
Prevention of rickets disease in children - Lack of vitamin D.

Pellagra disease - Symptoms - Signs

Pellagra disease - Symptoms and signs

Pellagra disease caused signs and symptoms manifest on skin, gastrointestinal system, mucous membranes, muscular and skeletal system, nervous system and vascular and renal system.

Early symptoms of Pellagra

Early signs and symptoms of pellagra manifest as loss of weight, weakness, fatigue, muscular and joint pains, backache, lassitude, headache, anxiety, irritability, depression, loss of appetite, indigestion, constipation, and skin lesions and rashes without any obvious causes.

Symptoms of pellagra disease on skin

Initial symptoms manifests as skin inflammations, lesions and rash with itching and burning sensation. Photodermatitis is one of the typical signs of the disease. The areas of skin exposed to sunlight become red and inflamed and show symptoms of sunburn. Later even heat and friction causes inflammation and dermatitis. The skin becomes dry and scaly. Further the edge between the rash and the unaffected skin is clearly demarcated.

The pellagra caused erythema may occur anywhere on the body where it is exposed to sunlight, friction or heat. The common regions of dermatitis are hands, arms, face, exposed neck, feet and lower legs. On the face of the affected patient, the sun exposed forehead, cheeks and nose get inflamed. The lips may also get inflamed and bleed; typical symptoms.

Depending upon the type of dress and exposure, the neck gets affected by the disease. The lesions on the exposed back of the hands of the patient appear like gloves. The exposed legs and feet are affected up to the edge of the pants or skirts by pellagra. The pressure points and genitals also may be affected by dermatitis.

In the later stages of pellagra, the skin becomes thick, scaly, hard and cracked. The skin becomes brown and dark with scaly dermatitis, bleeding at the blackened crusts and sloughing off at places. These areas of skin get easily infected and weeping sores appear. Further in this disease alopecia (loss of hair) are caused by pellagra. Angular stomatitis and Cheilosis are sometimes encountered as symptoms of niacin deficiency. swollen tongue and dermatitis on hands are symptoms and signs of pellagra
Photo dermatitis on hands and swollen tongue are symptoms and sign of pellagra disease (enlarge)

Symptoms and signs of disease on mucous membranes

The typical symptoms of pellagra on mucous membranes like mouth, tongue, nasal passage and in some cases vagina are that they become sore, red, thick, inflamed and swollen. Acute pain and burning sensation is experienced.

Signs of pellagra disease on the gastrointestinal system

Initially pellagra causes on the gastrointestinal system are excessive salivation, anorexia (lack of appetite), dyspepsia (indigestion), burning sensation in the throat, constipation and diarrhea. With the development of extremely painful sores and swelling in the mouth and the tongue the affected person will not able eat food properly leading to further .

Later signs like abdominal pain, abdominal bloating, nausea, vomiting and diarrhea with intestinal bleeding may follow if the deficiency of vitamin B3 (niacin) is not corrected. Gastritis and bloody diarrhea lead to infections and the patient may get dehydrated and become anaemic.

Signs of pellagra on the nervous system

The initial effect of pellagra disease on the central nervous system are insomnia (sleeplessness), anxiety, depression and apathy (indifference). The next stage of signs of pellagra are aggressive behaviour, headache, forgetfulness, progressive memory loss, confusion, disorientation, delusions, neuritis (inflammation of the nerves, paranoia (mental derangement) psychosis, and hallucinations (illusion of seeing and hearing things which are not present). The final stage signs of pellagra disease are delirium, dementia, tremor, stupor and coma.

Signs of pellagra on skeleto-muscular systems

In severe condition of pellagra disease symptoms like stiffness and inability to move arms and legs sets in. The patients also show signs like involuntary grasping and sucking movements , ataxia (lacking control over muscular movements) and fluid retention.

Pellagra disease, if not treated with therapeutic doses of vitamin B3 can become fatal. If not treated early, the signs and symptoms pellagra may not totally disappear.
Current topic:
Signs and symptoms of pellagra disease.