Hypervaccination, Autism, ADHD and Neurodevelopmental Disorders

Hypervaccination, Autism, ADHD and Neurodevelopmental Disorders

My daughter is expecting her third child, and our conversation sometimes turns to health topics, and the medical system itself as a danger to young children. The immediate threat to newborn children is hyper-vaccination, a term which describes the ever increasing CDC vaccination schedule, now over 100 shots. In 2017, the CDC schedule listed 51-54 shots or oral doses for 13 vaccines intended to prevent 16 diseases.The latest addition to the ACIP CDC childhood vaccination schedule is the messenger RNA Covid 19 vaccine. The state of Florida Department of Health advises against mRNA Covid vaccines for healthy children, contradicting the CDC. This outrageous act by the CDC ACIP commitee has no medical basis, has prompted Dr. McCullough to question the entire CDC vaccination schedule. In doing so, Dr McCullough found hypervaccination as the leading cause of immune dysregulation, citing over 200 peer reviewed articles linking immune dysregulation with neuropsychiatric disease such as ADD (Attention Deficit Disorder) [same as ADHD, Attention Deficit Hyperactivity Disorder], Asberger’s, and Autism Spectrum Disorder. This is further explained by Dr. Peter McCullough in an interview with Del BigTree on the HighWire.

Above header image courtesy of Aaron Siri

Dr. Peter McCullough says:

There has been an incredible acceleration and intensification of vaccines given to children…There are now over 200 peer reviewed papers suggesting that immune system dysregulation is related to neuropsychiatric diseases including ADD (Attention Deficit Disorder) , Asberger’s, Autism Spectrum Disorder. The leading cause of immune system dysregulation right now is “hyper-vaccination”, so there is great concern there. (1)

CDC Childhood Vaccine Schedule 2024 Compared to 1983

Watch the Video: Skip forward 9 minutes 30 seconds for a discussion of the childhood vaccine program. (1)

=========================================

This is a partial transcript of the interview starting at around 10 minutes :

Dr. Peter McCullough:

The straw that broke the camels back was when the CDC ACIP panel put the messenger RNA COVID vaccines, Pfizer and Moderna on the childhood vaccination schedule down to 6 months [of age]. If this group recommends that vaccine in the schedule, what else have they overlooked in terms of safety, or lack oi clinical rationale ? So, I started to take a careful look at the schedule. Personally, I took all the vaccines. I have (Dr. Peter McCullough) taken 69 vaccine shots in my life, including 40 flu shots, mandatory to be on medical staff. I am not an anti-vaxxer, but I am vaccine risk aware. Like many doctors I trusted the CDC and ACIP. This is what I have learned. There has been an incredible acceleration and intensification of vaccines given to children.

There are now over 200 peer reviewed papers suggesting that immune system dysregulation is related to neuropsychiatric diseases including ADD (Attention Deficit Disorder) , Asberger’s, Autism Spectrum Disorder. The leading cause of immune system dysregulation right now is “hyper-vaccination”, so there is great concern there.

I can tell you on the clinical efficacy side, all the vaccines appear to be fallible. Measles outbreaks for instance have occurred among fully vaccinated individuals. The same thing is true for Pertussis and Mumps.

We are not faced with compelling infectious disease threats right now, like Pertussis or Diphtheria, Polio, Hemophilus Influenza B. There were fewer than 100 cases of Hemophilus Influenza B, I believe 77 cases in a CDC publication, that is what the HIB vaccine is for. You know what? More than half of those were fully vaccinated.

The point is: We now have multiple papers including:

Anthony B Mawson, Pilot Comparative Study on the health of vaccinated and unvaccinated 6-12 year old U.S. children Journal of Translational Science 3, no. 3 (2017): 1-12, .

James Lyons-Weiler and Paul Thomas, “Relative Incidence of Office Visits and Cumulative Rates of Billed Diagnoses along the Axis of Vaccination,” International Journal of Environmental Research and Public Health 17, no. 22 (2020): 8674, [This Article has been RETRACTED]

Brian Hooker and Neil Z. Miller, “Analysis of Health Outcomes in Vaccinated and Unvaccinated Children: Developmental Delays, Asthma, Ear Infections and Gastrointestinal Disorders,” SAGE Open Medicine 8, (2020): 2050312120925344, doi:10.1177/2050312120925344.

All these studies suggest in today’s environment, today’s living conditions, and current context, that going natural, that is taking no vaccine, that children have healthier outcomes . They have lower rates of atopic dermatitis, asthma, lower rates of neuropsychiatric disorders that I have mentioned.

Right now, I am in line with the World Council for Health which in Sept 2023 came out with a recommendation to actually pause on the childhood vaccine schedule, and let us critically re evaluate and think through this. I could not in good conscience tell a parent to go ahead and follow the schedule now, particularly with the COVID 19 vaccines on the schedule.

Del Big Tree Question:

If we pause the child hood vaccine program , people will say you will cause a return of measles outbreak, and even worse, polio will come back, and small pox. What do you say about that?

Dr McCullough Answers:

Let’s take smallpox. That should be very responsive to Ticoviramat (TPOXX), an oral and IV drug which is very effective against monkeypox. We learned that in the pandemic. So if there was a sporadic case of smallpox, the availability of ticoviramat (TPOXX) handles that very well. I wouldn’t have any concerns there.

I think polio is a different issue. And fortunately, with polio , we have very good [waste] water supply testing. And we can get an idea if the three neurotropic strains of polio are even present in the [waste] water supply. (Author’s NOTE: this should read, waste water supply testing)

So we have surveillance, we have treatment. None of these vaccines are sufficiently compelling right now. The world has changed, and is not the same as it was in the 1960’s and 1970’s.

This idea that each child starting on the day of birth through age 18 takes well over a hundred injections, I think those days are over with.

Recent sentiment surveys, Kaiser Family Foundation being one, indicate probably a third of parents are really backing away from this intensive vaccine schedule.

============ END OF TRANSCRIPT #1 ===========================

Tanya Gaw (Action4Canada) Interviews Dr Peter McCullough

In this video interview, Dr. Peter McCullough discusses the harms of childhood vaccines. Autism is part of syndrome called ESSENCE disorders (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations) which include: attention deficit disorder (ADD, ADHD), autism spectrum disorder, Asperger syndrome, and cognitive and language disorders. These are neurodevelopmental/neuropsychiatric disorders. Dr. McCullough states that there are over 800 papers linking ESSENCE disorders to hypervaccination, the direct cause of exploding rates for Autism, ADHD, neurodevelopmental and chronic allergic disorders:

Partial Transcript of Above Interview:

Dr. Peter McCullough:

When I was a kid, and I am 60 years old [in the 1960’s], the rate of Autism was one in 10,000. Now it is one in 36 on the CDC web site. There is no childhood disease that is exploding in frequency at that rate. And autism is part of a collection of illnesses called the Essence Disorders (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations), and that includes attention deficit disorders [ADHD], Asbergers, Autism Spectrum Disorder, and then some cognitive and language disorders. But this whole group is exploding. And, they are neuropsychiatric, meaning it cant just be environmental, from cell phones or TV’s. There is something organic going on in the brain.

And so what we have learned over time. Some of the child hood diseases, such as German measles… if the pregnant mother had rubella, German measles, about ten percent of the babies would actually have autism, and this is back in the 1960’s before the rubella vaccine.

So we know that German measles is neurotrophic [goes to the brain and nervous system], so is mumps, so is measles, and polio.

A lot of the diseases we are vaccinating against, the [disease] organisms actually attack the brain, invoking an inflammatory response in the brain.

Currently there are about 200 papers now showing that autism is related to the immune system. The single greats perturbation of the immune system in children is vaccination. In fact it is hypervaccination. When I was a child there was just three shots, [containing] five antigens.

A child in the first year of life now is getting salvos of vaccines, and dozens and dozens of vaccines over the course of childhood, sometimes 6-12 at a time.

There are clear cut cases of the children having febrile seizures, near seizures, very high temperature, clonic jerking, doll’s eye reflex [oculocephalic reflex], then afterwards, they change. They don’t suckle, they don’t track the mothers eyes. The parents know, literally, the autism started after a round of vaccines. So, that literature is building. And then we have several papers, one by Gayle DeLong, (2011) is one of the most convincing ones, showing that just by combining diptheria , tetanus and pertussis, again this is hypervaccination, the rates of autism increased many fold.

In total about 800 papers out there linking the Essence Disorders to hypervaccination. No single vaccine itself does it. And no single congener [adjuvant, additive or preservative in the vaccine such as mercury or aluminum]. People have pointed to thimerosol, mercury. Some of the vaccines have it ,some don’t. Same thing with aluminum. I think it is related to the inflammation of hypervaccination, and it can happen with any vaccine, neonatal Hepatitis B, and the Gardasil [HPV] vaccine which is given later.

———————————– My Note Below ———————————–

[my note: Hepatitis B vaccine contains 50 mcg/ml of mercury and 500 mcg aluminum/ml, both neurotoxic heavy metals. In 2016, Dr. Junhua Yang injected Hep B vaccine into neonatal mice showing the vaccine impaired behavior and neurodevelopment of the mice.

See: Yang, Junhua, et al. “Neonatal-hepatitis-B-vaccination-impaired-the-behavior-and-neurogenesis-of-mice-transiently-in-early-adulthood..” Psychoneuroendocrinology 73 (2016): 166-176.

Dr. Junhua Yang writes:

This work reveals for the first time that early HBV vaccination induces impairments in behavior and hippocampal neurogenesis.This work provides innovative data supporting the long suspected potential association of HBV with certain neuropsychiatric disorders such as autism and multiple sclerosis (Gallagher and Goodman, 2010; Stubgen, 2012). end of author’s note]

In 2010, Dr. Carolyn Gallagher found 300 percent increase in autism diagnosis in male neonates injected with the Hepatitis B vaccine , compared to unvaccinated neonates, those vaccinated after first month, writing:

Boys vaccinated as neonates had threefold greater odds for autism diagnosis compared to boys never vaccinated or vaccinated after the first month of life….Gallagher, Carolyn M., and Melody S. Goodman. “Hepatitis B vaccination of male neonates and autism diagnosis, NHIS 1997–2002.” Journal of Toxicology and Environmental Health, Part A 73.24 (2010): 1665-1677.

Wang, Xiao, et al. “IL-4 mediates the delayed neurobehavioral impairments induced by neonatal hepatitis B vaccination that involves the down-regulation of the IL-4 receptor in the hippocampus.” Cytokine 110 (2018): 137-149.

July 26, 2018 : New Study: Hep B Vaccine “May Have Adverse Implications For Brain Development and Cognition” By JB Handley

———————- resume Dr. McCullough —————

Dr. Peter McCullough:

So, we are left with this uncomfortable feeling, we have got an autism epidemic on our hands, and maybe we created it through mass vaccinations.

You can ask the other question:” what about the kids who go natural. Prior to Covid in the United States it was 2.5 percent of parents went natural, no vaccines. Many times because they already had a child with autism, or a problem. Predictors of autism are older age of parents, siblings with autism, and low birth weight babies, premature babies, that’s it. So we knew that.

Now there are papers by Hooker, Miller and [Paul] Thomas, all showing that children who get no childhood vaccines have lower rates of allergic asthma, allergic dermatitis, need for tympanostomy tubes [to treat ear infections], tonsillitis, lower rates of ADD and Autism. In fact, non-existant.

Steve Kirsch and I testified in the Pennsylvania Senate, and Steve got on this topic. He said, “find me an Amish kid with autism.” They dont take any vaccines in the Amish, Yeah.

============ END of Transcript #2 ==========

Chart Autism Prevalence United States Now 1: 36 (2023),

Prevalence of Autism in 1970 was one in 10,000
Prevalence Now is one in 36.

Accelerating Autism Prevalence

Current Autism prevalence is ONE in 36 U. S. children diagnosed with autism. This is an 18% increase in prevalence rates reported by the CDC since 2021. This is a 417 percent increase since the year 2000.

Accelerating CDC Vaccination Schedule

The number of vaccine shots recommended from 1960’s vs. 2023, have gone from around 5 vaccine shots to around 87 shots by the time an 18 year old graduates. Vaccines are defined as “unavoidably unsafe” in the National Childhood Vaccine Injury Act (NCVIA) of 1986.

Corrupting Influence of Money: Clinics, pharmacies, hospitals are paid large sums of money to encourage vaccine uptake , money has influence. See previous article: Financial Kickbacks to Pediatricians for Vaccination Harms Children

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Charts from the Paul Tomas Study

The Paul Thomas study above quoted by Dr. Peter McCullough shows in graphic form this association of hypervaccination with childhood disorders: Asthma, Otitis Media, Eczema, Urticaria, Behavior Disorders and ADHD. See the chart below taken from Dr Paul Thomas study of his pediatrics office population: (8)(75)

Comparing the Health of Vaccinated (Orange Line) Vs Unvaccinated (Blue Line) Children:

Chart showing Vaccinations vs. ADHD

Here is the chart for ADHD vs. vaccination. Notice the dramatic difference between the unvaccinated children (NO ADHD – blue line) and the vaccinated children (Rising ADHD – orange line):

There May Be Self-Selection Bias in the Above Chart -The Social Construct

If ADHD and its treatment with stimulant drugs is considered a “social construct”, then one might suggest that mothers who accept hypervaccination would also accept labeling their child as ADHD and accept drug treatment with amphetamines or methylphenedate. These are chemically addictive, Class II controlled substances which are known to cause brain damage in animal studies. This is ignored by the medical system which claims these drugs are “safe and effective” in children for ADHD, an obvious falsehood. The mother’s circle of friends and family members, school teachers and psychologists may pressure the mother to accept stimulant drugs (amphetamines) for the child. After all, this is the mainstream medicine position.

On the other hand, mothers who reject hypervaccination who have unvaccinated children would resist labeling their children as ADHD and be more resistant to the mainstream medical use of ADHD drugs (amphetamines, methylphenidate and other stimulants), thus producing bias in the above data chart. These mothers would probably have a circle of supportive friends and family members who also feel the same way.

The Paul Thomas Story

Paul Thomas MD is a pediatrician in Oregon who compared the health of vaccinated vs. unvaccinated children in his office practice. This study showed increased childhood chronic disease in the vaccinated population. After publishing such a study in a peer review journal, you might think such a public service would be deserving of an award and a showing of gratitude. Quite the opposite, only a few months later, and Dr. Paul Thomas’s medical license was revoked and his publication was retracted. (8)(75)

Above Video: Dr. Paul Thomas presents his data, vaccinated vs unvaccinated health outcomes.

Being Persecuted for Being Right

I think Dr. Thomas is right, and he was persecuted for being right. The medical establishment, completely captured by the pharmaceutical industry, does not want this information out in public, and wielded their power and influence to crush Dr. Thomas.

Above video: Pennsylvania State Legislature Hearing – Steve Kirsch talks about Childhood Vaccines – Studies of Vaccinated vs Unvaccinated Children – Autism/ADHD Connection – Why the Amish have no Autism. State Senator Doug Mastriano.

ADHD the Second Greatest Threat to Children’s Health

This brings us to the topic of ADHD which was the subject of two previous newsletters:

Attention Deficit Disorder Exposed as Drug Marketing Ploy

ADHD Attention Deficit HyperActivity Syndrome Part Two

The Second Greatest Threat

In my opinion, after hypervaccination, the second greatest threat to the health of a child is ADHD treatment with drugs such as methylphenidate (Ritalin) and amphetamines (Adderal). Teachers and school psychologists notice the child is inattentive in class, impulsive, or fidgeting in the seat, or a “behavior problem”. The child is then labeled as ADHD, and treatment with brain stimulants follows. ADHD drugs such as amphetamines, methamphetamines and methylphenidate (MPH) have been studied extensively in animal models showing potential to produce brain damage depending on dosage and duration of treatment.

A Triumph of Drug Marketing and Disease Mongering

Disease marketing to the public by the drug industry to increase profits is called, “disease mongering”. The drug industry has used a marketing campaign of deceitful claims and representations to push addictive ADHD drugs to children.(76)

In 2009, Jonathan Leo, and Jeffrey Lacasse made a few observations about the ADHD drug industry, a rapidly expanding and highly lucrative growth industry in the US. ADHD is massively over-diagnosed. Amphetamine drugs used for treatment are Schedule II controlled substances, both addictive and harmful:

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.(77)

In 2014, Dr. Allen Frances, MD Chair, DSM-IV Task Force, Professor Emeritus, Duke University School of Medicine made this statement about ADHD disease mongering:

The Amphetamine/ Methylpheidate Epidemic. Chart Courtesy of Rasmussen, Nicolas (2008).

Today’s amphetamine epidemic is repeating the previous amphetamine epidemic of the 1960’s . Notice current peak amphetamine use is actually higher than previous peak in 1969 (Green ellipse and arrows). The 1969 peak was due soley to amphetamines, wheras the current peak in epidemic use is combination of methylphenidate (Ritalin) and amphetamines.

Above chart courtesy of Rasmussen, Nicolas. “America’s first amphetamine epidemic 1929–1971: a quantitative and qualitative retrospective with implications for the present.” American journal of public health 98.6 (2008): 974-985.

Conclusion:

As Dr. Peter McCullough so eloquently states in the above two interviews, we now have volumes of peer reviewed medical literature supporting the hypothesis that exploding rates of Autism, ADHD and other ESSENCE Diseases are directly related to neuro-inflammatiom from hypervaccination. If this is true, then treatment of ADHD with brain damaging drugs (Amphetamines and Methyphenidate) is an iatrogenic medical catastrophe which should be immediately halted. Where is the outrage?

The obvious correct path forward is, number one, impose strict restrictions on the use of Amphetamines in children and, secondly, eliminate hypervaccination in children by strongly rejecting the CDC childhood vaccination schedule, which after all, is the product a corrupt ACIP committee of the CDC (Center for Disease Control). For those interested, vaccine exemptions are available in most states.

Articles with Related Interest:

Click Here For Part Two of this series: ADHD Drugs and the Amphetamine Epidemic (not yet available- in progress)

HPV Vaccine, The Greatest Medical Scandal of Our Time

Curing Autism with Antibiotics

Aluminum in Vaccines and Autism

Donald Trump, RFK JR, Vaccines, Autism

ALL Autism Articles

Attention Deficit Disorder Exposed as Drug Marketing Ploy

ADHD Attention Deficit HyperActivity Syndrome Part Two

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)

Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663

my blog: www.jeffreydachmd.com
Natural Thyroid Toolkit by Jeffrey Dach MD
Cracking Cancer Toolkit by Jeffrey Dach MD
Heart Book by Jeffrey Dach MD
www.naturalmedicine101.com
www.bioidenticalhormones101.com
www.truemedmd.com
www.drdach.com

References:

1) DOCTORS CALL FOR HALT OF COVID, CHILDHOOD VACCINES The Highwire Del Bigtree and Dr Peter McCullough

Cardiologist & Epidemiologist, Peter McCullough, MD, joins Del on the heels of his World Council for Health appearance in which he boldly stated that the full childhood vaccine schedule should be placed on hold until safety can be properly assessed. And Dr. McCullough is not alone.
POSTED: October 20, 2023

Dr. Peter McCullough Transcript:

The straw that broke the camels back was when the CDC ACIP panel put the messenger RNA COVID vaccines, Pfizer and Moderna on the childhood vaccination schedule down to 6 months. If this group recommends that vaccine in the schedule, what else have they overlooked in terms of safety, or lack oi clinical rationale ? So, I started to take a careful look at the schedule. Personally, I took all the vaccines. I have (Dr. Peter McCullough) taken 69 vaccine shots in my life, including 40 flu shots, mandatory to be on medical staff. I am not an anti-vaxxer, but I am vaccine risk aware. Like many doctors I trusted the CDC and ACIP. This is what I have learned. There has been an incredible acceleration and intensification of of vaccines given to children.

The leading cause of immune system dysregulation right now is “hyper-vaccination”, so there is great concern there.

We are not faced with compelling infectious disease threats right now, like Pertussis or Diphtheria, Polio, Hemophilus Influenza B,

There were fewer than 100 cases of Hemophilus influenza B , I believe 77 cases in a CDC publication, that is what the HIB vaccine is for. You know what? More than half of those were fully vaccinated.

The point is: We now have multiple papers including:

Anthony R. Mawson, et al., “Pilot Comparative Study on the Health of Vaccinated and Unvaccinated 6 to 12-year-old U.S. Children,” Journal of Translational Science 3, no. 3 (2017): 1-12, doi:10.15761/JTS.1000186.

Del Big Tree Question: If we pause the child hood vaccine program , people will say you will cause a return of measles outbreak, and even worse, polio will come back, and small pox. What do you say about that?

Dr McCullough Answers:

I think polio is a different issue. And fortunately, with polio, we have very good [waste] water testing. And we can get an idea if the three neurotropic strains of polio are even present in the [waste] water supply. (Author’s NOTE: this should read, waste water testing)

So we have surveillance, we have treatment. None of these vaccines are sufficiently compelling right now. The world has changed, and is not the same as it was in the 1960’s and 1970’s.

This idea that each child starting on the day of birth through age 18 takes well over a hundred injections, I think those days are over with.

Recent sentiment surveys, Kaiser Family Foundation being one, indicate probably a third of parents are really backing away from this intensive vaccine schedule.

———————————————————— –

2) More than a third of parents oppose vaccine requirements in schools, KFF survey finds By Deidre McPhillips, CNN Fri December 16, 2022

More than a third of US parents say that vaccinating children against measles, mumps and rubella should be an individual choice and not a requirement to attend public school, even if that may create health risks, according to survey data published Friday by the Kaiser Family Foundation. That’s a notable increase from pre-pandemic times. A similar poll from the Pew Research Center found that 23% of parents opposed vaccine requirements in schools in 2019, but that’s now jumped to 35% in the KFF survey.

More than a third of parents oppose vaccine requirements in schools, KFF survey finds
By Deidre McPhillips, CNN December 16, 2022

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2) A Common-sense Approach to Childhood Vaccines is Now Needed
By World Council for Health September 5, 2023
References :

3) WCH meeting #101, August 28^th 2023. https://worldcouncilforhealth.org/multimedia/brian-hooker-vax-unvax/

4) Anthony R. Mawson et al., “Preterm Birth, Vaccination and Neurodevelopmental Disorders: A Cross-Sectional Study of 6- to 12-Year-Old Vaccinated and Unvaccinated Children,” Journal of Translational Science 3, no. 3 (2017): 1-8, doi:10.15761/JTS.1000187.

This paper explores the association between preterm birth, vaccination and NDD, based on a secondary analysis of data from an anonymous survey of mothers, comparing the birth history and health outcomes of vaccinated and unvaccinated homeschool children 6 to 12 years of age. A convenience sample of 666 children was obtained, of which 261
(39%) were unvaccinated, 7.5% had an NDD (defined as a learning disability, Attention Deficit Hyperactivity Disorder and/or Autism Spectrum Disorder), and 7.7% were born preterm. No association was found between preterm birth and NDD in the absence of vaccination, but vaccination was significantly associated with NDD in children born at term (OR 2.7, 95% CI: 1.2, 6.0). However, vaccination coupled with preterm birth was associated with increasing odds of NDD, ranging from 5.4 (95% CI: 2.5, 11.9) compared to vaccinated but non-preterm children, to 14.5 (95% CI: 5.4, 38.7) compared to children who were neither preterm nor vaccinated. The results of this pilot study suggest clues to the epidemiology and causation of NDD but question the safety of current vaccination practices for preterm infants. Further research is needed to validate and investigate these associations in order to optimize the impact of vaccines on children’s health.

5) Anthony R. Mawson, et al., “Pilot Comparative Study on the Health of Vaccinated and Unvaccinated 6 to 12-year-old U.S. Children,” Journal of Translational Science 3, no. 3 (2017): 1-12, doi:10.15761/JTS.1000186.

This study aimed 1) to compare vaccinated and unvaccinated children on a broad range of health outcomes, and 2) to determine whether an association found between vaccination and neurodevelopmental disorders (NDD), if any, remained significant after adjustment for other measured factors. A cross-sectional study of mothers of children educated at home was carried out in collaboration with homeschool organizations in four U.S. states: Florida, Louisiana, Mississippi and Oregon. Mothers were asked to complete an anonymous online questionnaire on their 6- to 12-year-old biological children with respect to pregnancy-related factors, birth history, vaccinations, physician-diagnosed illnesses, medications used, and health services. NDD, a derived diagnostic measure, was defined as having one or more of the following three closely-related diagnoses: a learning disability, Attention Deficient Hyperactivity Disorder, and Autism Spectrum Disorder. A convenience sample of 666 children was obtained, of which 261 (39%) were unvaccinated. The vaccinated were less likely than the unvaccinated to have been diagnosed with chickenpox and pertussis, but more likely to have been diagnosed with pneumonia, otitis media, allergies and NDD. After adjustment, vaccination, male gender, and preterm birth remained significantly associated with NDD. However, in a final adjusted model with interaction, vaccination but not preterm birth remained associated with NDD, while the interaction of preterm birth and vaccination was associated with a 6.6-fold increased odds of NDD (95% CI: 2.8, 15.5). In conclusion, vaccinated homeschool children were found to have a higher rate of allergies and NDD than unvaccinated homeschool children. While vaccination remained significantly associated with NDD after controlling for other factors, preterm birth coupled with vaccination was associated with an apparent synergistic increase in the odds of NDD. Further research involving larger, independent samples and stronger research designs is needed to verify and understand these unexpected findings in order to optimize the impact of vaccines on children’s health.

6) Brian Hooker and Neil Z. Miller, “Analysis of Health Outcomes in Vaccinated and Unvaccinated Children: Developmental Delays, Asthma, Ear Infections and Gastrointestinal Disorders,” SAGE Open Medicine 8, (2020): 2050312120925344, doi:10.1177/2050312120925344.

Objective: The aim of this study was to compare the health of vaccinated versus unvaccinated pediatric populations.
Methods: Using data from three medical practices in the United States with children born between November 2005 and June 2015, vaccinated children were compared to unvaccinated children during the first year of life for later incidence of developmental delays, asthma, ear infections and gastrointestinal disorders. All diagnoses utilized International Classification of Diseases–9 and International Classification of Diseases–10 codes through medical chart review. Subjects were a minimum of 3 years of age, stratified based on medical practice, year of birth and gender and compared using a logistic regression model.
Results: Vaccination before 1 year of age was associated with increased odds of developmental delays (OR = 2.18, 95% CI 1.47–3.24), asthma (OR = 4.49, 95% CI 2.04–9.88) and ear infections (OR = 2.13, 95% CI 1.63–2.78). In a quartile analysis, subjects were grouped by number of vaccine doses received in the first year of life. Higher odds ratios were observed in Quartiles 3 and 4 (where more vaccine doses were received) for all four health conditions considered, as compared to Quartile 1. In a temporal analysis, developmental delays showed a linear increase as the age cut-offs increased from 6 to 12 to 18 to 24 months of age (ORs = 1.95, 2.18, 2.92 and 3.51, respectively). Slightly higher ORs were also observed for all four health conditions when time permitted for a diagnosis was extended from ⩾ 3 years of age to ⩾ 5 years of age.
Conclusion: In this study, which only allowed for the calculation of unadjusted observational associations, higher ORs were
observed within the vaccinated versus unvaccinated group for developmental delays, asthma and ear infections.

Mawson et al.3 found a relationship between vaccination status
and learning disability and neurodevelopmental disorders.
Delong20 also reported a significant relationship to neurodevelopmental
disorders (autism and speech and language delay) when looking at the proportions of vaccine uptake in US children.

6A) Delong G. A positive association found between autism
prevalence and childhood vaccination uptake across the U.S. population. J Toxicol Environ Health A 2011; 74: 903–916.

The reason for the rapid rise of autism in the United States that began in the 1990s is a mystery. Although individuals probably have a genetic predisposition to develop autism, researchers suspect that one or more environmental triggers are also needed. One of those triggers might be the battery of vaccinations that young children receive. Using regression analysis and controlling for family income and ethnicity, the relationship between the proportion of children who received the recommended vaccines by age 2 years and the prevalence of autism (AUT) or speech or language impairment (SLI) in each U.S. state from 2001 and 2007 was determined. A positive and statistically significant relationship was found: The higher the proportion of children receiving recommended vaccinations, the higher was the prevalence of AUT or SLI. A 1% increase in vaccination was associated with an additional 680 children having AUT or SLI. Neither parental behavior nor access to care affected the results, since vaccination proportions were not significantly related (statistically) to any other disability or to the number of pediatricians in a U.S. state. The results suggest that although mercury has been removed from many vaccines, other culprits may link vaccines to autism. Further study into the relationship between vaccines and autism is warranted.

7) Brian Hooker and Neil Z. Miller, “Health Effects in Vaccinated versus Unvaccinated Children,” Journal of Translational Science 7, (2021): 1-11, doi:10.15761/JTS.1000459.

8) James Lyons-Weiler and Paul Thomas, “Relative Incidence of Office Visits and Cumulative Rates of Billed Diagnoses along the Axis of Vaccination,” International Journal of Environmental Research and Public Health 17, no. 22 (2020): 8674, [This Article has been RETRACTED]

Remarkably, zero of the 561 unvaccinated patients in the study had attention deficit hyperactivity disorder (ADHD) compared to 0.063% of the (partially and fully) vaccinated...There were no cases of ADHD in the unvaccinated group R1.2. Group B: Attention Deficit/Hyperactive Disorder and Behavioral Issues. Because there were no cases of ADHD in the unvaccinated group, the quartile analysis uses a comparison to the least vaccinated decile to avoid division by zero. Large increases were found in office visits among the vaccinated compared to the unvaccinated groups in outcomes in this group as well. The quartile representation shows large increases in ADHD and moderately large increases in behavioral issues (Figure 4B). Both of these conditions had highly significant relative incidences of office visit (ADHD, RIOV = 53.74; behavioral issues, 10.28) (p < 0.00001).Previous studies such as the Mawson study (2017) [9] reported high odds ratios for allergic rhinitis (30.1), learning disabilities (5.2), ADHD (4.2), autism (4.2), neurodevelopmental disorders (3.7), eczema (2.9), and chronic illness (2.4) but were limited because they were based on survey data.

9) Wakefield AJ, et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. The Lancet. 1998. doi.org/10.1016/S0140-6736(97)11096-0.

10) Turtles All The Way Down. Vaccine Science and Myth. 2022. Editor: Zoey O’Toole. Foreword by Mary Holland.

11) Kirsch S.If vaccines don’t cause autism, then how do you explain all this evidence? May 2023.

12) Vax-Unvax. Let the Science Speak. August 2023. Robert F. Kennedy Jr and Brian Hooker, PhD.

13) Countering the WHO’s “Big Catch-up” Global Campaign and Immunization Agenda 2030. WCH Statement. May 12, 2023.

14) Rejecting Monopoly Power over Global Public Health. WCH Policy Brief. May 2023.

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ADHD 2023

15) Batstra, Laura, Martin Whitely, and Sami Timimi. “ADHD: Science and society.” Frontiers in Psychiatry 13 (2023): 1129728.

If the science supporting ADHD diagnosis and treatments is weak and has not advanced significantly since 1980; What is driving increased ADHD diagnosis and treatment rates?

With the global ‘ADHD therapeutics market’ estimated to be worth US$29.56 billion in 2022—and expected to reach US$45.68 billion by 2027 (10)—perhaps the answer lies in thinking differently about ADHD. Instead of regarding it as an illness requiring medical intervention, it may be more insightful to understand ADHD as a marketable brand driven by economic and guild interests.

2017
16) Harding, Blake. “The Field Guide to ADHD: What They Don’t Want You to Know. Psychiatry–Theory, Applications and Treatments.” Online Submission (2017).

In the The Field Guide to ADHD: What They Don’t Want You to
Know, Harding confronts with unusual candor and painstaking effort one
of the most alarming and perilous crises of our time: ADHD. In
confronting this crisis, Harding forces us to reconsider the assumptions
underlying ADHD and how we think about medical diagnoses, disability,
health and authority. Harding unwraps these bewildering and conflicting
ADHD issues while investigating the spiraling amount of overdiagnosed cases of ADHD, many often highly medicated and taught to conform rather than to thrive, no matter the individual or societal cost.

As Harding passionately argues, policy makers, healthcare
professionals, parents and other stakeholders are not only supporting the overdiagnosis of ADHD, but fundamentally thinking about ADHD all wrong.

17) Gaidamowicz, Rima, et al. “ADHD-the scourge of the 21st century?.” Psychiatr Pol 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.

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ADHD Drug induced PSYCHOSIS

18) Mosholder, Andrew D., et al. “Hallucinations and other psychotic symptoms associated with the use of attention-deficit/hyperactivity disorder drugs in children.” Pediatrics 123.2 (2009): 611-616.

CONCLUSIONS. Patients and physicians should be aware that psychosis or mania arising during drug treatment of attention-deficit/hyperactivity disorder may represent adverse drug reactions.

19) Shibib, Shatha, and Nevyne Chalhoub. “Stimulant induced psychosis.” Child and adolescent mental health 14.1 (2009): 20-23.

Background: Stimulants are used as a first line option in the treatment of ADHD …The potential for psychotic side effects are well known, but reported as rare.

Method: We are reporting four cases of stimulant induced psychosis which presented over a 2 year period in a small community CAMHS setting.

Results: Our findings suggest that stimulant induced psychosis occurs. The symptoms in the early stages of the psychotic episode mimicked ADHD. Long acting preparations appeared to be a contributory factor to the development of psychotic side effects. Rechallenge with stimulant medication is described.

Conclusion: Psychosis is an important, unpredictable side effect of stimulant medication. Symptoms resolve with discontinuation of treatment. Remergence of ADHD symptoms are rapid and rechallenge is often indicated.

About 9-10 percent of kids treated with Stimulants develope psychosis.

20) Cherland, Esther, and Renée Fitzpatrick. “Psychotic side effects of psychostimulants: a 5-year review.” The Canadian Journal of Psychiatry 44.8 (1999): 811-813.

Of the 98 children treated with stimulant medication, 9 children
developed psychotic symptoms (Table 1).

Psychotic symptoms in the chart review appear to cluster in 3
groups: MPH-induced hallucinosis, slower-developing paranoia,
and mood-congruent psychotic symptoms. All 3 kinds
of psychotic side effects have been previously reported in
case reports ofchildren (4,5,8,16).

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Peter Breggin MD

21) 80% Of Population Takes Psychiatric Drugs and Gets Worse
they end up with “subsequent” “long-term socioeconomic difficulties” “including lower income, unemployment, and increased likelihood to live alone and to be unmarried.” Dr. Peter and Ginger Breggin Nov 5, 2023 SUBSTACK,

Studies in the United States with children started on low doses of Ritalin (methylphenidate) in the 1970s for minimal symptoms of ADHD showed they did very poorly long-term. They had a lifetime decline in quality of life compared to controls, including stunted growth, lower IQ, less education, more psychiatric hospitalizations and imprisonments, obesity, and a shorter lifespan. Ritalin became a gateway to becoming lifelong mental patients on psychiatric drugs of every sort. Other studies have shown brain shrinkage from stimulant drugs given to children. I have reviewed the scientific literature demonstrating these outcomes in: Psychiatric Drug Withdrawal: A Guide for Prescribers, Therapists, Patients, and their Families.2

These long-term catastrophes are primarily caused by drug-induced neurotoxicity 3 but also by the stigmatization and demoralization from doctors telling the children and their parents that the children are genetically defective, have biochemical balances, and need the drugs — lies to get them to take the neurotoxins.

For many years, evidence has been increasing that taking psychiatric drugs is among the most dangerous risks in modern society. For decades, I have been explaining and documenting that psychiatric drugs overall do much more harm than good. The drug-induced dysfunction or damage causes “medication spellbinding” 4 — the inability of patients to fully perceive the harm the drugs are doing to them.5

22) Breggin, P. R. (1999a). Psychostimulants in the treatment of children diagnosed with ADHD: Part 1–Acute risks and psychological effects. Ethical Human Sciences and Services, 1(1), 13-33.

23) Breggin, P. R. (1999b). Psychostimulants in the treatment of children diagnosed with ADHD: Part II–Adverse effects on brain and behavior. Ethical Human Sciences and Services, 1(3), 213-242.

24) Breggin, P. R. (2000). Confirming the hazards of stimulant drug treatment. Ethical Human Sciences and Services, 2(3), 203-204.

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25) 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.

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26) Confirming the hazards of stimulant drug treatment By Peter Breggin
International Journal of Risk and Safety in Medicine, vol. 13, no. 4, pp. 199-200, 2000

Until recently, no studies have systematically examined the rate of psychotic symptoms caused by routine treatment with stimulant drugs such as methylphenidate (Ritalin) and amphetamine (Dexedrine,
Adderall). Doctors who prescribe stimulant drugs often seem oblivious to the fact that they can cause psychoses, including manic-like and schizophrenic-like disorders. Without providing a scientific basis,
the literature often cites rates of 1% or less for stimulant-induced psychoses (reviewed in [1,2]). Recently on television I debated a well-known expert in child psychiatry who took the position that prescribed
stimulants “never” cause psychoses in children.

The rate of psychotic symptoms that first appear during stimulant treatment has recently been investigated in a 5-year retrospective study of children diagnosed with Attention Deficit Hyperactivity
Disorder (ADHD) [5]. Among 192 children diagnosed with ADHD at the Canadian clinic, 98 had been placed on stimulant drugs, mostly methylphenidate. Psychotic symptoms developed in more than 9%
of the children treated with methylphenidate. According to Cherland and Fitzpatrick, “The symptoms ceased as soon as the medication was removed” [5, p. 812]. No psychotic symptoms were reported among the children with ADHD who did not receive stimulants. The psychotic symptoms caused by methylphenidate included hallucinations and paranoia. The authors conclude that, due to poor reporting, the rate of stimulant-induced psychosis and psychotic symptoms was probably much higher. In my practice of psychiatry, I am frequently consulted about children who are taking three, four, and sometimes five psychiatric drugs, including medications that are FDA-approved only for the treatment of
psychotic adults. The drug treatment typically began when the children developed conflicts with adults at home or at school. In retrospect, the conflicts could easily have been resolved by interventions such as
family counseling or individualized educational approaches. Usually under pressure from a school, the parents instead acquiesced to put their child on stimulants prescribed by psychiatrists, family physicians,
or pediatricians. When these children developed depression, delusions, hallucinations, paranoid fears and other drug-induced reactions while taking stimulants, their physicians mistakenly concluded that the
children suffered from “clinical depression”, “schizophrenia” or “bipolar disorder” that had been “unmasked” by the medications. Instead of removing the child from the stimulants, these doctors mistakenly
prescribed additional drugs, such as antidepressants, mood stabilizers, and neuroleptics. Children who were put on stimulants for “inattention” or “hyperactivity” ended up taking multiple adult psychiatric drugs that caused severe adverse effects, including psychoses and tardive dyskinesia. It is time to recognize that the supposedly increasing rates of “schizophrenia”, “depression”, and “bipolar
disorder” in children in North America are often the direct result of treatment with psychiatric drugs. They should be classified as adverse drug reactions, not as primary psychiatric disorders. Doctors need to become more expert at identifying these adverse drug reactions in children and more aware of how and why to taper children from psychiatric medications [4]. When parents are willing to take a fresh approach to disciplining and caring for their children, or when the children’s school situation can be improved, it is usually possible to taper them off of all psychiatric medications. The parents are then relieved and
gratified to see their children increasingly improve with the removal of each drug. What is the answer to this widespread, unwarranted use of medication in the treatment of children? As long as we respond to the signals of conflict and distress in our children by subduing them with drugs, we will not address their genuine needs. As parents, teachers, therapists, and physicians we need to retake responsibility for our children [3].We must reclaim them from the drug companies and their advocates in the medical profession. At the same time, we must address the needs of our children on an individual and societal level. On the individual level, children need more of our time and energy. Nothing can replace the personal relationships that children have with us as their parents, teachers, counselors, or doctors. On a societal level, our children need improved family life, better schools, and more caring communities.

Peter R. Breggin, M.D.
Director, International Center for the Study of Psychiatry and Psychology
4628 Chestnut Street, Bethesda, MD 29814, USA

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27) Sacrificing Depth for Speed Dr. Sean Patrick Hatt, Integrative Psychology 2010

In spite of their seemingly ubiquitous presence, drugs used to treat ADHD are not at all similar to the caffeine in coffee or energy drinks. These are powerful pharmaceuticals that carry a long list of potentially serious risks, particularly in young people with still-developing brains.
Adverse drug reactions in stimulant formulas include impaired growth (Swanson, et al., 2007), insomnia, agitation, hypomania, mania, seizures, physical withdrawal, rebound effects, dependence (Breggin, 1999a, 1999b), and even psychosis (Breggin, 2000). Non-stimulant formulas also present safety problems, and their manufacturers were recently ordered by the United States Food and Drug Administration (FDA) to include a “black box” warning regarding the potential for increased suicidal ideation in adolescents (Carey, 2005). The black box was also subsequently ordered by the FDA for some popular stimulant formulas given an increased risk of sudden death (Pettypiece & Blum, 2006).

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Books:

28) 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)

29) 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)

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Anti-Oxidant treatment of ADHD

30) Verlaet, Annelies AJ, et al. “Rationale for dietary antioxidant treatment of ADHD.” Nutrients 10.4 (2018): 405.

Increasing understanding arises regarding disadvantages of stimulant medication in children with ADHD (Attention-Deficit Hyperactivity Disorder). This review presents scientific findings supporting dietary antioxidant treatment of ADHD and describes substantial alterations in the immune system, epigenetic regulation of gene expression, and oxidative stress regulation in ADHD.

As a result, chronic inflammation and oxidative stress could develop, which can lead to ADHD symptoms, for example by chronic T-cell-mediated neuroinflammation, as well as by neuronal oxidative damage and loss of normal cerebral functions.

Therefore, modulation of immune system activity and oxidant-antioxidant balance using nutritional approaches might have potential in ADHD treatment. The use of natural antioxidants against oxidative conditions is an emerging field in the management of neurodegenerative diseases. Dietary polyphenols, for example, have antioxidant capacities as well as immunoregulatory effects and, therefore, appear appropriate in ADHD therapy. This review can stimulate the development and investigation of dietary antioxidant treatment in ADHD, which is highly desired.

5.3. Pycnogenol
The herbal extract Pycnogenol®, derived from the bark of the French maritime pine (Pinus pinaster Aiton) [140], is composed of phenolic compounds, such as the monomers catechin and epicatechin,
as well as oligomeric and polymeric procyanidins [16,156]. An example of a procyanidin present in Pycnogenol® is procyanidin B1 (epicatechin-(4!8)-catechin) [157]. This extract is standardized to contain 70 5% (w/w) procyanidins [139,158]. Studies indicate high bioavailability of the individual components of Pycnogenol®. For example, 46% of catechinmetabolites (glucuronides and sulphates)were recovered in urine [139]. Oral Pycnogenol® ingestion was detectable in plasma after a single dose of 300 mg and multiple doses of 200 mg although detection times in plasma differ per compound. Metabolite M1 (-(3,4-dihydroxy-phenyl)–valerolactone) is formed by bacterial metabolism from catechin [157,159]. This indicates that the components of Pycnogenol® can be modified during digestion and absorption as well as by the liver [139], which can both increase and decrease the actual effect in vivo. Therefore, in vitro results need to be interpreted with caution.
Pycnogenol® has multiple pharmacological effects such as antihypertensive, anti-inflammatory and anti-diabetic effects [158]. Due to its antioxidant effect, it reduces oxidative stress and might be beneficial in ADHD [140]. Moreover, it was found to reduce histamine release from rat peritoneal mast cells [152]. Additionally, M1 is able to cross the BBB and other cell membranes, probably mediated by the GLUT-1 transporter [16,157]. This facilitated uptake also causes accumulation of M1, which is metabolized to glutathione adducts, in erythrocytes [157]. Most other external antioxidants are not effective in reducing oxidative stress in the brain, because they lack the ability to cross the BBB [62,160].

In children, Pycnogenol® administration caused positive effects on ADHD symptoms compared to placebo. Statistically significant enhanced concentration and reduced hyperactivity, as rated by the Child Attention Problems teacher rating scale, were found after 1 month of Pycnogenol® supplementation as well as improved visual-motoric coordination as rated by psychologists [16,140].

This effect could be related to a reduction of elevated catecholamine levels, as dopamine levels decreased in the urine of ADHD patients using Pycnogenol® and a trend of decreased epinephrine and norepinephrine levels was seen [5,14,16]. This could be linked to the stimulation of the enzyme endothelial nitric oxide synthase (eNOS), involved in the regulation of the release and uptake of norepinephrine and dopamine [16]. NO increase can also improve blood circulation in cerebral areas, which is impaired in ADHD [17].

However, on the contrary, inflammation is reduced by a suppression of iNOS [161]. In addition, Pycnogenol® increased the activity and expression of SOD, increased GSH levels and decreased GSSG levels, pointing towards less oxidative stress [162]. Also, an increase in
GSH reductase was found, which could explain the higher ratio of GSH/GSSG [140]. TAS levels of children with ADHD were increased to a normal level by Pycnogenol® administration [140,162],
while increased damage to DNA was lowered. It is therefore tempting to suggest that Pycnogenol® can be beneficial in ADHD because of its direct scavenging ability, chelating activity, stimulation of the DNA repair system and/or combinations thereof [140], but also due to its immune regulatory effects. However, this study had various limitations, including a short supplementation period and small placebo group [16].

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MPH is a Schedule II psychotropic controlled substance in same category as Fentanyl, Cocaine, Oxycontin

2013

31) Steiner, Dirk. “Unbagging Fidgety Philip. A pedagogical case pertaining a rethinking in dealing with syndromes of attention deficiency and/or hyperactivity in juveniles and infants.” RoSE–Research on Steiner Education 4.1 (2013).

An estimated ten to twelve million children are undergoing permanent medication with methylphenidate7 (MPH) in the United States at the present (Stolzer, 2012) 8.

Despite the questionable practice of putting children on a Schedule
II 9 categorised ‘psychotropic controlled substance’ (UN/INCB, 2003) as the remedy of choice—akin to a snort of cocaine 10, by the way—medicine very publically and quite literally won out over the critics and
those voicing misgivings—even though understandings and attempts at an explanation of the phenomenon of attention affecting syndromes have varied within scientific disciplines from the very beginning.

The so-considered ‘world-scale childhood and youth brain disorder of the new millennium’ so far, has only been manifested in a catalogue of behavioural patterns, such as ‘inattention’,‘impulsivity’, and, in some cases, ‘hyperactivity’ (ADHD Association, 2008)

Why, apparently, are such enormous numbers of our children suddenly reported to be ‘distracted’, ‘restless’, ‘hyperactive’—in brief—‘abnormal’? And where does this large-scale ‘genetically evoked brain defect’, effectively redefined as ‘ADHD’, the ‘most common disorder of childhood’ (Acosta et al., 2009; National Institutes of Health, 1998), suddenly come from? And what if attention affecting syndromes are in fact of environmental (i.e. socio-cultural) origin and are therefore a psychologic-pedagogical problem that has meanwhile been heavily—yet wrongfully—medicalised?

Now, almost three decades [now four decades] after its first distribution, the societal danger and damage which the medication-dominated approach—as well as the existence of an ‘ADHD’ in general—is causing, are becoming more and more evident , and pedagogical concerns, as well as socio-political scruples and misgivings—official levels included—are nowadays getting ever louder .

Despite all efforts to prove the necessity and raison d’être of methylphenidate [MPH] , this becomes fairly obvious if one realises the fact that MPH [methyl phenidate] is not a ‘remedy’ that would cure anything, on the contrary, it is a psychotropic, mind-altering drug that temporarily suppresses a medical condition in order to enable those affected to function again in contemporary society And since we are talking about a problem relating to the psyche, heavy, potentially addictive, mind-altering drugs, while suppressing symptoms in the first
instance, will only worsen the mental condition itself. This leads to the conclusion that Ritalin, by itself, can actually never constitute an appropriate solution to our societal problems (cf. Leuzinger-Bohleber, Brandl, & Hüther, 2006).

Considering the explosively propagating practice of diagnosing of ‘ADHD’ and prescribing of MPH, this logical fact seems to have been widely misunderstood. Realistically, MPH constitutes a very convenient—yet radical—solution that is ruining the lives of millions of young people and thus devastating our societies. This kind of thinking and acting actually constitutes a regression

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32) Corporate Coverup? Whistleblower Doctor Alleges Shire Pharmaceuticals Neglected ADHD Drug Monitoring

THE MILLENNIAL PRESS Question Everything Corporate Coverup? Whistleblower Doctor Alleges Shire Pharmaceuticals Neglected ADHD Drug Monitoring Posted by on October 8, 2023

After paying out $56.5 million as part of the settlement with federal and state governments in 2014 for allegedly misleading the public, US and state agencies by claiming Adderall would ‘normalize’ its users and Vyvanse would provide ‘less abuse liability’, a former executive from Shire Pharmaceuticals (now Takeda Pharmaceutical Company), in charge of Data Science, has taken legal action against the company. The whistleblower, Dr. Vincent Polito

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Industry Sponsored research

Three authors are employees of Shire Pharmaceuticals, primary products, Adderall and Vyvanse , ADHD drugs. Shire struck gold in 2019 when Takeda Pharmaceutical Company purchased it for $62 billion.

33) Shaw, M., et al. “Review of studies of ADHD: long-term outcomes with and without treatment.” European Psychiatry 26.S2 (2011): 579-579.

As awareness of ADHD has increased worldwide, interest has grown beyond the constellation of ADHD symptoms, to include long-term impact on people’s lives and society in general.
Objectives Examine the results of studies of long-term life consequences of ADHD.
Aims To identify areas of life affected long-term by ADHD and differences in outcomes with and without ADHD treatment.
Methods Following Cochrane guidelines, 12 databases were searched for studies published in English (1980–2010). Limiting criteria maximized study inclusion while maintaining high study rigor: (1) peer-reviewed, (2) primary study reports, (3) including a comparator condition, and (4) reporting long-term outcomes (mean 8 years, range 6 months-40 years from study start for prospective studies; subjects in adolescence or adulthood for retrospective or cross-sectional studies). The fully-defined electronic search yielded 4615 citations. Manual review based on titles and abstracts yielded 340 studies included in this analysis of outcomes.

Results The majority of studies (86%, 243 of 281; studies of untreated ADHD only) showed that untreated ADHD has substantial negative long-term outcomes, encompassing nine broad-ranging areas of life: non-medicinal drug use/addictive behaviour, antisocial behaviour, academic achievement, occupational achievement, public services use, self-esteem, social function, obesity, and driving outcomes.

In contrast, most studies including ADHD pharmacotherapy and/or non-pharmacotherapy (94%, 46 of 49) showed that compared with baseline or untreated ADHD, long-term outcomes improved or stabilized with treatment of ADHD.

Conclusions ADHD has notable negative long-term consequences, and this negative impact may be reduced with treatment of ADHD. Supported by Shire Development Inc.

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34) Shaw, Monica, et al. “A systematic review and analysis of long-term outcomes in attention deficit hyperactivity disorder: effects of treatment and non-treatment.” BMC medicine 10 (2012): 1-15.

Outcomes from 351 studies were grouped into 9 major categories: academic, antisocial behavior, driving, non-medicinal drug use/addictive behavior, obesity, occupation, services use, self-esteem, and social function outcomes. The following broad trends emerged: (1) without treatment, people with ADHD had poorer long-term outcomes in all categories compared with people without ADHD, and (2) treatment for ADHD improved long-term outcomes compared with untreated ADHD, although not usually to normal levels. Only English-language papers were searched and databases may have omitted relevant studies.
Conclusions

This systematic review provides a synthesis of studies of ADHD long-term outcomes. Current treatments may reduce the negative impact that untreated ADHD has on life functioning, but does not usually ‘normalize’ the recipients.

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++++++++++++++++ already copied over ++++++++++++++++

Methylphenidate

35) The Pharmacology of Cocaine, Amphetamines, and Other Stimulants
David A. Gorelick, MD, PhD Michael H. Baumann, PhD CHAPTER 10

All stimulants produce a similar range of psychological, behavioral, and physiologic effects, with the intensity and duration depending on potency, dose, route of administration, and duration of use (see Section 6, Chapter 46, “Management of Stimulant, Hallucinogen, Marijuana, Phencyclidine, and Club Drug Intoxication and Withdrawal”).

The initial effects—usually desired— include increased energy, alertness, and sociability; elation or euphoria; and decreased fatigue, need for sleep, and appetite (121). The intense pleasurable feeling has been described as a “total body orgasm” (122). These effects may occur after 5 to 20 mg of oral amphetamine, methamphetamine, or methylphenidate; 100 to 200 mg of oral cocaine; 40 to 100 mg of intranasal cocaine; or 15 to 25 mg of IV or smoked cocaine (122,123). Such single oral doses of stimulants improve cognitive and psychomotor performance in subjects whose performance has been impaired by fatigue, sleep deprivation, or alcohol, especially in tasks that require focused and sustained attention (vigilance) (123,124).

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MPH in mice- Brain Damage

Chronic use of MPH has long-term neurodegenerative consequences.

2012 Methylphenidate exposure induces dopamine neuron loss and activation of microglia

36) 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.

Methylphenidate (MPH) is a psychostimulant that exerts its pharmacological effects via preferential blockade of the dopamine transporter (DAT) and the norepinephrine transporter (NET), resulting in increased monoamine levels in the synapse. Clinically, methylphenidate is prescribed for the symptomatic treatment of ADHD and narcolepsy; although lately, there has been an increased incidence of its use in individuals not meeting the criteria for these disorders. MPH has also been misused as a “cognitive enhancer” and as an alternative to other psychostimulants. Here, we investigate whether chronic or acute administration of MPH in mice at either 1 mg/kg or 10 mg/kg, affects cell number and gene expression in the basal ganglia.

Through the use of stereological counting methods, we observed a significant reduction (∼20%) in dopamine neuron numbers in the substantia nigra pars compacta (SNpc) following chronic administration of 10 mg/kg MPH. This dosage of MPH also induced a significant increase in the number of activated microglia in the SNpc. Additionally, exposure to either 1 mg/kg or 10 mg/kg MPH increased the sensitivity of SNpc dopaminergic neurons to the parkinsonian agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Unbiased gene screening employing Affymetrix GeneChip® HT MG-430 PM revealed changes in 115 and 54 genes in the substantia nigra (SN) of mice exposed to 1 mg/kg and 10 mg/kg MPH doses, respectively. Decreases in the mRNA levels of gdnf, dat1, vmat2, and th in the substantia nigra (SN) were observed with both acute and chronic dosing of 10 mg/kg MPH. We also found an increase in mRNA levels of the pro-inflammatory genes il-6 and tnf-α in the striatum, although these were seen only at an acute dose of 10 mg/kg and not following chronic dosing.

Collectively, our results suggest that chronic MPH usage in mice at doses spanning the therapeutic range in humans, especially at prolonged higher doses, has long-term neurodegenerative consequences.

Enduring Changes in Neuro Glial Network

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

Repeated exposure to psychostimulant drugs induces complex molecular and structural modifications in discrete brain regions of the meso-cortico-limbic system. This structural remodeling is thought to underlie neurobehavioral adaptive responses. Administration to
adolescent rats of methylphenidate (MPH), commonly used in attention deficit and hyperactivity disorder (ADHD), triggers alterations of reward-based behavior paralleled by persistent and plastic synaptic changes of neuronal and glial markers within key areas of the reward circuits. By immunohistochemistry, we observe a marked increase of glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) expression and a down-regulation of glial glutamate transporter GLAST in dorso-lateral and ventro-medial striatum. Using electron microscopy, we find in the prefrontal cortex a significant reduction of the synaptic active zone length, paralleled
by an increase of dendritic spines. We demonstrate that in limbic areas the MPH-induced reactive astrocytosis affects the glial glutamatergic uptake system that in turn could determine glutamate receptor sensitization. These processes could be sustained by NO production and
synaptic rearrangement and contribute to MPH neuroglial induced rewiring.

repeated:

Methylphenidate (MPH) is a psychostimulant that exerts its pharmacological effects via preferential blockade of the dopamine transporter (DAT) and the norepinephrine transporter (NET), resulting in increased monoamine levels in the synapse. Clinically, methylphenidate is prescribed for the symptomatic treatment of ADHD and narcolepsy; although lately, there has been an increased incidence of its use in individuals not meeting the criteria for these disorders. MPH has also been misused as a “cognitive enhancer” and as an alternative to other psychostimulants. Here, we investigate whether chronic or acute administration of MPH in mice at either 1 mg/kg or 10 mg/kg, affects cell number and gene expression in the basal ganglia.

Through the use of stereological counting methods, we observed a significant reduction (∼20%) in dopamine neuron numbers in the substantia nigra pars compacta (SNpc) following chronic administration of 10 mg/kg MPH. This dosage of MPH also induced a significant increase in the number of activated microglia in the SNpc.

Conclusion

Collectively, our results suggest that chronic MPH usage in mice at doses spanning the therapeutic range in humans, especially at prolonged higher doses, has long-term neurodegenerative consequences.

MPH’s mechanism of action is to increase the availability of extracellular DA and NE in the synaptic cleft through blockade of the dopamine transporter (DAT) and norepinephrine transporter (NET) [12], [35], [36]

We found that chronic exposure to both 1 mg/kg and 10 mg/kg MPH increased the sensitivity of SNpc dopamine neurons to oxidative stress, based on a significantly increased SNpc dopamine neuron loss in mice administered MPH as compared to saline-treated control mice. Although the mechanism for this neuronal loss is unknown, a significant increase in MPH-induced activated microglia was observed; therefore, we hypothesize that an increase in free radical formation along with a concomitant neuroinflammatory response increases the sensitivity of the SNpc dopamine neurons to a later oxidative challenge. This conclusion is supported by a recent epidemiological study that showed that long-term amphetamine usage, which like MPH results in higher levels of striatal dopamine in the synaptic cleft, results in a significantly higher risk for developing Parkinson’s disease [51].

Taken together, our results suggest that chronic administration of methylphenidate in mice, at doses that approximate those at the higher therapeutic range in humans, results in a reduced expression of neurotrophic factors, increased neuroinflammation, and a small, but significant loss of SNpc dopamine neurons. These results can only be interpreted in the context on normal brain structure and function, and thus would have direct implications for the illicit/neurocognitive use of MPH. Since the underlying anatomy and biochemistry of ADHD has not been definitively characterized, our findings may or may not be generalizable to the vast majority of humans who are properly diagnosed with ADHD and are prescribed methylphenidate. Nevertheless, this work supports studies [51], [57], [58], [59] that demonstrate that drugs shown to increase the levels of dopamine in the synaptic cleft can contribute to degenerative changes in the basal ganglia.

38) Dendritic Spines:Wikipedia

A dendritic spine (or spine) is a small membranous protrusion from a neuron’s dendrite that typically receives input from a single axon at the synapse. Dendritic spines serve as a storage site for synaptic strength and help transmit electrical signals to the neuron’s cell body. Most spines have a bulbous head (the spine head), and a thin neck that connects the head of the spine to the shaft of the dendrite. The dendrites of a single neuron can contain hundreds to thousands of spines. In addition to spines providing an anatomical substrate for memory storage and synaptic transmission, they may also serve to increase the number of possible contacts between neurons.[1] It has also been suggested that changes in the activity of neurons have a positive effect on spine morphology.[2]

experimental findings that suggest a role for dendritic spine dynamics in mediating learning and memory,

In particular, long-term memory is mediated in part by the growth of new dendritic spines (or the enlargement of pre-existing spines) to reinforce a particular neural pathway. Because dendritic spines are plastic structures whose lifespan is influenced by input activity,[21] spine dynamics may play an important role in the maintenance of memory over a lifetime.

Neurogenesis: impact of juvenile mice MPH exposure on adult hippocampal neurogenesis. Decreased Adult neurogenesis in the hippocampus.= BRAIN DAMAGE !!!!

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

Background: The neural consequences of early-life exposure to methylphenidate (MPH; Ritalin) are of great interest given the widespread, and sometimes inappropriate, use in children. Here we examine the impact of juvenile MPH exposure on adult hippocampal neurogenesis.

Methods: Rats received MPH (2.0 mg/kg, intraperitoneal, twice daily) or saline (SAL) during preadolescence (postnatal days 20-35). Hippocampal cell proliferation (Experiment 1), neurogenesis (Experiment 2), and stress-induced changes in cell proliferation (Experiment 3) were assessed at several developmental stages including adulthood.

Results: Juvenile exposure to MPH did not alter proliferation at any developmental time point relative to control rats; however, exposure to MPH significantly decreased the long-term survival of newborn cells in adult rats, particularly in the temporal hippocampus. Although MPH-treated rats had higher levels of corticosterone after restraint stress, they did not show the expected greater decrease in hippocampal cell proliferation relative to control animals.

Conclusions: Early-life exposure to MPH inhibits the survival of adult-generated neurons in the temporal hippocampus and may reduce progenitor sensitivity to corticosterone-induced decreases in proliferation. These findings suggest that decreased adult neurogenesis is an enduring consequence of early-life exposure to MPH and are discussed for their relevance to humans.

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prolonged ADHD medication use at higher doses is significantly associated with smaller hippocampus volumes in specific subregions.

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

Structural neuroimaging studies comparing ADHD children to neurotypical children identified group differences in cortical and subcortical brain regions (Albajara Saenz, Villemonteix, & Massat, 2018). A landmark study by Shaw et al. 2007 reported a delay in peak cortical maturation of 3.5 years in children with ADHD, most apparent in prefrontal regions (Shaw et al., 2007). A mega-analysis by Hoogman et al. 2017 reported reduced volumes in the accumbens, amygdala, hippocampus, putamen, and overall brain in comparison to control children (Hoogman et al., 2017). However, there is considerable variability across neuroimaging studies in ADHD, as one meta-analysis found that only 25–50% of published reports had reproducible results (Frodl & Skokauskas, 2012). Since pharmacological agents are commonly used to treat ADHD symptoms, it is important to assess their impact on brain structure. If exposure to ADHD medication significantly alters brain structure measurements, it might provide partial explanation for the varying results across ADHD imaging studies.

Taken together, these studies do not provide evidence for abnormal brain development following exposure to ADHD medication. Rather, they highlight the confusing state of the literature where medication is reported as having either no effect on brain structure or as having a normalizing effect brain structure

studies have reported hippocampus volume reductions in adults with ADHD who had, during childhood, been treated with ADHD medication (Frodl and Skokauskas, 2012, Onnink et al., 2014). These findings were not observed in stimulant-naïve adults with ADHD. Frodl and Skokauskas (2012) have suggested that changes in smaller regions, such as the hippocampus, may go undetected as large threshold corrections for the whole brain are typically used (Frodl & Skokauskas, 2012). Moreover, in the relatively few studies that have included the hippocampus when assessing medication effects, no studies have sought to investigate subregions.

Five children with ADHD were concurrently prescribed anti-psychotics and were excluded from the final analysis (ADHD n = 101). The number of independent prescriptions for ADHD medication per child was one (n = 7), two (n = 34), three (n = 21), four (n = 18) and five (n = 21). A total of 315 prescriptions were included: Ritalin® (35.2%), Biphentin® (32.4%), Concerta® (22.6%), Vyvanse® (5.7%), Strattera® (2.5%) and Adderall® (1.6%).

Conclusions Although this study is cross-sectional, the results found within this sample of children show that prolonged ADHD medication use at higher doses is significantly associated with smaller hippocampus volumes in specific subregions.
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41) Svetlov, Stanislav I., Firas H. Kobeissy, and Mark S. Gold. “Performance enhancing, non-prescription use of Ritalin: a comparison with amphetamines and cocaine.” Journal of addictive diseases 26.4 (2007): 1-6.

Ritalin, known under chemical name methylphenidate (MPH), is a psychostimulant prescribed to treat attention-deficit/hyperactivity disorder (ADHD) and other conditions. Psychotropic effects and pharmacological pathways evoked by MPH are similar, but not identical to those produced by amphetamines and cocaine. Although not completely understood in detail, MPH psychostimulation is mediated by the increase of central dopamine (DA) and possibly norepinephrine (NE) and serotonin (ST) due to decrease of their re-uptake via binding to and inhibition of DA, NE, and ST transporters. Despite similarity in psychopharmacological effects, the rewarding/ reinforcing ability of MPH appears to be significantly lower than amphetamines and especially cocaine. MPH and similar medications have been widely used on College campuses and by students preparing for exams. Nicknamed ‘steroids for SATs,’ MPH and related medications are purchased without prescription and their use may even be encouraged by parents and tutors. However, while widely and safely used and administered for over forty years, Ritalin generated significant controversy including MPH abuse and addiction, and adverse reactions. It is now clear that treatment of ADD/ADHD with psychostimulants prevents drug abuse and addictions. Use by those without any medical or psychiatric diagnosis is increasing. In this mini-review, we discuss psychopharmacological and behavioral aspects, and outline neurochemical mechanisms that may provoke Ritalin abuse, addiction and adverse effects compared to amphetamines and cocaine.

42) Kim, Yong, et al. “Methylphenidate-induced dendritic spine formation and ΔFosB expression in nucleus accumbens.” Proceedings of the National Academy of Sciences 106.8 (2009): 2915-2920.

Methylphenidate is the psychostimulant medication most commonly prescribed to treat attention deficit hyperactivity disorder (ADHD). Recent trends in the high usage of methylphenidate for both therapeutic and nontherapeutic purposes prompted us to investigate the long-term effects of exposure to the drug on neuronal adaptation. We compared the effects of chronic methylphenidate or cocaine (15 mg/kg, 14 days for both) exposure in mice on dendritic spine morphology and ΔFosB expression in medium-sized spiny neurons (MSN) from ventral and dorsal striatum. Chronic methylphenidate increased the density of dendritic spines in MSN-D1 (MSN-expressing dopamine D1 receptors) from the core and shell of nucleus accumbens (NAcc) as well as MSN-D2 (MSN-expressing dopamine D2 receptors) from the shell of NAcc. In contrast, cocaine increased the density of spines in both populations of MSN from all regions of striatum. In general, the effect of methylphenidate on the increase of shorter spines (class 2) was less than that of cocaine. Interestingly, the methylphenidate-induced increase in the density of relatively longer spines (class 3) in the shell of NAcc was bigger than that induced by cocaine. Furthermore, methylphenidate exposure increased expression of ΔFosB only in MSN-D1 from all areas of striatum, and surprisingly, the increase was greater than that induced by cocaine. Thus, our results show differential effects of methylphenidate and cocaine on neuronal adaptation in specific types of MSN in reward-related brain regions.

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methylphenidate ADHD

MPH may induce long-lasting alterations in the adult mPFC GABAergic system when treatment was started at a young age.

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

First stimulant exposure at a young age is thus associated with lower baseline levels of GABA+ and increased responsivity in adulthood. This effect could not be found in patients that started treatment at an adult age. Hence, while adult stimulant treatment seems to exert no major effects on GABA+ levels in the mPFC, MPH may induce long-lasting alterations in the adult mPFC GABAergic system when treatment was started at a young age.

• Early stimulant exposure results in lower baseline PFC GABA levels in adulthood.
• Exposure at young age alters the GABAergic response to stimulants in adulthood.
• First exposure to stimulants in adulthood exerts no major effects.

In conclusion, our results demonstrate that MPH effects on GABA+ levels in ADHD patients are influenced by whether a subject had first started stimulant treatment in childhood or in adulthood. Our data thus suggest that long-lasting alterations may have occurred in GABAergic neurotransmission in the mPFC, selectively in subjects who had been first exposed to stimulant treatment early during childhood, but not in those who started medication only from later in their lives onward. Future studies are therefore warranted to assess the underlying mechanisms as well as the consequences of these lower GABA+ levels on cognitive and behavioral problems in ADHD.

44) Brookshire, Bethany R., and Sara R. Jones. “Chronic methylphenidate administration in mice produces depressive‐like behaviors and altered responses to fluoxetine.” Synapse 66.9 (2012): 844-847.

Methylphenidate (MPH) is a psychostimulant used in the treatment of attention-deficit/hyperactivity disorder in children and adults. Increasing abuse rates of this drug have raised questions regarding the effects of chronic, high-dose MPH administration. Although the effects of chronic MPH exposure have been well-documented in regard to reward-related behaviors in adolescent and adult animals, there are few studies of the effects of MPH on depressive-like behaviors and antidepressant responses, particularly in adult models. We examined the effects of chronic (14 days) high-dose (20 mg/kg i.p.) MPH exposure on locomotor activity and forced swim test behavior in C57Bl/6J mice. We show that MPH treatment ameliorates the locomotor suppression seen in response to fluoxetine. In addition, chronic MPH treatment produces depressive-like effects in the forced swim test, with decreased latency to first immobility and a trend toward increased immobility. These effects are reversed with acute fluoxetine administration, in contrast to saline-treated animals, which show no response to fluoxetine. The induction of depressive-like behaviors after chronic MPH treatment in adult mice is in agreement with previous studies in adolescent rats, and the marked alterations in fluoxetine responses implicate alterations in the serotonin system and possibly the dopamine system produced by MPH.

45) 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.

Background: Methylphenidate (MPH) is a stimulant prescribed for the treatment of attention-deficit/hyperactivity disorder (ADHD). Stimulant drugs can cause enduring behavioral adaptations, including altered drug sensitivity, in laboratory animals. We examined how early developmental exposure to stimulants affects behavior in several rodent models.

Methods: Rats received MPH or cocaine during preadolescence (P20-35). Behavioral studies began during adulthood (P60). We compared how early exposure to MPH and cocaine affects sensitivity to the rewarding and aversive properties of cocaine using place conditioning. We also examined the effects of early exposure to MPH on depressive-like signs using the forced swim test, and habituation of spontaneous locomotion, within activity chambers.

Results: In place-conditioning tests, early exposure to MPH or cocaine each made moderate doses of cocaine aversive and high doses less rewarding. Early MPH exposure also caused depressive-like effects in the forced swim test, and it attenuated habituation to the activity chambers.

Conclusions: Early exposure to MPH causes behavioral changes in rats that endure into adulthood. Some changes (reduced sensitivity to cocaine reward) may be beneficial, whereas others (increases in depressive-like signs, reduced habituation) may be detrimental. The effects of MPH on cocaine-related behaviors may be a general consequence of early stimulant exposure.

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ADHD and MTHFR

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46) Nancy Mullan, MD MTHFR+ and ADHD

Free ebook on MTHFR https://www.nancymullanmd.com/ebook-form

All of the symptoms of ADHD are associated with MTHFR mutations, including the impaired immunity that predisposes ADHD sufferers to have an increased incidence of ear infections. ADHD is on the autism spectrum, and 98% of individuals with Autism Spectrum Disorder have at least one MTHFR mutation

Diet is the foundation of heath no matter what you are trying to treat. Double handfuls of nutritional supplements will not overcome a problem with diet. The solution also involves getting genetic testing, subsequent additional testing to determine body biochemistry, and nutritional supplements to address the problems uncovered.
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47) Dr RoseAnn MTHFR and ADHD

The MTHFR genetic mutation is important in clinical conditions because it has been linked to various health issues, including ADHD, OCD, anxiety, and depression (Wan et. al., 2018).

Studies have suggested a possible connection between MTHFR genetic mutations and an increased risk for ADHD. The MTHFR gene plays a critical role in folate metabolism, which is essential for the production of neurotransmitters such as serotonin, dopamine, and norepinephrine. These neurotransmitters play important roles in regulating mood, attention, and behavior, and disruptions in their function have been implicated in the development of ADHD.

The mechanisms behind this association are not yet fully understood, but research suggests that MTHFR genetic mutations may lead to reduced folate metabolism, which in turn can impact neurotransmitter production and function. Reduced levels of neurotransmitters such as dopamine and norepinephrine have been implicated in ADHD, suggesting a possible link between MTHFR genetic mutations and the disorder.

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48) MTHFR: The Link Between ADD/ADHD, Folate, and Genetics June 28, 2016

Adolescents 13-18, Anxiety, Autism, Children 5-12, Vitamins and Supplements by Cori Burke, ND
Dr. Cori Burke is a Naturopathic Physician and graduate of the National University of Natural Medicine.
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MTHFR

49) Why ADHD & Learning Disabilities Can ‘Run in the Family’ & What You Can Do: Understanding the MTHFR Gene
info@lorrainedriscoll.com January 14, 2020

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Amphetamines

50) Selemon, Lynn D., et al. “Amphetamine sensitization alters dendritic morphology in prefrontal cortical pyramidal neurons in the non-human primate.” Neuropsychopharmacology 32.4 (2007): 919-931.

Amphetamine (AMPH) sensitization in the nonhuman primate induces persistent aberrant behaviors reminiscent of the hallmark symptoms of schizophrenia, including hallucinatory-like behaviors, psychomotor depression, and profound cognitive impairment. The present study examined whether AMPH sensitization induces similarly long-lasting morphologic alterations in prefrontal cortical pyramidal neurons. Three to 3½ years postsensitization, sensitized, and AMPH-naïve control monkeys were killed. Blocks of prefrontal cortex were Golgi-impregnated for elucidation of pyramidal dendritic morphology in layers II/superficial III (II/IIIs), deep III, and V/VI. In AMPH-sensitized animals as compared to AMPH-naïve controls, pyramidal dendrites in layer II/IIIs exhibited reduced overall dendritic branching and reduced peak spine density (22%) on the apical trunk. Across all layers, the distance from soma to peak spine density along the apical trunk was decreased (126.38±7.65 μm in AMPH-sensitized compared to 162.98±7.26 μm in AMPH-naïve controls), and basilar dendritic length was reduced (32%). These findings indicate that chronic dopamine dysregulation, consequent to AMPH sensitization, results in enduring, atrophic changes in prefrontal pyramidal dendrites that resemble the pathologic alterations described in patients with schizophrenia and may contribute to the persistence of schizophrenia-like behavioral changes and cognitive dysfunction associated with sensitization. These findings may also provide key insights into the etiologic origin of the pronounced behavioral disturbances and cognitive dysfunction associated with schizophrenia.

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Hippocampus

51) Arroyo-García, Luis Enrique, et al. “Amphetamine sensitization alters hippocampal neuronal morphology and memory and learning behaviors.” Molecular Psychiatry 26.9 (2021): 4784-4794.

An increase in the dopaminergic tone caused by AMPH sensitization generates oxidative stress, neuronal death, and morphological changes in the hippocampus that affect cognitive behaviors like short- and long-term memories.

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52) Tendilla-Beltrán, Hiram, Luis Enrique Arroyo-García, and Gonzalo Flores. “Amphetamine and the Biology of Neuronal Morphology.” Handbook of Substance Misuse and Addictions: From Biology to Public Health. Cham: Springer International Publishing, 2022. 1-24.

Amphetamines are widely used psychostimulants for both therapeutic and recreational purposes. These drugs enhance monoaminergic neurotransmission. Amphetamines increase dopamine, noradrenaline, and serotonin availability in the synaptic cleft, mainly by the reverse action of the monoamine transporters (MATs), which in physiological conditions are the main mechanism for monoamine recapture. Moreover, monoamines are closely related to the reward system, which is an ensemble of corticolimbic structures that hierarchizes sensory information according to motivation or pleasure. It has been widely studied the increased motor behavioral effects after repeated and intermittent amphetamine exposure, described as behavioral sensitization, which is part of the complex addictive behavior. Interestingly, amphetamines have neuroplasticity effects, since chronic exposure to these drugs hypertrophies the dendritic arbor and increases the number of dendritic spines in neurons of the corticolimbic system. Also, amphetamines induce oxidative stress. These neuronal impairments can be related to the memory and learning disturbances and ultimately to the behavioral sensitization induced by amphetamine exposure.

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Damage to dopaminergic neurons in striatum monkeys

53) 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.

Pharmacotherapy with amphetamine is effective in the management of attention-deficit/hyperactivity disorder (ADHD), now recognized in adults as well as in children and adolescents. 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. Furthermore, plasma concentrations of amphetamine associated with dopaminergic neurotoxicity in nonhuman primates are on the order of those reported in young patients receiving amphetamine for the management of ADHD. These findings may have implications for the pathophysiology and treatment of ADHD. Further preclinical and clinical studies are needed to evaluate the dopaminergic neurotoxic potential of therapeutic doses of amphetamine in children as well as adults.

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.

Reduces BDNF

55) Angelucci, Francesco, et al. “Chronic amphetamine treatment reduces NGF and BDNF in the rat brain.” European Neuropsychopharmacology 17.12 (2007): 756-762.

56) Advokat, Claire. “Literature review: Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD.” Journal of Attention Disorders 11.1 (2007): 8-16.

57) Bourgeois, Florence T., Jeong Min Kim, and Kenneth D. Mandl. “Premarket safety and efficacy studies for ADHD medications in children.” PLoS One 9.7 (2014): e102249.

Conclusions: Clinical trials conducted for the approval of many ADHD drugs have not been designed to assess rare adverse events or long-term safety and efficacy.

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2022

58) Mechler, Konstantin, et al. “Evidence-based pharmacological treatment options for ADHD in children and adolescents.” Pharmacology & Therapeutics 230 (2022): 107940.

statistically significant reduction in height and weight gain

Findings from longitudinal studies indicate that treatment with psychostimulants is associated with a statistically significant reduction in height and weight gain (Cortese et al., 2018; Faraone, Biederman, Morley, & Spencer, 2008; Greenhill et al., 2020; Swanson et al., 2017).

Lisdexamfetamine dimesylate is a prodrug that is metabolized to dextroamphetamine and is available as Vyvanse.

While short-term efficacy and safety of both stimulants and non-stimulants have been soundly demonstrated in various clinical trials (Banaschewski et al., 2006; Cortese et al., 2018; Faraone & Buitelaar, 2009; Padilha, Virtuoso, Tonin, Borba, & Pontarolo, 2018; Reed et al., 2016; Savill et al., 2015), a comparable extent of systematic assessments for longer-term outcomes is not yet available.

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59) Teixeira-Gomes, Armanda, et al. “The neurotoxicity of amphetamines during the adolescent period.” International Journal of Developmental Neuroscience 41 (2015): 44-62.

Amphetamine-type psychostimulants (ATS), such as amphetamine (AMPH), 3,4-methylenedioxymethamphetamine (MDMA), and methamphetamine (METH) are psychoactive substances widely abused, due to their powerful central nervous system (CNS) stimulation ability. Young people particularly use ATS as recreational drugs. Moreover, AMPH is used clinically, particularly for attention deficit hyperactivity disorder, and has the ability to cause structural and functional brain alterations. ATS are known to interact with monoamine transporter sites and easily diffuse across cellular membranes, attaining high levels in several tissues, particularly the brain. Strong evidence suggests that ATS induce neurotoxic effects, raising concerns about the consequences of drug abuse. Considering that many teenagers and young adults commonly use ATS, our main aim was to review the neurotoxic effects of amphetamines, namely AMPH, MDMA, and METH, in the adolescence period of experimental animals. Reports agree that adolescent animals are less susceptible than adult animals to the neurotoxic effects of amphetamines. The susceptibility to the neurotoxic effects of ATS seems roughly located in the early adolescent period of animals. Many authors report that the age of exposure to ATS is crucial for the neurotoxic outcome, showing that the stage of brain maturity has a strong importance. Moreover, recent studies have been undertaken in young adults and/or consumers during adolescence that clearly indicate brain or behavioural damage, arguing for long-term neurotoxic effects in humans. There is an urgent need for more studies during the adolescence period, in order to unveil the mechanisms and the brain dysfunctions promoted by ATS.

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60) Krasnova, Irina N., and Jean Lud Cadet. “Methamphetamine toxicity and messengers of death.” Brain research reviews 60.2 (2009): 379-407.

Methamphetamine (METH) is an illicit psychostimulant that is widely abused in the world. Several lines of evidence suggest that chronic METH abuse leads to neurodegenerative changes in the human brain. These include damage to dopamine and serotonin axons, loss of gray matter accompanied by hypertrophy of the white matter and microgliosis in different brain areas. In the present review, we summarize data on the animal models of METH neurotoxicity which include degeneration of monoaminergic terminals and neuronal apoptosis. In addition, we discuss molecular and cellular bases of METH-induced neuropathologies. The accumulated evidence indicates that multiple events, including oxidative stress, excitotoxicity, hyperthermia, neuroinflammatory responses, mitochondrial dysfunction, endoplasmic reticulum stress converge to mediate METH-induced terminal degeneration and neuronal apoptosis. When taken together, these findings suggest that pharmacological strategies geared towards the prevention and treatment of the deleterious effects of this drug will need to attack the various pathways that form the substrates of METH toxicity.

Concluding Remarks

In summary, the brains of human METH addicts, who abuse large doses of the drug, are characterized by a variety of neuropathological changes. These include degeneration of monoaminergic terminals, dysregulation of energy metabolism, evidence of oxidative stress, as well as microgliosis and reactive astrogliosis. The deleterious effects of the drug have been consistently replicated in animal models. These studies have helped to identify some of the pathways that form the mechanistic substrates for METH-induced damage to monoaminergic terminals. Similarly, recent investigations have clarified the bases for neuronal apoptosis caused by METH exposure in various regions of the mammalian brain. This knowledge is just beginning to impact on the thinking regarding how to best approach the development of potentially effective therapeutic strategies that will address the neurological and psychiatric deterioration observed in some METH addicts. The use of therapeutic agents that address solely the addictive properties of METH might not be sufficient to attenuate the varied neuropathological end-points caused by the use of the drug. One possibility might be the need to combine therapeutic anti-addictive drugs with neuroprotective agents within the same clinical setting where these patients are being treated. The combination of anti-addictive agents with the anti-manic drug, lithium, that has been shown to have neuroprotective properties (Chuang, 2004), might be a fruitful approach to the treatment of METH abusers. In any case, more studies are needed in order to further clarify strategies that might serve to promote recovery of monoaminergic systems in models of METH toxicity.

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61) Steinkellner, Thomas, et al. “The ugly side of amphetamines: short-and long-term toxicity of 3, 4-methylenedioxymethamphetamine (MDMA,‘Ecstasy’), methamphetamine and D-amphetamine.” (2011): 103-115.

Amphetamines exert their acute effects both in the central nervous system (CNS) and in peripheral tissues. The acute clinical outcome is dependent upon the dose administered and typically includes positively prescribed

subjective effects such as an increased state of arousal, euphoria, increased energy and talkativeness, but also negative emotions including anxiety, paranoia or auditory and visual hallucinations (Baylen and Rosenberg 2006; Cruickshank and Dyer, 2009).

The peripheral effects of amphetamines are primarily mediated by its interaction with the noradrenaline transporter (NAT) and are associated with an increase in extracellular noradrenaline (NA) concentrations. These effects include increases in heart rate, blood pressure, respiration rate, body temperature, psychomotor activation and reduced appetite (Boenisch and Bruess, 2006; Cruickshank and Dyer, 2009). It is the sympathomimetic stimulating effect of amphetamines which renders them attractive as doping agents (Docherty, 2008).

Amphetamines also increase locomotor activity, an effect which can be enhanced by the repeated administration of the drug. This hyperactivity is referred to as ‘behavioural sensitisation’ and is neurochemically correlated with an increase in striatal DA release. It can persist for several months following the last drug administration, thereby mimicking the sensitised states of human psychostimulant abusers (Paulson and Robinson, 1995; Pierce and Kalivas, 1997).

Taken together, these observations are consistent with a cellular model where amphetamine action in mesocorticolimbic dopaminergic neurons is the fundamental mechanism contributing to their reinforcing and addictive properties (Nestler, 2005; Kalivas, 2007).

Chronic METH abuse leads to the degeneration of monoaminergic terminals (Davidson et al., 2001; Krasnova and Cadet, 2009) and reduced DAT and DA levels in the striatum of mice, rats and monkeys (Anderson and Itzhak, 2006; Graham et al., 2008; Melega et al., 2008). Similar effects have been reported in people subjected to positron emission tomography (PET) (Volkow et al., 2001).

Amphetamines and psychotic episodes

One of the prime findings in amphetamine abuse is the induction of psychotic episodes that are almost indistinguishable from the positive symptoms seen in schizophrenic patients (Ujike and Sato, 2004; Hermens et al., 2009). This supports the conjecture that there might be a link between amphetamine abuse and the psychopathic traits observed in schizophrenia.

psychostimulants such as d-AMPH or METH can increase the susceptibility of users to psychotic symptoms either during acute amphetamine abuse or during withdrawal (Ujike and Sato, 2004; Hermens et al., 2009).

It has been recently shown that impulsive antisocial behaviours (a possible ‘negative symptom’ that can occur in schizophrenia) correlates with an increase in amphetamine-induced DA release in the NAc measured by [18F]fallypride PET and functional magnetic resonance imaging. These observations provide evidence for an association between substance abuse and psychopathic traits (Buckholtz et al., 2010). To obtain an animal model for the psychotic symptoms of schizophrenia, animals are subjected to amphetamine-induced sensitisation and observed during withdrawal periods after the sensitisation regimen (Paulson and Robinson, 1995; Peleg-Raibstein et al., 2009). Sensitised animals show an increase in subsequent amphetamine-induced DA release in the striatum and an increase in locomotor activity (Paulson and Robinson, 1995; Iwata et al., 1997). Thus, sensitisation is not only a model for addiction but also for psychosis (Gainetdinov et al., 2001).

Conclusions and future perspectives

Amphetamines are the second most commonly abused drugs in Europe after cannabis (EMCDDA, 2009) and the devastating effects of METH addiction are obvious in many parts of the world (Karila et al., 2010). All three drugs (METH, d-AMPH and MDMA) have been reported to induce psychotic episodes or ‘seizures’ in humans (Ujike and Sato, 2004; Karlsen et al., 2008). Furthermore, the loss of nigrostriatal dopaminergic neurons observed following repeated METH administration in animals has been associated with the pathogenesis of PD (Sonsalla et al., 1996; Harvey et al., 2000; Granado et al., 2010). These unintended (‘side’) effects should be carefully assessed when considering the long-term effects of amphetamine abuse on mental health and well-being.

Conversely, both d-AMPH and METH are used in the treatment of ADHD, narcolepsy and obesity. Likewise, MDMA abuse has been implicated in both the origin and treatment of PD (Morton, 2005; Sotnikova et al., 2005). Moreover, MDMA has even been suggested as a therapeutic aid in post-traumatic stress disorder (Morton, 2005). Long-term amphetamine administration has been shown to induce ample neurodegenerative side effects in animal models, thus rendering this the main cause for concern in humans following chronic amphetamine abuse.

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62) Edinoff, Amber N., et al. “Methamphetamine use: a narrative review of adverse effects and related toxicities.” Health Psychology Research 10.3 (2022).

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63) Angelucci, Francesco, et al. “Chronic amphetamine treatment reduces NGF and BDNF in the rat brain.” European Neuropsychopharmacology 17 (2007): 756-762.

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.
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Berberine

64) Mohseni, Fahimeh, et al. “Berberine hydrochloride improves cognitive deficiency through hippocampal up-regulation of neurotrophins following inhalant self-administration of methamphetamine.” Iranian Journal of Basic Medical Sciences 26.1 (2023): 23.

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ALA and Lithium Reversed Amphetamine increased locomotor activity and reversed the decrease in BDNF.

65) Macêdo DS, et al. Effects of alpha-lipoic acid in an animal model of mania induced by d-amphetamine. Bipolar Disord 2012: 14: 707–718.

Objectives: Oxidative stress and neurotrophic factors are involved in the pathophysiology of bipolar disorder (BD). Alpha-lipoic acid (ALA) is a naturally occurring compound with strong antioxidant properties. The present study investigated ALA effects in an amphetamine-induced model of mania.

Methods: In the reversal protocol, adult mice were first given d-amphetamine (AMPH) 2 mg/kg, intraperitoneally (i.p.) or saline for 14 days. Between days 8 and 14, the animals received ALA 50 or 100 mg/kg orally, lithium (Li) 47.5 mg/kg i.p., or saline. In the prevention paradigm, mice were pretreated with ALA, Li, or saline prior to AMPH. Locomotor activity was assessed in the open-field task. Superoxide dismutase (SOD) activity, reduced glutathione (GSH), and thiobarbituric acid-reactive substance (TBARS) levels were evaluated in the prefrontal cortex (PFC), hippocampus (HC), and striatum (ST). Brain-derived neurotrophic factor (BDNF) levels were measured in the HC.

Results: ALA and Li prevented and reversed the AMPH-induced increase in locomotor activity. Prevention model: ALA and Li co-administration with AMPH prevented the decrease in SOD activity induced by AMPH in the HC and ST, respectively; ALA and Li prevented GSH alteration in the HC and TBARS formation in all brain areas studied. Reversal model: ALA reversed the decrease in SOD activity in the ST. TBARS formation was reversed by ALA and Li in all brain areas. Furthermore, ALA reversed AMPH-induced decreases in BDNF and GSH in the HC.

Conclusions: Our findings showed that ALA, similarly to Li, is effective in reversing and preventing AMPH-induced behavioral and neurochemical alterations, providing a rationale for the design of clinical trials investigating ALA’s possible antimanic effect.

=======================

Low-Dose Nutritional Lithium for ADHD James Greenblatt, MD

66) Why Low-Dose Nutritional Lithium Should Be an Option for ADHD James Greenblatt, MD

I continue to prescribe low-dose nutritional lithium to my patients. I use the treatment to stabilize mood. To help with addictions. To slow or stop memory loss in seniors. And I use it to effectively ease or erase irritability, anger, and aggression in children with ADHD.

67) Lithium, The Magic Mineral That Charges Cell Phones and Preserves Memory By James Greenblatt, MD, and Kayla Grossmann, RN Townsend Letter, October 2015

A 4-year-old boy, Peter, had severe ADHD. Even at this young age, he was shunned by other children, and his parents were asked to remove him from preschool. It was easy to observe his aggressive behaviors in my office. A trace mineral analysis from a hair sample revealed no detectable lithium. I prescribed 250 mcg of lithium in liquid form. Peter’s annoying aggressiveness diminished. He became able to make friends, and eventually he began to participate cooperatively with other children in a new preschool.

Shawn at age 8 was often in trouble for bullying. Although he had been diagnosed with ADHD, stimulants had not been helpful. His trace mineral analysis showed no detectable lithium. On 2 mg of lithium orotate, he showed significant improvement, and he lost interest in bullying other children.

68) Nutritional Lithium and Memory Preservation By James Greenblatt, MD07/01/2019

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69) Greenblatt, James, Jennifer Dimino, and Winnie T. Lee. “OPCs for the Treatment of ADHD: A Functional Medicine Approach By James Greenblatt, MD 04/05/2020 May 8th, 2023 No Comments 13 min read.”

OPCs (Pycnogenol) for the Treatment of ADHD: A Functional Medicine Approach

Science has demonstrated that OPCs directly benefit brain networks, neuron-to-neuron signaling, biochemical changes and metabolic processes that have been identified as underlying factors for many of the symptoms of ADHD. While it is speculative just how exactly OPCs improve cognitive function among individuals with ADHD, the available literature supports OPCs as a safe, naturally occurring, and therapeutic adjunct treatment that can improve cognitive performance and minimize the hallmark ADHD symptoms of hyperactivity and inability to focus. Their use as medicine over thou- sands of years is testament to their efficacy and safety, and modern research has corroborated that they are in- deed effective and safe.

In over three decades of using OPCs to treat patients with ADHD, we have never observed any negative side effects associated with OPC supplementation. Instead, we have observed patients whose thinking becomes progressively clearer once they start taking OPCs. Count- less patients have also reported an improved ability to concentrate and maintain focus, a steady improvement in their ability to read, write, and listen, and parents of patients have shared anecdotal stories about improvements in behaviors at home and performance in school.

Buy Lithium Orotate 1 mg Capsules:
Lithium (orotate) 1 mg from Pure Encapsulations
Dosage is 2 mg/ day which is similar to average dietary intake

Buy Lithium Liquid from WellnessOne on Amazon :

Buy Pycnogenol Pure Encapsulations
Pycnogenol (OPC) proanthocyanidin extract, maritime pine bark.

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+++++++++++ Already copied OVer ++++++++++++++++++++++

Dr Breggin ADHD drugs / Kids

70) Peter Breggin, MD – ADHD Kids – A Lifelong Road to Tragedy.
Simple Truths about Psychiatry Vol. 8

i’m peter bregen i’m a psychiatrist and this is one in my series of simple truths about psychiatry i’ve already talked to you about stimulant drugs for children and now i want to talk to you about adhd or attention deficit disorder but first remember that stimulant drugs don’t cure anything they don’t fix anything they don’t improve anything they cause biochemical imbalances in the brain that make children docile that take away their
spontaneity and make them obsessively focus on things that they don’t care about there’s no evidence that stimulant drugs improve anything past the first few weeks when they subdue behavior, there’s no improvement in academic performance, social life, how people feel about themselves, sports. these drugs should not be given to children that’s the vast weight of scientific evidence that you can find in my books like psychiatric drug withdrawal and brain disabling treatments in psychiatry but now let’s go on to what is adhd.

i want you to imagine you know maybe in your late twenties or thirties that you went back to school was it fun do you remember going back to school and thinking wow it was great not too many of us think like that in fact let’s suppose somebody said you could have a six-figure salary for 20 years and retire and all you would have to do is everything you did in school you would just sit all day long in hard chairs with a desk in front of
you you’d have one person teaching you all day long you’d have to raise your hand to go to the bathroom you wouldn’t be able to socialize would
you do that for 20 years even for a good retirement you see adhd is about what we’re trying to make our children do that they’re not comfortable willing or able to do.
if you look in the diagnostic manual for what are the criteria for adhd they’re about kids who are uncomfortable in class the criteria include things like fidgeting in chairs, squirming in chair, cutting off the teacher to answer questions before she’s finished asking them,
not standing in line, being too active.

what happened is that the drug companies actually created the diagnosis adhd to sell it to teachers and say we have a medication that will get rid of all your difficulties in your classroom they held workshops they work to the department of education to do it now is adhd a disease well it can’t be a disease because think about it what might make a child say fidget in class or be hyperactive in class or interrupt the teacher. why it could be almost anything. it could be that the child’s behind in class and uneasy and anxious because they can’t keep up it might be that the child’s the
opposite of that that the child’s way ahead of class that the child’s thinking about things far beyond what’s going on in the classroom and is bored it could be that the teacher is boring. well maybe the teacher’s been depressed for years. maybe the teacher doesn’t know how to have moral authority, get the kids to quiet down, and listen to her or maybe the child’s going through a divorce at home and is just anxious and fidgety and nervous and needy or maybe the child’s malnourished maybe the child has an underlying problem like head injury from sports.

because that can give you all the same kinds of activities.
in other words this list of behaviors doesn’t mean anything in my experience it means the parents aren’t disciplining the child properly and within minutes in my office the child’s quieted down because i’m giving intense attention really caring about the child i’m interested in what the child has to say and the parents learn how to engage a child right in front of their eyes or the child doesn’t have any problem at all but school is boring i’ve even seen children turn around overnight with a change of teacher.

so adhd is not a disease, it’s not a disorder, but once you start giving a child drugs for adhd you create all kinds of diseases and disorders children get depressed on the drugs, they get psychotic on the drugs. they lose weight, get skinny, weakened and fatigued on the drugs they lose interest in socializing on the drugs which is one of the main effects that the teachers often see as positive because the kid’s not trying to socialize in class anymore let me say in a word there’s no disorder there’s no disease. the drugs just flattened behavior the great news is is that if your child has adhd like symptoms your child is almost certainly either perfectly normal and bored in school or needs his parents to learn to discipline him better while also providing unconditional love.

read my book talking back to ritalin or the ritalin factbook you’ll find everything i’m saying is documented with dozens of references and you’ll find better approaches to helping your child be the normal kid he really is thank you

71) Dr Breggin ADHD drugs PART ONE: watch you tube video

1) ADHD drugs suppress over all human growth, suppressing growth hormone cycles, brain is not growing normally

2) ADHD drugs are highly addictive: schedule II DEA
same as morphine, cocaine, fentanyl.

3) Changes the brain: animal studies show peristent, permanent brain damage

4) Drug Label says do not give to child who is agitated or depressed.

5) Adverese effects of ADHD drugs: many children become depressed, start having Insomnia, anxiety, OCD disorder.

6) average pediatriciian does not recognize these adverse effects.

apathy anxiety depression insomnia are drug adverse effects.They will give a second drug !!! Kid gets depressed….doctor gives antidepressant….inducing increased suicidality, suicidal behavior. Kid is now on 3-4-5 drugs. Then they will add anti psychotic drugs.

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72) Part 2 Dr Breggin on ADHD Drugs

Features of ADHD: hyperactivity, inattention, impulsivity. There is no common disease process. ADHD is a list of behaviors that make trouble to teachers. Drugs include:

Amphetamines
amphetamine
dextroamphetamine
lisdexamfetamine

Brand names :
Adderall XR (generic available)
Dexedrine (generic available)
Dyanavel XR
Evekeo
ProCentra (generic available)
Vyvanse

Methamphetamine (Desoxyn)
Methylphenidate works by blocking the reuptake of norepinephrine and dopamine in your brain.Transdermal patch under the brand name Daytrana.

Aptensio XR (generic available)
Metadate ER (generic available)
Concerta (generic available)
Daytrana
Ritalin (generic available)
Ritalin LA (generic available)
Methylin (generic available)
QuilliChew
Quillivant

On drug, brain is suppressed by psychiatric drug

Studies on Chimps with ADHD meds:

Chimps stop being spontaneous and stop trying to esccape.
Thats what we do to our children. Make them good caged children.
They become zombie like. The spirit is dimished.
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73) Leslie, Douglas L., et al. “Temporal association of certain neuropsychiatric Disorders Following Vaccination of children and adolescents: a Pilot case–control study.” Frontiers in Psychiatry (2017): 3.

Background: Although the association of the measles, mumps, and rubella vaccine with autism spectrum disorder has been convincingly disproven, the onset of certain brain-related autoimmune and inflammatory disorders has been found to be temporally associated with the antecedent administration of various vaccines. This study examines whether antecedent vaccinations are associated with increased incidence of obsessive–compulsive disorder (OCD), anorexia nervosa (AN), anxiety disorder, chronic tic disorder, attention deficit hyperactivity disorder, major depressive disorder, and bipolar disorder in a national sample of privately insured children.

Methods: Using claims data, we compared the prior year’s occurrence of vaccinations in children and adolescents aged 6–15 years with the above neuropsychiatric disorders that were newly diagnosed between January 2002 and December 2007, as well as two control conditions, broken bones and open wounds. Subjects were matched with controls according to age, gender, geographical area, and seasonality. Conditional logistic regression models were used to determine the association of prior vaccinations with each condition.

Results: Subjects with newly diagnosed AN were more likely than controls to have had any vaccination in the previous 3 months [hazard ratio (HR) 1.80, 95% confidence interval 1.21–2.68]. Influenza vaccinations during the prior 3, 6, and 12 months were also associated with incident diagnoses of AN, OCD, and an anxiety disorder. Several other associations were also significant with HRs greater than 1.40 (hepatitis A with OCD and AN; hepatitis B with AN; and meningitis with AN and chronic tic disorder).

Conclusion: This pilot epidemiologic analysis implies that the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals. These findings warrant further investigation, but do not prove a causal role of antecedent infections or vaccinations in the pathoetiology of these conditions. Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines.

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74) Hepatitis B – Vaccine Risk Statement (VRS) Hepatitis B Vaccine: Is It Safer Than Hepatitis B?

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75) Dr. Thomas’s Journey of Awakening The Problem with Thomas’s Book ‘The Vaccine-Friendly Plan’ by Jeremy Hammond This chart from his study: James Lyons-Weiler and Paul Thomas, “Relative Incidence of Office Visits and Cumulative Rates of Billed Diagnoses along the Axis of Vaccination,” International Journal of Environmental Research and Public Health 17, no. 22 (2020): 8674, [This Article has been RETRACTED]

ADHD Drug Marketing

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

77) 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

78) 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, MD Chair, DSM-IV Task Force, Professor Emeritus, Duke University School of Medicine, Durham, NC. February 12, 2014

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+++++++++ GOOD IMAGES ++++++++++

79) Carias, Emily, et al. “Chronic oral methylphenidate treatment increases microglial activation in rats.” Journal of Neural Transmission 125 (2018): 1867-1875.

In vitro autoradiography using [3H] PK 11195 was performed to measure microglial activation…These findings indicate that chronic MP results in widespread microglial activation immediately after treatment and following the cessation of treatment in some brain regions.

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80) Quintero, Javier, José R. Gutiérrez-Casares, and Cecilio Álamo. “Molecular characterisation of the mechanism of action of stimulant drugs lisdexamfetamine and methylphenidate on ADHD neurobiology: A review.” Neurology and Therapy 11.4 (2022): 1489-1517. ADHD pathophysiology is largely unknown.

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neuron and astrocyte loss in the hippocampus of juvenile rats. see also (36)

81) Schmitz, Felipe, et al. “Methylphenidate causes behavioral impairments and neuron and astrocyte loss in the hippocampus of juvenile rats.” Molecular neurobiology 54 (2017): 4201-4216.

Results showed that chronic methylphenidate administration
caused loss of astrocytes and neurons in the hippocampus
o f juvenile rats. BDNF and pTrkB immunocontents and NGF levels were decreased, while TNF-α and IL-6 levels, Iba-1 and caspase 3 cleaved immunocontents (microglia marker and active apoptosis marker, respectively) were increased.

Both exploratory activity and object recognition memory were impaired by methylphenidate. These findings provide additional evidence that early-life exposure to methylphenidate can have complex effects, as well as provide new basis for
understanding of the biochemical and behavioral consequences
associated with chronic use of methylphenidate during central nervous system development.

ADHD is a complex neuropsychiatric disease characterized mainly by high levels of inattention, hyperactivity, and impulsivity [1–3]. However, recent studies have reported a large increase in the incidence of MPH misuse among young adults and
students who do not meet the criteria for ADHD, in search of cognitive enhancement [4, 5], in preschool children with 2–4 years of age [6, 7].

======================

Dopamine Transporter Levels

82) 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.

=====================

83) Hsu, Sanford Pc, et al. “Long-term challenge of methylphenidate changes the neuronal population and membrane property of dopaminergic neuron in rats.” Neurochemistry international 122 (2019): 187-195.

The number of dopaminergic neurons in the substantia nigra (SN), the serotonergic neurons in the dorsal raphe nucleus, and the cholinergic neurons in the tegmental nucleus significantly decreased as compared with Normal group, whereas the noradrenergic neurons in the locus coeruleus substantially increased.

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84) Zhang, X., et al. “Discontinuation of methylphenidate after long-term exposure in nonhuman primates.” Neurotoxicology and Teratology 97 (2023): 107173.

The blockage of the dopamine transporter (DAT) and the norepinephrine transporter (NET) by MPH may help with
ADHD symptoms by boosting monoamine levels in the synapse.

This study demonstrates that 6 months after cessation of long-term, chronic MPH treatment, there are no significant neurochemical or neural metabolic changes in the central nervous system (CNS) of non-human primates (NHPs) and suggests that microPET imaging is helpful in assessing the status of biomarkers of neurochemical processes linked to chronic CNS drug exposure.

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85) Ludolph, A. G., et al. “Methylphenidate exerts no neurotoxic, but neuroprotective effects in vitro.” Journal of neural transmission 113 (2006): 1927-1934.

86) Volz, T. J. “Neuropharmacological mechanisms underlying the neuroprotective effects of methylphenidate.” Current Neuropharmacology 6.4 (2008): 379-385.

Lithium neuroprotection from Methylphenidate – BDNF

87) Motaghinejad, Majid, et al. “The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF.” Neurotoxicology 56 (2016): 40-54.

88) Mehrafza, Shafagh, et al. “Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways.” Iranian Journal of Basic Medical Sciences 22.8 (2019): 856.

89) List of studies showing MPH impairs hippocampus neurogenesis: Neurogenesis hippocampus methylphenidate

==============================

Chart of amphetamine/methylphenidate use

90) Rasmussen, Nicolas. “America’s first amphetamine epidemic 1929–1971: a quantitative and qualitative retrospective with implications for the present.” American journal of public health 98.6 (2008): 974-985.

When a drug is treated not only as a legal medicine but as a virtually harmless one, it is difficult to make a convincing case that the same drug is terribly harmful if used nonmedically. This is what happened in the 1960s and is presumably happening today. Thus, to end their rampant abuse, amphetamines had to be made strictly controlled substances and their prescription sharply curtailed. Today, amphetamines are widely accepted as safe even for small children, and this return of medical normalization inevitably undermines public health efforts to limit amphetamine abuse.

Methylphenidate was first synthesized in 1944 and was approved for medical use in the United States in 1955.

he study found that about one third of “habituated or addicted” medical Dexamyl users were in fact physically dependent.50 Taken together with the prevalence estimates in the previous paragraph, this outcome implies extensive iatrogenic amphetamine addiction in the early 1960s—that is, 2.2% to 3.3% of all patients receiving amphetamine prescriptions in a given year.51

In the early 1960s, amphetamines were still widely accepted as innocuous medications. Apart from vast numbers of middle-aged, middle-class patients receiving low-dose prescriptions from family doctors to help them cope with their daily “duties,” in much the same way that their doctors prescribed minor tranquilizers,61 a significant quasi-medical gray market in amphetamines had developed.

The first amphetamine epidemic was iatrogenic, created by the pharmaceutical industry and (mostly) well-meaning prescribers. The current amphetamine resurgence began through a combination of recreational drug fashion cycles and increased illicit supply since the late 1980s

On the basis of treatment admissions data, methamphetamine abuse doubled in the United States from 1983 to 1988, doubled again between 1988 and 1992, and then quintupled from 1992 to 2002.89 According to usage surveys, during 2004, some 3 million Americans consumed amphetamine-type stimulants of all kinds nonmedically, twice the number of a decade earlier. As noted, 250000 to 350000 of them were addicted.90 Thus, in terms of absolute numbers, the current epidemic has now reached approximately the same extent and severity as that of the original epidemic at its peak in 1970, when there were roughly 3.8 million past-year nonmedical amphetamine users, about 320 000 of whom were addicted (Table 1). (Of course, the national population then was about 200 million compared with 300 million today, meaning that in relative terms today’s epidemic is only two thirds as extensive.)

Another striking similarity between present and past epidemics relates to the role of pharmaceutical amphetamines. Although illicitly manufactured methamphetamine launched the current epidemic, in step with rising amphetamine abuse in recent years, the United States has seen a surge in the legal supply and use of amphetamine-type attention deficit medications, such as Ritalin (methylphenidate) and Adderall (amphetamine). American physicians, much more than those in other countries, apparently are again finding it difficult to resist prescribing stimulants that patients and parents consider necessary, or at least helpful, in their struggle with everyday duties.91 According to DEA production data, since 1995, medical consumption of these drugs has more than quintupled, and in 2005, for the first time exceeded amphetamine consumption for medical use at the epidemic’s original peak: 2.5 billion 10-mg amphetamine base units in 1969 vs 2.6 billion comparable units in 2005.92 Thus, just as the absolute prevalence of amphetamine abuse and dependency have now reached levels matching the original epidemic’s peak, so has the supply of medical amphetamines (Figure 1 ▶).

+++++ PET images of Loss of DAT in Basal Ganglia +++++++++++++++
91) Volkow, Nora D., et al. “Loss of dopamine transporters in methamphetamine abusers recovers with protracted abstinence.” Journal of Neuroscience 21.23 (2001): 9414-9418.

Methamphetamine is a popular drug of abuse that is neurotoxic to dopamine (DA) terminals when administered to laboratory animals. Studies in methamphetamine abusers have also documented significant loss of DA transporters (used as markers of the DA terminal) that are associated with slower motor function and decreased memory.

The DA transporter increases with abstinence could indicate that methamphetamine-induced DA transporter loss reflects temporary adaptive changes (i.e., downregulation), that the loss reflects DA terminal damage but that terminals can recover, or that remaining viable terminals increase synaptic arborization. Because neuropsychological tests did not improve to the same extent, this suggests that the increase of the DA transporters was not sufficient for complete function recovery. These findings have treatment implications because they suggest that protracted abstinence may reverse some of methamphetamine-induced alterations in brain DA terminals.

Methylphenidate binding in Meth users

Fig. 1 Brain images of the distribution volume of [11C]d-threo-methylphenidate in a control and a METH abuser. Images shown were obtained at the level of the striatum (images to the left) and the cerebellum (images to the right), and they are from a normal control and a METH abuser evaluated twice, during short and protracted abstinence. Notice the significant increases in binding in striatum in the METH abuser with protracted abstinence.

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Striatum

92) Bamford, Ian J., and Nigel S. Bamford. “The striatum’s role in executing rational and irrational economic behaviors.” The Neuroscientist 25.5 (2019): 475-490.

The striatum is a cluster of interconnected nuclei that form a part of the basal ganglia. It is involved in decision making functions, such as motor control, emotion, habit formation, and reward.

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+++++++++++ Nice PET SCAN IMAGES ++++++++++++++++++++++++

93) 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.

Brain scans show an increase in dopamine transporter levels (more red) after 12 months of treatment with methylphenidate in ADHD patients. Scans of control subjects with no treatment are shown for comparison.

Figure 1. Averaged dopamine transporter availability images.

Averaged dopamine transporter availability images of ADHD (n = 18) and control (n = 11) subjects prior to and after 12 months oral MP treatment as well as baseline and 12 follow up scans of control subjects. The images are scaled with respect to the maximum value (distribution volume ratio) obtained on the ADHD subjects at follow up visit and presented using the rainbow scale. Red represents the highest value and dark violet represents the lowest value.

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 [and MPH], 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.

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).

94) Long-Term ADHD Treatment Increases Brain Dopamine Transporter Levels, May Affect Drug Efficacy
Twelve-month treatment may impact adult ADHD patients’ response to methylphenidate May 15, 2013

The researchers found that adults with ADHD who had been prescribed the drug methylphenidate for a period of 12 months had a 24% increase in the density of the dopamine transporter in some brain regions, which after treatment was significantly higher than in adults without ADHD who had not been treated with the drug. Prior to the 12-month treatment, there were no significant differences in the two groups’ dopamine transporter levels. The authors conclude that the elevated dopamine transporter density, suggested by some as a biological test for diagnosis of ADHD, may be a consequence of chronic treatment rather than a marker for the disorder. These findings may offer an explanation for discrepancies in the literature describing dopamine transporter levels in ADHD patients, as differences in dopamine transporter levels in the brain may be due to differences in prior treatment.

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95) 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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96) If vaccines don’t cause autism, then how do you explain all this evidence? by Steve Kirsch
We see an odds ratio of 5 when comparing autism in vaxxed vs. unvaxxed in MULTIPLE studies. The before:after odds are even more extraordinary. How can we ignore all this evidence? Steve Kirsch Jun 17, 2023

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97) How Do Vaccines Cause Autism? Past discoveries that can help us understand the current wave of neurological spike protein injuries. A Midwestern Doctor Jul 21, 2023

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98) 130 studies linking vaccines to neurological and autio-immune disease

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99) First-Ever Peer-Reviewed Study of Vaccinated vs Unvaccinated Children Shows Vaccinated Kids Have a Higher Rate of Sickness, 470% Increase in Autism 2017 Mark Blaxill, Age of Autism

Mawson Study

Vaccinated children were significantly more likely than the unvaccinated to have been diagnosed with a neurodevelopmental disorder: most notably, the risk of being affected by an Autism Spectrum Disorder (ASD) was 4.7 fold higher in vaccinated children; as well, ADHD risk was 4.7 fold higher and learning disability risk was 3.7 fold higher. Overall, the vaccinated children in the study were 3.7 times more likely to have been diagnosed with some kind of neurodevelopmental disorder.

100) ADHD, Chronic Fatigue Syndrome, and Autism – What Do They Have in Common?January 1, 2016 by Allene Edwards Last updated on: May 18, 2016

Conclusion If we are to stop the current epidemic of neurological and autoimmune diseases including ADHD, CFS, and autism, we have to stop poisoning our bodies and our children’s bodies with chemicals and heavy metals. …The numbers don’t lie. ADHD, CFS, and autism are the result of our polluted lives and a vaccine schedule that would defy common sense even if our vaccines were safe and effective. Too many of us are sick. Too many children are sick. It’s time we stand up and demand change.

101) Leslie, Douglas L., et al. “Temporal association of certain neuropsychiatric Disorders Following Vaccination of children and adolescents: a Pilot case–control study.” Frontiers in Psychiatry (2017): 3.

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102) Childhood “Immunizations”: The High Risks of Vaccine Injury – Tanya Gaw w/ Dr. Peter McCullough

Summary by Tanya Gaw the founder of ‘Action4Canada’: “Dr. Peter McCullough discusses the harms of childhood vaccines in this clip from the Empower Hour. Dr. McCullough states that autism is part of a collection of illnesses called ESSENCE disorders (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations) which include: attention deficit disorder, autism spectrum disorder, Asperger syndrome, and cognitive and language disorders. These are neurodevelopmental/neuropsychiatric disorders. He states that there are over 800 papers linking ESSENCE disorders to hyper vaccination. Listen to this clip and become vaccine risk aware.”

103) Medical Litereature search for : hepatitis B vaccination autism

104) Medical Literature Search for: aluminum vaccination autism

105) Medical Literature search for: immune dysfunction autism spectrum disorders

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Mandatory Vaccination is a Result of Left Wing Pharma-Fascism

106) The Rise of Pharma Fascism and the Ruination of the Commons
By Toby RogersToby Rogers October 8, 2023 Brownstone Institute

Vaccines are ineffective and dangerous

The large gains in life expectancy and declines in infectious disease in the 20th century happened before the introduction of mass vaccination campaigns. Improved living standards, sewers, water treatment facilities, food safety, organized solid waste disposal, along with “improvements in housing and decreased crowding in US cities” are responsible for “nearly 90% of the decline in infectious disease mortality among U.S. children.” That’s not me talking, that’s a review of a century of public health data published in Pediatrics. In an earlier era, when public health focused on large public works projects, health improved. Now that public health focuses almost exclusively on promoting vaccines, health and well-being have plummeted.

107) Guyer, Bernard, et al. “Annual summary of vital statistics: trends in the health of Americans during the 20th century.” Pediatrics 106.6 (2000): 1307-1317.

The major declines in child mortality that occurred in the first third of the 20th century have been attributable to a combination of improved socioeconomic conditions in this country and the public health strategies
to protect the health of Americans. These public health measures included the establishment of local health departments in nearly all of the states. State and local health departments implemented these
public health measures including water treatment, food safety, organized solid waste disposal, and public education about hygienic practices. These improvements in water and food safety and purity are linked to the major decline in diarrheal diseases seen in the early years of the century.44 Similarly, improvements in housing and decreased crowding in US cities are linked to the reductions in mortality
from tuberculosis and other diseases attributable to person-to-person airborne transmission.43 Vaccination, while first used in the 18th century,
became more widely implemented in the middle part of the century. Vaccines against diphtheria, tetanus, and pertussis became available during the late 1920s but only widely used in routine pediatric practice after World War II.Thus vaccination does not account for the impressive declines in mortality seen in
the first half of the century.

108) Why I’m an abolitionist Toby Rogers Sep 15, 2022

Over the last three decades, Dr. Aaby and his team have studied the non-specific effects of the other vaccines administered in Guinea-Bissau. His findings in connection with the DTP vaccine — the most widely administered vaccine in the world — are the most shocking. Across multiple studies, Dr. Aaby found that children vaccinated with DTP have 5 times higher (95% CI: 1.53–16.3) all-cause mortality than children who were not injected with DTP.He and his team also found sex effects — girls were more likely to die following DTP vaccination than boys.

Modern Eugenics in Indiana 1907

During a sad chapter in our history, modern eugenics argued for and actually practiced “Artificial Selection ” on our fellow humans by weeding out the “unfit”.

The state of Indiana passed a Eugenics inspired sterilization law in 1907. The law was struck down in 1921 by the Indiana Supreme Court after 2500 people had been involuntarily sterilized by the state. Sterilization of institutionalized patients continued to the mid-1970’s in 33 states. In all, about 60,000 Americans were involuntarily sterilized. The topic of Eugenics is still active, as this article on the Huff Post demonstrates.

The History of Eugenics by Mark Crispin Miller

The Connection between Eugenics and Vaccination:

AN example of the above was found by Catholic Doctors in Kenya during a tetanus vaccination campaign, finding the tetanus vaccine vials to contain HCG, the pregnancy hormone. By adding HCG to the tetanus vaccine, this creates vaccination against HCG, and autoimmunity to HCG, thus inducing miscarraiges, serving as an anti-fertility treatment.

Kenyan Catholic Doctors Association speak: Tetanus vaccination campaign is all about population control

Part Three: July 2023. Professor Mark Crispin Miller, propaganda studies at New York University – 2020: A PROPAGANDA MASTERPIECE, PART THREE – THE COUP OF 1963 TO COVID 2021. A professor in propaganda studies at New York University,

Click Here for Part One and Part Two:

2020: A Propaganda Masterpiece Parts 1&2 | Perspectives on the Pandemic | by Mark Crispin Miller

109) A Mother of Triplets’ Heartbreaking Story If vaccines don’t cause autism, then what caused these triplets to develop autism less than 24 hours after the shot? A heartbreaking story if you haven’t seen it. ‘They Lost Their Smiles’: A Mother of Triplets’ Heartbreaking Story All three of Brenda McDowell’s triplets, she attests, ‘shut down’ within hours of each other after receiving their routine pneumococcal vaccines — later to be diagnosed with Autism Spectrum Disorder.

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One thought on “Hypervaccination, Autism, ADHD and Neurodevelopmental Disorders”

just a thought on November 13, 2023 at 9:05 AM said:

If the info in the following video is correct, there are a few vaccines that actually benefit us in ways other than protecting us from disease (2 if I heard her correctly)

https://m.youtube.com/watch?v=_d8PNlXHJ48

Unfortunately, drug companies want to change how they produce their vaccines, which may adversely affect even those.

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Hypervaccination, Autism, ADHD and Neurodevelopmental Disorders

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