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Small red blood cells could indicate cancer — ScienceDaily

Having abnormally small red blood cells — a condition known as microcytosis — could indicate cancer, according to new research led by a University of Exeter student working with a world-leading team.

Medical Sciences student Rhain Hopkins was lead author of the study of more than 12,000 UK patients aged over 40, which found that the cancer risk in males was 6.2 per cent, compared to 2.7 per cent in those without microcytosis.

The research, funded by Cancer Research UK and NIHR and published in BJGP, found that in females, the risk of cancer was 2.7 per cent in those with microcytosis, compared to 1.4 per cent without.

Of more than 108,000 followed within the Clinical Practice Research Datalink records, 12,289 patients with microcytosis were followed up. Of those, 497 developed cancer within a year.

Microcytosis is related to iron deficiency and with genetic conditions which affect haemaglobn in the blood. Similarly, iron deficiency has been identified as a feature of some cancers, particularly colorectal. Microcytosis is easily identified in a routine blood test.

Rhian Hopkins was working with Exeter’s cancer diagnosis team as part of her Professional Training Year, which gives Medical Sciences students practical experience of research. As lead author of the paper, she said: “Research targeted at diagnosing cancer earlier is so important in reducing the burden of this devastating disease. The identification of risk markers, such as microcytosis, that are relevant to a range of cancers, can have a real impact in primary care. Being part of this research has been a very rewarding experience and getting my first paper published is such a massive achievement.”

Professor Willie Hamilton, at the University of Exeter Medical School, who oversaw the research, said: “Overall, the risk of cancer in patients with microcytosis was still low, however our research indicates a need to investigate cancer. In two patients with cancer out of three the possibility of cancer is fairly easy to identify. For the other third, symptoms are often vague, and don’t clearly point to cancer. For these patients GPs have to use more subtle clues to recognise that cancer may be present. Small red cells have long been recognised with colon cancer, but this study shows that they are a much broader clue, alerting the doctor to the small possibility of one of several possible cancers.”

Dr Elizabeth Shephard, who supervised Rhian, said: “Rhian was a dedicated, proactive and enthusiastic student and an absolute pleasure to work with. As part of her Professional Training Year (PTY), Rhian undertook this standalone project of investigating the role of microcytosis as a possible early marker of cancer. She taught herself to use Stata statistical analysis software, and with guidance learned how to build the database from which to run the analyses. She also analysed the data and wrote up the paper for publication, making a meaningful contribution to the potentially life-saving area of cancer diagnosis.

“The PTY placement is a fantastic opportunity for undergraduates to gain valuable research work experience — and for academics to work with bright students. I wouldn’t hesitate to recommend the programme.”

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What Is Anisocytosis? Red Blood Cells and Why Their Size Matters

‌A simple blood smear can tell your doctor a lot about your health. It allows them to observe the number, size, and shape of your blood cells. Sometimes it can lead to a diagnosis of anisocytosis. This means that your red blood cells (RBCs) are of mixed sizes. Normally, red blood cells should be about the same size. 

Any abnormality of your red blood cells is significant because of the important role they play in your body. Scientists are still investigating anisocytosis and its relationship with disease.

Red Blood Cells and What They Do

Red blood cells are the most abundant blood cells in your body. They make up almost half of your blood’s volume. They grow in your bone marrow and take about 7 days to mature. A hormone called erythropoietin controls the production of your RBCs, which are also known as erythrocytes.

Red blood cells are uniquely suited for their twin jobs. These include carrying oxygen from your lungs to the rest of your body and returning with the carbon dioxide that you exhale. A protein called hemoglobin inside RBCs transports the oxygen and carbon dioxide. 

Red blood cells are shaped like disks that are thinner in the middle. They resemble doughnuts without the hole. They don’t need a thick middle because they have no nuclei. This shape allows them to fold over so they can fit through your narrowest blood vessels.

The lack of a nucleus means that red blood cells don’t live long. Their life span is just 3 months. They perform such important jobs in your body that abnormalities in size, shape, and number will seriously affect your health. 

Measuring Anisocytosis

Anisocytosis is diagnosed using a measurement called red blood cell distribution width (RDW). A high RDW value means that the variation in the size of your red blood cells is higher than normal. A high RDW value can be caused by cells that are larger than normal, smaller than normal, or both.

Your healthcare provider will combine the results of your RDW test with other tests to make decisions about your health. A high RDW value doesn’t always mean that you are ill. RDW values increase with age and can be higher in certain ethnic groups. They may also increase during the later stages of pregnancy and after physical exercise.

Anemias and Anisocytosis

Blood disorders known as anemias are the most common cause of anisocytosis. It’s important to remember that anemia is not a diagnosis. Instead, it is a symptom of an underlying problem.

Common signs and symptoms of anemia include:

Anemia is treated by addressing its cause. Sometimes that means taking supplements or changing your diet. You may need blood transfusions if your level of red blood cells gets too low. Some types of anemia can require a bone marrow transplant.

Kinds of Anemia

Anisocytosis may be present in several types of anemia, including the following.

Iron deficiency anemia. Red blood cells may be abnormally small and pale in this type of anemia. Iron deficiency is most often caused by blood loss. Insufficient iron in your diet or a problem absorbing the iron you consume can also cause it.

Vitamin deficiency anemia. A shortage of vitamin B12 or folate or both can cause this anemia. It is also known as megaloblastic anemia because some of the red blood cells are large and abnormally shaped.

Some kinds of anemia do not have anisocytosis as a symptom. These are called normocytic because the red blood cells are of normal size. An RDW test is still helpful here. It can rule out some types of anemia.

Other Conditions Associated With Anisocytosis

Researchers have discovered that many conditions besides anemia are associated with anisocytosis as measured by an RDW test. In fact, a high RDW value has been associated with a higher overall death rate.

Doctors aren’t sure whether anisocytosis plays a role in the deterioration of health or if it is simply a marker of illness. Is it a cause or an effect? Could it be used more widely in the diagnosis of illness? Can it even predict outcomes? Scientists are interested in these questions.  

Other than anemia, some conditions that are associated with anisocytosis include:

Cardiovascular disease. Many people with atrial fibrillation, coronary artery disease, and other heart problems have higher than normal RDW scores. This indicates anisocytosis.

Liver disease. One study suggested that RDW could be used to predict 3-month mortality in people with liver disease. Another study found that high RDW values were related to poor outcomes from hospitalization.

Kidney disease. In one study of people with acute kidney failure, high RDW scores were identified in people who died within 28 days. A study of patients with kidney disease showed that RDW scores increased as people experienced more serious stages of the disease.

Colorectal cancer. Persons with colorectal cancer had lower overall survival rates when they had high RDW scores, showing anisocytosis. This was true whether the test was done before surgery or after.

Alpha Thalassemia (for Parents) – Nemours KidsHealth

Thalassemias

Thalassemias are a group of blood disorders that affect the way the body makes hemoglobin. Hemoglobin is a protein found in red blood cells that carries oxygen throughout the body. It’s made up of alpha globin and beta globin.

The body contains more red blood cells than any other type of cell, and each has a life span of about 4 months. Each day, the body produces new red blood cells to replace those that die or are lost from the body.

With thalassemia, the red blood cells are destroyed at a faster rate, leading to anemia, a condition that can cause fatigue and other complications.

Thalassemias are inherited conditions — they’re carried in the genes and passed on from parents to children. People who are carriers of a thalassemia gene show no thalassemia symptoms and might not know they’re carriers. If both parents are carriers, they can pass the disease to their kids. Thalassemias are not contagious.

While there are many different types of thalassemias, the main two are:

  1. Alpha thalassemia: when the body has a problem producing alpha globin
  2. Beta thalassemia: when the body has a problem producing beta globin

When the gene that controls the production of either of these proteins is missing or mutated, it results in that type of thalassemia.

About Alpha Thalassemia

Normally, each person has four genes for alpha globin. Alpha thalassemia happens when one or more of the genes that control the making of alpha globins is absent or defective. It can cause anemia ranging from mild to severe and is most commonly found in people of African, Middle Eastern, Chinese, Southeast Asian, and, occasionally, Mediterranean descent.

Some children with alpha thalassemia have no symptoms and require no treatment. Others with more severe cases need regular blood transfusions to treat anemia and other symptoms.

A child can only get alpha thalassemia by inheriting it from his or her parents. Genes are “building blocks” that play an important role in determining physical traits and many other things about us.

Humans are made up of trillions of cells that form the structure of our bodies and carry out specialized jobs like taking nutrients from food and turning them into energy. Red blood cells, which contain hemoglobin, deliver oxygen to all parts of the body.

All cells have a nucleus at their center, which is kind of like the brain or “command post” of the cell. The nucleus directs the cell, telling it to grow, mature, divide, or die. The nucleus contains DNA (deoxyribonucleic acid), a long, spiral-shaped molecule that stores the genes that determine hair color, eye color, whether or not a person is right- or left-handed, and many more traits. DNA, along with genes and the information they contain, is passed down from parents to their children during reproduction.

Each cell has many DNA molecules, but because cells are very small and DNA molecules are long, the DNA is packaged very tightly in each cell. These packages of DNA are called chromosomes, and each cell has 46 of them. Each package is arranged into 23 pairs — with one of each pair coming from the mother and one from the father. When a child has alpha thalassemia, there is a change in chromosome 16.

Alpha globin is made on chromosome 16. So, if any gene that tells chromosome 16 to produce alpha globin is missing or mutated, less alpha globin is made. This affects hemoglobin and decreases the ability of red blood cells to transport oxygen around the body.

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Types of Alpha Thalassemia

Alpha globin is made by four genes and one or more can be mutated or missing, so there are four kinds of alpha thalassemia:

  1. One missing or abnormal gene makes a child a silent alpha thalassemia carrier. Silent alpha thalassemia carriers have no signs or symptoms of the disease, but are able to pass thalassemia on to their children.
  2. Two missing or mutated genes is a condition called alpha thalassemia minor or having alpha thalassemia trait. Children with this condition may have red blood cells that are smaller than normal (microcytosis) and sometimes very slight anemia.

    People with alpha thalassemia minor usually don’t have any symptoms at all, but can pass thalassemia on to their children. The two abnormal genes can be on the same chromosome (called the cis position) or one on each chromosome (called the trans position). If two genes on the same chromosome are affected, the person can pass along a two-gene defect to his or her child. This situation is much more common in people of Asian descent.

  3. Three missing or mutated genes is called hemoglobin H disease. Signs and symptoms will be moderate to severe.
  4. Four missing or mutated genes is a condition known as alpha thalassemia major or hydrops fetalis. This almost always leads to a fetus dying before delivery or a newborn baby dying shortly after birth. However if this disease is suspected because of a history in the family, it can be diagnosed prenatally. Sometimes, if treatment is initiated before the baby is even born, the baby can survive.

Complications

In addition to anemia and hydrops fetalis, severe cases of alpha thalassemia and hemoglobin H disease can lead to serious complications, especially if untreated. Complications of alpha thalassemia include:

  • Excess iron. When children have alpha thalassemia, they can end up with too much iron in their bodies, either from the disease itself or from getting repeated blood transfusions. Excess iron can cause damage to the heart, liver, and endocrine system.
  • Bone deformities and broken bones. Alpha thalassemia can cause bone marrow to expand, making bones wider, thinner, and more brittle. This makes bones more likely to break and can lead to abnormal bone structure, particularly in the bones of the face and skull.
  • Enlarged spleen. The spleen helps fight off infections and filters out unwanted materials, such as dead or damaged blood cells, from the body. Alpha thalassemia can cause red blood cells to die off at a faster rate, making the spleen work harder, which makes it grow larger. A large spleen can make anemia worse and may need to be removed if it gets too big.
  • Infections. Children with alpha thalassemia have an increased risk of infection, especially if they’ve had their spleens removed.
  • Slower growth rates. The anemia resulting from alpha thalassemia can cause children to grow more slowly and also can lead to delayed puberty.
p

Symptoms

The signs and symptoms of alpha thalassemia vary depending on the type that a child has and how severe it is. Children with alpha thalassemia trait and those who are silent carriers have no symptoms at all.

Some of the more common symptoms of alpha thalassemia include:

  • fatigue, weakness, or shortness of breath
  • a pale appearance or a yellow color to the skin (jaundice)
  • irritability
  • deformities of the facial bones
  • slow growth
  • a swollen abdomen
  • dark urine

Diagnosis

In most cases, alpha thalassemia is diagnosed before a child’s second birthday or through newborn screening, a blood test given when the child is first born. Children with alpha thalassemia major may have a swollen abdomen or symptoms of anemia or failure to thrive.

If the doctor suspects alpha thalassemia, he or she will take a blood sample for testing. Blood tests can reveal red blood cells that are pale, varied in shape and size, or smaller than normal. They also can detect low red blood cell counts and cells with an uneven distribution of hemoglobin, which causes them to look like a bull’s-eye when seen through a microscope.

Blood tests also can measure the amount of iron in the blood, evaluate hemoglobin, and test a child’s DNA for abnormal hemoglobin genes.

If both parents are carriers of the alpha thalassemia disorder, doctors can conduct tests on a fetus before birth. This is done through either:

  • chorionic vilius sampling, which takes place about 11 weeks into pregnancy and involves removing a tiny piece of the placenta for testing
  • amniocentesis, which is usually done about 16 weeks into the pregnancy and involves removing a sample of the fluid that surrounds the fetus

Treatment

The amount of treatment that alpha thalassemia requires depends on how severe the symptoms are. For those with alpha thalassemia trait or silent carriers with only mild anemia from time to time, no medical treatment is necessary.

However, the blood counts in alpha thalassemia trait look a lot like the blood counts in iron deficiency anemia, which is a very common disorder. It’s important for doctors to know when children have alpha thalassemia trait so that they do not treat them with iron if it’s not needed.

Doctors also might recommend a folic acid supplement for kids with hemoglobin H disease to help the body make new red blood cells. In addition, these kids may require an occasional blood transfusion, particularly after surgery.

Less commonly, children with severe cases of hemoglobin H disease may require regular blood transfusions their entire lives to keep them healthy. During blood transfusions, they’re given blood from donors with matching blood types. Over time, this can cause a build-up of iron in the body, so kids who receive frequent blood transfusions may have to take medications to remove excess iron from their bodies.

Currently, the only cure for thalassemia is a procedure called a bone marrow transplant (also called a stem cell transplant). Bone marrow, which is found inside bones, produces blood cells. In a bone marrow transplant, a person is first given high doses of radiation or drugs to destroy the defective bone marrow. The bone marrow is then replaced with cells from a compatible donor, usually a healthy sibling or other relative. Bone marrow transplants carry many risks, so they usually are done only in the most severe cases of thalassemia.

Because living with alpha thalassemia can be challenging, people who are carriers of alpha thalassemia trait may want to seek genetic counseling if they’re considering having children.

If your child has alpha thalassemia, support groups are available to help your family cope with the obstacles presented by the disease.

Evaluation of Microcytosis – American Family Physician

1. Hematologic diseases. In: Wallach J. Interpretation of Diagnostic Tests. 8th ed. Boston, Mass.: Little Brown and Company; 2006:385–419….

2. Richardson M.
Microcytic anemia [published corrections appear in Pediatr Rev. 2007;28(7):275, Pediatr Rev. 2009;30(5):181, and Pediatr Rev. 2007;28(4):151]. Pediatr Rev.
2007;28(1):5–14.

3. World Health Organization, Centers for Disease Control and Prevention. Assessing the iron status of populations. http://www.who.int/nutrition/publications/micronutrients/anaemia_iron_deficiency/9789241596107.pdf. Accessed June 7, 2009.

4. Beutler E,
Waalen J.
The definition of anemia: what is the lower limit of normal of the blood hemoglobin concentration? Blood.
2006;107(5):1747–1750.

5. Moreno Chulilla JA,
Romero Colás MS,
Gutiérrez Martín M.
Classification of anemia for gastroenterologists. World J Gastroenterol.
2009;15(37):4627–4637.

6. Guralnik JM,
Eisenstaedt RS,
Ferrucci L,
Klein HG,
Woodman RC.
Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood.
2004;104(8):2263–2268.

7. Thomas C,
Thomas L.
Anemia of chronic disease: pathophysiology and laboratory diagnosis. Lab Hematol.
2005;11(1):14–23.

8. Jain S,
Kamat D.
Evaluation of microcytic anemia. Clin Pediatr (Phila).
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9. Hershko C,
Skikne B.
Pathogenesis and management of iron deficiency anemia: emerging role of celiac disease, helicobacter pylori, and autoimmune gastritis. Semin Hematol.
2009;46(4):339–350.

10. Adamsom J, Longo D. Anemia and polycythemia. In: Fauci AS, Braunwald E, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008:355–362.

11. Muhe L,
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2000;5(11):805–810.

12. AlFadhli SM,
Al-Awadhi AM,
AlKhaldi D.
Validity assessment of nine discriminant functions used for the differentiation between iron deficiency anemia and thalassemia minor. J Trop Pediatr.
2007;53(2):93–97.

13. Ntaios G,
Chatzinikolaou A,
Saouli Z,

et al.
Discrimination indices as screening tests for beta-thalassemic trait. Ann Hematol.
2007;86(7):487–491.

14. Demir A,
Yarali N,
Fisgin T,
Duru F,
Kara A.
Most reliable indices in differentiation between thalassemia trait and iron deficiency anemia. Pediatr Int.
2002;44(6):612–616.

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Iron deficiency and erythropoiesis: new diagnostic approaches. Clin Chem.
2003;49(10):1573–1578.

16. Recommendations to prevent and control iron deficiency in the United States. Centers for Disease Control and Prevention. MMWR Recomm Rep.
1998;47(RR-3):1–29.

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18. Guyatt GH,
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1992;7(2):145–153.

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Investigating iron status in microcytic anaemia. BMJ.
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2007;75(5):671–678.

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2008;28(4):422–430.

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Erythrocyte indices

Erythrocyte indices

 Erythrocyte indices


When a patient has a lower
than normal hemoglobin, it is important to determine whether
red blood cells are of normal size and if they have a normal concentration of
hemoglobin. These measurements, known as erythrocyte or red
blood cell indices
, provide important information about various types
of anemias.

Mean corpuscular
volume (MCV)
measures the mean or average size of individual red blood
cells. To obtain the MCV, the hematocrit is divided by the
total RBC count. The MCV is an indicator of
the size of red blood cells. If the MCV is low, the cells are
microcytic or smaller than normal. Microcytic red blood cells are seen in iron
deficiency anemia, lead poisoning and the genetic diseases thalassemia major
and thalassemia minor. If the MCV is high, the cells are macrocytic,
or larger than normal. Macrocytic red blood cells are associated with pernicious
anemia and folic acid deficiencies. If the MCV is within the
normal range, the cells are referred to as normocytic. A patient who has anemia
from an acute hemorrhage would have a normocytic anemia.

Mean corpuscular
hemoglobin (MCH)
measures the amount, or the mass, of hemoglobin present
in one RBC. The weight of hemoglobin in an average cell is obtained by dividing
the hemoglobin by the total RBC count. The
result is reported by a very small weight called a picogram (pg).

Mean corpuscular
hemoglobin concentration (MCHC)
measures the proportion of each cell
taken up by hemoglobin. The results are reported in percentages, reflecting
the proportion of hemoglobin in the RBC. The hemoglobin is
divided by the hematocrit and multiplied by 100 to obtain the
MCHC.

The MCH
and the MCHC are used to assess whether red blood cells are
normochromic, hypochromic, or hyperchromic. An MCHC of less
than 32% or an MCH under 27 %.
indicates that the red blood cells are deficient in hemoglobin concentration.
This situation is most often seen with iron deficiency anemia.

Normal values for erythrocyte
indices
are:

  • MCV:
    • MCV values
      are higher in newborns and infants
    • Men: 80-98
      fl (femoliters)
    • Women: 96-108
      fl
  • MCH – 17-31
    pg (picograms)
  • MCHC- 32-36%

Anemias can be classified
using erythrocyte indices in the following way:

  • MCV, MCH and
    MCHC normal
    — normocytic, normochromic anemia — most often caused
    by acute blood loss
  • Decreased MCV,
    MCH, and MCHC
    — microcytic, hypochromic anemia — most often caused
    by iron deficiency
  • Increased MCV,
    variable MCH and MCHC
    — macrocytic anemia — most often caused
    by Vitamin B12 deficiency (due to pernicious anemia) and folic acid deficiency

Abnormal erthryocyte
indices
are helpful to classify types of anemia. However, diagnosis
must be based on the patient’s history, physical examination, and other diagnostic
procedures.


© RnCeus.com

 

Microcytosis – an overview | ScienceDirect Topics

Classification

Anemias are classified by the average size, designated as the mean corpuscular volume (MCV), of the red blood cell (RBC). Microcytosis (MCV < 80), normocytosis (MCV = 80–100), and macrocytosis (MCV > 100) are characterizations used to classify anemias.

Failure of RBC production is noted when the reticulocyte count, the number of immature RBCs produced by the bone marrow, is low. While a high reticulocyte count is an expected compensatory response to an anemic state, it is only seen in hemolytic anemia and anemia secondary to acute hemorrhage.

Iron deficiency anemia is typically microcytic with a low to normal reticulocyte count. However, early iron deficiency may present with normocytic anemia and should therefore not be excluded immediately in a patient with an MCV in the normal range (Rose and Berliner, 2010). Other laboratory characteristics of iron deficiency anemia aside from microcytosis and low iron include a peripheral blood smear with hypochromic red blood cells, decreased MCHC, decreased serum ferritin, decreased reticulocyte hemoglobin, and lastly increased total iron binding capacity (TIBC). Transferrin saturation refers to the ratio of serum iron to transferrin concentration. This ratio is typically 20%, but is decreased in iron deficiency due to a decrease in serum iron and increase in TIBC. This is useful because iron deficiency can be distinguished from chronic inflammatory conditions in which there is a decrease in both iron and TIBC (Rose and Berliner, 2010).

Soluble or serum transferrin receptor (sTfR) is a measure of erythropoietic activity and is typically increased in iron deficiency anemia. However, serum ferritin is more specific for iron deficiency than sTfR levels. One study demonstrated a false negative rate of 36% in predicting iron deficiency anemia (Schrier, 2014a). Because ferritin is an acute phase reactant, it will increase in the presence of inflammation. For example, a patient with iron deficiency along with rheumatoid arthritis may have a falsely normal ferritin value. Inflammation typically increases ferritin threefold and it is useful to divide the patients ferritin by three. A ferritin by this method of 20 or less suggests concurrent iron deficiency (Schrier, 2014a).

The red blood cell distribution width (RDW) is the variation in values about the MCV and is elevated in iron deficiency anemia. A normal RDW value ranges between 11.5% and 14.5% and indicates a homogenous population of red blood cells. However, it must be noted that a normal RDW does not exclude the possibility of cells much larger or much smaller than the rest of the red blood cells or that the main population is normal. An elevated RDW suggests anisocytosis, or an increase in variability of red blood cell size (Schrier and Landaw, 2014b).

It is important to differentiate iron deficiency anemia from anemia of chronic disease and thalassemia. While both iron deficiency and anemia of chronic disease present with low iron, the TIBC is low with a normal or increased ferritin in anemia of chronic disease. In beta thalassemia minor, the ferritin is normal or increased, the RDW is typically normal, the hemoglobin A2 is increased (it is often decreased in iron deficiency), and the production of red cells is normal or increased in thalassemia while it is decreased in profound iron deficiency. A patient with thalassemia often presents with a family history including anemia, possible splenomegaly, and target cells or teardrop cells on a blood smear (Schrier, 2014a).

Possible Causes of High or Low Red Blood Cell Count

Red blood cells transport oxygen to all parts of the body. Read on to learn how nutrition affects red blood cell health, the optimal range for red blood cells, and the pros and cons of having high or lower levels of red blood cells.

Red Blood Cell Indices

Red blood cell indices are part of the complete blood count test. Each marker provides specific information about red blood cell health, which may be useful for diagnosing nutrient deficiencies and diseases.

Hemoglobin, hematocrit, and red blood cell indices are the initial laboratory tests used to diagnose and classify anemia.

Mean Corpuscular Volume (MCV)

Mean corpuscular volume (MCV) is a measurement of the average size (volume) of each red blood cell [1].

The normal values for MCV are 87 ± 7 fl (80 – 94 fl).

When red blood cells are smaller than normal (microcytic), the MCV is decreased. Low MCV is typical of a number of conditions, including:

When red blood cells are larger than normal (macrocytic), the MCV is increased. High MCV is typical of a number of conditions, including:

  • Newborns and infants
  • Megaloblastic anemias (folate deficiency anemia and vitamin B12 deficiency anemia) [12, 13]
  • Reticulocytosis – increased red blood cell production (congenital hemolytic anemia and acute blood loss) [14]
  • Alcoholism [15]
  • Liver disease [16]
  • Hypothyroidism [17]
  • Aplastic anemia [16]
  • Myelodysplastic syndrome [16]
  • Acute leukemia [16]
  • Drugs (methotrexate, antiretroviral, anticonvulsive, and sulfasalazine) [16]

These are not necessarily exhaustive lists of potential causes of high and low MCV, and they shouldn’t be used to self-diagnose anything. Your doctor will look at your MCV, other lab markers, and other symptoms to determine an appropriate diagnosis and treatment plan.

Mean Corpuscular Hemoglobin (MCH)

MCH quantifies the average amount of hemoglobin per red blood cell [1].

The normal values for MCH are 29 ± 2 picograms (pg) per cell (27-31 pg/cell).

Values of MCH typically mirror MCV results: small red blood cells have a lower MCH, and large red blood cells have a higher MCH. Thus, MCH is often increased and decreased in the same conditions as the MCV.

Mean Corpuscular Hemoglobin Concentration (MCHC)

MCHC indicates the amount of hemoglobin per unit volume of the red blood cell [1].

MCHC is the hemoglobin content divided by the volume of the red blood cell.

The normal values for MCHC are 34 ± 2 g/dl of red blood cells (32 – 36 g/dl).

Decreased MCHC values (hypochromia, or paler red blood cells) are seen in conditions such as iron deficiency anemia, vitamin B6 deficiency, and thalassemia [3, 8].

Increased MCHC values (hyperchromia, or darker color red blood cells) are seen in conditions such as autoimmune hemolytic anemia, in burn patients, and hereditary spherocytosis [18, 19].

Again, your doctor is best positioned to determine the underlying cause of irregular MCHC and to help you develop an appropriate treatment or management plan.

Red Cell Distribution Width (RDW)

RDW measures the variability of the red blood cell volume [1].

The normal value for RDW is 13 ± 1.5% (11.5 – 14.5%).

The RDW is often normal (homogenous red blood cell size) in healthy people and also in:

  • Leukemia [20]
  • Aplastic anemia [20]

Doctors may therefore use RDW along with a battery of other tests to help them differentiate aplastic anemia from some other types of anemia.

High values (heterogenous red blood cells) indicate high variation in size (anisocytosis) of red blood cells. The RDW is often increased in:

  • Vitamin B12 deficiency [12]
  • Folate deficiency [21]
  • Iron deficiency anemia [22, 23]
  • Blood transfusions [24]
  • Thalassemia [25]
  • Sideroblastic anemia (abnormal red blood cells because the body cannot correctly incorporate iron into hemoglobin) [25]
  • Alcoholism [26]
  • Liver disease [27]
  • Leukemia [28]

This is not necessarily an exhaustive list of potential causes of high RDW, and it shouldn’t be used to self-diagnose anything. Your doctor will look at your RDW, other lab markers, and other symptoms to determine an appropriate diagnosis and treatment plan.

No disease states have been identified in which the RDW is decreased [20].

RBC Count

RBC count is an estimate of the number of red blood cells per liter of the patient’s blood [29].

4.7 to 6.1 x 1012/L in adult men

4.2 to 5.4 x 1012/L in adult women

3.8 to 6.0 x 1012/L in children

Normal values may vary depending on the individual laboratory, the age of the patient, physical activity, and other factors [30].

If your RBC count is outside the normal range, talk to your doctor to determine the underlying cause and develop a management plan, if appropriate.

Red Blood Cell Production

All blood cells originate from common parent cells called hematopoietic stem cells. In adults, blood cells are produced mainly in the bone marrow. Certain substances control the production of blood cells. The hormone erythropoietin or EPO, is produced in the kidneys and promotes the production of red blood cells [31].

The process by which red blood cells are produced is called erythropoiesis. This process relies on a number of nutrients and hormones to be efficient [32, 33]:

  • Metals: iron, copper [34], zinc, manganese
  • Vitamins: B12, folate, vitamins C, E, B6, thiamine (vitamin B1), riboflavin
  • Amino acids
  • Hormones: SCF (stem cell factor), IL-3, GM-SCF (granulocyte-macrophage stem cell factor), erythropoietin (EPO), androgens, and thyroxine.

How Are Red Blood Cells Disposed of in the Body?

Red blood cells have a life cycle of about 120 days. When they are too old or damaged, they are broken down in the bone marrow, spleen or liver.

Used up heme is broken down as a component of bile, which is excreted in the intestine [35].

What is Anemia?

Having a low level of red blood cells can diminish the ability of the blood to transport oxygen, which can cause the heart to come under strain as it works to get enough oxygen to the tissues [36].

Anemia can happen with lower red blood cell count or when red blood cells don’t contain enough hemoglobin [36].

In anemia, the body doesn’t get enough oxygen-rich blood. As a result, you may feel tired or weak. You also may have other symptoms, such as shortness of breath, dizziness, headaches, pale skin, chest pain, and coldness in the hands or feet [36, 37].

Severe or long-lasting anemia can damage your heart, brain, and other organs in your body. Very severe anemia may even cause death [36, 37].

What Causes Anemia?

Anemia is often a symptom that indicates another underlying condition. It’s important to talk to your doctor to identify the possible causes of your anemia and develop an appropriate treatment plan [36, 37].

The three main causes associated with anemia are:

  • Blood loss
  • Lack of red blood cell production
  • Higher rates of red blood cell destruction
  • Inflammation

For some people, the condition is caused by more than one of these factors [38]. Read this post on iron to learn more about anemia.

Inflammation and Anemia

The pro-inflammatory cytokines, IL-1, TNF-α, IFN-γ, and IL-6, inhibit red blood cell production in anemia [39].

IL-8 triggers the death (apoptosis) of red blood cells. RBCs are particularly sensitive to systemic inflammatory changes [40].

Symptoms of Anemia

Anemia is associated with a number of symptoms, which may indicate to your doctor that this test is appropriate. This is not necessarily an exhaustive list; someone with anemia count may have several of these symptoms in addition to others not listed here. Furthermore, these symptoms may not necessarily indicate anemia. Your doctor is best positioned to determine the appropriate blood tests, other labs, and treatment options.

That said, symptoms associated with anemia may include [41, 36, 37]:

  • Headaches
  • Dizziness
  • Weakness
  • Shortness of breath and problems breathing while lying down
  • Double or blurred vision and blind spots
  • Unexplained itching (especially after a warm bath), reddened face, and a burning feeling on your skin (especially your hands and feet)
  • Bleeding from your gums and heavy bleeding from small cuts
  • Unexplained weight loss
  • Fatigue (feeling tired)
  • Excessive sweating
  • Coldness in the hands and feet
  • Pale skin
  • Chest pain
  • Very painful swelling in a single joint, usually the big toe (called gouty arthritis)
  • Bone pain (in rare cases)
  • Increased probability of blood clots (impending danger of heart attack or stroke).
  • Slowed blood flow also prevents enough oxygen-rich blood from reaching your organs. This can lead to angina (chest pain or discomfort) and heart failure. The high levels of red blood cells can lead to stomach ulcers, gout, or kidney stones.
  • Some people may develop myelofibrosis. This is a condition in which your bone marrow is replaced with scar tissue. Abnormal bone marrow cells may begin to grow out of control which can lead to acute myelogenous leukemia (AML), a cancer of the blood and bone marrow. This disease can worsen very quickly [42].
  • Arrhythmias or irregular heartbeats
  • Heart damage and possibly heart failure
  • Organ damage
  • In people who have cancer or HIV/AIDS, anemia can worsen prognosis and reduce the effectiveness of treatments.
  • People who have kidney disease with anemia are more likely to have heart problems [43]

Increased RBC count is independently (but weakly) associated with the risk of cardiovascular events [44].

Elderly patients with depression and low blood cell count may respond better to some medications such as fluoxetine [45].

Health Benefits of Having a Higher RBC Count

An increased number of red blood cells, to a certain extent, allows the body to transport more oxygen to muscles and therefore increase stamina and performance [46].

Conditions Associated With Low RBC Count

The conditions listed here are commonly associated with low RBC count but may indicate another condition or cause another set of symptoms. Work with your doctor or other health care professional for an accurate diagnosis.

1) Iron, Vitamin B6, B12, and/or Folic Acid deficiency

Approximately one-third of the world’s population is anemic, and the majority of these cases are due to iron deficiency [47].

A diet that lacks iron, folic acid, or vitamin B12 can prevent your body from making enough red blood cells. Your body also needs small amounts of vitamin C, riboflavin, and copper to make red blood cells [38].

Conditions that make it hard for your body to absorb nutrients also can prevent your body from making enough red blood cells [38].

Iron deficiency interferes with hemoglobin synthesis [48, 49], so iron deficiency results in reduced hemoglobin in red blood cells. Iron deficiency also results in more variable red blood cell size (>20% RDW), and smaller (low MCV) and paler red blood cells (low MCH) [48, 49].

Nutrient deficiency of either folate or vitamin B12 results in enlarged red blood cells (megaloblastic anemia), with an MCV increased to a range of 105 to 160 fl [49].

2) Inflammation and Infection

Some chronic diseases can cause anemia [37].

Anemia of inflammation is the second most common cause of anemia after iron deficiency. It is associated with acute and chronic infections, sepsis, malignancies, autoimmune disorders, and chronic kidney disease [39].

Some cancer treatments may damage the bone marrow or damage the red blood cells’ ability to carry oxygen. If the bone marrow is damaged, it can’t make red blood cells fast enough to replace the ones that die or are destroyed [37].

People who have HIV/AIDS may develop anemia due to secondary infections or medicines used to treat their diseases [37].

3) Pregnancy

Anemia can occur during pregnancy due to low levels of iron, folic acid, and/or vitamin B12 [37].

Anemia of pregnancy is considered a global health problem, affecting almost 50% of pregnant women [50].

During the first 6 months of pregnancy, the fluid portion of a woman’s blood increases faster than the number of red blood cells. This makes the blood thinner and can lead to anemia [37].

4) Smoking in Pregnancy

Smoking generally increases red blood cell count [51]. However, in pregnancy, smoking lowers red blood cell count which might create a hypoxic condition for the fetus [52].

Neonates born to smoking mothers had lower red blood cell counts, lower hemoglobin, and lower serum cobalamin levels [53].

5) Blood Loss

Blood loss is the most common cause of anemia, especially iron-deficiency anemia. Blood loss can be short term or persist over time.

Heavy menstrual periods or bleeding in the gut or urinary system can cause blood loss. Surgery, injury, or cancer also can cause blood loss [37].

6) Alcohol

Alcohol consumption decreases the red blood cell count, with even the lowest consumption producing a significant decrease in men [54]. In another study that showed similar results, there was a correlation between decreased RBCs and the duration of dependence [55].

7) Overhydration

Overhydration is rare, but can also occur in patients with impaired kidney function. The blood has more volume, but the number of blood cells is unchanged, resulting in a lower red blood cell count or concentration [56].

8) Low Erythropoietin

Your body needs the hormone erythropoietin to make red blood cells. This hormone is produced by the kidneys and stimulates the bone marrow to make more red blood cells [37].

Anemia is a common complication of chronic kidney diseases, due to reduced erythropoietin production by the kidneys [57, 58].

9) Enlarged or Diseased Spleen

The spleen is an organ that removes worn-out red blood cells from the body. If the spleen is enlarged or diseased, it may remove more red blood cells than normal, causing anemia [37].

10) Inherited and Acquired Conditions

Hereditary conditions such as sickle cell anemia or thalassemias can cause your body to destroy too many red blood cells, causing anemia [37].

Immune disorders, infections, certain medicines, or reactions to blood transfusions, can increase red blood cell destruction and cause hemolytic anemia [59].

Some infants are born without the ability to make enough red blood cells. This condition is called aplastic anemia. Infants and children who have aplastic anemia often need blood transfusions to increase the number of red blood cells in their blood [37].

Acquired conditions or factors, such as certain medicines, toxins, and infectious diseases, also can cause aplastic anemia [37].

11) Periodontal Disease

The progression of periodontal disease is associated with a decrease in red blood cell counts [60].

Chronic gum inflammation (periodontitis) is associated with a lower red blood cell count, which tends to improve after periodontal treatment [61].

Conditions Associated With High RBC Count

The conditions listed here are commonly associated with low RBC count but may indicate another condition or cause another set of symptoms. Work with your doctor or other health care professional for an accurate diagnosis.

High red blood cell count may be caused by low oxygen levels, kidney disease, or other problems.

1) Low Oxygen Levels or Hypoxia

Your body may increase red blood cell production to compensate for any condition that results in low oxygen levels, including:

  • Living at high altitude [62]
  • A condition present at birth that reduces the oxygen-carrying capacity of red blood cells (hemoglobinopathy) [63]
  • Obstructive sleep apnea [64]
  • Cystic fibrosis [65]
  • Cor pulmonale [65]
  • Congestive heart failure [65]

2) Obesity

Obesity has been linked with higher RBC count as well as a number of other elevated blood markers, though researchers are not sure why [66].

3) Bone Marrow Overproduction

  • Polycythemia vera (when the bone marrow produces too many red blood cells) [67]
  • Other myeloproliferative disorders (abnormal growth of blood cells in the bone marrow) [68]

4) Dehydration

If the liquid component of the blood is decreased, as in dehydration, the red blood cell count increases. Basically, the red blood cells become more concentrated, although their actual number stays the same [69].

5) Performance-Enhancing Drugs

Certain drugs stimulate the production of red blood cells, including:

  • Anabolic steroids [70]
  • Blood doping (transfusion) [71]
  • Injections of erythropoietin [72]

6) Cold Exposure

Swimming in cold water can increase erythropoiesis (red blood cell production) [73].

In the elderly, red blood cell count was increased in the cold [74].

7) Smoking

Smoking increases red blood cell count except in pregnant women [51, 75, 76].

Further Reading

90,000 Anemia of Chronic Disease – MyPathologyReport.ca

What is anemia of chronic disease?

Anemia of chronic disease is a type of anemia that results from another long-term medical condition that prevents the body from producing normal red blood cell counts. Conditions that commonly lead to anemia in chronic disease include chronic inflammatory conditions, long-term infections (such as HIV or tuberculosis), kidney disease, and cancer.

Anemia means a decreased amount of hemoglobin in the blood. This may be due to a decrease in the number of red blood cells in the blood or a decrease in the amount of hemoglobin in each red blood cell. Because the body uses oxygen to produce energy, a person with anemia has less oxygen in their blood, which can make them tired or short of breath.

red blood cells

Blood contains many different types of cells. These cells include immune cells and red blood cells (erythrocytes).Red blood cells are responsible for carrying oxygen from the lungs to the rest of the body and for carrying carbon dioxide back to the lungs. They trap oxygen and carbon dioxide using a special protein called hemoglobin.

Red blood cells form in a part of the bone called the bone marrow. When young red blood cells mature in the bone marrow, they produce hemoglobin. Your body needs iron to make hemoglobin for red blood cells. At the end of this process, red blood cells enter the bloodstream.Normal, healthy red blood cells circulate in the bloodstream for about 120 days before they are removed and their iron is recycled to form new red blood cells.

The extra iron is stored in a specialized protein called ferritin. The amount of ferritin will change as the amount of iron in your body changes. For example, a person with low levels of iron in their body will have low levels of ferritin in their blood.

How do these conditions cause anemia of chronic disease?

Most of these conditions can cause anemia due to decreased levels of a protein called erythropoietin (EPO) in the body.EPO is produced by the kidneys and acts as a signal to the bone marrow to produce more red blood cells. All of these conditions can reduce the amount of EPO produced by the kidneys, and some can inhibit the bone marrow’s response to EPO, resulting in fewer red blood cells produced in the bone marrow. Chronic inflammation can also cause anemia due to a decrease in the amount of new iron absorbed from food or how it can be used by the body.

How do doctors test for anemia in chronic disease?

A blood test can be used to detect anemia in chronic conditions.When examined under a microscope, red blood cells are usually of normal size (normocytic), although in some cases they may be smaller than normal (microcytic). Ferritin levels in the blood will be normal or elevated even if iron stores are reduced. Other iron tests can help determine if there is an iron deficiency, as anemia in chronic disease and anemia in iron deficiency can occur at the same time.

Rosemary Tremblay-LeMay, MD, FRCPC, updated 8 March 2021

Biology, physiology, medicine, transfusiology, stem cells, erythrocytes, pluripotency

Blood donors may soon be unnecessary. Scientists have finally managed to create red blood balls from embryonic stem cells, causing them to lose their nucleus. Cells without a nucleus, unable to divide, are probably the safest cell therapy, and it is from this that the widespread use of stem cells in practice can begin. If legislation allows.

Even taking into account the negative results of blood transfusions of dogs, sheep and monkeys to humans, as well as attempts to use milk of various animals instead of blood serum, transfusiology remains one of the most “successful” areas of practical medicine.For more than three centuries of development, its methods have practically not changed.

In addition to the gradual improvement of the instrumentation, the followers of the founder of this field of medicine James Blundell “only” discovered blood groups, guessed to separate and use the components of this liquid connective tissue separately, preserve them, and also use saline and acellular fluids to replenish the lost volume.

Now the creation of red blood cells from embryonic stem cells can be safely included in this list.

Robert Lanza, and so famous even outside the scientific community, together with colleagues found a way to grow red blood cells in cell culture.

Red blood cells (red blood cells)

blood cells of humans, vertebrates and some invertebrates (echinoderms). The main function of red blood cells is to transport oxygen from the lungs to the tissues of the body, and transport carbon dioxide (carbon dioxide) in the opposite …

It would seem that red blood cells were discovered and studied a century ago.Although they do not have the same resistance to changes in salinity or acidity of the solution as blood leukocytes, red blood cells exist perfectly outside the bloodstream. They are easy to freeze and unfreeze, you can even “inflate” them with water, like balloons, and fill them with any substance through the pores.

Nevertheless, they still have one “drawback”: they do not share.

Actually, the study of the development of erythrocytes and blood cells in general became the first theory of stem cells.Back in 1908, exactly one hundred years ago, Alexander Maksimov suggested the existence of a hypothetical “predecessor”, and several decades later the hemangioblast cell was isolated from the bone marrow.

From this precursor cell, not only red and white blood cells are formed, but even the endothelium, which lines all blood vessels without exception. Until recently, in practice, it was possible to use only the last two possibilities. Endothelial progenitor cells provoke vascular growth, allowing the treatment of circulatory disorders.Leukocytes are successfully used in a variety of “cell vaccines” due to their ability to actively divide.

But with the cultivation of the precursors of red blood cells for a long time nothing happened.

Red blood cell formation (erythropoiesis)

occurs in the bone marrow of the skull, ribs and spine, and in children – also in the bone marrow at the endings of the long bones of the arms and legs. Before entering the blood, erythrocytes successively go through several stages of proliferation and…

Although everything in our body is unique, the adult red blood cell is especially unique. It does not have a nucleus, and together with the nucleus, it loses the ability to divide. Ribosomes and the entire protein-synthesizing apparatus disappear, but even more space for hemoglobin appears, depending on the conditions of storing oxygen or carbon dioxide.

Such economy allows to divide the functions of erythrocytes in space: their reproduction is the lot of the bone marrow, but in the vessels there are already fully functioning cells, which do not have to compete for a place with young ones.

Despite the numerous variants of “artificial blood”, it has not yet been possible to effectively replace the erythrocyte mass in daily clinical practice.

It is not only about the transfer of gases: erythrocytes are involved in maintaining the constancy of acidity and viscosity properties of blood. So, until today, the only way has been the procurement and preservation of donated blood, which, of course, do not have time to cope with the growing needs of the “industry”.

Attempts to grow erythrocytes from stem cells were also made, but they remained unsuccessful: even if a precursor was obtained as a result of division, the specialists could not get it to get rid of the nucleus.

Lanza and his colleagues have successfully met this challenge.

And not only with her.

They proposed to grow embryonic stem cells (ESCs) in the appropriate microenvironment: in this case, on stromal cells obtained from the bone marrow, which form a corresponding “niche” in the body. Coupled with a “cocktail” of growth factors that direct development in the right direction, this led Lanza to the appearance of the above-mentioned hemangioblasts, and then – and red blood cells.

Embryonic stem cells

have the property of pluripotency, that is, they can differentiate into any cells that make up the body – cells of endoderm, mesoderm and ectoderm. This property distinguishes them from multipotent stem cells, which …

Scientists, of course, consider the loss of a nucleus to be their main success. Firstly, this contributed to the maximum approximation to the properties of the erythrocyte for the “assimilation” of gases: the saturation curves completely coincided.Secondly, with the loss of the nucleus, the cells decreased in size, which is necessary for normal movement through capillaries, the diameter of which is often smaller than the erythrocytes themselves.

Thirdly, the absence of a nucleus and the concomitant inability to divide is a guarantee of peace of mind for potential recipients, because the ability to form tumors still remains one of the main scientific barriers to the use of ESC products.

However, the authors of publication in Blood still have work to do.To begin with, they plan to increase the yield, ranging from 10 to 100 billion cells per maternal colony of ESCs. What took scientists several weeks, in the body happens in a few minutes: every second the red bone marrow releases about 2.5 million red blood cells into the channel.

In addition, the composition of erythrocytes, as expected, turned out to be close to embryonic, and not to adults. The fact is that by 4–5 months after birth, hemoglobin is gradually replaced from fetal to adult.Of course, this does not happen in each erythrocyte separately, but due to a change in generations of blood cells. In the experiment described above, scientists obtained fetal, although in some cases the content of high-grade beta-globin reached 20%.

The prospects are the most tempting. After all, now you can save on numerous tests for viruses, bacteria and other vector-borne infections, which, among other things, do not have one hundred percent efficiency and reliability.

There are two problems so far: the ban on the practical use of ESCs and their products, and in addition, the lack of a cell line that would give ideal donor erythrocytes of the first (O) blood group, and such cells can be transfused to anyone.

Although if we assume that ESCs will ever be introduced into clinical practice, this will begin with the reproduction of erythrocytes: cells without a nucleus practically do not carry any genetic load, and therefore their introduction is as safe as possible for the recipient. At least in comparison with other technologies offered today.

However, it is still very far from the practical use of embryonic stem cells. And, for example, in Russia the problem of donated blood is extremely acute.

Especially now. In August, many donors go on vacation, and childhood illnesses do not know vacations and vacations, many children need donors every day. Their life depends on it in the most literal sense. If you are able to donate blood for sick children, you can contact the organization “Donors for Children” by contacting the donor program coordinator by phone in Moscow (495) 5172286 or by e-mail [email protected] Here they will explain to you what recommendations and contraindications to donation are and will give you the addresses of hospitals and transfusion stations.

Donors are still needed.

90,000 Altitude adaptation. How does the human body adapt to life in the mountains

Frankly speaking, the body of an average person is extremely poorly adapted to the conditions of high mountains. Evolution clearly did not create us for this. The formation of the biological appearance of Homo sapiens did not take place at the transcendental Himalayan heights – in some miserable hundreds of meters above sea level. Therefore, our body tolerates only a small range of atmospheric pressures well, and human life at altitudes of 2500 meters or more runs into a number of problems.With increasing altitude, atmospheric pressure decreases exponentially. For example, at an altitude of five thousand meters, it is only about half of the normal pressure at sea level. As the total air pressure drops, the pressure of each of its components (partial pressure), including oxygen, decreases. This means that a climber at a five-kilometer altitude with every breath will get half the oxygen than a boring man living at sea level.

View of Mount Everest.Its height is 8848 meters above sea level. Photo: ValentinoPhotography / Photodom / Shutterstock

Most often climbers are faced with acute mountain sickness – the author of these lines experienced its symptoms. The mechanism of its development has not yet been fully understood, but it probably has common roots with another dangerous enemy of climbers – high-altitude cerebral edema.

Under conditions of low atmospheric pressure and lack of oxygen (hypoxia), a chain of processes occurs in the brain that leads to impaired blood circulation, mild edema and an increase in intracranial pressure.To one degree or another, mountain sickness appears in almost all climbers, and most often its symptoms disappear after a few days. If it comes to high-altitude cerebral edema, the climber’s life is in mortal danger and an immediate evacuation is required.

Another truly paradoxical altitude sickness is high-altitude pulmonary edema. Nature is always economical, and the mechanism of hypoxic vasoconstriction (scientifically – vasoconstriction) works in our body to optimize the blood supply to the respiratory organ.With different body positions, different parts of the lung can be compressed and receive less air. If some part of the lung lacks oxygen, then the vessels in it contract. Ideally, this should lead to a redistribution of blood flow between areas of the lungs and provide the body with a maximum supply of oxygen in any situation. This is what happens at normal atmospheric pressure. And in the mountains, with acute hypoxia, this mechanism leads to a convulsive contraction of the entire vascular network of the lungs, which further complicates the already difficult extraction of oxygen from rarefied air.At the same time, vasoconstriction raises the pressure in the vessels, forcing blood plasma to leak through the capillary walls. As it fills the lumens of the alveoli, it foams with each breath and reduces the effective lung volume. High-altitude pulmonary edema is extremely life-threatening and overtakes an average of 4% of climbers above 4500 meters.

Mount Kankar-Punsum. Its height is 7,570 meters above sea level. Probably the highest unconquered peak in the world. Photo: Gradythebadger / Wikipedia

Red blood cells, erythrocytes, are a key component of the body’s oxygen transport system.It is they, or rather the protein hemoglobin, with which they are crammed to the eyeballs, that captures oxygen in the lungs, carries it throughout the body and gives it to the tissues in the capillaries of our organs. After one to two weeks of being at an altitude, the number of erythrocytes, and hence the hemoglobin content in the blood, increases. At the same time, its oxygen capacity and human resistance to hypoxia grow. But until now the phenomenon of rapid acclimatization remained unclear. Why is it often that only a few days spent at a height are put on the feet of a person suffering from acute mountain sickness? A recent article published in the Journal of Proteome Research, sheds light on this process.It turns out that all the most exciting events in these first few days at altitude occur not outside, but inside our erythrocytes.

Physiologists have long known that hemoglobin binds oxygen more efficiently in a more alkaline environment (with an increase in pH value), and oxygen release occurs better with an increase in acidity (low pH). Carbon dioxide dissolves in the blood and gives a weak carbon dioxide. In this case, carbon dioxide is formed in the tissues, and is removed from the body in the lungs with exhalation.It turns out that a large amount of carbon dioxide in the tissues makes hemoglobin give oxygen more readily, and its low concentration in the lungs, on the contrary, stimulates hemoglobin to capture oxygen. This effect is called the Bohr effect by physiologists. It works great at sea level, but in the mountains this graceful natural mechanism starts to fail. With altitude, the air pressure, and hence the partial pressure of carbon dioxide in it, rapidly decreases. Carbon dioxide is removed from the blood, and the blood is alkalized.Hemoglobin begins to give up bound oxygen in tissues worse and worse. The way out of this situation is obvious: you urgently need to acidify the blood, or at least the cytoplasm of erythrocytes. Research has shown that this is how it happens.

If the erythrocyte is in a state of normoxia, that is, it is normally supplied with oxygen, the decomposition of glucose in it proceeds along the pentose phosphate pathway. This path is a cascade of biochemical reactions, due to which the substance NADP • H is synthesized – a very valuable reducing molecule.It is necessary for the erythrocyte to repair the constantly oxidized cell membrane. Indeed, a huge stream of an aggressive oxidant – oxygen – continuously passes through the membrane, literally charring its phospholipid molecules.

Elbrus Volcano is the highest mountain peak in Russia and Europe. Its height is 5642 meters above sea level. Photo: LxAndrew / Wikipedia

In parallel, there is another major metabolic pathway – glycolysis, which generates energy and produces an acid metabolic product – lactic acid.However, with normoxia, it is maximally inhibited. This is due to the fact that the enzymes necessary for its implementation are firmly bound to the membrane protein, which has a strange name – the anionic transport protein of band 3 (it is called so because when erythrocyte proteins are separated by gel electrophoresis it was found in the third band ).

And now the owner of our erythrocytes is in the highlands, and he begins to lack oxygen – hypoxia. As soon as there is enough oxygen-free hemoglobin in the cell, it interacts with the protein in lane 3, releasing glycolysis enzymes, which begin to break down glucose into lactic acid.The very next day after climbing to an altitude, this shift begins to slowly but surely increase the content of lactic acid in the cell, compensating for the lack of carbon dioxide and forcing hemoglobin to better give oxygen to the tissues. By the beginning of the third week at altitude, these metabolic changes reach a plateau, and the climber’s acclimatization can be considered complete.

In general, the uniqueness of the highlands is that it put a person in difficult conditions, to which it was absolutely impossible to develop cultural adaptation.Warm clothes, a roof over your head and a fire in the hearth are simple and will perfectly protect you from cold and bad weather. But what about the lack of oxygen? Gas cylinders and pressure chambers offer a high level of technology that has become available only in the last 100 years. But the restless evolution has always been difficult to confuse. And where technology was powerless, ruthless natural selection came to the rescue. Thousands of years of high altitude living have provided the indigenous peoples of mountainous regions with unique mechanisms of resilience.

The Andean and Tibetan types of adaptation are the most studied. The indigenous population of the Andes – the Quechua and Aymara Indians – have more lung capacity and a lower respiration rate at altitude than those from below. In comparison with the inhabitants of the plain and even with the Tibetans, there are much more red blood cells in their blood, which carry oxygen, and therefore hemoglobin. This allows their blood to more efficiently capture oxygen in the lungs and carry it to the tissues.

A Quechua woman on salt terraces in the Peruvian Andes.Photo: Christian Vinces / Photodom / Shutterstock

Genetic analyzes show the heredity of these traits, but at the same time they are all very similar to the changes occurring in the human body, recently settled in the highlands. Quechua and Aymara came to the Andes about 11 thousand years ago. This time was barely enough for the beginning of evolutionary processes. This “superficial” type of adaptation has led to the fact that Quechua and Aymara feel at altitude much more confident than the inhabitants of the plain. But at the same time it brought its own problems.Among the indigenous population of the Andes, there is a high prevalence of a condition called chronic mountain sickness (not to be confused with acute!). The high content of red blood cells in the blood leads to its thickening and increases the pressure in the vessels of the lungs. The already moderate rate of respiration, characteristic of Aymara and Quechua, decreases with age, leading to a constant lack of oxygen and an even greater increase in the hemoglobin content. Chronic mountain sickness appears only during long life in the highlands, usually in old age, and disappears when you move down.

Much deeper adaptations were found among the highlanders of Central Asia. It turned out that the Tibetans and ethnically close to them Sherpas have a sharply increased respiratory rate. At the same time, contrary to expectations, their hemoglobin is only slightly increased – 16.9 g / 100 ml, while the norm is 13-15 g for a person at sea level. At the same time, compared to ordinary people, their tissues produce almost twice as much nitric oxide – one of the main vasodilating factors in the human body. That is why their capillary bed is much wider than that of residents of lower regions.And most importantly, it helps them avoid one of the main physical problems of all climbers – hypoxic vasoconstriction. Normally, for most Tibetans and Sherpas, this reflex, fatal for climbers, does not work at all. Therefore, high-altitude pulmonary edema is rare in them.

Porter in Nepal. Photo: Rickson Davi Liebano / Photohouse / Shutterstock

Research shows that the indigenous people of Tibet and the Himalayas migrated to these places about 25,000 years ago. This time of evolution was already enough to adapt their organisms to the harsh mountain conditions at a qualitatively better level than that of the Andes Indians.Studies of the genome of Tibetans have shown that they have peculiar variants of the genes EGLN1, PPARA and EPAS1, encoding proteins that are involved in the maturation of new red blood cells. EPAS1 turned out to be another most important gene of this series. Tibetan variants of these genes appear to block excess red blood cell production without causing chronic altitude sickness. However, the most exciting thing was revealed when analyzing single-nucleate polymorphisms – differences in the structure of a gene for a single nucleotide. It turned out that the Tibetan variant of the EPAS1 gene, associated with a reduced hemoglobin content in the blood, is unique and coincides with the variant of this gene found in the Denisovan human genome.The same mysterious hominid, whose finger phalanx was found in the Denisova cave in Altai and who managed to leave his mark on the Melanesian genome and, as we now know, helped the Tibetans adapt to the harsh mountain conditions.

Dmitry Lebedev

July 3 – Alcoholism Prevention Day

“There is no such organ in the human body that would not be destroyed

from any dose of alcohol. But the brain suffers the most.”Uglov F.G.

Alcohol, getting into the human body, gets the highest concentration in the brain. If the concentration of alcohol in the blood is taken as 1, then in the liver it will be 1.45, in the cerebrospinal fluid – 1.5, and in the brain – 1.75.

After a person has consumed alcohol, he gets into the blood. In the blood, under the influence of alcohol, there is an intense gluing (agglutination) of red blood cells – erythrocytes, which provide the tissues of the body with oxygen.

In the normal state, the outer surface of erythrocytes is covered, as it were, with a thin layer of lubricant, which becomes electrified when rubbed against the walls of blood vessels. Each of the erythrocytes carries a unipolar negative charge, and therefore they have the initial property of repelling each other. Alcohol removes this protective layer and relieves electrical stress. As a result, red blood cells, instead of repelling, begin to stick together.

For large vessels in the arm or leg, this gluing does not pose a great danger, since these glues, although they consist of many up to a thousand erythrocytes, are still smaller than the cross-section of the vessel and can freely move through it.But in small vessels, you can immediately notice gluing visually, for example, a reddish complexion and nose in someone who has taken alcohol. In chronic alcoholics, you can even distinguish a reddish mesh of dead blood vessels on the face.

The human brain consists of 15 billion nerve cells – neurons, and each neuron feeds its own microcapillary.

The microcapillary has a very thin section and for the normal nutrition of the neuron, erythrocytes can only squeeze in one row.And when alcoholic gluing of erythrocytes comes to the base of the microcapillary, it clogs it, it takes 7-9 minutes and the next human brain cell dies irrevocably. After each so-called “moderate drink”, a new graveyard of dead neuronal cells appears in a person’s head. The normal functioning of the cerebral cortex is disrupted and therefore a person becomes stupid (drunk).

After the death of neurons, the body gives a signal to the adrenal glands to release serotonin into the blood, which, entering the place of dead nerve cells, dissolves them to the point where decay products can be excreted from the body with the help of the kidneys in the form of a component of urine.This is the tragedy of the “deceived brain” – neurons and nerve cells of the brain die, and the person experiences the illusion of “pleasure”.

Changes in the structure of the brain occur even with moderate alcohol consumption. Swedish scientists have established that after 4 years of so-called “moderate” drinking, the brain is shrunken due to the death of billions of cortical cells. In “moderate drinkers”, a shriveled brain is found in 85% of cases.

Having understood the mechanism of brain destruction, it will be clear the plausibility of such a scientific aphorism: “He who drinks wine and beer, he urinates in the morning with his own brains.” Moreover, I drank a lot of beer – I drained a lot of brains, I drank a little – I did not drink much, but I didn’t care, since this is the nature of the interaction of alcohol with the human body.

The described changes in the substance of the brain are irreversible. They leave behind a deep trace in the form of loss of small and smallest structures of the brain, which inevitably and inevitably affects its function.

Much of the current situation is due to the fact that most people do not fully know the truth about alcohol and its properties. Hence, in particular, the recognition and support by them of “cultural” wine drinking, which supposedly saves a person from the destructive effects of alcoholic beverages. Previously, such ideas had some justification: then many objective scientific data on alcohol had not yet been obtained, and therefore even some scientists believed that small doses of alcoholic beverages did not have any significant effect on a person and that, while fighting drunkenness, it is necessary to widely educate the “culture” of drinking among the population.Now, when extensive medical research and medical practice have proven significant harm to humans of the smallest alcoholic doses, talking about the “culture” of alcohol consumption means one way or another to justify the further spread of drunkenness.

How does alcohol affect brain function? What happens to the person? Why is his personality, character and behavior changing so dramatically? This issue has been studied in detail by psychiatrists and physiologists. It has been established that alcohol (in all drinks containing it: vodka, cognac, liqueurs, wine, beer, etc.)acts on the body, its nervous system in the same way as other narcotic substances and typical poisons, such as chloroform, ether, opium in all its varieties, etc.

Recent studies on the effect of small doses of alcohol on humans have put in the hands of physicians invaluable materials. It has been established that any dose of alcohol, no matter how small it is, has an effect on the central nervous system. In particular, after taking a small dose of alcohol of about 60 grams, the right hemisphere of the human brain, which is “responsible” for making decisions, is inhibited. What does this oppression mean? First of all, a person noticeably increases the time for processing information, the biocurrents of the brain change significantly, which leads to nervous irritations, nervous fatigue.

And it is illusory to a person that he feels better, that everything is working out for him, and a calming release has come. This is precisely the insidiousness of alcohol as a drug. External deceit, illusion conceals a definitely negative action.

Alcohol hinders mental processes.In this case, more complex mental processes suffer first of all and simple mental functions retain their effect longer, especially those that are associated with motor representations. As for the motor acts, they are initially accelerated, but this acceleration depends on the relaxation of the inhibitory impulses, and an inaccuracy is immediately noticed in the motor acts.

After drinking, alcohol stays in the human brain for 20 to 90 days. All this time, the work of the higher centers of the brain does not enter the normal course.

It is widely believed that alcohol has a stimulating, reinforcing and revitalizing effect on a person, but all these phenomena, upon deeper study, turn out to be nothing more than a lesion of certain parts of the brain. Paralysis in the mental sphere includes, in particular, a person’s loss of attentiveness and sound thinking.

Under the influence of alcohol, mental centers are paralyzed, which dramatically affects those processes that we call judgment and criticism.Feelings that are not held back by criticism begin to prevail in a person. He becomes too frank and sociable, frivolous, loses the ability to subtly assess the environment, ceases to notice danger. The relaxing effect of alcohol is found in dulling pain sensations, feelings of fatigue, and also in dulling mental pain, for example, melancholy and anxiety. Excessive liveliness and gesticulation, boasting are also a consequence of the onset of paralysis of consciousness and will: correct, reasonable barriers have been removed that keep the sober from useless movements and thoughtless, absurd waste of energy.

With the deepening of alcoholic anesthesia in humans, not only the cells of the cerebral cortex are inhibited, but also the subcortical nodes, the cerebellum. When very large doses of alcohol are taken, a severe dysfunction of the central nervous system occurs with the involvement of the spinal cord and medulla oblongata. Deep anesthesia and coma develops.

The use of alcohol inevitably leads to the degradation of a person, his abilities for creative thinking, synthesis are dulled, and then these higher properties of the human brain disappear altogether.

Neurologist UZ 22 City Polyclinic Makarevich ML

A standard blood test determines the risk of death from COVID-19

Scientists have found that a routine CBC can predict the outcome of COVID-19. It also helps to understand how the patient is responding to treatment and, if necessary, to adjust the therapy.

The achievement is described in a scientific article published in the JAMA Network Open journal.

Patients experience COVID-19 in very different ways. In some, the disease is mild or even asymptomatic, while others receive severe complications or even die. In general, the risk is higher for the elderly and those with chronic illnesses, but this is the “average hospital temperature”. And a pensioner can safely recover, just as a student can die. Accordingly, in order to effectively combat the disease, it is necessary to understand how serious the risk is for this particular patient, and preferably before he is taken to intensive care.

A new study has shown that the criterion can be a parameter obtained from a routine clinical blood test. More precisely, the relative width of the distribution of erythrocytes by volume (red blood cell distribution width, or RDW).

Let us explain. A typical human erythrocyte has a volume of 80–100 femtoliters. But some of these cells may be slightly larger or slightly smaller. The distribution width is a parameter that shows how many unusually large and / or small red blood cells are in the patient’s blood.The normal distribution width is 11-15%. But with some diseases, it increases.

The disease caused by the SARS-CoV-2 coronavirus affects the size of red blood cells.

A group led by John Higgins of Harvard Medical School studied RDW’s link to heart disease, cancer and diabetes. When the COVID-19 pandemic broke out, researchers quickly switched to patients with this diagnosis.

Scientists examined 1,641 adults hospitalized with a diagnosis of COVID-19 from March 4 to April 28, 2020 in Boston.The sample included people of different ages and races and almost equally consisted of men and women.

Higgins and colleagues wondered if there was a relationship between RDW and the severity of a new disease. At the same time, RDW was considered to be increased above 14.5%.

Scientists have indeed discovered such a connection. Mortality among patients with increased RDW was 31% (!), While among patients with normal RDW – “only” 11%.

Moreover, patients in whom the RDW increased right in the hospital died even more often.That is, this easily identifiable indicator allows you to track whether the patient is getting better or worse.

The found pattern persisted even when the authors adjusted for the age of the patients and for common diseases such as hypertension and diabetes.

We emphasize that the sample consisted of hospitalized people, that is, only patients with severe enough symptoms were included in it. This explains the 11% mortality rate even among participants with normal RDW.

If we take into account the known mild cases, it turns out that the mortality rate of COVID-19 is much lower: about 1% (which, however, is still ten times more than that of ordinary flu).

Why the severity of the disease is associated with the diversity of the size of red blood cells remains unclear. Perhaps it is a systemic inflammation caused by a cytokine storm. Scientists plan to study this issue in more detail in the future.

By the way, earlier Vesti.Ru talked about an unusual way to diagnose coronavirus.We also wrote about domestic tests for COVID-19.

90,000 Thirty trillion human defenders – Science – Kommersant

Red blood cells have always been considered, although the most important, but very simply arranged part of the blood: an oxygen carrier, and that’s it. Recent work by American biologists has shown that in fact, red blood cells have many more functions. So far, we can talk about a total of 17.

The average person circulates 30 trillion red blood cells.During maturation, these blood components are deprived of the main elements of the cell – they lose both DNA and organelles. Until recently, erythrocytes were somewhat condescending to be just sacs for transporting hemoglobin. Yes, this is an extremely responsible function, its lack leads to serious problems of the body, but only one.

The discoveries of the last three years show that red blood cells perform much more tasks than simply delivering oxygen to organs and tissues.Pulmonologist-resuscitator Neilam Mangalmurti of the University of Pennsylvania School of Medicine and her team found that red blood cells fix microdamages in the body, and can also capture suspicious nucleic acids (DNA and RNA), signaling the presence of foreign agents in human blood. Red blood cells also know how to report unpleasant findings to the immune system.

More than that. Red blood cells regulate the content of nitric oxide in the blood, and this substance controls the size of the lumen of the vessels: it increases the throughput or decreases it.

Researchers have found similar properties of red blood cells in other living things besides humans – in fish and birds. Some species use red blood cells for protection: they “attack” the pathogens found in the body.

How do erythrocytes perform this role? As Mangalmurti’s team found out, they contain a molecular sensor, more precisely, a toll-like receptor (TLR9, a receptor with one membrane component). This receptor recognizes the presence of foreign hereditary information and attaches to the recognized nucleic acid molecule with a pair of nucleotide bases – cytosine and guanine.(Damaged human cells release such nucleotides, and bacterial DNA is also rich in them, so they can be recognized.) In response, a strong reaction of the immune system occurs, previously it was assumed that this is all a matter of leukocytes. But it turned out that erythrocytes, having identified a stranger, react: you can call it the word “wrinkle”, although what wrinkles a tiny object can have!

Researchers speculate that such a red blood cell response could alert the immune system to foreign DNA or tissue damage.In mice, scientists were able to establish that erythrocytes, “captured” foreign nucleic acid, can cause generalized inflammation in the body. In humans, this inflammation is called sepsis.

The newly discovered functions of erythrocytes can explain a common complication in hospitalized patients. “Almost all intensive care patients are anemic by the third day in the intensive care unit,” says Mangalmurti. When blood passes through the spleen, immune cells called macrophages usually engulf the old and damaged red blood cells, while the good ones are not.Healthy cells are marked with a special protein that can be called “don’t eat me” – and the macrophage really does not absorb them.

“We can now say that red blood cells have immune function in humans and other mammals,” says Mangalmurti. In her opinion, in most cases, cells serve as cleaners: they do not allow potentially dangerous DNA into the body, which enters the bloodstream from many of the body’s cells. But during infection or after injury, such DNA can literally take up all of the bloodstream.

The red blood cells then sacrifice themselves, prompting the macrophages to “eat” them, warning the immune system and causing inflammation. But if the macrophages run wild and consume too many red blood cells, anemia can result.

The materials of the article “DNA Binding to Tlr9 Expressed by Red Blood Cells Promotes Innate Immune Activation and Anemia” were used; L. K. Metthew Lam, Sophia Murphy, Dimitra Kokkinaki, Alessandro Venosa, Scott Sherrill-Mix, Carla Casu, Stefano Rivella, Aaron Weiner, Jeongho Park, Sunny Shin, Andrew E.Vaughan, Beatrice H. Hahn, Audrey R. Odom John, Nuala J. Meyer, Christopher A. Hunter, G. Scott Worthen, Nilam S. Mangalmurti; Science Translational Medicine October 2021

Leonty Krivov

90,000 Iron in the diet | Memorial Sloan Kettering Cancer Center

This information explains how to take in the right amount of iron to maintain your health.

Iron is a mineral that the body needs to make red blood cells.Red blood cells store oxygen and carry it throughout the body. Iron is also found in many proteins and enzymes that help maintain health.

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Daily iron intake

The National Academy of Sciences recommends iron intake based on age and gender. These recommendations are summarized in the table “Recommended daily iron intake”. Iron is measured in milligrams (mg).

Recommended daily intake of iron
Age Men Women
7-12 months 11 mg 11 mg
1-3 years 7 mg 7 mg
4-8 years 10 mg 10 mg
9-13 years old 8 mg 8 mg
14-18 years old 11 mg 15 mg
19-50 years old 8 mg 18 mg
51 and older 8 mg 8 mg

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Iron deficiency anemia

If your body does not get enough iron, you may develop iron deficiency anemia.This can happen if:

  • Your diet lacks iron;
  • You are receiving chemotherapy or radiation therapy;
  • you have a chronic illness;
  • You have lost some blood, for example during surgery or in an accident.

Iron additives

If you have low iron levels, your healthcare professional may prescribe an iron supplement to help normalize iron levels quickly.The amount of iron your healthcare professional recommends may be higher than the amount listed in the Recommended Daily Allowance for Iron table.

Ingesting large amounts of iron may cause stomach irritation and constipation (when bowel movements occur less frequently than usual). Tell your healthcare provider if you have these or any other problems while taking iron. Do not take iron supplements without consulting your healthcare professional.

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How to read food labels

Figure 1. Food label

Eat foods high in iron to maintain normal iron levels. Information on the iron content of foods is given on the label in the nutritional table (see Figure 1). On food labels, the amount of iron is indicated as a percentage (%) of the daily intake.The daily intake of iron is 18 mg.

  • If your daily intake is 5% or less, the food is considered to be a poor source of iron.
  • If the intake is 10–19% of the RDA, the food is considered to be a good source of iron.
  • If the intake is 20% or more of the RDA, the food is considered to have an increased iron content.

To accurately calculate the amount of iron in a food, multiply the daily iron intake (18 mg) by the percentage of the daily value in 1 serving of the food.For example, if the product label states that it contains 50% of the daily iron intake, then multiply 18 mg by 50%. One serving of this product contains 9 mg of iron.

Daily iron intake is provided as a guideline. You may need more or less of it. Use the chart above and check with your healthcare professional to find out how much iron you need to consume each day.

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How to help the body absorb iron

Animal iron, or heme iron, is best absorbed by the body.Plant-based iron, or non-heme iron, is less absorbed by the body.

You can help your body absorb more iron by doing the following.

  • Eat foods or supplements with both iron and vitamin C with a single meal. Examples of foods with a higher vitamin C content are oranges, other citrus fruits, tomatoes, broccoli, and strawberries.
  • Eat foods with iron from both animal and plant sources.
  • For foods with a high iron content, use a cast iron skillet.
  • If your healthcare provider has prescribed iron supplements for you, ask them if you should take 2-3 small doses or 1 large dose. Your body will absorb more iron if you take smaller doses distributed throughout the day.

Some actions make it difficult for the body to absorb iron. Follow the guidelines below.

  • If you drink coffee or tea, drink it between meals, not during them. This applies to all types of coffee and tea, including regular coffee, decaffeinated coffee, black and green tea.
  • Do not consume more than 30 grams of fiber per day.
  • Do not consume foods that are high in calcium (such as dairy products or calcium-fortified juices) and high in iron at the same time.

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How to choose foods with iron content

Sources of iron of animal origin
Source Iron quantity
Beef, meat and offal, spleen, 3 oz (90 g) 33.5 mg
Chicken Liver, 3 oz (90 g) 11.6 mg
Cuttlefish, 3 oz. (90 g) 9.2 mg
Oysters, 3 oz. (90 g) 7.8 mg
Mussels, 3 oz. (90 g) 5.7 mg
Liver sausage pate, ¼ cup (70 ml) 4.9 mg
King Crab, 3 oz (90 g) 2.5 mg
Shellfish, 3 oz. (90 g) 2.4 mg
Beef Shoulder, 3 oz (90 g) 2.4 mg
Ground beef, 3 oz (90 g) 2.3 mg
Lamb, 3 oz. (90 g) 1.5 mg
Canned Anchovies, 1 oz (30 g) 1.3 mg
Chicken, 3 oz. (90 g) 0.9 mg
Turkey drumstick, 3 oz (90 g) 0.9 mg
Pork, 3 oz. (90 g) 0.8 mg
Egg, 1 large 0.8 mg
Salmon, 3 oz. (90 g) 0.6 mg
Scallops, 3 oz. (90 g) 0.5 mg
Turkey breast, 3 oz. (90 g) 0.5 mg
Shrimp, 3 oz (90 g) 0.3 mg
Sources of iron of plant origin
Source Iron quantity
Total ® , ¾ cup (210 ml) 18 mg
Grapenuts ® , 1/2 cup (140 ml) 16.2 mg
Multigrain Cheerios ® , ¾ cup (210 ml) 6.1 mg
Cream of Wheat ® , ½ cup (140 ml) 6 mg
Sesame seeds, ¼ cup (70 ml) 5.2 mg
Fiber One ® , ½ cup (140 ml) 4.5 mg
Raising Spice Oatmeal, ¾ cup (210 ml) 4 mg
Dried apricots, ½ cup (140 ml) 3.8 mg
Wheat germ, ½ cup (140 ml) 3.6 mg
Lima beans, ½ cup (140 ml) 2.9 mg
Mixed nuts, ½ cup (140 ml) 2.5 mg
Red beans, ½ cup (140 ml) 2.5 mg
Sunflower seeds, ½ cup (140 ml) 2.4 mg
Walnuts, 1/2 cup (140 ml) 2 mg
Cooked spinach, ½ cup (140 ml) 1.9 mg
Dark Chocolate, 60-69%, 1 oz (30 g) 1.8 mg
Black beans, ½ cup (140 ml) 1.8 mg
Raisins, ½ cup (140 ml) 1.5 mg
Dried figs, ½ cup (140 ml) 1.5 mg
Chickpeas, ½ cup (140 ml) 1.4 mg
Wheat bread, 1 slice 1 mg
Molasses, 1 tablespoon 1 mg

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Consultation with a dietitian

If you have questions or concerns about food intake while in the hospital, ask for a referral to a dietitian.If you have questions about your diet after you leave the hospital, call 212-639-7312 to make an appointment with your dietitian.

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