The truth about ADHD

ADHD is always a popular topic … and an apoplexic topic. Any mention of ADHD seems to induce everyone within ear-shot to uncontrollably expectorate their half-baked opinion on the subject, like the Tourette’s syndrome of ignorance.

I’ve heard them all over the years …

ADHD is over diagnosed.
ADHD is just a label for bad parenting.
ADHD is caused by sugar.
ADHD is caused by food colouring / preservatives / gluten / (any other fad ‘toxin’)
ADHD is cured by diet / meditation / supplements / swiss balls.
ADHD medication (Ritalin) is overused / irresponsible / lazy parenting / harmful / ungodly.
ADHD doesn’t exist in France.
ADHD doesn’t exist at all.

I could go on, but if I do, I’m just going to get myself in a tizz.

ADHD is the new AIDS. There is so much misinformation and discrimination surrounding ADHD in our modern enlightened society that the stigma is worse than the actual illness, which really says something about how badly ADHD is treated in our communities.

One of the cruellest aspects of the cultural mismanagement of ADHD is the fact that it maligns the sufferers while simultaneously isolating them from much needed support. Saying that children with ADHD should just behave themselves, or parents of children with ADHD should just have better parenting skills is victim blaming at its worst.

In order to counter the prevalent ignorance of ADHD, even just a little, I want to give a crash course on the science so that at least somewhere on the searchable web, there is a counterbalance to the thousands of misinformed arm-chair ‘experts’ whose only experience with ADHD is reading the misguided perspectives of other so-called ‘experts’.

ADHD stands for Attention Deficit Hyperactivity Disorder.

The current formal definition that must be matched to have a diagnosis of ADHD is:

  1. Inattention: Six or more symptoms of inattention for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of inattention have been present for at least 6 months, and they are inappropriate for developmental level:
    * Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities.
    * Often has trouble holding attention on tasks or play activities.
    * Often does not seem to listen when spoken to directly.
    * Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., loses focus, side-tracked).
    * Often has trouble organizing tasks and activities.
    * Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as schoolwork or homework).
    * Often loses things necessary for tasks and activities (e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
    * Is often easily distracted
    * Is often forgetful in daily activities.
  1. Hyperactivity and Impulsivity: Six or more symptoms of hyperactivity-impulsivity for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for the person’s developmental level:
    * Often fidgets with or taps hands or feet, or squirms in seat.
    * Often leaves seat in situations when remaining seated is expected.
    * Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling restless).
    * Often unable to play or take part in leisure activities quietly.
    * Is often “on the go” acting as if “driven by a motor”.
    * Often talks excessively.
    * Often blurts out an answer before a question has been completed.
    * Often has trouble waiting his/her turn.
    * Often interrupts or intrudes on others (e.g., butts into conversations or games)

In addition, the following conditions must be met:
– Several inattentive or hyperactive-impulsive symptoms were present before age 12 years.
– Several symptoms are present in two or more setting, (e.g., at home, school or work; with friends or relatives; in other activities).
– There is clear evidence that the symptoms interfere with, or reduce the quality of, social, school, or work functioning.
– The symptoms do not happen only during the course of schizophrenia or another psychotic disorder.
– The symptoms are not better explained by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder.

(http://www.cdc.gov/ncbddd/adhd/diagnosis.html)

In Australia, ADHD cannot be formally diagnosed by anyone other than a paediatrician or a psychiatrist. So even as an experienced GP, I can’t officially diagnose it. The school counsellor or local naturopath can’t diagnose it. You can’t just pluck it out of the air. The diagnosis can only come from a medical specialist with at least a decade of university level training.

The official prevalence rate of ADHD (the number of people with a current diagnosis) is only 5%. According to some US based community surveys, nearly a half of those children are not on medication for it (http://www.cdc.gov/ncbddd/adhd/data.html). So much for Ritalin being overprescribed.

Stimulants vs nothing

ADHD is a predominantly genetic disorder which leads to specific structural deficiencies in the brain. Children with ADHD have a significant global reduction in the volume of grey matter, most prominently in a part of the brain called the right lentiform nucleus. These changes usually improve with age and improve with stimulant medication. There is also evidence of changes to the shape and size of other brain structures such as the amygdala and the thalamus (areas of the brain integral to sensory and emotional processing). Early evidence also exists which suggests changes in the white matter pathways connecting a number of critical brain regions. Studies investigating brain development have estimated that the frontal lobe development of ADHD children lags that of normal children by an average of about three years.

These changes in the brain are not caused by the child’s behaviour, since other studies have shown the same changes in the brains of unaffected first degree relatives (brothers or sisters), just to a milder degree.

Modern functional imaging techniques show that the brains of children with ADHD have abnormally low functioning in most of the brain structures related to attention and planning (numerous areas of the frontal cortex as well as the basal ganglia, thalamus and parietal cortices). At the same time, there is extra activity in portions of the brain related to the Default Mode Network (the day-dreaming part of your brain). So children with ADHD have brains in which the ‘day-dreaming’ network activity persists into, or emerges during, periods of task-related activity. This takes processing power away from the competing task-specific processing causing a deficit in performance. Studies show that Ritalin normalises this dysfunction.

The best evidence suggests that dopamine is the main neurotransmitter involved in ADHD. Other neurotransmitters are likely to be involved but the evidence is still being confirmed. Medications like Ritalin improve ADHD symptoms by increasing the amount of dopamine that the nerve cells have access to, improving the clarity of the signal between them.

Underlying all of these neural changes are genetics. While there have been no specific genes discovered in research thus far, twin studies have demonstrated a heritability of ADHD of up to 76%. The most significant environmental factors that are responsible for the remainder of the influence on ADHD are not nutritional factors such as sugar or food additives, but are low birth weight/prematurity and exposure to smoking during pregnancy.

Are there any better treatments for ADHD other than stimulants like Ritalin? Other non-stimulant medications are available although at this stage, Ritalin and Dexamphetamine still out-perform them. Cognitive therapies may mimic some of the brain changes of Ritalin but it is not clear whether the effectiveness of cognitive therapies are equal to or better than the stimulant medications. What is clear is that Ritalin doesn’t lead to a euphoric state (a “drug high”) when given orally. So children can not get addicted to Ritalin when used responsibly.

In summary, ADHD exists. It’s caused by the interaction of a number of genes and some environmental factors such as those related to prematurity, low birth weight and maternal smoking, which alter the growth and development of the brain, specifically the grey matter of the frontal cortex, the basal ganglia and thalamus, and the pathways which connect them. These structural changes cause the day-dreaming part of the brain to be more active and the attention and planning parts of the brain to be less active.

ADHD is not caused by food additives or sugar. There is no evidence that autoimmunity plays a significant part. Forcing your child to consume bone broth or stop eating gluten will not cure them.

ADHD is not caused by bad parenting. Ritalin is not evil. Medications like Ritalin and Dexamphetamine have been shown to improve the functioning of children with ADHD and improve their underlying neurological deficits.

It’s time to cut the crap. Our culture needs to stop victimising the child with ADHD and their parents, who already suffer enough from the ADHD without ignorant busy-bodies and self-titled experts chiming in and making their suffering even more pronounced. It’s time to stop judging those who choose the best for their child by medicating them, who do so in spite of the unfair and ill-informed criticism of everyone from their mother-in-law to the milkman when they do. It’s time to remove the stigma from one of the most common psychiatric disorders of childhood so that every child has an equal chance of growing into an adult that can realise their full potential.

That’s the truth about ADHD.

Bibliography:

Cortese, S. (2012). The neurobiology and genetics of Attention Deficit/Hyperactivity Disorder (ADHD): what every clinician should know. Eur J Paediatr Neurol, 16(5), 422-433. doi: 10.1016/j.ejpn.2012.01.009

Gluten mad!

Tonight as I was browsing Facebook again, I came across an article a person had posted on gluten. The article claimed that gluten is connected to depression, and indeed, nearly every other neurological disorder for good measure.

Gluten is a protein found in certain grains like wheat, barley and rye. Gluten also makes foods taste better and improves their texture, so it’s often added to everything else.

The “gluten is toxic” meme is a very catchy one that’s doing the rounds again. I first heard of the idea that gluten is the cause of nearly every disease when I was in medical school, when every person I knew who’d seen a naturopath was told they had gluten intolerance and were conned into an unappetising and restrictive diet which didn’t make any of them better.

The same meme is now making it’s way back around again now that the low-fat, sugar-free, zucchini broth-type diet fads are waning.

The proposed link between depression, anxiety and gluten is a new twist to the old story. But with depression becoming a preeminent disease in the 21st century, the link doesn’t surprise me.

So what does the evidence say? Is gluten the culprit behind the modern scourge of mental illness?

I certainly don’t think so, at least according to my interpretation of the medical literature. As far back as 2001, researchers studying the mental health of patients with coeliac disease noted that coeliac disease patients had much higher levels of anxiety and depression than healthy matched controls (up to about three to six times greater in one study), and after a year on a gluten free diet, there were no changes to the rates of anxiety and depression (Addolorato et al., 2001).

In more recent times, larger studies have been performed. Hauser, Janke, Klump, Gregor, and Hinz (2010) confirmed higher levels of anxiety in German female coeliac patients who were on a gluten free diet, compared to the normal controlled population. Mazzone et al. (2011) showed that children with coeliac disease on gluten-free diets for about 7 years on average still showed an increased rate of anxiety and depression symptoms and showed higher scores in “harm avoidance” and “somatic complaints” as compared to healthy control subjects.

A larger cross sectional survey was performed in the Netherlands in 2013, on 2265 adults with coeliac disease (van Hees, Van der Does, & Giltay, 2013). That survey showed that a significantly higher proportion of those with coeliac disease, despite being on a strict gluten free diet, reporting a higher rate of anxiety and depression compared to the general population. It also showed (albeit in a smaller subgroup of respondents) that poor adherence with a gluten free diet did not affect the likelihood of depressive symptoms.

To be fair, cross sectional surveys and longitudinal cohorts aren’t necessarily the strongest form of evidence, but it is the best we’ve currently got. There was a recent randomised controlled trial, a stronger form of evidence, looking at the effect the introduction of gluten had on depressive symptoms in people who did not have coeliac disease but reported gluten sensitivity and were controlled on a gluten free diet (Peters, Biesiekierski, Yelland, Muir, & Gibson, 2014). While this showed some worsening of depressive symptoms in those subjects given gluten, the exposure was short, the effect was moderate, and the results should be considered cautiously given the small number of subjects reduced the power of the study.

Given the weight of evidence, I can’t help but be sceptical of books touting the ‘gluten = depression’ theory, books like “Grain Brain”. It’s author, American neurologist Dr David Perlmutter, attests that more than 38 different diseases are caused by gluten, including autism and depression. If you believe the celebrity chiropractor who reviewed Perlmutter’s work (http://www.glutenfreesociety.org/gluten-free-society-blog/gluten-leaky-brain-the-connection-to-depression/), increased intestinal permeability and intestinal dysbiosis (“leaky gut” and bad gut bacteria) combine to increase inflammation in the blood and in the brain, causing depression.

But correlation does not equal causation. Just because brain diseases, inflammation and gut problems tend to occur together does not prove that gut problems cause inflammation and brain problems. Rather, the evidence suggests that it’s the other way around, with all of the processes linked to genetics.

For example, autism is related to a number of genes that both reduce the proteins that help nerve cells grow branches (Won, Mah, & Kim, 2013), and at the same time, switch on a low grade form of inflammation (Onore, Careaga, & Ashwood, 2012). I believe it’s the pre-existing inflammation that adds to the cellular dysfunction of the brain and at the same time, promoting low grade inflammation of a number of organs, including the gut. It’s the pre-existing inflammation that causes the gut to become “leaky”, not the “leaky” gut causing the inflammation.

Because if gluten was the primary cause, then why do people with coeliac disease who do not eat gluten report more depressive and anxious symptoms than control groups who do eat gluten? Why would those with coeliac disease who are eating sporadic gluten be just as depressed as those patients who do not?

If you don’t have coeliac disease, then gluten free diets are just like Amway products. You really don’t need them, and you could probably do much better without them. All you’re really doing is just making someone else obscenely rich.

Not only are you wasting your money, but you might also be harming your health by eating gluten free foods, since most foods that are stripped of gluten are also stripped of most of their other nutrients.

As Nash and Slutzky (2014) summarise, “Every major change in our diet carries with it the possibility of unforeseen risks. Many readers — the general public, as well as medical professionals — accept what they read at first glance. Myths have been part of our medical lore for millennia. Those jumping on the gluten-free/high-fat bandwagon may be disappointed when their symptoms are not mitigated; more critically, they may be at increased risk for other, more dangerous ailments.”

If you really think you feel better off gluten, then talk to your doctor or registered dietician to make sure you remain healthy off it.

References

Addolorato, G., Capristo, E., Ghittoni, G., Valeri, C., Masciana, R., Ancona, C., & Gasbarrini, G. (2001). Anxiety but not depression decreases in coeliac patients after one-year gluten-free diet: a longitudinal study. Scand J Gastroenterol, 36(5), 502-506.

Hauser, W., Janke, K. H., Klump, B., Gregor, M., & Hinz, A. (2010). Anxiety and depression in adult patients with celiac disease on a gluten-free diet. World J Gastroenterol, 16(22), 2780-2787.

Mazzone, L., Reale, L., Spina, M., Guarnera, M., Lionetti, E., Martorana, S., & Mazzone, D. (2011). Compliant gluten-free children with celiac disease: an evaluation of psychological distress. BMC Pediatr, 11, 46. doi: 10.1186/1471-2431-11-46

Nash, D. T., & Slutzky, A. R. (2014). Gluten sensitivity: new epidemic or new myth? Every major change in our diet carries with it the possibility of unforeseen risks. Am J Cardiol, 114(10), 1621-1622. doi: 10.1016/j.amjcard.2014.08.024

Onore, C., Careaga, M., & Ashwood, P. (2012). The role of immune dysfunction in the pathophysiology of autism. Brain Behav Immun, 26(3), 383-392. doi: 10.1016/j.bbi.2011.08.007

Peters, S. L., Biesiekierski, J. R., Yelland, G. W., Muir, J. G., & Gibson, P. R. (2014). Randomised clinical trial: gluten may cause depression in subjects with non-coeliac gluten sensitivity – an exploratory clinical study. Aliment Pharmacol Ther, 39(10), 1104-1112. doi: 10.1111/apt.12730

van Hees, N. J., Van der Does, W., & Giltay, E. J. (2013). Coeliac disease, diet adherence and depressive symptoms. J Psychosom Res, 74(2), 155-160. doi: 10.1016/j.jpsychores.2012.11.007

Won, H., Mah, W., & Kim, E. (2013). Autism spectrum disorder causes, mechanisms, and treatments: focus on neuronal synapses. Front Mol Neurosci, 6, 19. doi: 10.3389/fnmol.2013.00019