Inherited, abnormal genes account for a small proportion of leukemia cases (Alter BP 2003; Bischof O et al 2001; Fong CT et al 1987). However, in most cases, the DNA damage that eventually results in the onset of leukemia is brought about by interactions between genes, age, and a variety of environmental or lifestyle factors such as nutrition and exposure to chemicals (Greaves MF 2004; Irons RD et al 1996).
Age. Since up to 70 percent of leukemia cases are in those over 50, age can be considered the biggest risk factor for developing leukemia (Fenech MF et al 1997; Russell RM 2000a). The chromosomes of white blood cells in older people are more fragile than those in young adults and are more vulnerable to the types of DNA damage (e.g., free radical damage) known to cause leukemia (Esposito D et al 1989; Mendoza-Nunez VM et al 1999).
A diet rich in fruits and vegetables and other antioxidants can help guard against DNA damage caused by free radicals (Ames BN et al 1993). However, the ability of the elderly to repair DNA damage is poor and is associated with suboptimal micronutrient status (Ames BN 1998; Fenech MF et al 1997). The metabolism of elderly people is altered in such a way that while they continue to efficiently absorb macronutrients such as fats and proteins, absorption of micronutrients such as vitamin B12 and vitamin D is compromised, leading to malnutrition (Russell RM 2000a). Suboptimal levels of micronutrients can cause DNA damage associated with leukemia and limit the ability to repair this damage (Ames BN 1998; Ames BN 1999).
Nutrition. Diets lacking in essential micronutrients are as detrimental as cigarette smoking in the cause of cancer and can cause the same kind of DNA damage as exposure to radiation (Ames BN 1998). Deficiencies is several micronutrients, including folic acid and vitamins B12 and B6, may contribute to leukemia (Ames BN 1999).
Folic acid deficiency causes chromosome breaks (Fenech MF et al 1997) and is a risk factor in the development of ALL. In folic acid deficiency, efforts to repair damaged DNA are compromised and lead to breakages in genes (chromosome breaks) (Ames BN 1999; Skibola CF et al 2002; Wickramasinghe SN et al 1994). Deficiencies in vitamins B12 and B6 are thought to act in the same way as folic acid deficiency in increasing the risk for both adult and childhood ALL (Ames BN 1999).
There is a possible relationship between the restricted nutrient intake of slimming diets and the development of acute leukemia (Visani G et al 1997). Another theory is that phenol and hydroquinone, chemicals mainly ingested from meat and protein-rich diets, known to produce DNA damage, and antibiotics, may cause leukemia (McDonald TA et al 2001).
Chemotherapy. Chemotherapy, used for the treatment of other cancers, can cause DNA damage and make increase the risk of developing some form of leukemia. For example, chemotherapy for the treatment of other cancers is the major recognized cause of AML in the young, referred to by clinicians as secondary or treatment-related AML (Felix CA 1998). Treatment-related AML is associated with therapy for breast cancer, ovarian cancer, Hodgkin’s disease and non-Hodgkin’s lymphoma, and accounts for up to 20 percent of AML cases (Kaldor JM et al 1990; Smith MA et al 1996). Treatment with epipodophyllotoxins (etoposide and teniposide) is associated with development of secondary AML (Hawkins MM 1991; Pedersen-Bjergaard J et al 1991). Cyclosporine A, used to treat suppressed red blood cell production, is associated with the development of secondary leukemia (Yamauchi T et al 2002).
Radiation. Exposure to high doses of radiation causes leukemia by inducing DNA damage through translocations (Kamada N et al 1987). Population studies show a link between radiation exposure from nuclear testing between 1951 and 1962 in the United States and the onset of leukemia (Archer VE 1987; Johnson CJ 1984). The incidence of leukemia was high in the United States in the years during and immediately after the nuclear testing. Utah showed high increases (up to five times the norm) in leukemia rates, which persisted as late as the 1980s (Archer VE 1987; Johnson CJ 1984). Exposure to radiation is linked to acute and myeloid leukemia in children (Archer VE 1987). The association between radiation exposure and leukemia was noted in survivors of the atomic bomb in Japan (Ichimaru M et al 1991) and in people who lived near the nuclear reactors in the Chernobyl disaster of 1986 (Noshchenko AG et al 2002). Leukemia caused by radiation typically appears 10 years after exposure (Tilyou SM 1990).
Chemicals. Long-term or occupational exposure to benzene is a cause of acute leukemia (Austin H et al 1988; Rinsky RA et al 1981). Long-term exposure to herbicides, pesticides, and other agricultural chemicals is linked to an increased risk of developing leukemia (Meinert R et al 2000). Hair dyes contain chemicals that cause cancer and are associated with leukemia (Sandler DP 1995), particularly the long-term use of permanent dyes (Rauscher GH et al 2004).
Smoking. Cigarette smoke contains leukemia-causing chemicals like benzene (Korte JE et al 2000). Although smoking in the young is associated with modest increases in the risk of developing leukemia, in those over 60 smoking is associated with a twofold increase in risk for AML and a threefold increase in the risk for ALL (Sandler DP et al 1993).
Genetics. Children with Down’s syndrome have a 10 to 20 times higher risk of developing leukemia than the general population (Fong CT et al 1987). This risk is not confined to childhood years and extends through adulthood. There are also inherited disorders, such as Fanconi’s anemia and Bloom’s syndrome, that are characterized by genetic instability and inability to repair DNA damage and are associated with an increased risk of leukemia (Alter BP 2003; Bischof O et al 2001).
Viruses. Acute T cell leukemia is associated with infection by the human T cell leukemia virus (HTLV); human lymphotrophic virus-1 causes leukemia in humans. In infected individuals, HTLV proteins attach themselves to proteins in the lymphocytes responsible for regulating cell growth and corrupt their functions resulting in the uncontrolled cell growth of leukemia (Uchiyama T 1997). This type of leukemia is rare in the United States and is generally found in Asia and parts of the Caribbean.
Symptoms associated with leukemia include weakness, fatigue, unexplained weight loss, pain, (abdominal, bone, and joint), abnormal bleeding, infection, fever, excessive bruising, and enlarged spleen, lymph nodes, and liver.
The first step in diagnosing leukemia is a complete blood count (CBC). With a diagnosis of leukemia, further testing of cell samples obtained by bone marrow aspiration or lumbar puncture determines the specific type of leukemia. Specific treatment is then targeted for leukemia based upon a number of factors, including results of genetic tests and leukemic cell sub-type.
What You Have Learned So Far
- Leukemia is a collective name for cancers of the white blood cells that grow, multiply, and change uncontrollably
- It occurs through damage to the genes, such as chromosome translocations or mutations
- Leukemia can be chronic or acute and occur in myeloid or lymphocytic white blood cells
- Risk factors for leukemia include environmental or lifestyle factors such as nutrition, smoking, exposure to chemicals, viruses, radiation, and previous chemotherapy or radiotherapy treatment for other cancers
- Diagnosis is made from results of blood and bone marrow tests
- Leukemia is more prevalent in the aged who have altered metabolism causing micronutrient deficiencies and reduced bone marrow function (Chatta GS et al 1996)
- Vitamin D3, curcumin, green tea, and soy extracts help support healthy cell growth, function, and maturation in patients with leukemia