ADHD Causes

Attention-deficit hyperactivity disorder (ADHD) is associated with the neurological function of the brain. Strongly linked to genetic and environmental influences, researchers have yet to identify an exact cause. That said, researchers have found links between these potential cause and risk factor to attention deficit disorder:

• Genetics
• Neurotransmission impairment
• Brain abnormalities
• Dietary factors
• Perinatal/neonatal influences
• Thyroid dysfunction
• Trauma
• Societal
• Environmental factors

Genetics

ADHD is strongly associated with genetics. One in four children with ADHD has a close relative with the disorder whereas, parents and siblings of ADHD kids are two to eight times more likely to develop the disorder themselves.¹ Molecular genetic studies have identified several genes that are believed to be associated with the disorder including those involved with the release, reuptake and transformation of dopamine and norepinephine. That said, of genes that have been identified, none have been found to have much effect, leading researchers to conclude that the disorder is likely linked to several.²

ADHD is believed to have a heritability rate of 76 percent. However, how much of the disorder is nature over nurture is questionable. Some researchers estimate that between 40 and 80 percent of the genetic variance for personality may be nature-based.³ Thus while ADHD has a strong genetic influence, environmental factors such as food additives, toxins and excessive stimulation play a significant in the disorder’s development and evolution.

Neurotransmission

ADHD symptoms are believed to be associated with what is known as the executive functions of the brain.⁴ Acting as a conductor, the executive functions prioritize, integrate and regulate the brain’s other cognitive processes such as planning, mental flexibility, abstract thinking, rule acquisition, initiating actions (both appropriate and inappropriate) and selecting relevant information.⁵ Non-localized, these executive functions are linked through a complex nerve network that communicates through neural transmission. A problem with the network of the chemicals used to send and receive messages can cause a breakdown in communication.

In his book Attention Deficit Disorder: The Unfocused Mind of Children and Adults, Thomas E. Brown suggests that ADHD is the result of a defunct network. Thus, even in the case where the individual has an ample supply of the chemical that fuel the system—neurotransmitters—messages still aren’t getting through. According to Brown, this conclusion is supported by more than 200 well-controlled medication studies that show that stimulants temporarily reestablish this circuitry:

The results from these many medication studies clearly indicate that ADD syndrome is essentially a chemical problem, specifically an impairment in the brain’s management system. Just as diabetes is a disease that reflects impairments in the body’s processing of insulin, ADD syndrome is a disorder that reflects impairments in the brain’s processing of dopamine and norepinephrine.⁶

Brain abnormalities

The brains of individuals diagnosed with ADHD are different than those in people without the disorder. One study showed that the brains of children with ADHD were slightly reduced, particularly in the prefrontal cortex on the left-hand side of the brain.⁷ Additional studies show abnormalities in the fiber pathways that connect the frontal lobes and the cerebellum.⁸ ADHD has also been linked to decreased levels of blood flow to the brain and low levels of cerebral glucose. In a 1990 study using proton emission topography (PET), researchers found that cerebral glucose metabolism was 8.1 percent lower in adults who had been diagnosed with ADHD as children than in normal adults.⁹ However, when the authors of this study repeated it three years later with adolescents, no significant differences were found between the “hyperactive” and “normal” brain.¹⁰

Diet

An exhaustive number of studies have linked ADHD to dietary factors such as low levels of essential fatty acids, mineral deficiencies, synthetic additives, food additives and refined sugar.

• Essential Fatty Acids (EFAs): EFAs play an important role in the development of the protective surface coating that insulates the nerve fibers. Indeed, dietary intake is directly related to EPA levels in the nerves. As early as 1981, researchers observed that children who were hyperactive, particularly boys, struggled to absorb and metabolize essential fatty acids. They also found that many of the foods that the hyperactive children reacted to contained substances blocked the conversion of EPAs to eicosanoids, the signaling molecules used in the regulation of the central nervous system. Additionally, EPA supplementation relieved many of their symptoms.¹¹ A great deal of research is now underway to verify the link between EPA supplementation and the reduction of ADHD symptoms.

• Mineral deficiencies: Children with ADHD have a greater propensity to be deficient in zinc, iron and magnesium.
  • Zinc is vital in the growth of the developing brain. In addition to helping maintain the ongoing functioning of the brain, it plays a role in the production and modulation of serotonin and the metabolizing of dopamine. In a paper summarizing the finding of nine zinc studies conducted around the world, the authors found that not only were children more likely to be low in zinc but lower zinc levels also correlated to the severity of their symptoms.¹² High Fructose Corn Syrup consumption also results in lowered zinc levels.
  • Important for the structure and function of the central nervous system, iron plays a role in neurotransmission and is associated with cognitive development. Studies show that not only are children with ADHD more likely to be low in iron but that the severity of their symptoms correlated to lower iron levels. Iron deficiency is also linked to a higher rate of absorption of lead and restless leg syndrome.¹³
  • Suboptimal levels of magnesium have been linked to reduced energy metabolism, synaptic nerve cell signaling and cerebral blood flow. Several studies have linked children to low levels of magnesium.¹⁴

• Food allergies, additives, preservatives and dyes: The link between ADHD and food intolerance remains controversial. In 1982, the U.S. National Institute of Health concluded that elimination diets helped just 5 percent of children diagnosed with ADHD. However, more recent studies suggest that children’s reactions to certain foods and additives may be more pronounced.¹⁵ Additional, Dr. Benjamin Feingold has shown that 50 percent of hyperactive respond favorably to his elimination diet which recommends eating only those foods free of artificial flavors, dyes, preservatives and salicylates (a commonly used preservative derived from salicylic acid).¹⁶

• Refined sugars: The role of refined sugars in ADHD is hotly debated. Whereas numerous studies show no connection between the consumption of refined sugars and behavior, one study showed that children with ADHD are more likely to be hypoglycemic. In a study of 261 children, 74 percent were found to have abnormal levels of glucose tolerance.¹⁷ Metabolically, these children’s pancreases’ were releasing an abnormal amount of insulin to metabolize the sugar. As a result, their high insulin levels caused their epinephrine and norepinephrine levels to spike resulting in ADHD-like symptoms. While void in nutrients, sugar calls on a number of nutrients in its processing. Thus, sugar may play an indirect role in ADHD by robbing the body of the nutrients needed to support the cognitive functions of the brain.¹⁸

Perinatal/Neonatal Factors

Children born to women who smoke or drank during their pregnancy may be at risk of developing ADHD. Additional perinatal risks include moderate-to-severe physical illness during gestation, symptoms of miscarriage and/or premature delivery and respiratory infections. ADHD has also been linked to a number of issues related to a child’s birth and first month of life. Premature babies are at a greater risk of developing ADHD as are infants who suffer from seizures, decreased levels of oxygen to the brain, mild speech retardation, brain injuries and fever. Finally, studies show that infants who are exposed to lead or manganese and/or are weaned prior to three months are at a higher risk for ADHD.¹⁹

Thyroid Dysfunction

Thyroid hormones are vital to the regulation of nerve maturation. Research shows that roughly 50 to 70 percent of children who are resistant to thyroid hormones have ADHD. Similarly, studies showed that the offspring of rats that had hypothyroidism were more likely to be hyperactive and restless, and prone to panic. (Hypothyroidism is when the thyroid fails to make enough hormones.) Similarly, in a study comparing the children born to women from “moderately iodine deficient” versus “marginally iodine deficient” areas at the time of gestation underscores the critical role of the thyroid of warding off the symptoms of ADHD. The study showed that whereas none of the children bore to the mothers living in the marginally iodine sufficient area developed ADHD, a total of 68.7 percent of children born to the mothers from the moderately iodine deficient area did.²⁰

Trauma

Children with ADHD are more likely to be abused than children without the disorder. According to Thomas E. Brown, author of Attention Deficit Disorder: The Unfocused Mind in Children and Adults, children with ADHD may be more at risk of emotional and/or physical abuse from fed-up friends and family members. In a study of girls with ADHD, a significantly higher number reported having been abused than those in the control groups.²¹ Similarly, researchers found that a greater number of children living in conflict zones such as the Gaza Strip were more likely to have ADHD than those living in areas free of conflict.²² Research shows that abuse is also more prevalent in ADHD adults. In a controlled study of 57 adults, emotional abuse and neglect was more common among the ADHD adults whereas sexual abuse and neglect was more common among the women with the disorder.²³

Societal

A fair amount of evidence suggests that ADHD is a manufactured diagnosis. Child and adolescent psychiatrist Dr. Sami Timimi points out that there is no known cause for ADHD and there exists no specific cognitive, medical and/or neurological markers for diagnosing it. In addition, there is no specific treatment for ADHD and stimulation medication has been said to have the same effect on otherwise normal children. Finally, stimulation medication has generated huge profits for the pharmaceutical industry. “Thus the mainstream dogma on ADHD is contaminated and misleading.” Under the current medical model, ADHD becomes a convenient scapegoat for parents and teachers to shirk from their responsibilities as caretakers and for the community members to disregard societal flaws such as the loss of the extended family, the pressure on schools, the breakdown in the moral authority of adults and increasingly frenetic pace of family life.²⁴

Mercury exposure is among the most commonly cited environmental factors that can contribute to ADD and ADHD, and can also contribute to autism. Mercury is a biproduct of many industrial and waste plants and is can cause individuals problems in functioning including attention deficit disorders.

Often cited in fish, foods with high mercury levels should be avoided so as not to consume too much mercury. Ironically, low levels of omega 3 fatty acids can also contribute to ADD/ADHD, and some of the foods with high omega 3 amounts include fish. Therefore, it is important to know about the fish you consume:

How high are the levels of mercury in the particular kind of fish you are eating? - Some fish have higher levels of mercury, on average, than others. The American Heart Association states that Salmon, Sardines Clams, Crab, Scallops, and Sole have among the lowest levels of mercury, while swordfish, shark, golden bass/snapper and mackerel have some of the highest.²⁵ In general, fish that are predators who live longer have more of a chance of building up mercury levels in their tissues (hence the reason shark and swordfish are among those with the highest levels of mercury)

In what kind of environment did the fish live? - If fishing or farming of fish occurs near industrialized plants, the water may be contaminated with high levels of mercury that are released into the air and can then accumulate in streams and ponds near the plants. The Environmental Protection Agency recommends reading their Fish Advisory Website²⁶ or checking with your state or local health department for information about fish caught near your home.

How was it caught? - Perhaps less applicable to the mercury discussion, it is good to remember how a fish is caught when deciding whether or not to consume it. The repercussions of catching or farming fish in an unhealthy manner include personal or group sickness to the fish or humans, and damage to the natural environment. The Monterey Bay Aquarium's Seafood Watch program offers great information on how to shop for sustainably caught or farmed seafood. They have also partnered with Whole Foods to provide a sustainably caught seafood purchasing experience in their stores. Ask your fish purveyors if they carry sustainably caught/farmed products, and purchase these fish!

What kind of packaging did it come in? - The packaging of fish or any food, like plastic, tin, aluminum etc. is important to note as these can affect the food itself, the person consuming it, and the health of the environment.

Read more about mercury exposure and autism.

1. Chris D. Meletis, N.D. and Nieske Zabriskie, N.D., “Attention-Deficit Hyperactivity Disorder,” Alternative and Complementary Therapies 14, no. 5 (October 2008): 235–241.
2. Aliyah Baruchin, “Nature, Nurture and Attention Deficit,” The New York Times, March 12, 2008, http://health.nytimes.com/ref/health/healthguide/esn-adhd-expert.html
3. Rob Santich, “Attention deficit hyperactivity disorder,” (presentation, the National Herbalists Association of Australia’s 6th annual conference, Canberra, Australia, September 2007).
4. Thomas E. Brown, Ph.D., Attention Deficit Disorder: The Unfocused Mind in Children and Adults, (New Haven and London: Yale University Press, 2005): 10.
5. Donald T. Stuss and Robert T. Knight, Principles of Frontal Lobe Function, Oxford: Oxford University Press, 2002.
6. Thomas E. Brown, Ph.D., Attention Deficit Disorder: The Unfocused Mind in Children and Adults, (New Haven and London: Yale University Press, 2005): 91.
7. Amy L. Krain and Francisco Xavier Castellanos, “Brain Development and ADHD,” Clinical Psychology Review 26, no. 4 (August 2006): 433–444.
8. Kate Johnson, “Abnormal Brain Anatomy Found in ADHD,” Pediatric News, January 2005, http://findarticles.com/p/articles/mihb4384/is139/ain29155375/?tag=rel.res1
9. Alan Zamekin, et al., “Cerebral Glucose Metabolism in Adults with Hyperactivity of Childhood Onset,” The New England Journal of Medicine 323, no. 20 (November 15, 1990): 1361–1366.
10. “Zamekin’s Research on ADHD,” Audiblox, http://www.learninginfo.org/adhd-research.htm
11. Rob Santich, “Attention Deficit Hyperactivity Disorder,” (presentation, the National Herbalists Association of Australia’s 6th annual conference, Canberra, Australia, September 2007).
12. Natalie Sinn, “Nutritional and Dietary Influences on Attention Deficit Hyperactivity Disorder,” Nutrition Reviews 66, no. 10 (2008): 558–568.
13. Natalie Sinn, “Nutritional and Dietary Influences on Attention Deficit Hyperactivity Disorder,” Nutrition Reviews 66, no. 10 (2008): 558–568.
14. Natalie Sinn, “Nutritional and Dietary Influences on Attention Deficit Hyperactivity Disorder,” Nutrition Reviews 66, no. 10 (2008): 558–568.
15. Chris D. Meletis, N.D. and Nieske Zabriskie, N.D., “Attention-Deficit Hyperactivity Disorder,” Alternative and Complementary Therapies 14, no. 5 (October 2008): 235–241.
16. Rob Santich, “Attention deficit hyperactivity disorder,” (presentation, the National Herbalists Association of Australia’s 6th annual conference, Canberra, Australia, September 2007).
17. Rob Santich, “Attention deficit hyperactivity disorder,” (presentation, the National Herbalists Association of Australia’s 6th annual conference, Canberra, Australia, September 2007).
18. “The Role of Sugar in ADHD,” ADD ADHD Advances, September 6, 2004, http://addadhdadvances.com/sugar.html
19. Chris D. Meletis, N.D. and Nieske Zabriskie, N.D., “Attention-Deficit Hyperactivity Disorder,” Alternative and Complementary Therapies 14, no. 5 (October 2008): 235–241.
20. Chris D. Meletis, N.D. and Nieske Zabriskie, N.D., “Attention-Deficit Hyperactivity Disorder,” *Alternative and Complementary Therapies *14, no. 5 (October 2008): 235–241.
21. Allison M. Brisco-Smith and Stephen P. Hinshaw, “Linkages Between Child Abuse and Attention Deficit/Hyperactivity Disorder in Girls: Behavioral and Social Correlates,” Child Abuse & Neglect 30, no. 11 (November 2006): 1239–1255.
22. Thomas Miller, El-Masri Mustafa, Allod Federico and Samir Qouta, “II: Emotional and behavioural problems and trauma exposure of school-age Palestinian children in Gaza: Some preliminary findings.” Medicine, Conflict and Survival 15, no. 4 (1999): 368-378.
23. Julie J. Rucklidge, Deborah L. Brown, Susan Crawford and Bonnie J. Kaplan, “Retrospect Reports of Childhood Trauma in Adults with ADHD,” Journal of Attention Disorders 9, no. 4 (May 2006): 631–641.
24. Sami Tamimi, “ADHD is Best Understood as a Cultural Contruct,” The British Journal of Psychiatry 184 (2004): 8–9.
25. http://www.americanheart.org/presenter.jhtml?identifier=3013797
26. http://water.epa.gov/scitech/swguidance/fishshellfish/outreach/advice_index.cfm