ADHD Drugs, the Good, Bad and Ugly

ADHD Drugs, The Good, Bad and Ugly

by Jeffrey Dach MD

In adults, brain stimulant drugs such as amphetamines and methylphenidate have been used and abused for decades by adults to stimulate the brain to obtain greater wakefulness, more rapid thinking, and more fluent verbal ability, etc. Methylphenidate (MPH) and cocaine have similar mechanisms of action. Both block dopamine and norepinephrine transporters, thus preventing re-uptake into the pre-synaptic neuron. This leads to greater accumulation of both dopamine and norepinephrine within the synaptic space, amplifying the post-synaptic signal. (See Schematic Diagram Below) (37)

Above Image: pink DAT = Dopamine Transporters involved in reuptake of dopamine. D1 and D2 are dopamine receptors at the post-synaptic neuron.  Blue dots are dopamine contained within vesicles within presynaptic neuron or released freely into synaptic  space. Above image courtesy of :  Véronneau-Veilleux, Florence, et al,2022. (37) (3)

Header Image at top courtesy of Volkow, Nora,(2012): PET scan of brain using tracer agent which shows activity of Dopamine Transporters in Basal Ganglia. Note reduced activity in Basal Ganglia after I.V. methylphenidate infusion indicating the drug blocks dopamine transporters. PET scans before and after Intravenous MP shows reduced Dopamine receptor availability in striatum for both untreated (naive) and chronically treated patients, reflecting increased Dopamine availability at the synaptic spaces elicited by the drug. (2)

ADHD Drugs Therapeutic Efficacy in Children

ADHD Drugs Are Toxic to Children’s Sensitive Brains

As discussed in my previous newsletter, adults have been using brain stimulants such as amphetamines and cocaine since the 1940’s as performance enhancing drugs, either obtained over-the-counter, a doctor’s prescription or from the street. Methylphenidate can be considered similar to cocaine in mode of action on the brain, since both block the DAT, Dopamine Transporters involved in re-uptake of dopamine into the pre-synaptic neuron, thus increasing dopamine levels within the synaptic space, and amplifying the post-synaptic signal. Amphetamines also increase vesicular release of dopamine in addition to blocking DAT. Both drugs also increase nor-epinephrine levels.

A Triumph of Clever Advertising over Common Sense

Left image: Note dramatic increasing ADHD prescription rates in the UK 1995–2015,courtesy of Renoux, Christel, et al. 2016. Fig 3. (38)

Stimulant drug use in children for ADHD is a new twist made possible by massive drug company advertising which increased methylphenidate use in the U.S. by 800 per cent from 1994 and 1999. Without the benefit of long term safety studies, drug company marketing convinced doctors, teachers and school psychologists that it is perfectly safe to prescribe highly addictive Schedule II brain stimulant drugs to children. DEA Schedule II is reserved for the most addictive and dangerous drugs in medicine, such as cocaine, fentanyl and oxycontin. In 2014, Dr. Allen Frances, the psychiatrist who chaired the DSMIV task force, (the manual for mental health disorders, and the “bible” for psychiatrists), wrote:

Drug companies were given the means, the motive,and the message to disease monger ADHD and blow it up out of all proportion.They succeeded beyond all  expectations in achieving a triumph of clever advertising over common sense. (11-13)

Follow the Money – ADHD is a Growth Industry

In 2023, the global ADHD therapeutics market for  methylphenidate and amphetamines is 32 billion dollars and expected to grow to 50 billion by 2028. These huge profits are powered by deceptive drug marketing, rigged, faked, or biased drug studies and old fashioned greed. The ADHD drug epidemic is still expanding, damaging the young brains of three generations of children. (20)

Opposite Effect In Children

Brain stimulants have the desired effect in adults, in whom they stimulate the brain as expected, serving as performance enhancing drugs. However, when stimulant drugs are used in children, they have quite the opposite effect, causing depression of brain activity, an obvious indicator of toxic overdose. According to Dr. Peter Breggin, a child psychiatrist with extensive experience treating ADHD kids, this drug toxicity is the “therapeutic effect” of ADHD drugs in children, and the explanation for “suppression of spontaneous and social behaviors”, depression and apathy as drug effects. ADHD drugs are useful for controlling behavior. However, there is no improvement in academic performance for kids on ADHD brain stimulants. (21-24)

In 1999, Dr. Peter Breggin writes:

The “therapeutic” effects of stimulants are a direct expression of their toxicity. Animal and human research indicates that these drugs often suppress spontaneous and social behaviors while promoting obsessive/compulsive behaviors. These adverse drug effects make the psychostimulants seemingly useful for controlling the behavior of children, especially in highly structured environments that do not attend to their genuine needs.(4)

Drug of Choice for ADHD

In ADHD kids, amphetamines and methylphenidate (Ritalin) are considered the drug of choice, transforming a misbehaved child exhibiting inattention, hyperactivity and impulsivity into a docile “zombie-like” child, now considered well-behaved by the teachers in the classroom.This seemingly miraculous remission in the child’s ADHD symptoms of hyperactivity, inattentiveness and impulsivity is a direct result of suppression of prefrontal cortical activity. This “therapeutic effect” of the ADHD drugs in children is actually a result of toxic over-dose which suppresses activity in the prefrontal cortex. In adults, ADHD drugs serve as performance enhancement drugs. In children, however, ADHD drugs merely affect behavior, without any enhancement in academic performance.(21-24)

Electrophysiology Studies in Mice of Pre-Frontal Cortex on Methylphenidate

In 2013, fourteen years after Dr. Peter Breggin’s observations about methylphenidate effects in ADHD kids, Dr. Kimberly Urban showed that Dr. Breggin was quite correct. Electrophysiology studies of prefontal cortex neurons in juvenile and adult mice treated with methylphenidate (Ritalin) showed that while adult mice respond normally to brain stimulants at commonly used therapeutic doses, juvenile mice with developing brains are hypersensitive to this same dosage, resulting in toxic over-dose which suppresses rather than stimulates brain activity. (1)

Even Extremely Small Doses Are Toxic in Children

Dr. Kimberly Urban even reduced the methylphenidate to extremely small dosages in juvenile mice, finding the same paradoxical effect. The neurons of the frontal cortex were still suppressed. See Dr. Kimberly Urban’s chart below: (1)

Above image from Fig 1 (Urban, 2013): MPH=Methylphenidate (Ritalin).

A) Juvenile Mice: Upper Frame Left side, Blue Ellipse and Arrow: Comparison of action potentials in prefrontal cortex neurons in juvenile mice (upper frame) and adult mice (lower frame) injected with single dose saline upper graph, and single dose methylphenidate lower chart. Notice decreased frequency of action potential spikes after MPH in juvenile mice, indicating depression of brain activity in PFC (PreFrontal Cortex) from single dose MPH.

A) Juvenile Mice: Upper Frame Right Side: Green Ellipse/Arrow shows action potential spikes after chronic saline (Green Ellipse and Arrow) or after chronic MPH (Red Ellipse and Arrow). Notice chronic MPH use decreases frequency of spikes, which then stops short, indicating severe depression of prefrontal cortex neurons in juvenile mice.

B) Adult Mice Lower Frame: Green Arrow and Ellipse shows chronic Saline given to Adult mice (serving as controls), while Red Arrow and Ellipse shows Chronic MPH administration to the adult mice. Notice chronic MPH dosage increases frequency of action potential spikes in adult mice compared to saline controls indicating increased stimulation of PFC neurons, the opposite of the depressive effect in juvenile mice.

Long Term Brain Alterations

In addition to confirming Dr. Breggin’s observations 14 years earlier, Dr. Urban found long term and possibly permanent alteration in brain chemistry, and function from chronic methylphenidate use in juvenile mice, raising the question of chronic brain alteration in children on ADHD drugs. This is also known as brain damage. Ample animal and human studies in the medical literature support this notion that long term use of ADHD drugs may cause alteration in brain chemistry, function, and behavior, some of which may remain permanent. (3-10)(14-19)

In 2017, Dr. Kimberly Urban writes:

Adolescent MPH [Methyphenidate] exposure was found to reduce social play, impair pattern learning and reversal learning, increase locomotor hyperactivity, and response to cocaine, sometimes lasting into adulthood. Early exposure to MPH has also been shown to result in increased anxiety lasting into adulthood and alter circadian rhythms. (18-19)

ADHD Child Brain Drug Tolerance – The Drugs Stop Working

Above images PET SCAN courtesy of Wang, (2013): Green Arrow shows baseline activity. Red arrow shows increased DAT activity in striatum after 1 year of MPH use in ADHD children. .  Averaged dopamine transporter availability (DAT) images. Averaged dopamine transporter availability images of ADHD (n = 18) and control (n = 11) subjects prior to and after 12 months oral MP  (Methylphenidate) treatment as well as baseline and 12 follow up scans of control subjects. (35)

Developing Drug Tolerance

In 2019, Dr. James M. Swanson, professor of pediatrics at University of California, Irvine, an expert on methylphenidate (MPH) in ADHD writes that ADHD children build up a tolerance to MPH in the long term (1-3 years), and require larger doses of MPH (or drug holiday) to overcome tolerance and restore efficacy. Note drug tolerance for MPH is similar to tolerance for other addictive drugs such as opiates requiring larger doses over time or drug holidays to restore efficacy. (36)

Dr. Gene-Jack Wang’s PET Scan Study in AHDH Children on MPH

The explanation for drug tolerance to methylphenidate (MPH) over time is shown by the 2013 PET study by Dr. Gene-Jack Wang (see above images). The PET scans use a tracer that shows DAT (Dopamine Transporter) availability in the brain. Note most of activity is in the striatum (basal ganglia). Note upper right images: follow up visit scan after 12 months of MPH use, the ADHD children using MPH show increased activity for DAT in the striatum (Red Arrow) compared to baseline (Green Arrow) and controls.  This means DAT (Dopamine Transporters) have increased. The brains of ADHD children on MPH compensate by increasing the number of Dopamine Transporters, serving to reduce the amount of excess dopamine at the synaptic cleft. This creates drug tolerance over time, and explains why MPH beneficial effects on ADHD behavior are only short term. The drug stops working in the long term (1-3 years). (35)

Methylphenidate Increased DAT in Mice

In 2013, Dr. Erin Calipari confirmed in studies using mice, Methylphenidate increased DAT (Dopamine Transporter) expression. (52)

Increased DAT Causes Dopamine Toxicity and Neuron Loss

When Dopamine Transporters are increased for any reason, toxic dopamine levels accumulate in the terminal end of the neuron causing neuron cell death. Dopamine is a mitochondrial toxin and inhibits Complex I of the mitochondrial respiratory chain. Males are more susceptible to this adverse effect, compared to females protected by higher estrogen levels. (45) (52-59)

Damage to Dopaminergic Nerve Endings in the Striatum

In addition to upregulation of DAT (Dopamine Transporters) in the striatum, something much worse happens. In 2005, Dr. George Ricaurte studied amphetamine use in non-human primates (monkeys) at doses equivalent to those used for Adult ADHD, finding  damage to the terminal endings of dopaminergic neurons in the striatum (basal ganglia), writing:

Here we demonstrate that amphetamine treatment, similar to that used clinically for adult ADHD, damages dopaminergic nerve endings in the striatum of adult nonhuman primates. (42-43)

In 2012, Dr. Shankar Sadasivan studied methylphenidate use in mice finding similar loss of dopaminergic neurons in the basal ganglia. In addition there was microglia activation indicating inflammatory response. (59)

Adderall Addiction Treatment Centers Are Very Busy

If ADHD drugs are so safe, then why do we have tens of thousands of busy Adderal Addiction Treatment Centers? A Google search for Adderal Addiction Center yields two hundred million hits. Take a Look.

Analogy with the Opioid Epidemic

I see the current ADHD drug epidemic analogous to the Opioid epidemic. Opiates were abused for decades, and finally the pendulum swung the other way finally reigning in Oxycontin sales by Purdue Pharmaceuticals, owned by the Sackler family. The ADHD drug marketing playbook bears a striking resemblance to the Purdue/Oxycontin marketing playbook. Eventually, the massive iatrogenic harm to our children will be recognized and the ADHD drug epidemic will come to an end. We will look back and wonder how this could have gone on so long. (25-36)

The Scourge of the 21st Century

In 2018, Dr. Rima Gaidamowicz called ADHD “the scourge of the 21st century”, invented by doctors and pharmacists to tame misbehaving children while maximizing profit from drug treatments. Dr. Rima Gaidamowicz writes:

Those who question ADHD existence argue that this disorder is likely temperament and parenting matter, rather than the illness, and that the diagnosis and treatment of this illness can be a matter invented by doctors and pharmacists, the aim of which is to tame individuals disregarding public standards of conduct and get the maximum profit from medicines in the treatment of this illness. (60)

Methylphenidate and Cocaine have same mechanism of action. Note below image shows the mechanism of action of cocaine is identical to methylphenidate. They both block the Dopamine Transporters.

Above image: Cocaine in the brain: In the normal neural communication process, dopamine is released by a neuron into the synapse, where it can bind to dopamine receptors on neighboring neurons. Normally, dopamine is then recycled back into the transmitting neuron by a specialized protein called the dopamine transporter. If cocaine is present, it attaches to the dopamine transporter and blocks the normal recycling process, resulting in a buildup of dopamine in the synapse, which contributes to the pleasurable effects of cocaine. courtesy of the NIDA of NIH:

Conclusion: In 1999, Dr Peter Breggin made observations about the effects of brain stimulants on ADHD children, namely the therapeutic effect is a direct result of drug toxicity. Later in 2013, Dr. Breggin was shown to be quite correct by Dr. Kimberly Urban’s painstaking electrophysiology studies in mice. These studies and others show that the juvenile brain is hypersensitive to the effect of brain stimulants, producing the paradoxical effect of brain suppression. When stimulant drugs are given to adults, they stimulate the brain and serve as performance enhancers. However, when given to children, these drugs have the opposite effect, suppressing and depressing brain function. This is the definition of drug toxicity. Even small doses of ADHD brain stimulant drugs are toxic to children. This toxicity accounts for the “therapeutic effect” in ADHD children, and may result in long-term and even permanent alterations in brain chemistry and function. Another disturbing observation was made by Dr. Wang using PET scans showing Dopamine Transporter activity increases after chronic MPH administration. The ADHD child brain develops MPH tolerance by upregulating Dopamine Transporters. Knowing this, why would any parent want to do this to their child’s brain?  Think of it this way. Would you give your child cocaine to manage his/her behavior in the classroom, which will only work short term for a year or so? Ritalin (methylphenidate) is essentially the same drug as cocaine. They both block dopamine transporters. In my opinion, the medical use of brain stimulants in children is an iatrogenic catastrophe which should be halted immediately. (1-41)

ADHD is BS – “Mockumentary” Starring Australian Comedian Peter Rowsthorn

TRIGGER WARNING – If you are certain that amphetamines are good for impulsive/inattentive children DON’T WATCH ADHD is BS. This mockumentary stars Australian comedian Peter Rowsthorn (aka Brett for Kath and Kim) as American ‘ADHD expert’ Professor Chip Cash. Prof Cash parrots all the usual BS that will help the ADHD Industry sell US$22.5billion+ in drugs (primarily amphetamines for use by children) in 2021. Watch ADHD is BS, have a laugh, and then get serious and do something to help end this profitable, hypocritical, pseudo-scientific, twenty-first century form of child abuse.

Recommended Books:

Finally Focused: The Breakthrough Natural Treatment Plan for ADHD That Restores Attention, Minimizes Hyperactivity, and Helps Eliminate Drug Side Effects Paperback – May 9, 2017  by James Greenblatt MD (A Psychiatrist who treats ADHD children)

Talking Back to Ritalin: What Doctors Aren’t Telling You About Stimulants and ADHD Paperback – September 1, 2001 by Peter R. Breggin MD (A Psychiatrist who treats ADHD children)

An Anatomy of Addiction: Sigmund Freud, William Halsted, and the Miracle Drug, Cocaine Paperback – Illustrated, July 3, 2012 by Howard Markel (Author)

Seitler, Burton Norman. “ADHD: What We’ve Been Told Ain’t Necessarily So.” Deconstructing ADHD: Mental Disorder or Social Construct? 3 (2022): 119.

Jeffrey Dach MD
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Articles with Related Interest:

Attention Deficit Disorder Exposed as Drug Marketing Ploy

ADHD Attention Deficit HyperActivity Syndrome Part Two

The ADHD Drug Epidemic Amphetamines and Methylphenidate

Hypervaccination ADHD Autism and Neurodevelopmental Disorders

ADHD Attention Deficit Syndrome Part Two

Attention Deficit Disorder Exposed as Drug Marketing Ploy

Lithium Orotate the great Protector

More on Anti-Inflammatory Effects of Chinese Skullcap

References:

1) Urban, Kimberly R., and Wen-Jun Gao. “Methylphenidate and the juvenile brain: enhancement of attention at the expense of cortical plasticity?.” Medical hypotheses 81.6 (2013): 988-994.

(1A) Urban, Kimberly R., and Wen-Jun Gao. “Psychostimulants as cognitive enhancers in adolescents: more risk than reward?.” Frontiers in Public Health 5 (2017): 260.

adolescent MPH exposure was found to reduce social play, impair pattern learning and reversal learning, increase locomotor hyperactivity, and response to cocaine, sometimes lasting into adulthood (57–60). Early exposure to MPH has also been shown to result in increased anxiety lasting into adulthood and alter circadian rhythms (61–65).

These results suggest that there is an age-dependent effect of MPH in the PFC, and that the juvenile brain may be hypersensitive to the effects of psychostimulants, and even a low dose may push the healthy developing brain into a hyperdopaminergic and hyperadrenergic state.

Thus, psychostimulants given at low doses similar to those used to treat ADHD may indeed provide an effective and largely safe cognitive enhancement, as the PFC of adults has finished maturing (11, 12, 99).

However, in the adolescent brain, levels of DA and NE are naturally higher, as the PFC development is ongoing and synaptic pruning has not been completed; thus, adding psychostimulants likely pushes the levels of DA and NE beyond the optimal range and into excessive levels (12). This is consistent with impairments in pattern learning and object-memory, reduced pyramidal neuron activity, and reduced NR2B-containing NMDA receptor levels seen in our studies

Until the research is completed to give us a more thorough understanding of the drugs’ actions in the developing PFC, off-label use of psychostimulants and nootropics may present more risk than reward for adolescents.

(1B) Urban, Kimberly R., Barry D. Waterhouse, and Wen-Jun Gao. “Distinct age-dependent effects of methylphenidate on developing and adult prefrontal neurons.” Biological psychiatry 72.10 (2012): 880-888.

(1C) Urban, Kimberly R., and Wen-Jun Gao. “Performance enhancement at the cost of potential brain plasticity: neural ramifications of nootropic drugs in the healthy developing brain.” Frontiers in systems neuroscience 8 (2014): 38.

2) Volkow, Nora D., et al. “Methylphenidate-elicited dopamine increases in ventral striatum are associated with long-term symptom improvement in adults with attention deficit hyperactivity disorder.Journal of neuroscience 32.3 (2012): 841-849. Headre image is Fig1. Averaged DA D2/D3 receptor availability (BPND) images for the [11C]raclopride scans done after intravenous placebo and after intravenous MP (iv-MP) for the treatment-naive and long-term treatment conditions. Intravenous MP reduced DA D2/D3 receptor availability in striatum in both conditions, reflecting the DA increases elicited by the drug.

3) Loureiro-Vieira, Sara, et al. “Methylphenidate effects in the young brain: friend or foe?.” International Journal of Developmental Neuroscience 60 (2017): 34-47.

Above Image Courtesy of Dr Sara Loureiro-Vieira, (2017) : Fig. 2. Methylphenidate (MPH) Mechanism of Action on Monoamine Neurotransmitters. MPH binds to and blocks the dopamine and norepinephrine transporters which inhibits the re-uptake of  dopamine and norepinephrine into the pre-synaptic nerve ending. The increase of  Dopamine and Norepinephrine in the synaptic space leads to enhanced postsynaptic signalling. (3)

Dr. Peter Breggin on the Safety and Efficacy of ADHD Drugs

4) Breggin, Peter R. “Psychostimulants in the treatment of children diagnosed with ADHD: Risks and mechanism of action.” International Journal of Risk & Safety in Medicine 12.1 (1999): 3-35.

Millions of children in North America are diagnosed with attention deficit/hyperactivity disorder and treated with psychostimulants such as methylphenidate, dextroamphetamine, and methamphetamine. These drugs produce a continuum of central nervous system toxicity that begins with increased energy, hyperalertness, and overfocusing on rote activities. It progresses toward obsessive/compulsive or perseverative activities, insomnia, agitation, hypomania, mania, and sometimes seizures. They also commonly result in apathy, social withdrawal, emotional depression, and docility. Psychostimulants also cause physical withdrawal, including rebound and dependence. They inhibit growth, and produce various cerebral dysfunctions, some of which can become irreversible. The “therapeutic” effects of stimulants are a direct expression of their toxicity. Animal and human research indicates that these drugs often suppress spontaneous and social behaviors while promoting obsessive/compulsive behaviors. These adverse drug effects make the psychostimulants seemingly useful for controlling the behavior of children, especially in highly structured environments that do not attend to their genuine needs.

5) Sadasivan, Shankar, et al. “Methylphenidate exposure induces dopamine neuron loss and activation of microglia in the basal ganglia of mice.” PloS one 7.3 (2012): e33693.

6) Cavaliere, Carlo, et al. “Methylphenidate administration determines enduring changes in neuroglial network in rats.” European Neuropsychopharmacology 22.1 (2012): 53-63.

7) Lagace, Diane C., et al. “Juvenile administration of methylphenidate attenuates adult hippocampal neurogenesis.” Biological psychiatry 60.10 (2006): 1121-1130.

8) Fotopoulos, Nellie H., et al. “Cumulative exposure to ADHD medication is inversely related to hippocampus subregional volume in children.” NeuroImage: Clinical 31 (2021).

9) Solleveld, Michelle M., et al. “Age-dependent, lasting effects of methylphenidate on the GABAergic system of ADHD patients.” NeuroImage: Clinical 15 (2017): 812-818.

10) Carlezon Jr, William A., Stephen D. Mague, and Susan L. Andersen. “Enduring behavioral effects of early exposure to methylphenidate in rats.” Biological psychiatry 54.12 (2003): 1330-1337.

The Manipulation of Data and Attitudes about ADHD

11) Leo, Jonathan, and Jeffrey Lacasse. “The Manipulation of Data and Attitudes about ADHD: A Study of Consumer Advertisments.” Rethinking ADHD: from brain to culture (2009): 287-312.

Between 1994 and 1999, the production of Ritalin increased eight hundred percent, with ninety percent of it being consumed in the United States

ADHD has been the subject of considerable controversy over the years. It has no biological diagnostic markers; it has been theorized to be over-diagnosed in Western countries; and it can be treated by both
psychosocial and pharmacological interventions. In addition, the most popular treatments for ADHD are Schedule II pharmaceuticals – psychostimulant drugs, such as methylphenidate or amphetamine, which carry both addictive properties and the risk of iatrogenic harm, and are largely prescribed to a vulnerable population

12) Leo, Jonathan, and Jeffrey R. Lacasse. “The New York Times and the ADHD epidemic.” Society 52 (2015): 3-8.

Drug companies were given the means, the motive,and the message to
disease monger ADHD and blow it up out of all proportion.They succeeded beyond all  expectations in achieving a triumph of clever advertising over common sense.  Allen Frances, Chair, DSMIIV, February 12, 2014

13) These Are The Ridiculous Ads Big Pharma Used To Convince Everyone They Have ADHD Richard Feloni Dec 16, 2013, 3:29 PM EST

14) Bolaños, Carlos A., et al. “Antidepressant treatment can normalize adult behavioral deficits induced by early-life exposure to methylphenidate.” Biological psychiatry 63.3 (2008): 309-316.

15) Achat-Mendes, C., K. L. Anderson, and Y. Itzhak. “Methylphenidate and MDMA adolescent exposure in mice: long-lasting consequences on cocaine-induced reward and psychomotor stimulation in adulthood.” Neuropharmacology 45.1 (2003): 106-115.

16) Carlezon Jr, William A., Stephen D. Mague, and Susan L. Andersen. “Enduring behavioral effects of early exposure to methylphenidate in rats.Biological psychiatry 54.12 (2003): 1330-1337.

17) Bolanos, Carlos A., et al. “Methylphenidate treatment during pre-and periadolescence alters behavioral responses to emotional stimuli at adulthood.” Biological psychiatry 54.12 (2003): 1317-1329.

Results: The MPH-treated animals were significantly less responsive to natural rewards such as sucrose, novelty-induced activity, and sex compared with vehicle-treated control animals. In contrast, MPH-treated animals were significantly more sensitive to stressful situations, showed increased anxiety-like behaviors, and had enhanced plasma levels of corticosterone.

Conclusions: Chronic exposure to MPH during development leads to decreased sensitivity to rewarding stimuli and results in enhanced responsivity to aversive situations. These results highlight the need for further research to improve understanding of the effects of stimulants on the developing nervous system and the potential enduring effects resulting from early-life drug exposure.

18) Urban, Kimberly R., and Wen-Jun Gao. “Psychostimulants as cognitive enhancers in adolescents: more risk than reward?.” Frontiers in Public Health 5 (2017): 260.

The current dearth of knowledge on the dose–response curve, metabolism, and cognitive outcomes in adolescents following methylphenidate or other psychostimulant exposure may be perpetuating a perception of these drugs as “safe” when that might not be true for developing brains.

The first stimulant approved for ADHD treatment AMPH (Adderall©) blocks reuptake but also increases vesicular release of DA; the effect on DA release is the main action at low doses

stimulant medications seem to improve cognitive function in an inverted-U curve manner, with lower doses improving and higher doses impairing various aspects of cognition

adolescent MPH exposure was found to reduce social play, impair pattern learning and reversal learning, increase locomotor hyperactivity, and response to cocaine, sometimes lasting into adulthood (57–60). Early exposure to MPH has also been shown to result in increased anxiety lasting into adulthood and alter circadian rhythms (61–65).

The current dearth of knowledge on the dose–response curve, metabolism, and cognitive outcomes in juveniles and adolescents following MPH or other psychostimulant exposure may be perpetuating a perception of these drugs as “safe” for any age when that might not be true.

19) Urban, Kimberly R., et al. “A clinically-relevant dose of methylphenidate enhances synaptic inhibition in the juvenile rat prefrontal cortex.” Journal of reward deficiency syndrome and addiction science 2.3 (2017): 69.

Taken together, these results suggest that MPH administration to a healthy juvenile may enhance excitation of GABAergic interneurons; thus shifting the excitation-inhibition balance in the prefrontal cortex towards inhibition, and depressing overall prefrontal cortical activity. Our findings also indicate that the adolescent brain is more sensitive to MPH than previously thought, and dose ranges need to be reconsidered for age as well as size.

20) Market Data Forecast: Global ADHD therapeutics market is 32 billion in 2023 and is expected to grow to 50 billion by 2028.

Academic Performance

21) de Faria, Joyce Costa Melgaço, et al. ““Real‐world” effectiveness of methylphenidate in improving the academic achievement of Attention‐Deficit Hyperactivity Disorder diagnosed students—A systematic review.” Journal of Clinical Pharmacy and Therapeutics 47.1 (2022): 6-23.

the available evidence does not support the establishment of adequate conclusions about the real benefits of methylphenidate in the academic improvement of ADHD students.

22) Watson, G. L., Andrea Powell Arcona, and David O. Antonuccio. “The ADHD drug abuse crisis on American college campuses.” Ethical Hum Psychol Psychiatry 71 (2015): 5-21.

Although popularly viewed as “academic steroids,” there is no evidence that ADHD medications promote complex cognitive functioning or scholarship. To the contrary, compelling new evidence indicates that ADHD drug treatment is associated with deterioration in academic and social-emotional functioning.

23) Cregin, Dennis, et al. “The Adderall Epidemic: A Proposed Cyclic Relationship between ADHD Medication Use, Academic Performance, and Mental Distress.” Impulse (19343361) 18.1 (2021).

A total of 879 individuals completed an anonymous Google Form survey that was administered at colleges/universities in the U.S. using social media platforms. The survey included questions regarding frequency of ADHD medication use, symptoms experienced, perception of safety, GPA, and general demographic information. Our results indicate that the use of ADHD medication is significantly correlated with a self-reported low GPA as well as an increase in reported mental health side effects (including depression,anxiety, and panic attacks) and physical side effects (including sleep disturbances, fatigue, headaches, and weight loss). Conversely, belief in the efficacy of ADHD medications in aiding academic performance was negatively correlated with a self-reported high GPA. It thus appears that the use of non-prescription ADHD medications is not associated with increased academic performance. Furthermore, mental and physical symptoms related to illicit ADHD medication use are likely to contribute to the observed poor academic performance. It is therefore recommended that college student populations are educated on these findings to decrease illicit use of ADHD medications as study aids.

===== No increment in academic learning =============

24) Pelham, William E., et al. “The effect of stimulant medication on the learning of academic curricula in children with ADHD: A randomized crossover study.” Journal of consulting and clinical psychology 90.5 (2022): 367-380.

Results: Medication had large, salutary, statistically significant effects on children’s academic seatwork productivity and classroom behavior on every single day of the instructional period. However, there was no detectable effect of medication on learning the material taught during instruction: Children learned the same amount of subject-area and vocabulary content whether they were taking OROS-MPH or placebo during the instructional period.

Acute effects of OROS-MPH on daily academic seatwork productivity and classroom behavior did not translate into improved learning of new academic material taught via small-group, evidence-based instruction. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

25) Meier, Barry. Pain killer: an empire of deceit and the origin of America’s opioid epidemic. Random House, 2018.

26) Posner, Gerald. Pharma: Greed, lies, and the poisoning of America. Simon and Schuster, 2021.

27) Chow, Ronald. “Purdue Pharma and OxyContin–A Commercial Success But Public Health Disaster.” Harvard Public Health Review 25 (2019).

28) Schatman, Michael E., and Lynn R. Webster. “The health insurance industry: perpetuating the opioid crisis through policies of cost-containment and profitability.” Journal of Pain Research (2015): 153-158.

29) Schwartz, Stephan A. “America′ s Deadly Opioid Epidemic from Which Everyone But the Users Profits.” Explore: The Journal of Science and Healing (2017).

30) Arteaga, Carolina, and Victoria Barone. A Manufactured Tragedy: The Origins and Deep Ripples of the Opioid Epidemic. Working paper. http://www. carolina. com/s/Opioids_ArteagaBarone_Jan2022. pdf, 2022.

31) Gale, Arthur H. “Drug company compensated physicians role in causing America’s deadly opioid epidemic: When will we learn?.” Missouri medicine 113.4 (2016): 244.

32) Morreale, Mary. “Why Is the Pendulum Swinging? The Opiate Epidemic in the USA: Dreamland: The True Tale of America’s Opiate Epidemic. By Sam Quinones; Bloomsbury Press; New York; 2015; ISBN: 978-1-62040-250-4; pp. 384; $28 (hardcover).” (2016): 839-840.

33) Edgell, Caitlyn. “It’s Time to Finish What They Started: How Purdue Pharma and the Sackler Family Can Help End the Opioid Epidemic.” Penn St. L. Rev. 125 (2020): 255.

34) Gale, Arthur. “Sacklers Sacked But Purdue Still Caused Opioid Epidemic.” Missouri Medicine 119.2 (2022): 109.

====== Chronic MPH Increases DAT Transporters ========

35) Wang, Gene-Jack, et al. “Long-term stimulant treatment affects brain dopamine transporter level in patients with attention deficit hyperactive disorder.” PloS one 8.5 (2013): e63023.

Discussion  This study shows that long-term treatment with MPH up-regulated DAT availability in the ventral striatum, providing the first evidence of DAT neuroplasticity after long-term treatment with a clinically relevant dose of MPH in the human brain. DAT is responsible for recycling DA from the extracellular space into the pre-synaptic terminal [14]. The DAT levels in the membrane are regulated by the concentration of extracellular DA; DAT levels decrease when extracellular DA is low and increase when extracellular DA is high [15]. Repeated administration of a variety of stimulant drugs (e.g., cocaine, amphetamine) has been shown to change DAT expression in  preclinical models. These studies show different results for stimulant drugs that are DAT blockers, such as cocaine, from those of stimulant drugs that are DA releasers, such as methamphetamine and amphetamine. Cocaine, which like MPH blocks DAT, temporarily increases the expression of DAT after chronic administration [16]. Indeed humans, postmortem and imaging studies have shown increased DAT (20–50%) in the striatum of chronic cocaine abusers when compared with controls [17], [18]. These increases are positively correlated with the severity of cocaine use and can recover with detoxification. This is consistent with an adaptation response to compensate for chronic increases in extracellular DA secondary to repeated cocaine intoxication.

Similarly, subchronic MPH treatment results in an attenuation of DA release in rodents, which was ascribed to either an upregulation of DAT or enhanced autoreceptor sensitivity [19]. In ADHD adults we also recently showed that long-term treatment with clinical doses of MPH resulted in an attenuation of MPH induced DA increases in the striatum [20]. Similar to treatment with other DAT blockers the increased expression of DAT in the striatum after long term MPH treatment in this study might reflect an accelerated clearance of synaptic DA in response to chronic DA enhancement from long-term exposure to MPH [14]. In this study the clinical measures at follow-up were obtained while subjects were under the influence of the medication (MPH), which explains the significant improvement in all of the clinical symptoms. However it would have been desirable to test them also when they were not under the effects of MPH (i.e. in the morning prior to medication intake) to assess if the upregulation of DAT after chronic MPH was associated with impaired performance.

Few studies have investigated the behavioral consequences of long-term exposure to MPH and the extent to which chronic exposure results in tolerance is still a matter of debate. Indeed, studies on the chronic effects of MPH have reported conflicting results with some documenting sensitization to the locomotor effects of MPH [21], others tolerance [22], and others no changes [23]. The reasons for these discrepancies are likely to reflect differences in doses, conditions of drug administration and age of the animals. The findings on the effects of chronic MPH (using doses that are therapeutically relevant), on the rewarding effects of drugs of abuse are also not consistent. Whereas one study reported that MPH pretreatment in preadolescence or in adulthood decreased the rewarding effects of cocaine (as assessed by conditioned place preference) later in life [24], two others [25], [26] reported that chronic MPH treatment in adolescence or in adulthood enhanced cocaine’s reinforcing effects (as assessed by cocaine self-administration and the latency for acquisition of self-administration). These behavioral changes are likely to reflect in part changes in brain DA activity since DA is involved both in locomotor activity as well as the rewarding effects of cocaine. In this study, even though the ADHD subjects did not show more hyperactivity as compared to the controls prior to MPH treatment, the SWAN scores for the hyperactivity/impulsivity dimension in the ADHD subjects were significantly reduced after long-term MPH treatment.

We hypothesize that the increased DAT availability is a compensation for the pharmacologic occupancy of DAT (estimated to be greater than 50%) [27] and the increased elevations in synaptic DA. The results of this prospective treatment study and theory of DAT plasticity suggest that some of the discrepancies in the literature regarding the levels of DAT in ADHD may reflect treatment histories. Note also that in some instances the results are confounded by measuring DAT while the pharmacological effects of MPH are still present [28], which would result in lower measures of DAT availability secondary to DAT occupancy by MPH. Thus we postulate that decreased synaptic levels of DA might drive the changes in DAT levels reported in ADHD (which vary to maintain equilibrium of synaptic DA levels in brain).

Here we report an upregulation of DAT secondary to long-term treatment with stimulant medication, which could result in further decreases in dopaminergic signaling when the individual with ADHD is not medicated (i.e. over weekend holidays). To the extent that reduced DA release in ADHD is associated with inattention [29], this could result in more severe inattention and the need for higher doses of medication. Though there is limited literature on loss of efficacy of stimulant medication with long-term treatment this is an area that merits further investigation. Studies are necessary to test if DAT down-regulate after MPH discontinuation and the time necessary for their recovery.

36)  Swanson, JM. Debate: are stimulant medications for attention-deficit/hyperactivity disorder effective in the long term? J Am Acad Child Adolesc Psychiatry. 2019; 58(10):936–938.

James Swanson: Sparse data from RCT studies suggest long-term effectiveness of long-term treatment-as-usual diminishes over time and is small for continuing treatment when long-term is specified as 1 year.

long-term observational follow-up studies indicate a history of treatment with stimulant medication is not associated with long-term effectiveness for long time periods (3 to 10 years).

Dissipation may be due to insufficient continued increases in daily dose in the long-term follow-up (as the approved maximum is approached) to overcome long-term tolerance hypothesized to accumulate with extended consistent treatment. A positron emission tomography (PET) study of long-term treatment with methylphenidate for 1 year showed that density of dopamine transporters in ventral striatal brain regions increased by 24%, suggesting a possible neural mechanism underlying long-term tolerance.11=  11. Wang GJ, Volkow ND, Wigal T et al. Long-term stimulant treatment affects brain dopamine transporter level in patients with attention deficit hyperactive disorder. PLoS One 2013;8(5):e63023.

In long-term treatment, daily doses beyond the approved maximum may be required to maintain effectiveness, but in most clinical practices, this is not acceptable. Also, consistent treatment is recommended, but stopping and restarting may release tolerance and offer a more effective method of long-term treatment.

The literature clearly documents short-term effectiveness (that certainly justifies clinical treatment), but critical studies also indicates effectiveness diminishes over time and in the long-term (defined as > 3 years) the average residual or continuing effects of treatment-as-usual are no longer clinically significant.

37) Véronneau-Veilleux, Florence, et al. “A mechanistic model of ADHD as resulting from dopamine phasic/tonic imbalance during reinforcement learning.” Frontiers in Computational Neuroscience 16 (2022): 849323.

38) Renoux, Christel, et al. “Prescribing trends of attention‐deficit hyperactivity disorder (ADHD) medications in UK primary care, 1995–2015.” British journal of clinical pharmacology 82.3 (2016): 858-868.
Figure 3 Attention‐deficit hyperactivity disorder prescription rates in the UK Clinical Practice Research Datalink, 1995–2015, stratified by drugs.

39) Volkow, Nora D., et al. “Methylphenidate and cocaine have a similar in vivo potency to block dopamine transporters in the human brain.” Life sciences 65.1 (1999): PL7-PL12.

40) Volkow, N. D., et al. “Comparable changes in synaptic dopamine induced by methylphenidate and by cocaine in the baboon brain.” Synapse 31.1 (1999): 59-66.

41) Volkow, Nora D., et al. “Is methylphenidate like cocaine?: Studies on their pharmacokinetics and distribution in the human brain.” Archives of general psychiatry 52.6 (1995): 456-463.

42) Effect of ADHD Medications on the Brain Medically reviewed by Puya Yazdi, MD Written by Carlos Tello, PhD (Molecular Biology) Last updated: November 3, 2021

43) Ricaurte, George A., et al. “Amphetamine treatment similar to that used in the treatment of adult attention-deficit/hyperactivity disorder damages dopaminergic nerve endings in the striatum of adult nonhuman primates.” Journal of Pharmacology and Experimental Therapeutics 315.1 (2005): 91-98.

44) Top Neuroscientist Explains How Big Pharma’s Adderall Is Essentially Crystal Meth David Rainoshek, MA Feb 22, 2016

45) Is Adderall the True ‘Gateway Drug’?
Medication can be a lifeline for people with ADHD. But hustle culture has normalized amphetamine abuse in the pursuit of productivity and achievement
C. Brian Smith Mel Magazine

45) Miyazaki I, Asanuma M. Dopaminergic neuron-specific oxidative stress caused by dopamine itself. Acta Med Okayama. 2008;62(3):141-50.

Dopamine and its metabolites containing 2 hydroxyl residues exert cytotoxicity in dopaminergic neuronal cells, primarily due to the generation of highly reactive dopamine and DOPA quinones.

46) Angelucci F, Gruber SH, El khoury A, Tonali PA, Mathé AA. Chronic amphetamine treatment reduces NGF and BDNF in the rat brain. Eur Neuropsychopharmacol. 2007;17(12):756-62

Amphetamines (methamphetamine and d-amphetamine) are dopaminergic and noradrenergic agonists and are highly addictive drugs with neurotoxic effect on the brain. In human subjects, it has also been observed that amphetamine causes psychosis resembling positive symptoms of schizophrenia. Neurotrophins are molecules involved in neuronal survival and plasticity and protect neurons against (BDNF) are the most abundant neurotrophins in the central nervous system (CNS) and are important survival factors for cholinergic and dopaminergic neurons. Interestingly, it has been proposed that deficits in the production or utilization of neurotrophins participate in the pathogenesis of schizophrenia. In this study in order to investigate the mechanism of amphetamine-induced neurotoxicity and further elucidate the role of neurotrophins in the pathogenesis of schizophrenia we administered intraperitoneally d-amphetamine for 8 days to rats and measured the levels of neurotrophins NGF and BDNF in selected brain regions by ELISA. Amphetamine reduced NGF levels in the hippocampus, occipital cortex and hypothalamus and of BDNF in the occipital cortex and hypothalamus. Thus the present data indicate that chronic amphetamine can reduce the levels of NGF and BDNF in selected brain regions. This reduction may account for some of the effects of amphetamine in the CNS neurons and provides evidences for the role of neurotrophins in schizophrenia.

47) Adderall Risks: Much More Than You Wanted To Know
Posted on December 28, 2017 by Scott Alexander

Trying to discover the risks of Adderall is a kind of ridiculous journey. It’s ridiculous because there are two equal and opposite agendas at work. The first agenda tries to scare college kids away from abusing Adderall as a study drug by emphasizing that it’s terrifying and will definitely kill you. The second agenda tries to encourage parents to get their kids treated for ADHD by insisting Adderall is completely safe and anyone saying otherwise is an irresponsible fearmonger. The difference between these two situations is supposed to be whether you have a doctor’s prescription. But what if you are the doctor, trying to decide who to prescribe it to? Then what? All they tell you in medical school is to give it to the people who actually have ADHD – which, I repeat, is kind of meaningless.

48) From Nazi Blitzkriegs to ADHD Treatment: What Stimulant Drugs Can and Cannot Do by Bruce E. Levine CounterPunch Feb 9, 2023

49) Theanine and ADHD: Literature Search on Google Scholar

50) Lithium and ADHD : Literature Search in Google Scholar

51) Lithium and Attention Deficit Disorder

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Methylphenidate increases DAT expression – MICE

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52) Calipari, Erin S., et al. “Methylphenidate amplifies the potency and reinforcing effects of amphetamines by increasing dopamine transporter expression.” Nature communications 4 (2013): 2720.

Methylphenidate (MPH) is commonly diverted for recreational use, but the neurobiological consequences of exposure to MPH at high, abused doses are not well defined. Here we show that MPH self-administration in rats increases dopamine transporter (DAT) levels and enhances the potency of MPH and amphetamine on dopamine responses and drug seeking behaviors, without altering cocaine effects. Genetic over-expression of the DAT in mice mimics these effects, confirming that MPH self-administration-induced increases in DAT levels are sufficient to induce the changes. Further, this work outlines a basic mechanism by which increases in DAT levels, regardless of how they occur, are capable of increasing the rewarding and reinforcing effects of select psychostimulant drugs, and suggests that individuals with elevated DAT levels, such as ADHD sufferers, may be more susceptible to the addictive effects of amphetamine-like drugs.

————————————— –

Dopamine transporter over-expressing (DAT-tg) mice display spontaneous loss of midbrain dopamine neurons

53)  Masoud, S. T., et al. “Increased expression of the dopamine transporter leads to loss of dopamine neurons, oxidative stress and l-DOPA reversible motor deficits.” Neurobiology of disease 74 (2015): 66-75.

In this study, we report that over-expression of DAT is capable of triggering oxidative stress, dopamine neuron loss and L-DOPA reversible motor deficits in DAT-tg mice

we characterized transgenic mice that over-express the dopamine transporter selectively in dopamine neurons. We report that dopamine transporter over-expressing (DAT-tg) mice display spontaneous loss of midbrain dopamine neurons that is accompanied by increases in oxidative stress markers, 5-S-cysteinyl-dopamine and 5-S-cysteinyl-DOPAC.

Collectively, our findings demonstrate that even in neurons that routinely handle dopamine, increased uptake of this neurotransmitter through the dopamine transporter results in oxidative damage, neuronal loss and LDOPA reversible motor deficits.

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54) Gerlach, Manfred, Edna Grünblatt, and Klaus W. Lange. “Is the treatment with psychostimulants in children and adolescents with attention deficit hyperactivity disorder harmful for the dopaminergic system?.” ADHD Attention Deficit and Hyperactivity Disorders 5 (2013): 71-81.

The available findings in non-human primates support the notion that the administration of amphetamine and methylphenidate with procedures simulating clinical treatment conditions does not lead to long-term adverse effects in regard to development, neurobiology or behaviour as related to the central dopaminergic system.
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55) Miller, Gary W., et al. “Dopamine transporters and neuronal injury.” Trends in pharmacological sciences 20.10 (1999): 424-429.

Indeed, it appeared that neurones that expressed higher levels of DAT were more susceptible to the neurotoxic effects of MPP1 than those expressing lower levels (Refs 17, 18). There is also evidence of a correlation between DAT expression and the extent of cellular damage in transfected cells expressing different levels of DAT (Refs 19, 20). In addition to exogenous toxins like MPTP, there are several putative endogenous toxins, such as dopamine itself…High levels of cytosolic dopamine have been shown to inhibit mitochondrial respiration and cause autooxidation of dopamine and free radical formation21,22…Animals that did not express DAT were immune to damage to the dopamine system,

56) Storch, A., A. C. Ludolph, and J. Schwarz. “Dopamine transporter: involvement in selective dopaminergic neurotoxicity and degeneration.” Journal of neural transmission 111 (2004): 1267-1286.

Dopaminergic toxicity of its active metabolite 1-methyl-4-pyridinium (MPP(+)) is mediated by the DAT through accumulation into DA neurons, where it inhibits mitochondrial complex I activity.

57)  Miller, D. B., et al. “The impact of gender and estrogen on striatal dopaminergic neurotoxicity.” Annals of the New York Academy of Sciences 844 (1998): 153-165.

estrogen has neuroprotective properties in this model of striatal dopaminergic neurotoxicity.

58) Ben‐Shachar, Dorit, Roza Zuk, and Yelena Glinka. “Dopamine neurotoxicity: inhibition of mitochondrial respiration.” Journal of neurochemistry 64.2 (1995): 718-723.

These results suggest that catecholamines can cause toxicity not only by inducing an oxidative stress state but also possibly through direct interaction with the mitochondrial electron transport system.

59) Sadasivan, Shankar, et al. “Methylphenidate exposure induces dopamine neuron loss and activation of microglia in the basal ganglia of mice.” PloS one 7.3 (2012): e33693.

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Those who question ADHD existence argue that this disorder is likely temperament and parenting matter, rather than the illness, and that the diagnosis and treatment of this illness can be a matter invented by doctors and pharmacists, the aim of which is to tame individuals disregarding public standards of conduct and get the maximum profit from medicines in the treatment of this illness.

60) Gaidamowicz, Rima, et al. “ADHD-the scourge of the 21st century?.” Psychiatria polska 52.2 (2018): 287-307.

Currently, attention deficit hyperactivity disorder (ADHD) is intensively studied by world medical community, its understanding expands, for example, it has now been diagnosed not only in children but also in adults. On the other hand, ADHD raises a number of discussions on the need of its treatment and, if there is a need, how it shall be treated, it is doubtful whether this disorder overall exists, because its “morphological component” has not been identified so far, and all the symptoms of ADHD, including anxiety, concentration difficulties, motor hyperactivity, cognitive disorders or social disadaptation, can be found in a number of mental disorders and somatic diseases. Modern attention, emotional and behavioral changes can be considered as a result of changing human social portrait. Those who question ADHD existence argue that this disorder is likely temperament and parenting matter, rather than the illness, and that the diagnosis and treatment of this illness can be a matter invented by doctors and pharmacists, the aim of which is to tame individuals disregarding public standards of conduct and get the maximum profit from medicines in the treatment of this illness. Due to the fact that ADHD is diagnosed more often, it is even called the twenty-first-century scourge. In this article we will review the historical aspect of formation of ADHD diagnosis, illness etiology, comorbidity with other mental and somatic diseases as well as treatment necessity and opportunities, paying attention to adult ADHD as well.

61) Lange, Klaus W. “The treatment of attention deficit hyperactivity disorder has no proven long-term benefits but possible adverse effects.” Movement and Nutrition in Health and Disease 1 (2017).

In summary, treatment of ADHD has no proven beneficial impact on long-term outcomes but may be associated with various adverse effects.

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One thought on “ADHD Drugs, the Good, Bad and Ugly

  1. K2 and thyroid and get your D3 walking outside, as much as possible. Skip the drugs.
    Your doctor might not know this and I have only seen one supplement made this way but always with D3. Also if possible, get off all grains and try raw dairy (I would give this a good try before running to the doctor) and before giving dairy up altogether. Show your doctor this link from June 2022:
    ADHD and thyroid disorders: Are they linked? – Medical News Today Jun 30, 2022 Diagnosis Misdiagnosis Treatment Seeking medical advice Outlook Thyroid disorders and ADHD have overlapping symptoms. Studies also suggest that there is an association between thyroid.

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