Vitamins and chronic illness: Sorting out the true from the false!

What is vitamin D?

Vitamin D is not a true vitamin. In fact, vitamins cannot be synthesized by the body (they are only provided by food). Nevertheless, vitamin D is provided through the sun's rays. Therefore, it is actually a pre-hormone. Vitamin D is comes in two forms: D2 (only in plants) and D3 (in plants and animals). These two forms, after transformation by the body (notably thanks to UV rays), make it possible to obtain active vitamin D (calcitriol).

In developed countries, the people most at risk of deficiency are alcoholics, people who do not get enough sunlight and those suffering from chronic intestinal conditions (who may experience reduced absorption or vitamins). Furthermore, vitamin D is fat-soluble; therefor, patients undergoing treatment for obesity or high cholesterol (whose aim is to lower the intestinal absorption of fat) are also likely to be deficient. This vitamin has a number of benefits, particularly in terms of bone mineralization.

Furthermore, vitamin D also has an effect on the immune system. It stimulates innate immune cells (macrophages and dendritic cells) as well as adaptive immune cells via Th2 lymphocytes in particular (which play an anti-inflammatory role).

If you'd like to know more about the link between vitamin D and the immune system, feel free to read the following articles:

What impact does vitamin D have on multiple sclerosis?

Why do we need vitamin D?

What is the link between vitamin D and osteoporosis?

Osteoporosis is an age-related bone disease, corresponding to a decrease in bone mass. This decrease leads to increased bone fragility. A fall from a standing height or a simple impact can lead to a fracture. Rare cases of spontaneous fractures have also been reported. The most affected bone areas are the wrists, the femoral neck (the "ball" that sits in the hip socket) and the vertebrae. 

Throughout life, the skeleton is slowly destroyed and rebuilt (4 to 5 times in total) in order to maintain an optimal bone density. Bone density increases until about the age of 20. Then, around the age of 35, it slowly decreases. During menopause, due to the decrease in the secretion of hormones such as estrogen, there is a drop of about 30% in this density. On average, one woman in three is affected by osteoarthritis after menopause. Around the age of 70, however, bone loss is almost identical between men and women. 

In addition, osteoporosis can be caused by other conditions such as hyperthyroidism or by treatments like cortisone derivatives, in which case it is known as secondary osteoporosis. 

Bone mineralization, which enables bone renewal and strength, is regulated by three hormones: 

• Calcitonin, which has a hypocalcemic effect by lowering kidney absorption of calcium and bone reabsorption (destruction of old bone releasing calcium);
• Parathyroid hormone (PTH), a hormone secreted by the parathyroid glands, is hypophosphoremic and hypercalcemic. In fact, it decreases the kidney reabsorption of phosphorous (hypophosphoraemia) while increasing that of calcium and increasing bone resorption;
• Finally, vitamin D has a hypercalcemic and hyperphosphoremic action. It increases the intestinal absorption of phosphorus and especially calcium, increases bone mineralization and inhibits the action of PTH.
  
  

Thus, a vitamin D deficiency causes bone demineraliaation leading, in the long term, to osteoporosis.

What is vitamin B?

Vitamin B12 (or cobalamin) is the largest and most complex of the B vitamins. It is obtained from food, particularly meat, fish and eggs.

It is involved in the proper functioning of the immune system and contributes to a normal energy metabolism. Vitamin B12 also enables the production of myelin. Myelin is the sheath surrounding axons (fibrous extensions of neurons), which acts like a sheath around an electric wire. It therefore serves to ensure efficient transmission of information. Demyelination (destruction of myelin) causes serious neurological disorders. The symptoms of multiple sclerosis (MS) are also due to the destruction of myelin by immune cells. However, the role of vitamin B12 in MS has not been proven - if there indeed is a role for vitamin B12 in MS, it is likely to be a minor one. 

Finally, cobalamin is essential for the production of DNA constituents. Without it, cell replication is affected, causing dysfunction, particularly in tissues with a high rate of renewal, such as blood cells or the digestive tract.

Finally, cobalamin is essential in the production of DNA components. Without it, it will have an impact on cell replication causing malfunctions, especially in tissue with a high renewal rate such as the blood cells or digestive tract.

What is the link between vitamin B and pernicious anemia or Biermer's disease?

Biermer's disease or pernicious anemia is an autoimmune condition causing vitamin B12 deficiency. It is a rare disease, affecting about 0.1% of the general population, of whom most are women.

The disease is characterized by the appearance of three syndromes:

• A progressive onset anemic syndrome (pernicious anemia), which is generally well tolerated and may have few functional symptoms. The main symptoms of this syndrome are pale skin, fatigue, a loss of appetite, shortness of breath, etc.
• A digestive syndrome, due to the hypersecretion of gastrin (a hormone responsible for the secretion of gastric fluids), characterized by nausea, vomiting, pain, etc.
• A characteristic neurological syndrome: this syndrome is defined by:
• A neuro-anemic syndrome, also called "subacute combined degeneration of spinal cord", "Lichtheim's disease" or "Putnam-Dana syndrome", resulting in areflexia (loss of reflexes), paresthesia (tingling) or even paralysis;
• Neuropsychiatric disorders characterized by drowsiness, memory problems, a depressive state and hallucinations.
  
  

The treatment of this condition is straightforward, simply by supplementing with vitamin B12. Unfortunately, this supplementation must be continued throughout life.

What is vitamin A?

Vitamin A or retinol is, like other vitamins, only provided by the diet. It plays an important role in vision, particularly in the adaptation of the eye to darkness, but also in the health of the skin, mucous membranes and the proper functioning of the immune system. This vitamin is also involved in bone growth and embryo development.

What is the link between vitamin A and xerophthalmia?

Vitamin A is stored in the liver. Retinol deficiency is associated with malnutrition in children and liver malfunction or malabsorption of the vitamin in adults. Without it, the renewal of visual pigments is compromised.

The result is a condition called xerophthalmia, a condition in which the eye fails to produce tears, eventually leading to reduced visual acuity and even blindness. 

The disease develops rapidly and is characterized by several stages:

• XN - Night blindness
• X1A - Conjunctival xerosis: Dryness of the conjunctival mucosa (the tissue lining the white part of the eye) which becomes dull.
• X1B - Bitot's spots: Appearance of slightly raised white deposits.
• X2 - Corneal xerosis: A dull and hazy appearance of the cornea. Up to this stage, high-dose vitamin A supplementation can reverse or preserve loss of vision.
• X3A & B - Corneal ulcer/keratomalacia: Stage X2 (corneal xerosis) can lead to corneal ulceration and melting if not treated quickly.
• XS - Corneal scar due to xerophthalmia: Scarring of the cornea, which can cause pain, sensitivity to light, and loss of vision.
• XF - Xerophthalmic fundus: Functional and structural changes in the retina can be observed, the cornea may soften and necrosis may lead to loss of the eyeball.

A varied diet (vitamins are found in meat, vegetables, etc.) can help to overcome vitamin deficiencies. It is also advisable to have regular blood tests to identify any deficiencies.

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