Methylphenidate side effect, use for adhd, Ritalin
January 20 2018 by Ray Sahelian, M.D.

Pediatrics. 2016. Stimulant Medication and Psychotic Symptoms in Offspring of Parents With Mental Illness. Stimulants, such as methylphenidate, are among the most commonly used medications in children and adolescents. Psychotic symptoms have been reported as rare adverse reactions to stimulants but have not been systematically inquired about in most previous studies. Family history of mental illness may increase the vulnerability to drug-induced psychotic symptoms. We examined the association between stimulant use and psychotic symptoms in sons and daughters of parents with major mood and psychotic disorders. We assessed psychotic symptoms, psychotic-like experiences, and basic symptoms in 141 children and youth, who had 1 or both parents with major depressive disorder, bipolar disorder, or schizophrenia, and of whom 24 (17%) had taken stimulant medication. Psychotic symptoms were present in 62% of youth who had taken stimulants compared with 27% of participants who had never taken stimulants.

Heart palpitations
Ritalin, a popular drug for treating attention-deficit hyperactivity disorder (ADHD), increases the risk of an abnormal heart rhythm. Children and teens who are prescribed methylphenidate -- sold under the brand names Ritalin, Daytrana and Concerta -- have a an increased risk of arrhythmias

Bone loss, osteoporosis
Commonly prescribed drugs to treat attention-deficit hyperactivity disorder ADHD may affect bone density. Young people who take stimulants such as methylphenidate (Ritalin, Concerta) and Adderall have lower bone density than their peers. This could have serious consequences later in life.

Women who take Ritalin or Concerta for attention-deficit/hyperactivity disorder (ADHD) have a small increased risk of having a baby with a heart defect if Ritalin/Concerta (methylphenidate) was taken by the mother-to-be.

Methylphenidate and weight loss
Weight loss is known to be a potential side effect of methylphenidate. Methylphenidate  increases brain levels of the chemical dopamine, which is involved in feelings of pleasure and "reward." Dopamine levels increase in response to food, and some research has suggested that people with normally low dopamine levels may be more vulnerable to becoming overweight because of the reward value they get from food. Dr. Gary S. Goldfield and his colleagues at the University of Ottawa in Canada had 14 adults take either a dose of methylphenidate or a placebo shortly before offering the volunteers a buffet lunch. The volunteers' pre-lunch hunger ratings were no different whether they took methylphenidate or the placebo, the drug did cause them to eat less. On average, they ate 11 percent fewer calories, and 17 percent less fat. Since methylphenidate did not affect hunger, this suggests it might have dampened the rewarding effects of the food, according to the researchers. Dr. Gary S. Goldfield is conducting a longer-term clinical trial to see whether methylphenidate does in fact spur weight loss, and whether its effects on dopamine explain the benefit. American Journal of Clinical Nutrition, August 2007.

J Clin Psychopharmacol. Feb 12 2014. Methylphenidate Enhances Cognitive Performance in Adults With Poor Baseline Capacities Regardless of Attention-Deficit/Hyperactivity Disorder Diagnosis.

Front Synaptic Neurosci. 2014 Jan 21. Juvenile methylphenidate reduces prefrontal cortex plasticity via D3 receptor and BDNF in adulthood. Early drug intervention in childhood disorders aims to maximize individual potential in the short- and long-term. Consistently, juvenile exposure to psychostimulants, such as methylphenidate (MPH), reduces risk for substance use in animals and sub-populations of individuals with attention deficit hyperactivity disorder (ADHD). We investigated the effects of MPH on brain plasticity via dopamine receptor D3 (D3R) and brain-derived neurotrophic factor (BDNF) expression in developing rats. These data suggest a sensitive window of vulnerability to modulation of BDNF expression around adolescence, and that compared to normal animals, juvenile exposure to MPH permanently reduces prefrontal BDNF transcription and translation upon cocaine exposure in adulthood by a D3R-mediated mechanism.