What are the symptoms of calcium deficiency?

The calcium level in blood can be moderately low without causing any symptoms. However, if levels of calcium are low for long periods, people may develop dry scaly skin, brittle nails, and coarse hair.

A long-term calcium deficiency can lead to dental changes, cataracts, alterations in the brain, and osteoporosis, which causes the bones to become brittle.

Other symptoms of calcium deficiency include rickets, osteomalacia, scurvy, tetany, parathyroid hyperplasia, stunted growth, laryngospasm.

Deficiency of calcium lowers the body resistance and for the children become as easy prey to respiratory and intestinal infections.

Poor calcium intake affects mostly bone and muscle. Rickets occurs in children when the amount of calcium accretion per unit of bone matrix is deficient.

Hypocalcemia may result in tetany, a condition characterized by intermittent muscle contractions that fail to relax, especially in muscles of the arms and legs. Hypocalcemia is often detected by routine blood tests before symptoms become obvious. Doctors measure the total calcium level (which includes calcium bound to albumin) and the albumin level in blood to determine whether the level of unbound calcium is low.
What are the symptoms of calcium deficiency?

Hypervitaminosis A

Acute hypervitaminosis A results from ingestion of very large amounts of the vitamin during a relatively short period of time.

Chronic hypervitaminosis A in humans is more common than acute hypervitaminosis A. Serum levels of vitamin A are generally more than 3.49 umol/liter and there are increased levels of the unbound retinol resulting in a change in the ration of free retinal to retinal bound to RBP as well as increase in retinyl esters.

A symptoms of acute hypervitaminosis A include nausea, vomiting, double or blurred vision, increased intracranial pressure, headache, dizziness, skin desquamation, and muscle in-coordination.

Chronic hypervitaminosis A can result from high intakes of vitamin A over long period of time and/or in connection with liver or kidney disease.

The effects of hypervitaminosis A on the liver, the primary storage site for vitamin A, are multiple. They include fat storing cell hyperplasia and hyper trophy, fibrogenesis, sclerosis of veins, portal hypertension and congestion in perisinusoid cells, which leads to hepatocellular damage and cirrhosis o a cirrhosislike hepatic disorder.

Vitamin A in very large doses is known to be teratogenic in many animals. Excessive intake of vitamin A has also been associated with human congenital abnormalities in some cases reports although a causal relationship has not been established.

High intakes should be avoided by pregnant women. Hypervitaminosis A in pregnant women can lead to fetal abnormality, but such cases are very rare. Levels of vitamin A intake associated with hypervitaminosis A varies according to the health and size of the person.

As little as 12,000 IU per day, given to small children for an extended period, has been reportedly led to toxicity symptoms.

Hypervitaminosis A may result from acute ingestion of about 500,000 IU of vitamin A by an adult, or from a chronic daily intake of about 100,000 IU. Cases of hypervitaminosis A caused by natural food sources are rare but they have a very long history.

It has been hypothesized that pathological changes found in a Homo erectus skeleton from 1.5 million years ago were caused by hypervitaminosis A attributable to the consumption of carnivore livers.
Hypervitaminosis A

Toxicity of manganese

Toxicity of manganese compounds appears to depend upon type of manganese ion presents and the oxidation state of manages.

It has been suggested that manganese cations are more toxic than the anion forms.

In 1901 research showed that manganese toxicity could result in neurological damage in humans.

However, it was not until a series of reports in the 1930s and 1940s describing a high incidence of manganese toxicity in manganese mine workers that manganese toxicity was recognized as a significant health workers. Chronic inhalation exposure of humans to high levels may result in a syndrome called manganism and typically begins with feelings of weakness and lethargy and progresses to other symptoms such as gait disturbances, clumsiness, tremors, speech disturbances, a mask-like expression, and psychological disturbances.

Additionally, individuals with liver failure are at greater risk for toxicity because manganese homeostasis is maintained largely by the liver through excretion in the bile.

Manganese toxicity secondary to liver failure is characterized by manganese accumulation within the liver and other organs such as the brain; accumulation in the brain results in neurologic abnormalities.

Psychological changes including mental irritability, headaches, nervousness, compulsive actions, and hallucinations can occur.
Toxicity of manganese

Protein deficiency symptoms

The nutritional disease kwashiorkor was first described in the medical literature in the 1930s and a very tentative suggestion made that it might due to dietary protein deficiency.

In protein deficiency, when the diet supplies too little protein or lacks a specific essential amino acid relative to the others, the body slows it synthesis of proteins whole increasing its breakdown of body tissue protein to liberate the amino acids it needs to build other proteins of critical importance.

The first sign of protein deficiency is likely to be weak muscles – the body tissue most reliant on protein.

A protein deficiency may also show up in the blood. Red blood cells live for only 12 days. Protein is needed to produce new ones.

People who do not get enough protein may become anemic, having fewer red blood cells than they needed.
Protein deficiency symptoms

What are the causes of hypervitaminosis A?

Vitamin A is required for vision. Epithelial cells (those cells present in the lining of body cavities and in the skin and glands) require vitamin A.

This vitamin also required for resistance to infection.  Toxicity has been usually associated with abuse of vitamin A supplements rather than from ingestion of food sources.

Toxicity has been observed in people who have either chronically or acutely consumed more than 10 times the RDA. Some people take large doses of vitamin A hoping for improved vision, increased resistance to disease, improved skin and the like.

Acute hypervitaminosis A is caused by a single massive dose, or a limited number do large doses taken during a short period.  Chronic hypervitaminosis A results from continued ingestion of high doses for month or even years.

Symptoms of hypervitaminosis A include dryness of the skin, headache, anorexia, weakness, hair loss, joint pain, vomiting, irritability, enlarge liver and spleen, and in babies, a bulging fontanelle and increase intracranial pressure.
What are the causes of hypervitaminosis A?

Symptoms of osteoporosis

The term ‘osteoporosis’ was first coined in the nineteenth century in France and Germany as a histological description of aged human bone, emphasizing its apparent porosity.

The signs and symptoms in osteoporosis are vague, in that an individual may be developing osteoporosis, or may have early or well established osteoporosis and be unaware until they sustain fracture.

Usually the first symptoms will manifest themselves in the form of acute pain in the mid to low back region.

Back pain is one of the most frequent reasons for seeking medical advice, and every case of acute or chronic back pain must ne thoroughly investigated.

Other more dramatic symptoms are fractures of rib, hip or wrist or a combination of these, having occurred without definitely traceable traumatic cause.

Pain obviously associated with such fractures and so may be regarded as a symptom of the disease, although the presence of osteoporosis in itself should not be a cause of pain.

In advance cases there may be deformities such as loss of height or a bent spine. The bones tend to break easily from even minor accidents or trivial strains.

Symptoms of osteoporosis