Anisocytes as seen in the Live Blood Analysis Training Course – often associated with B12 deficiency and a common cause of fatigue.

 Anisocytes – often associated with B12 deficiency

We are now on week 4 of the Live Blood Analysis Training Course and studying anisocytes – often associated with B12 deficiency and a common cause of fatigue.

Our tutor explains that the fatigue is due to 2 factors:

1) Vitamin B12 deficiency causes anemia, which then reduces the amount of oxygen that can be carried by the red blood cells which can result in fatigue.

2) The change in size of the cell also leads to fatigue:

A normal RBC is usually 6-8 microns in size and the diameter a capillary is 5-10 microns. Gas exchange is facilitated by close contact between the RBC membranes and the capillary wall as the RBCs squeeze to pass through.

This squeezing effect does not occur when the RBCs are smaller than normal as they simply slip through.

Larger than normal RBCs fold to pass through, which also reduces contact with the capillary wall.

So the RBCs can’t carry as much oxygen as they should, due to a reduced haemoglobin level, and they can’t exchange the oxygen they do carry because they’re not the optimal size for gas exchange at a cellular level.

More info on Anisocytes:

Appearance:

Red blood cells that vary in size, some larger than normal (Macrocytes) and some smaller than normal (Microcytes).

Relevance:

In normal live samples all the RBCs should generally be the same size. Anisocytosis is significant if the RBCs exhibit more than the normal variation of size with the presence of microcytes and/or macrocytes.

Implications:

♦ Vitamin B12 and folic acid deficiency. ♦ Iron deficiency (microcytes and target cells). ♦ Liver disease. ♦ Poor absorption. ♦ Food allergy. ♦ Megaloblastic anaemia, pernicious anaemia and aplastic anaemia.   ♦ Hypothyroidism.

Associated Symptoms:  

♦ Lassitude ♦ Dizziness ♦ Weakness ♦ Poor concentration ♦ Pallor  ♦ Shortness of breath ♦ Increased heart rate ♦ Palpitations

Medical Perspective:

Macrocytes in substantial numbers are observed in patients with megaloblastic anemias (vitamin B12 and folic acid deficiency), often with considerable anisocytosis (with some microcytes present as well).

In addition, macrocytes may be prominent in individuals with erythroleukemia, myelodysplastic disorders, acquired sideroblastic anemia and with antimetabolite or androgen drug therapy.

A lesser degree of macrocytosis is seen commonly in alcoholic patients. Macrocytosis may also be seen in individuals with a high reticulocyte count.

A predominance of hypochromic microcytic cells is found in iron deficiency anemia, thalassemia, and hereditary sideroblastic anemia and in some patients with the anemia of chronic disease and with lead intoxication.

For individuals with mild anemia, the degree of microcytosis is usually substantially greater in patients with thalassemia minor than those with iron deficiency.

Interventions:

♦ Sublingual vitamin B12 – 1000ug daily (e.g. Solgar: vitamin B12) ♦ Folic acid and/or vitamin B-Complex ♦ Chelated Iron supplement (when target cells observed) ♦ Trace minerals ♦ Chlorophyll-rich foods: Chlorella, spirulina, wheat grass juice / powder, barley grass juice / powder, alfalfa tablets, green leafy vegetables, blackstrap molasses, beetroot, beansprouts.

Anisocytosis is almost always associated with nutritional deficiencies that can be corrected by optimal nutrition, unless the problem is genetic.

Emphasis is placed on the supplements listed above, as well as the dietary recommendations.

Generally, the more severe anemias are accompanied by the most severe anisocytosis, which are often seen in severe hepatic degeneration.

If severe anisocytosis is noted, correlate with the other clinical information and the dried layered test to establish the probability of liver disease.

Consider sending the patient for a LFT (Liver Function Test) and an abdominal ultrasound to determine the nature and extent of liver disease.

From here, a natural treatment approach can be planned and implemented.  

Copyright Dr Okker R. Botha, Johannesburg, South Africa, 2009

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