Apologies for any typos, any feedback on where gaps need to be filled in would be much appreciated.
Related Series:
Are psychiatric drugs driving dementia rates?
Efficacy and safety of psychiatric drugs
Fertility and Birth Rates have been falling or stagnant since the 1970’s
A ‘New’ Normal? An Updated Look at Fertility Trends Across the Globe
Basically, countries with birth rates above 1.6 or 1.7 children per woman experienced fertility declines. Countries with birth rates below that saw more stability or even increases. What we appear to be seeing is a global convergence around fertility rates of 1.6 or 1.7 children. This is not just a rich-world phenomenon. Birth rates in Mexico are around 1.9 to 2 kids per woman, so below the rate needed to sustain Mexico’s current population levels. Brazil’s birth rate is even lower, at 1.75, similar to Colombia’s at 1.77. Costa Rica is even lower, at 1.66. El Salvador, Argentina, and Venezuela are all just barely “breaking even” demographically. Other countries like Guatemala are higher but falling fast. Across the Pacific, Sri Lanka, Bangladesh, and India are all around 2 or 2.2 kids per woman, while Malaysia has fallen to about 1.8. Thailand is even lower, at 1.5 kids per woman. Even Muslim countries like Turkey (2), Iran (1.8), and Tunisia (2.1) have near-replacement fertility, with speedy declines still ongoing.
NCHS – Births and General Fertility Rates: United States
I don’t know how to save a filter, but you can dimension by year, measure by crude birth rate.
Births: Provisional Data for 2020(PDF)
The provisional number of births for the United States in 2020 was 3,605,201, down 4% from the number in 2019 (3,747,540) (Tables 1–3 and Figure 1). This is the sixth consecutive year that the number of births has declined after an increase in 2014, down an average of 2% per year, and the lowest number of births since 1979.
Fertility rates are below replacement rate
Replacement level fertility and future population growth
Replacement level fertility is the level of fertility at which a population exactly replaces itself from one generation to the next. In developed countries, replacement level fertility can be taken as requiring an average of 2.1 children per woman.
Psychiatric Drug Use has greatly increased since the 1970’s
Adult Utilization of Psychiatric Drugs and Differences by Sex, Age, and Race
Overall, 16.7% (95% CI, 15.9%-17.5%) of 242 million US adults reported filling 1 or more prescriptions for psychiatric drugs in 2013, including 12.0% (95% CI, 11.3%-12.7%) reporting antidepressants; 8.3% (95% CI, 7.7%-8.9%) filling prescriptions for anxiolytics, sedatives, and hypnotics; and 1.6% (95% CI, 1.4%-1.8%) taking antipsychotics.
Total Number of People Taking Psychiatric Drugs in the United States
All Psychiatric Drugs All Ages 76,940,157
Psychiatric Drug Use Impairs Sexual Function even after discontinuation
Some patients report a certain degree of natural improvement over a period of time – sometimes months or years after stopping the antidepressant. However, many fail to recover to any significant degree with some having had the problem for over 20 years without any improvement. For some people, PSSD may be permanent.
Post-SSRI sexual dysfunction & other enduring sexual dysfunctions
These enduring post-treatment syndromes may interface with tardive dyskinesia linked to antipsychotic drugs in the 1960s. Antipsychotics can cause dyskinesias on treatment, which ordinarily resolve when treatment is stopped. Dyskinesias can also emerge on withdrawal but clear up in time. Tardive dyskinesia is a syndrome that involves dyskinetic movements centred on the jaw and lower facial area, which can emerge on treatment but become more marked when treatment stops. The syndrome can endure for years or decades afterwards. These legacy effects of antidepressants and antipsychotics have some interface with withdrawal syndromes linked to these drugs. Withdrawal to opioids and alcohol is viewed as limited to a few weeks, having features not found during administration of the drug and as ordinarily responding to re-institution of treatment. Antidepressant and antipsychotic withdrawal however is linked to dysthymia, which may appear to be continuous with the original problem but can be demonstrated in healthy volunteers given these drugs, as well as to other sensory and autonomic disturbances. These states can last for months or longer, opening up a possible link between enduring sexual syndromes and other legacy effects of antidepressants and antipsychotics (Healy and Tranter, Reference Healy and Tranter1999).
Persistent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors
SSRIs can cause long-term effects on all aspects of the sexual response cycle that may persist after they are discontinued. Mechanistic hypotheses including persistent endocrine and epigenetic gene expression alterations were briefly discussed
Antidepressants and sexual dysfunction: a history
Meanwhile 10% of people of sexually active years in developed countries are on antidepressants chronically.17 Nearly 20% of the population, therefore, may not be able to make love the way they want. In some deprived areas, the figure may be much higher. Some likely comfort themselves with the thought that once they stop treatment, they will get back to normal, when in fact they may be even less able to function.
The overall severity of symptoms improved for 45% and worsened or remained the same for 37% of respondents after discontinuing treatment with serotonin reuptake inhibitors. Only 12% of respondents reported being counseled regarding potential sexual dysfunction while taking antidepressants. The majority rated the effect of PSSD on their quality of life as extremely negative (59%) or very negative (23%).
Substance/Medication-Induced Sexual Dysfunction DSM-V
The prevalence of antidepressant-induced sexual dysfunction varies in part depending on the specific agent. Approximately 25%-80% of individuals taking monoamine oxidase inhibitors, tricyclic antidepressants, serotonergic antidepressants, and combined serotonergic-adrenergic antidepressants report sexual side effects. Approximately 50% of individuals taking antipsychotic medications will experience adverse sexual side effects, including problems with sexual desire, erection, lubrication, ejaculation, or orgasm.
Post SSRI Sexual Dysfunction (PSSD) is an under-researched syndrome involving the persistence of sexual (but sometimes also, cognitive and emotional) side effects of SSRIs that continue after the discontinuation of the SSRI. This is a support and discussion community for people who may have this condition. Please read our rules and stickied posts before posting.
Rates of “autism” and “ADHD” have greatly increased over the last 40 years
The prevalence of autism diagnosis (herein referred to interchangeably as autism, ASD, or autism/ASD) has risen at least 30- to 40-fold over the last 2 decades (figure).
Data and Statistics About ADHD
About 1 in 6 (17%) children aged 3–17 years were diagnosed with a developmental disability, as reported by parents, during a study period of 2009-2017. These included autism, attention-deficit/hyperactivity disorder, blindness, and cerebral palsy, among others. The estimated number of children ever diagnosed with ADHD, according to a national 2016 parent survey is 6.1 million (9.4%).
ACE: Health – Neurodevelopmental Disorders
From 1997 to 2017, the proportion of children ages 5 to 17 years reported to have ever been diagnosed with attention-deficit/hyperactivity disorder (ADHD) increased from 6.3% in 1993 to 10.7% in 2017. For the years 2014–2017, the percentage of boys reported to have ADHD (14.6%) was higher than the rate for girls (6.5%). This difference was statistically significant.
Trends in the Prevalence of Developmental Disabilities in U. S. Children, 1997–2008
Over the last 12 years, the Prevalence of DDs has increased 17.1%—that’s about 1.8 million more children with DDs in 2006–2008 compared to a decade earlier; Prevalence of autism increased 289.5%; Prevalence of ADHD increased 33.0%; and, Prevalence of hearing loss decreased 30.9%.
Psychiatric Drug Use Causes DNA Fragmentation in Sperm and Low Sperm Count
Effect of antidepressant medications on semen parameters and male fertility
In addition, the number of men having elevated sperm DNA fragmentation of >30% increased from 10% at baseline to 50% post-treatment (odds ratio 9, confidence interval 2.3–38).
A North American prospective study of depression, psychotropic medication use, and semen quality
Recent use of psychotropic medications was associated with worse semen quality, and this association was confounded by a history of depression diagnosis. The observed association between depression and semen volume showed little mediation by psychotropic medication use.
With more chronic exposure, cells adapt by an unknown hypothetical process that results in more permanent modifications to DNA methylation and chromatin structure, leading to enduring alteration of a given epigenetic network. Therefore, any epigenetic side-effect caused by a drug may persist after the drug is discontinued. It is further proposed that some iatrogenic diseases such as tardive dyskinesia and drug-induced SLE are epigenetic in nature. If this hypothesis is correct the consequences for modern medicine are profound, since it would imply that our current understanding of pharmacology is an oversimplification. We propose that epigenetic side-effects of pharmaceuticals may be involved in the etiology of heart disease, cancer, neurological and cognitive disorders, obesity, diabetes, infertility, and sexual dysfunction.
Patients treated with selective serotonin reuptake inhibitors had a mean of 8.1% ± 5.4% normal forms per ejaculate. A significant increase in the amount of denatured single strand DNA in total cellular DNA was found in patients treated with selective serotonin reuptake inhibitors compared with that in controls (43.2% ± 11.4% vs 21.4% ± 10.6%, p = 0.01). Each semen analysis parameter significantly correlated with treatment duration. Selective serotonin reuptake inhibitors can impair semen quality and damage sperm DNA integrity.
Semen Parameters are Unrelated to BMI But Vary With SSRI Use and Prior Urological Surgery
No consistent relationship was observed between increasing BMI and sperm concentration, motility, or morphology, although the testosterone levels trended downward with increasing BMI; there was a suggestion for decreased sperm concentration in current smokers. Men treated with combination SSRI and other psychotropic agent therapy (n = 12) had significantly reduced sperm motility (P = .009).
The antidepressant Sertraline inhibits CatSper Ca2+ channels in human sperm
We show that the list of synthetic, non-physiological CatSper modulators also includes common drugs like SSRIs. These drugs have been on the market for decades and their toxicity profile, as well as their therapeutic window, is well known. Although there is no doubt about the safety of these drugs, our findings suggest that Sertraline and perhaps other SSRIs might have side effects that have thus far been unexplored. The drug’s action on CatSper impairs sperm function and might thereby iatrogenically disturb the fertilization process in vivo, lowering the fecundity of males, females, or both.
FDA-approved medications that impair human spermatogenesis
The most common effect of these drugs was epididymitis, although there were various other causes of spermatogenic failure induced by these drugs, many of which have been substantiated in peer-reviewed publications. For example, tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs), such as clomipramine and paroxetine, can lead to significant but reversible suppression of spermatogenesis. Some drugs have the potential to induce substantial elevation of the serum prolactin level, which suppresses the gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion. Most antipsychotic agents block dopamine in the CNS, leading to suppression of the hypothalamic-pituitary-gonadal axis, thereby affecting hormone signaling and subsequent spermatogenesis.
SNPs are a leading etiology for “autism” and “ADHD”
The proportion of ASD explained by SNPs has been estimated to be between 17 and 60%, thus their contribution should not be neglected. However, the functions of the genetic variants that are responsible for the association with ASD remain poorly characterized. As such, we do not yet fully understand how to translate information on ASD-associated SNPs into specific biological mechanisms that can be therapeutically targeted to alleviate the symptoms and complications of ASD.
Identification of common genetic risk variants for autism spectrum disorder
Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes.
Epidemiological research has reported that attention-deficit hyperactivity disorder (ADHD), anxiety, bipolar disorder (BD), schizophrenia (SCZ), and unipolar depression (UD) are multimorbid conditions that are typically accompanied by cognitive advantages or deficits, suggesting that common biological mechanisms may underlie these phenotypes. Genome-wide association studies (GWAS) have identified single-nucleotide polymorphisms (SNPs) associated with psychiatric disorders and cognitive functioning.
Genetics of attention deficit hyperactivity disorder
These studies also show that about a third of ADHD’s heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD’s heritability.
This study suggested the genetic architecture of ADHD comprises both common and rare variants. Some common causal variants are likely to be shared between Han Chinese and Caucasians. Complex neurodevelopmental networks may underlie ADHD’s etiology.
Genetic Markers of ADHD-Related Variations in Intracranial Volume
This is the first genome-wide study to show significant genetic overlap between brain volume measures and ADHD, both on the global and the single variant level. Variants linked to smaller ICV were associated with increased ADHD risk.
Associations between psychiatric medication use and neuropsychiatric disorders by country
List of countries by antidepressant consumption
Assuming this is accurate:
- Iceland –
ADHD: https://onlinelibrary.wiley.com/doi/full/10.1111/bcpt.12243
Rising trend for both
2. Australia –
Autism: https://www.aihw.gov.au/reports/disability/autism-in-australia/related-material
Autism: https://journals.sagepub.com/doi/10.1177/0004867415595287
Rising trend for both
3. Portugal
ADHD: https://www.actamedicaportuguesa.com/revista/index.php/amp/article/view/1616/1198
Autism: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1469-8749.2007.00726.x
Rising trend for both
4. United Kingdom
Rising trend for both. ADHD prevalence has increased from ~3.2% to ~17.6% in 30 years.
5. Canada
ADHD: https://journals.sagepub.com/doi/10.1177/0706743717714468
Rising trend for both. Autism prevalence increased 3x between 2000 and 2015. ADHD prevalance increased 3x between 1999 and 2012.
6. Sweden
ADHD: https://journals.sagepub.com/doi/10.1177/1087054714554617
Rising trend for both. Similar jumps. This is getting depressing
7. Belgium
Rolled into EU stuff, will need to go through the data in more detail
8. Denmark
ADHD: https://vbn.aau.dk/ws/portalfiles/portal/316415095/PHD_Christina_Mohr_Jensen_E_pdf.pdf
Autism: https://jamanetwork.com/journals/jamapediatrics/fullarticle/380557
Rising trend for both.
9. Spain
ADHD: https://systematicreviewsjournal.biomedcentral.com/articles/10.1186/s13643-019-0967-y
Rising trend for both.
10. New Zealand
ADHD: No prevalence available
Autism: No prevalence available
No prevalence, might be able to pull by medication prescriptions, will look later.
11. Finland
Autism: https://www.tandfonline.com/doi/abs/10.3109/08039488.2013.861017
Finland had an earlier massive jump than most countries, stabilized then jumped again when second generation antidepressants started arriving.
Overall: There’s a clear link between prevalance and position on this list. Will probably make a table with prevalence rates.
So far, there’s a pretty clear trend between this list and rising prevalence rates among each age cohort.
Alternate Theories
Microplastics
Microplastics: A Threat for Male Fertility
Evidence regarding MPs toxicity and epidemiology is emerging. Data are still preliminary but suggest that ingested MPs bio-accumulate in mammalian tissue, including the testis, with outcomes on semen quality in rodents, as a consequence of inflammatory state and oxidative stress damage. Effects depend on the size and molecular structure of MPs, thus attention must be given to evaluating their risks to humans and the environment.
Breakdown of social structures/marriage
Birth Control
Further Questions
Is the male/female imbalance in “ASD” and “ADHD” an artifact of increased sperm fragmentation due to psychiatric drug use?
Is the highly heterogeneous denovo mutation etiology of “autism” a result of psychiatric drug use damage to DNA?
Is the mixed heritability of many psychiatric conditions an artifact of psychiatric drug use?
Is there a relationship between prevalence of use and birth rates?
Do certain classes of drugs impart more risk than others?