Why are Western countries below the replacement birth rate?
For context, this is a question I answered on Quora
It is declining below replacement birth rate levels outside of the west as well. India’s birth rate just declined below replacement levels in the past few years.
China continues to have below replacement level birth rates despite suspending the one child policy 10 years ago. South Korea and Japan have the lowest birth rates in the world. Russia has a lower below replacement level birth rate than the U.S. despite being substantially poorer and less educated.
Source: Our World in Data: Fertility Rates by Country
Iran has below replacement level birthrates despite being a repressive theocracy.
So do several countries in Latin America such as Mexico, El Salvador, Costa Rica, Cuba, Colombia, Brazil and Peru despite having much lower standards of living and education.
Americas Quarterly: Latin America's Fertility Decline is Accelerating
The fact that this is happening outside the west in areas that are much poorer, less educated and more authoritarian contradicts the convenient ready made narrative that this is solely a result of cultural changes or woman being college educated. Those are correlates not causative factors of declining fertility. The reality is that we are being slowly poisoned with a slurry of endocrine disrupting chemicals (EDCs) and genotoxins that are making people less fertile and making changes to our hormones that can change people’s behavior. The multinational conglomerates that are doing the poisoning would like you to believe in the false narrative that this is only a western problem caused by cultural shifts and women going to college and using contraceptives. That is what their billionaire owned shitlib media puppets who they pay off through sponsorships will tell you. Reality is that EDCs including micro and nano plastics, polyfluoroalkyls, phthalates, bisphenols, and pesticide residues are destroying human reproductive health and likely altering sexual behavior.
Ubiquitous Micro and Nano plastics are destroying Fertility
A growing body of evidence suggests that microplastics and nanoplastics disrupt multiple hormonal axes (HPG, HPT, HPA), leading to reproductive dysfunction, thyroid abnormalities, developmental toxicity, oxidative stress, decreased sperm quality, and immunotoxicity.
A rodent experiment in male mice in which some subjects were exposed to polystyrene microplastics for 28 days found that the exposure group had lower sperm counts and motility, lower testosterone levels, experienced a higher loss of spermatogenic cells, and had more multinucleated gonocytes compared to the control group, once again evidencing the endocrine disrupting and reproductive toxicity of micro and nano plastics for males.
A separate experiment in female mice in which some subjects were exposed to the same polystyrene microplastics as the male mice for 35 days found that the exposure groups had elevated inflammatory cytokine levels, particularly Interleukin-6 in the ovaries, increased oxidative stress, reduced survival of superovulated oocytes and lower oocytes quality, reduced mitochondrial membrane potential and disrupted calcium homeostasis evidencing evidencing the endocrine disrupting and reproductive toxicity of micro and nano plastics for females.
A scoping review of rodent experiments in which subjects were exposed to micro and nano plastics through various routes of administration (n = 31) found that males exposed to micro and nanoplastics exhibit sperm deformities, testicular inflammation, and decreased testosterone levels, while exposed females demonstrate ovarian inflammation, altered oocyte quality, and disruptions in hormone profiles. They also found that exposure during pregnancy is linked to cross-generational developmental disorders and metabolic abnormalities in progeny. In both sexes plastic toxicity appears to interfere with reproductive endocrine function, disrupt steroidogenesis, and induce oxidative stress in reproductive tissues.
Ubiquitous plasticizers are destroying fertility
As I mentioned in a prior post two years ago, a group of common plasticizers called phthalates, which mimic estrogen, progesterone and androgen in the human endocrine system, have been linked with lower testosterone, lower sperm counts and worse sperm motility in men with higher urinary concentrations as well as preterm labor, low birth weight babies, and even miscarriages.
PFAs/PFOs endocrine disruption
A combined in vitro and cohort study investigating the effects of perfluorooctanoic acid (PFOA) on progesterone activity in human endometrial cells and reproductive outcomes in young women from the Veneto region of Italy (n = 146) and a control group (n = 1,080) found that PFOA exposure increased rate of irregular menstrual periods (29.5% vs 21.5%, p = 0.022) and delayed age at menarche (+164 days, p = 0.006). Genetically, PFOA exposure resulted in dysregulation of progesterone activated genes.
A cohort study conducted among adolescents and young adults recruited from a mass urine screening population between 1992 and 2000 (n = 540) found, through collected blood samples analyzed for serum concentrations of PFAS (including PFOA, PFOS, and PFUA) using high-sensitivity UPLC-MS/MS, that higher serum concentrations of PFOA, PFOS, and PFUA are associated with lower serum concentrations of sex hormone-binding globulin, follicle-stimulating hormone, and testosterone, especially among females aged 12–17 years. Follicle-stimulating hormone levels were significantly lower in association with PFOS in males and PFUA in females within the same age range.
A systematic review and meta-analysis assessing the impact of PFAS exposure on female fertility using population-based studies (n = 13) found that PFOA exposure is associated with a 33% increase in female infertility.
A systematic review of human population studies and toxicological research on PFAS exposure and ovarian function found that PFA exposure is associated with delayed puberty onset, irregular menstrual cycles, longer cycle lengths, earlier menopause onset, and lower estrogen and androgen levels. Animal experiments confirmed that PFAs can cross the blood–follicle barrier, disrupt ovarian folliculogenesis and hormone production and reduce ovarian reserve.
A narrative review of existing epidemiological and experimental studies on the association between exposure to PFOA and PFOS (types of PFAS) and male infertility notes that PFOS and PFOA exposure have been associated with lower testosterone levels, lower sperm count and motility.
A comprehensive review of both human epidemiological studies and animal experimental research regarding PFAS exposure and effects on sperm found that PFAS exposure is associated with reduced sperm count, abnormal morphology, and lower motility in humans and testicular and epididymal damage in animal models, impairing spermatogenesis and sperm quality. Mechanistic studies found alterations in membrane fluidity, activation of stress-response signaling pathways, and disruption of hormonal and cellular processes crucial to sperm function.
Bisphenols Endocrine Disruption
A comprehensive review of the effects of Bisphenol A on human reproductive health found that BPA exposure is associated with sperm alterations, hormone level changes, and testicular atrophy in males and is correlated with hormonal imbalances, diminished ovarian reserve, and a higher risk of reproductive disorders including fibroids, polycystic ovarian syndrome (PCOS), endometriosis, and infertility in females.
A mini-review of toxicological and epidemiological studies published between 2013 and 2016 that included human exposure, animal models and mechanistic studies of bisphenol endocrine disruption found that BPA analogs have similar endocrine disrupting effects to BPA itself in its interactions with estrogen and androgen receptors.
A scoping review conducted according to PRISMA guidelines, synthesizing findings across toxicological, in vitro, and in vivo studies, including human observational research (n = 107) found that 94% of in vitro studies reported at least one adverse outcome in oocyte health, 86% of in vivo studies (animal models) found adverse effects on follicle development or chromosome alignment, and >50% of human observational studies found associations between higher urinary BPA levels and reduced antral follicle count or oocyte yield in IVF patients.
Of course, none of the evidence of individual endocrine disruption and toxicity takes into account possible synergistic toxicity from being exposed to all of these chemicals on a daily basis, so what has thus far been found is probably an underestimate of the damage being done.