In case you have been missing it, the number people getting diagnosed with ADHD (kids but especially adults), is going up at an alarming rate.
I now regularly have adults coming in and out of the blue announcing they are on ritalin post a diagnosis of ADHD.
Note, the data below is up to 2018, and since then IME, the diagnoses have gone berserk.
Adults:
Children
Now, in the past, we were probably under-diagnosing it, and now I cannot help but wonder if we are over diagnosing it.
In private schools, 42% of students get extra time in exams due to neuro-divergence, versus the still far too high 26.5% in state schools.
Plus, there is the issue of treatment.
There is no discussion about anything other than ritalin (Methlyfenidate) or atomoxetine.
Certainly, no discussion of long-term side effects, which, given these are long-term drugs, needs considering.
Let’s consider what they both do and then look at the pathways.
Methylfenidate is a dopamine and noradrenaline reuptake inhibitor. So, by slowing down the breakdown of them, it increases the levels in the synapse.
Atomoxetine only stops the reuptake of noradrenaline.
Let’s look at the balance and the pathways.
The dopamine, noradrenaline pathway looks like this, with the start using the essential amino acid, phenylalanine.
The key part here is, the enzyme that converts phenylalanine to tyrosine AND tyrosine to DOPA, which are both IRON dependent.
Thus, low iron (ferritin under 50 ng/ml, for some people under 80-100 ng/ml), will not make enough DOPA (from phenylalanine and tyrosine) to then go on and make enough DOPAMINE and NORADRENALINE to have normal concentration and focus.
So we can theorise from mechanistic first principles, if the drugs used to improve the symptoms of ADHD work by raising DOPAMINE and NORADRENALINE, then if we are low in IRON and cannot make normal levels, then this may be a cause of ADHD symptoms.
Hence, there is a subgroup of people with “ADHD” (arguable a misdiagnosis), where it was secondary to low cellular iron (always without anaemia, which usually needs ferritin to be below 15 ng/ml, if not lower).
You increase iron, and the symptoms improve/resolve.
Hence, articles like this:
Let’s look at some data and note, the literature is mixed, BECAUSE not all ADHD (or symptoms of ADHD) is really low iron, affecting the end amount of dopamine and noradrenaline.
For example, some people have an issue with the dopamine receptor DRD4 or the enzyme that converts dopamine to noradrenaline, DBH.
Not sure whose genes these are…..😙
So, are lower ferritin levels associated with more ADHD and stronger severity?
Yes, say most studies (though not all agree).
“Children with ADHD had significantly lower serum ferritin levels and higher levels of both symptom severity and functional impairment compared to healthy controls. Ferritin levels were negatively correlated with ADHD symptom severity”
“Multiple regression analysis indicated that CPRS Hyperactivity score was significantly associated with ferritin level”
Now, association is not causation, but mechanistically this makes sense that iron could be involved in those without a genetic predisposition (aka a mis-diagnosis) and those with the genes AND low iron (ferritin).
So let’s take a look at an intervention study.
80 kids with ADHD and ferritin under 30 ng/ml, given either 80 mg of ferrous sulphate (which is 16 mg of actual IRON), vs placebo for 12 weeks.
Key to note before we discuss the results is that the treatment group on iron only achieved mean ferritin of 30 ng/ml.
Still well below the minimum of 50, if not for some at 100 ng/ml. Thus we could potentially expected even better results with higher doses.
Note the clear improvement, but also note, this is not a “cure” per se.
For your patients, use IN health Iron bisglycinate, which is superior to ferrous sulphate/fumerate is every way
– Even with 64% less iron, a 24 mg iron bisglycinate capsule beat a 66 mg ferrous fumerate by 96%.
And wayyyy less side effects.
For your patients, we can now test this easily with OPTIMAL TESTING.
But we still need to look at this in a more systematic approach.
My low tech approach is to get their amino acids up with more protein, aiming for 1.5-2 g of protein per KG of body weight – more protein = more phenylalanine and tyrosine = more potential to make dopamine and noradrenaline.
Which is easy terms is 2 palms of protein at each meal (see attached)
Most people are nowhere near this.
SIMPLE COLLAGEN is an easy way to increase overall protein, just add it to food like soup, or porridge or even just water, it is so pure, it has almost zero flavour.
And you can also give TYROSINE 1000 mg x3 daily to directly feed the dopamine to the noradrenaline pathway.
Maybe add some magnesium with B6.
If only someone had read the literature and had made a formula with both in already….😙
Add some vitamin D and you have a good stack.
For prevention, get pregnant women on CHOLINE (that’s why it is part of the Optimal Pregnancy TRIO.
Note, restless leg syndrome is also a marker for sub-optimal iron, as is chronic pain, all mediated by low production of dopamine, noradrenaline and serotonin.
Check out the full info on restless legs here:
