Can Vitamin B12 Deficiency Make You Tired?

The term “asthenia” derived from the Greek, means absence of strength or vigor. It is a complex symptom that simultaneously encompasses the physical and the psychic in a global way, is subjective and involves a set of vague sensations, different for each individual which is perceived and expressed through the nervous and the muscular system. From the physiological point of view, you can consider fatigue as the tiredness that occurs after the efforts, and asthenia as the same sensation, but without efforts to justify it.

In the asthenia, you can identify three different components that participate in a different grade according to the case: 1) laziness, faintness, lack of vigor and the need to rest before tasks that did not produced them previously; 2) generalized weakness: anticipated sense of difficulty in initiating and maintaining an activity; and 3) mental fatigue: characterized by altered concentration, memory loss and emotional lability.

Although fatigue is a common reason for consultation as a single symptom, it sometimes appears as a component of a clear subjacent disease.

It is not infrequent that it is a symptom, ailment or complaint repeated over time, in different consultations, with the same or different professionals and, in general, without the doctor’s response.

Fatigue may be normal when an intense effort is made, but when it is not related to the performed behaviors, it is called “pathological” fatigue.

It is a symptom that can occur during the period of convalescence of different diseases and surgeries. All people have experienced the feeling of asthenia, for example during viral infections. In these cases, the obvious relationship with a disease of clear diagnosis makes the asthenia is not, by itself, a cause for concern. Very different is the situation in which the asthenia dominates the clinical presentation and compromises the usual activities, enclosing the threat of potentially serious diseases.

Can Vitamin B12 Deficiency Make You Tired?

Vitamin B12 deficiency is manifested clinically by general symptoms such as weakness, pallor, and megaloblastic macrocytic anemia, also gastrointestinal symptoms such as nausea, vomiting, severe anorexia, glossitis, diarrhea and malabsorption of nutrients and for neurological symptoms among, which paresthesias in the limbs are highlighted, incoordination and loss of vibratory sensitivity. This deficiency is practically non-existent in humans by poor intake (except perhaps for strict vegetarians) because most foods are rich in vitamin B12 and the daily requirement is very low (about 1 ug for 24 hours). Therefore, it is clear to conclude that this lack is always secondary to a variety of nonspecific entities or to some specific genetic disorders.

Once the vitamin reaches the stomach it is combined with a mucoprotein secreted by the parietal cells called “intrinsic factor.” The complex intrinsic factor-vitamin B12 is then formed, which upon arrival at the ileum is captured by special receptors existing there. Subsequently, it is released into the portal circulation where it is taken up by the transcobalamin II globulin responsible for transporting it to the liver.

Pernicious anemia (prototype of vitamin B12 deficiency) is a specific disorder due to the absence of parietal cells of the gastric mucosa that are responsible for producing the intrinsic factor, essential for the absorption of the vitamin. Other nonspecific gastrointestinal disturbances may produce the same effects, such as the decrease or absence of iatrogenic parietal cells (gastrectomy), the alteration of the ileal mucosa, the absorption site of vitamin B12 (tropical sprue, enteropathy gluten, resection of the terminal ileum), of the presence of flora or parasites that compete with the host in the use of the vitamin (blind loop syndrome, diverticulosis, diphilobotrium latum infestation), or pancreatic-chronic disease, in which case the pathophysiology of malabsorption of vitamin B12 is not well known.

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