Qualified Liability

Architecture for decentralized systems on Ethereum

[Qualified Liability @JoshDavisWrites]

A well regulated community, being necessary to the security of a free State, the right of the people to contract and establish charters, shall not be infringed.

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

They knew the window. They knew how common it was. They knew treatment had to happen early. They just decided not to screen for it anyway.

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

They knew the window. They knew how common it was. They knew treatment had to happen early. They just decided not to screen for it anyway.

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

They knew the window. They knew how common it was. They knew treatment had to happen early. They just decided not to screen for it anyway.

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

[Qualified Liability @JoshDavisWrites]

In 2020, ACOG put “universal screening for thyroid disease in pregnancy is not recommended” in its highest evidence tier, Level A, meaning “good and consistent scientific evidence.” The stated reason was that identifying and treating maternal subclinical hypothyroidism had not been shown to improve pregnancy outcomes or child neurocognitive outcomes. But that reason does not reach the conclusion. Universal thyroid screening does not only detect subclinical hypothyroidism; it also detects overt hypothyroidism and overt hyperthyroidism, which ACOG itself says should be treated to minimize adverse outcomes. Even stranger, ACOG graded its broad negative recommendation against universal screening as Level A, while its own alternative—targeted testing in women with risk factors or clinical suspicion—was only Level C, meaning consensus/expert opinion [1].

The RCT problem is worse. The major null neurocognitive trials, CATS and Casey/MFMU, are often used to argue against universal screening, but they mostly tested treatment that began too late to answer the early-screening question [2–4]. The lead author of CATS later coauthored a review stating that treatment in the major RCTs began at 13–18 weeks, “after the critical neurodevelopmental period,” and therefore may have been too late to affect fetal brain development [4]. A 2019 Lancet Diabetes & Endocrinology cohort made the timing issue biologically concrete: the association between maternal TSH and child brain morphology was strongest early and was no longer detectable after about 14 weeks [5]. Meanwhile, positive but imperfect evidence, such as Ma 2015, reported lower miscarriage after screening/intervention for subclinical hypothyroidism [6]. So the honest guideline sentence would have been: “Evidence is limited, timing-sensitive, and conflicting.” Instead, the message became a confident recommendation against universal screening. That is not good science communication.

* Guideline-body problem: uncertainty about subclinical hypothyroidism was used to reject universal screening for all thyroid disease, including overt disease that guideline bodies agree should be treated [1,7].
* RCT problem: late-treatment trials do not answer whether preconception or very early first-trimester screening and treatment would improve outcomes [2–5].
* Science-communication problem: “has not been shown” or “no evidence” made a contested, timing-sensitive literature sound settled, despite positive but limited pregnancy-outcome evidence and cost-effectiveness evidence [6,8].
* Accountability problem: nobody has to prove bad faith first. The narrow question is whether a Level A recommendation against universal screening is actually supported by “good and consistent scientific evidence.” On this record, that level of certainty looks unearned.

References / source guide

[1] American College of Obstetricians and Gynecologists. Practice Bulletin No. 223: Thyroid Disease in Pregnancy. Obstetrics & Gynecology. 2020;135(6)–e274. DOI: 10.1097/AOG.0000000000003893. See also Practice Bulletin Summary No. 223, Obstetrics & Gynecology. 2020;135(6):1496–1499. Key point: ACOG places “Universal screening for thyroid disease in pregnancy is not recommended because identification and treatment of maternal subclinical hypothyroidism has not been shown to result in improved pregnancy outcomes and neurocognitive function in offspring” under Level A recommendations, while “indicated testing” for women with personal/family history, type 1 diabetes, or clinical suspicion appears under Level C recommendations.

[2] Lazarus JH, Bestwick JP, Channon S, Paradice R, Maina A, Rees R, Chiusano E, John R, Guaraldo V, George LM, Perona M, Dall’Amico D, Parkes AB, Jooman M, Wald NJ. Antenatal Thyroid Screening and Childhood Cognitive Function. New England Journal of Medicine. 2012;366(6):493–501. DOI: 10.1056/NEJMoa1106104. Commonly referred to as the CATS trial. Key point: a major RCT finding no significant child-IQ benefit from screening/treatment as implemented; important for later guideline discussions, but treatment timing is central to interpreting what it actually tested.

[3] Casey BM, Thom EA, Peaceman AM, Varner MW, Sorokin Y, Hirtz DG, Reddy UM, Wapner RJ, Thorp JM Jr, Saade G, Tita ATN, Rouse DJ, Sibai B, Iams JD, Mercer BM, Tolosa J, Caritis SN, VanDorsten JP, Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal–Fetal Medicine Units Network. Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy. New England Journal of Medicine. 2017;376(9):815–825. DOI: 10.1056/NEJMoa1606205. Key point: another major null neurocognitive RCT; mean randomization/treatment timing was in the second trimester range, so it is not a clean test of very early first-trimester screening/treatment.

[4] Taylor PN, Zouras S, Min T, Nagarahaj K, Lazarus JH, Okosieme OE. Thyroid Screening in Early Pregnancy: Pros and Cons. Frontiers in Endocrinology. 2018;9:626. DOI: 10.3389/fendo.2018.00626. PMCID: PMC6209822. Key point: this review, coauthored by John H. Lazarus, states that levothyroxine in major RCTs was initiated at a median gestational age of approximately 13–18 weeks, after the critical neurodevelopmental period, and therefore possibly too late to affect fetal brain development.

[5] Jansen TA, Korevaar TIM, Mulder TA, White T, Muetzel RL, Peeters RP, Tiemeier H. Maternal Thyroid Function During Pregnancy and Child Brain Morphology: A Time Window-Specific Analysis of a Prospective Cohort. The Lancet Diabetes & Endocrinology. 2019;7(8):629–637. DOI: 10.1016/S2213-8587(19)30153-6. Key point: maternal TSH was associated with child total gray matter and cortical gray matter volume most strongly in early pregnancy; after about 14 weeks’ gestation, TSH was no longer associated with child brain morphology.

[6] Ma L, Qi H, Chai X, Jiang F, Mao S, Liu J, Zhang S, Lian X, Sun X, Wang D, Ren J, Yan Q. The Effects of Screening and Intervention of Subclinical Hypothyroidism on Pregnancy Outcomes: A Prospective Multicenter Single-Blind, Randomized, Controlled Study of Thyroid Function Screening Test During Pregnancy. Journal of Maternal-Fetal & Neonatal Medicine. Published online 2015. DOI: 10.3109/14767058.2015.1049150. Key point: reported that screening/intervention for subclinical hypothyroidism significantly reduced miscarriage. Important limitation: cluster/randomization-by-center and unequal baseline characteristics mean this is not definitive proof that screening works, but it is enough to show the evidence record was not empty.

[7] Stagnaro-Green A, Dong A, Stephenson MD. Universal Screening for Thyroid Disease During Pregnancy Should Be Performed. Best Practice & Research Clinical Endocrinology & Metabolism. 2020;34(4):101320. DOI: 10.1016/j.beem.2019.101320. Key point: argues that evidence for universal screening for overt thyroid disease stands independently from the unresolved debate over subclinical hypothyroidism and thyroid autoimmunity.

[8] Dosiou C, Barnes J, Schwartz A, Negro R, Crapo L, Stagnaro-Green A. Cost-Effectiveness of Universal and Risk-Based Screening for Autoimmune Thyroid Disease in Pregnant Women. Journal of Clinical Endocrinology & Metabolism. 2012;97(5):1536–1546. DOI: 10.1210/jc.2011-2884. Key point: universal first-trimester screening was cost-effective compared with risk-based screening and no screening; importantly, the analysis remained favorable even under scenarios where subclinical hypothyroidism treatment benefit was minimized or excluded.

[Qualified Liability @JoshDavisWrites]

If you wanted to read:
ACOG Committee Opinion No. 381: Subclinical Hypothyroidism in Pregnancy
You are told “This document has been withdrawn or is no longer available. Please contact the Resource Center at the American College of Obstetricians and Gynecologists”

The contents of this opinion letter are damning.

ACOG’s own guidelines acknowledged:
“Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize thyroid hormone, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy.“

They also knew how common the problem was. The guidelines stated:
“The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening.“

And crucially, they acknowledged the timing window for treatment:
“Maternal thyroxine is particularly critical early in pregnancy because the fetal thyroid gland cannot synthesize iodothyronines until after 10 weeks of gestation. Treatment may be ineffective only if given after this time.“

Yet, despite acknowledging all three facts:
(1) the critical window,
(2) the prevalence of the condition, and
(3) the window for effective treatment, ACOG stated:
“Data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available... Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.“

They knew the window. They knew how common it was. They knew treatment had to happen early. They just decided not to screen for it anyway.

[Qualified Liability @JoshDavisWrites]

In 2020, ACOG put “universal screening for thyroid disease in pregnancy is not recommended” in its highest evidence tier, Level A, meaning “good and consistent scientific evidence.” The stated reason was that identifying and treating maternal subclinical hypothyroidism had not been shown to improve pregnancy outcomes or child neurocognitive outcomes. But that reason does not reach the conclusion. Universal thyroid screening does not only detect subclinical hypothyroidism; it also detects overt hypothyroidism and overt hyperthyroidism, which ACOG itself says should be treated to minimize adverse outcomes. Even stranger, ACOG graded its broad negative recommendation against universal screening as Level A, while its own alternative—targeted testing in women with risk factors or clinical suspicion—was only Level C, meaning consensus/expert opinion [1].

The RCT problem is worse. The major null neurocognitive trials, CATS and Casey/MFMU, are often used to argue against universal screening, but they mostly tested treatment that began too late to answer the early-screening question [2–4]. The lead author of CATS later coauthored a review stating that treatment in the major RCTs began at 13–18 weeks, “after the critical neurodevelopmental period,” and therefore may have been too late to affect fetal brain development [4]. A 2019 Lancet Diabetes & Endocrinology cohort made the timing issue biologically concrete: the association between maternal TSH and child brain morphology was strongest early and was no longer detectable after about 14 weeks [5]. Meanwhile, positive but imperfect evidence, such as Ma 2015, reported lower miscarriage after screening/intervention for subclinical hypothyroidism [6]. So the honest guideline sentence would have been: “Evidence is limited, timing-sensitive, and conflicting.” Instead, the message became a confident recommendation against universal screening. That is not good science communication.

* Guideline-body problem: uncertainty about subclinical hypothyroidism was used to reject universal screening for all thyroid disease, including overt disease that guideline bodies agree should be treated [1,7].
* RCT problem: late-treatment trials do not answer whether preconception or very early first-trimester screening and treatment would improve outcomes [2–5].
* Science-communication problem: “has not been shown” or “no evidence” made a contested, timing-sensitive literature sound settled, despite positive but limited pregnancy-outcome evidence and cost-effectiveness evidence [6,8].
* Accountability problem: nobody has to prove bad faith first. The narrow question is whether a Level A recommendation against universal screening is actually supported by “good and consistent scientific evidence.” On this record, that level of certainty looks unearned.

References / source guide

[1] American College of Obstetricians and Gynecologists. Practice Bulletin No. 223: Thyroid Disease in Pregnancy. Obstetrics & Gynecology. 2020;135(6)–e274. DOI: 10.1097/AOG.0000000000003893. See also Practice Bulletin Summary No. 223, Obstetrics & Gynecology. 2020;135(6):1496–1499. Key point: ACOG places “Universal screening for thyroid disease in pregnancy is not recommended because identification and treatment of maternal subclinical hypothyroidism has not been shown to result in improved pregnancy outcomes and neurocognitive function in offspring” under Level A recommendations, while “indicated testing” for women with personal/family history, type 1 diabetes, or clinical suspicion appears under Level C recommendations.

[2] Lazarus JH, Bestwick JP, Channon S, Paradice R, Maina A, Rees R, Chiusano E, John R, Guaraldo V, George LM, Perona M, Dall’Amico D, Parkes AB, Jooman M, Wald NJ. Antenatal Thyroid Screening and Childhood Cognitive Function. New England Journal of Medicine. 2012;366(6):493–501. DOI: 10.1056/NEJMoa1106104. Commonly referred to as the CATS trial. Key point: a major RCT finding no significant child-IQ benefit from screening/treatment as implemented; important for later guideline discussions, but treatment timing is central to interpreting what it actually tested.

[3] Casey BM, Thom EA, Peaceman AM, Varner MW, Sorokin Y, Hirtz DG, Reddy UM, Wapner RJ, Thorp JM Jr, Saade G, Tita ATN, Rouse DJ, Sibai B, Iams JD, Mercer BM, Tolosa J, Caritis SN, VanDorsten JP, Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal–Fetal Medicine Units Network. Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy. New England Journal of Medicine. 2017;376(9):815–825. DOI: 10.1056/NEJMoa1606205. Key point: another major null neurocognitive RCT; mean randomization/treatment timing was in the second trimester range, so it is not a clean test of very early first-trimester screening/treatment.

[4] Taylor PN, Zouras S, Min T, Nagarahaj K, Lazarus JH, Okosieme OE. Thyroid Screening in Early Pregnancy: Pros and Cons. Frontiers in Endocrinology. 2018;9:626. DOI: 10.3389/fendo.2018.00626. PMCID: PMC6209822. Key point: this review, coauthored by John H. Lazarus, states that levothyroxine in major RCTs was initiated at a median gestational age of approximately 13–18 weeks, after the critical neurodevelopmental period, and therefore possibly too late to affect fetal brain development.

[5] Jansen TA, Korevaar TIM, Mulder TA, White T, Muetzel RL, Peeters RP, Tiemeier H. Maternal Thyroid Function During Pregnancy and Child Brain Morphology: A Time Window-Specific Analysis of a Prospective Cohort. The Lancet Diabetes & Endocrinology. 2019;7(8):629–637. DOI: 10.1016/S2213-8587(19)30153-6. Key point: maternal TSH was associated with child total gray matter and cortical gray matter volume most strongly in early pregnancy; after about 14 weeks’ gestation, TSH was no longer associated with child brain morphology.

[6] Ma L, Qi H, Chai X, Jiang F, Mao S, Liu J, Zhang S, Lian X, Sun X, Wang D, Ren J, Yan Q. The Effects of Screening and Intervention of Subclinical Hypothyroidism on Pregnancy Outcomes: A Prospective Multicenter Single-Blind, Randomized, Controlled Study of Thyroid Function Screening Test During Pregnancy. Journal of Maternal-Fetal & Neonatal Medicine. Published online 2015. DOI: 10.3109/14767058.2015.1049150. Key point: reported that screening/intervention for subclinical hypothyroidism significantly reduced miscarriage. Important limitation: cluster/randomization-by-center and unequal baseline characteristics mean this is not definitive proof that screening works, but it is enough to show the evidence record was not empty.

[7] Stagnaro-Green A, Dong A, Stephenson MD. Universal Screening for Thyroid Disease During Pregnancy Should Be Performed. Best Practice & Research Clinical Endocrinology & Metabolism. 2020;34(4):101320. DOI: 10.1016/j.beem.2019.101320. Key point: argues that evidence for universal screening for overt thyroid disease stands independently from the unresolved debate over subclinical hypothyroidism and thyroid autoimmunity.

[8] Dosiou C, Barnes J, Schwartz A, Negro R, Crapo L, Stagnaro-Green A. Cost-Effectiveness of Universal and Risk-Based Screening for Autoimmune Thyroid Disease in Pregnant Women. Journal of Clinical Endocrinology & Metabolism. 2012;97(5):1536–1546. DOI: 10.1210/jc.2011-2884. Key point: universal first-trimester screening was cost-effective compared with risk-based screening and no screening; importantly, the analysis remained favorable even under scenarios where subclinical hypothyroidism treatment benefit was minimized or excluded.

[Qualified Liability @JoshDavisWrites]

In 2020, ACOG put “universal screening for thyroid disease in pregnancy is not recommended” in its highest evidence tier, Level A, meaning “good and consistent scientific evidence.” The stated reason was that identifying and treating maternal subclinical hypothyroidism had not been shown to improve pregnancy outcomes or child neurocognitive outcomes. But that reason does not reach the conclusion. Universal thyroid screening does not only detect subclinical hypothyroidism; it also detects overt hypothyroidism and overt hyperthyroidism, which ACOG itself says should be treated to minimize adverse outcomes. Even stranger, ACOG graded its broad negative recommendation against universal screening as Level A, while its own alternative—targeted testing in women with risk factors or clinical suspicion—was only Level C, meaning consensus/expert opinion [1].

The RCT problem is worse. The major null neurocognitive trials, CATS and Casey/MFMU, are often used to argue against universal screening, but they mostly tested treatment that began too late to answer the early-screening question [2–4]. The lead author of CATS later coauthored a review stating that treatment in the major RCTs began at 13–18 weeks, “after the critical neurodevelopmental period,” and therefore may have been too late to affect fetal brain development [4]. A 2019 Lancet Diabetes & Endocrinology cohort made the timing issue biologically concrete: the association between maternal TSH and child brain morphology was strongest early and was no longer detectable after about 14 weeks [5]. Meanwhile, positive but imperfect evidence, such as Ma 2015, reported lower miscarriage after screening/intervention for subclinical hypothyroidism [6]. So the honest guideline sentence would have been: “Evidence is limited, timing-sensitive, and conflicting.” Instead, the message became a confident recommendation against universal screening. That is not good science communication.

* Guideline-body problem: uncertainty about subclinical hypothyroidism was used to reject universal screening for all thyroid disease, including overt disease that guideline bodies agree should be treated [1,7].
* RCT problem: late-treatment trials do not answer whether preconception or very early first-trimester screening and treatment would improve outcomes [2–5].
* Science-communication problem: “has not been shown” or “no evidence” made a contested, timing-sensitive literature sound settled, despite positive but limited pregnancy-outcome evidence and cost-effectiveness evidence [6,8].
* Accountability problem: nobody has to prove bad faith first. The narrow question is whether a Level A recommendation against universal screening is actually supported by “good and consistent scientific evidence.” On this record, that level of certainty looks unearned.

References / source guide

[1] American College of Obstetricians and Gynecologists. Practice Bulletin No. 223: Thyroid Disease in Pregnancy. Obstetrics & Gynecology. 2020;135(6)–e274. DOI: 10.1097/AOG.0000000000003893. See also Practice Bulletin Summary No. 223, Obstetrics & Gynecology. 2020;135(6):1496–1499. Key point: ACOG places “Universal screening for thyroid disease in pregnancy is not recommended because identification and treatment of maternal subclinical hypothyroidism has not been shown to result in improved pregnancy outcomes and neurocognitive function in offspring” under Level A recommendations, while “indicated testing” for women with personal/family history, type 1 diabetes, or clinical suspicion appears under Level C recommendations.

[2] Lazarus JH, Bestwick JP, Channon S, Paradice R, Maina A, Rees R, Chiusano E, John R, Guaraldo V, George LM, Perona M, Dall’Amico D, Parkes AB, Jooman M, Wald NJ. Antenatal Thyroid Screening and Childhood Cognitive Function. New England Journal of Medicine. 2012;366(6):493–501. DOI: 10.1056/NEJMoa1106104. Commonly referred to as the CATS trial. Key point: a major RCT finding no significant child-IQ benefit from screening/treatment as implemented; important for later guideline discussions, but treatment timing is central to interpreting what it actually tested.

[3] Casey BM, Thom EA, Peaceman AM, Varner MW, Sorokin Y, Hirtz DG, Reddy UM, Wapner RJ, Thorp JM Jr, Saade G, Tita ATN, Rouse DJ, Sibai B, Iams JD, Mercer BM, Tolosa J, Caritis SN, VanDorsten JP, Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal–Fetal Medicine Units Network. Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy. New England Journal of Medicine. 2017;376(9):815–825. DOI: 10.1056/NEJMoa1606205. Key point: another major null neurocognitive RCT; mean randomization/treatment timing was in the second trimester range, so it is not a clean test of very early first-trimester screening/treatment.

[4] Taylor PN, Zouras S, Min T, Nagarahaj K, Lazarus JH, Okosieme OE. Thyroid Screening in Early Pregnancy: Pros and Cons. Frontiers in Endocrinology. 2018;9:626. DOI: 10.3389/fendo.2018.00626. PMCID: PMC6209822. Key point: this review, coauthored by John H. Lazarus, states that levothyroxine in major RCTs was initiated at a median gestational age of approximately 13–18 weeks, after the critical neurodevelopmental period, and therefore possibly too late to affect fetal brain development.

[5] Jansen TA, Korevaar TIM, Mulder TA, White T, Muetzel RL, Peeters RP, Tiemeier H. Maternal Thyroid Function During Pregnancy and Child Brain Morphology: A Time Window-Specific Analysis of a Prospective Cohort. The Lancet Diabetes & Endocrinology. 2019;7(8):629–637. DOI: 10.1016/S2213-8587(19)30153-6. Key point: maternal TSH was associated with child total gray matter and cortical gray matter volume most strongly in early pregnancy; after about 14 weeks’ gestation, TSH was no longer associated with child brain morphology.

[6] Ma L, Qi H, Chai X, Jiang F, Mao S, Liu J, Zhang S, Lian X, Sun X, Wang D, Ren J, Yan Q. The Effects of Screening and Intervention of Subclinical Hypothyroidism on Pregnancy Outcomes: A Prospective Multicenter Single-Blind, Randomized, Controlled Study of Thyroid Function Screening Test During Pregnancy. Journal of Maternal-Fetal & Neonatal Medicine. Published online 2015. DOI: 10.3109/14767058.2015.1049150. Key point: reported that screening/intervention for subclinical hypothyroidism significantly reduced miscarriage. Important limitation: cluster/randomization-by-center and unequal baseline characteristics mean this is not definitive proof that screening works, but it is enough to show the evidence record was not empty.

[7] Stagnaro-Green A, Dong A, Stephenson MD. Universal Screening for Thyroid Disease During Pregnancy Should Be Performed. Best Practice & Research Clinical Endocrinology & Metabolism. 2020;34(4):101320. DOI: 10.1016/j.beem.2019.101320. Key point: argues that evidence for universal screening for overt thyroid disease stands independently from the unresolved debate over subclinical hypothyroidism and thyroid autoimmunity.

[8] Dosiou C, Barnes J, Schwartz A, Negro R, Crapo L, Stagnaro-Green A. Cost-Effectiveness of Universal and Risk-Based Screening for Autoimmune Thyroid Disease in Pregnant Women. Journal of Clinical Endocrinology & Metabolism. 2012;97(5):1536–1546. DOI: 10.1210/jc.2011-2884. Key point: universal first-trimester screening was cost-effective compared with risk-based screening and no screening; importantly, the analysis remained favorable even under scenarios where subclinical hypothyroidism treatment benefit was minimized or excluded.

[RT @RT_com]

‘If you’re ANTI-PEDOPHILES, if you are against what is going on in GAZA, then we really are actually on the right side’ — Candace Owens after interview with Ana Kasparian

'We’re on the same side’

[Qualified Liability @JoshDavisWrites]

@EnesSaltk7 I love this :)
https://t.co/sLGl3BfdF9

Best exporter out there and it's 100% free. 2 months ago I could print to PDF no problem. when I woke up and found out that doesn't work anymore and you can't copy all the text on the screen I had a mental breakdown. Thank you!

[Qualified Liability @JoshDavisWrites]

@TOEwithCurt Nevermind I'm just not online very much I guess...
https://t.co/GLLVmchTM1

[Qualified Liability @JoshDavisWrites]

Well it would help me to appreciate your perspective if I could understand what the motivations are to generate sock puppet accounts... yes I'm aware that controlling sock puppets is valuable for controlling narratives... but it's not like there's a TOE conspiracy that needs to be "controled."

[Qualified Liability @JoshDavisWrites]

Gary keeps saying we need to move past slogans and start doing the prep work to design these taxes correctly, so I built this database/index as a public navigation guide for anyone who wants to understand what makes wealth-tax policy hard, where past designs failed, and what a serious anti-evasion architecture would need to solve.

Gary mentions Gabriel Zucman will be on the show next week, this database starts with him it includes Thomas Piketty, Emmanuel Saez and many more. 112 primary sources ranked and indexed for anyone who wants to actually query the evidence.

Wealth Tax Policy & Global Evasion Strategy Database + Index (guide)
Resources you can use to better understand tax policy:
[Wealth Tax Policy Navigation Guide] (https://t.co/177LWFS8RX)
[Wealth Tax Policy NotebookLM Database](https://t.co/V4dOpXhQzb)

[Mykhailo Rohoza @MykhailoRohoza]

“After 2027, there will be no way back.”
Elon Musk said this in a podcast with Lex Fridman — a line that was later cut. When asked “Why?”, he fell silent for almost a minute. Then he quietly said: “It’s not a catastrophe. It’s a transition.”
The transcript left behind three themes that gave him away: autonomous intelligence, loss of meaning, and energy dependence. It all sounded like a forecast — but now reads like a diagnosis of the era.
The first sign is the collapse of attention.
Musk said humanity will stop thinking in cycles. Planning for the future will shrink to the horizon of updates. People will stop building and start simply replacing. MIT research confirms: a generation born after 2000 holds attention for about 8 seconds — less than a goldfish. Musk called this “cultural Alzheimer’s.” We’re not losing memory — we’re losing the ability to think.
The second sign is artificial intelligence that no longer obeys.
Musk said: “When a system starts correcting humans, the time of linear logic is over.” Even now, algorithms decide who we date, what we buy, and what we think about. This isn’t a machine uprising — it’s dissolution into convenience. People won’t notice the moment when choice becomes an option, not a right.
The third sign is energy dependence.
Musk explained: civilization can no longer survive even a day without electricity. By 2027, in his view, the balance will shift — energy will become currency, and control over it will become power. From that moment on, everything non-autonomous will disappear. This isn’t an apocalypse — it’s a change of biological form.
At the end, he said a line that didn’t make it on air:
“Technology is stronger than us, but not smarter. As long as we have meaning, we are alive. Lose it — and we become code.”
Then, after a pause, he added:
“We must learn to be human before systems learn to be gods.”
Are you ready for the transition — or already living in a world where choices are made for you?

[Qualified Liability @JoshDavisWrites]

@worstall @garyseconomics S,Z, Pikietty = wrong
Milanovic = correct
This is just too simple a narrative for a topic of this complexity I'm afraid.

[Qualified Liability @JoshDavisWrites]

From their 2016 QJE paper, they state: "not all assets generate taxable investment income—main homes and pensions, in particular, do not".
* Gold: Generates zero cash income, yet has value. Cannot be capitalized from income streams.
* Vacant land: Generates zero income but has wealth. Cannot be capitalized.
* Bitcoin: Zero income stream (unless staked/lent), yet represents wealth. Cannot be capitalized.
* Art collections: Billionaires hold billions in art generating zero taxable income
* Unrealized stock appreciation: A stock rising from $100 to $1,000 without paying dividends generates zero income to capitalize
* Tax-exempt municipal bonds: Explicitly excluded from their taxable income calculations

Too many forms of wealth to name here don't have income streams not to mention those forms of wealth which do have income streams on the black and grey market.

[Qualified Liability @JoshDavisWrites]

global capital income inequality (income from interest, dividends, rents, and pensions) can decline simultaneously while wealth inequality increases. This is because:
Wealth is not income and income is not wealth.
Global wealth in 2020 was approximately $250 trillion, while annual capital income flow was only about $6 trillion. So the wealth stock is roughly 41 times larger than the annual income flow.

[Qualified Liability @JoshDavisWrites]

overtreatment carries its own risks, while strict conservatism can too.

Cite a single RCT that ties overtreatment to miscarriages, none exists. You only have observational data and the abundance of observational data demonstrates there are far greater risks to first trimester hypothyroidism than first trimester hyperthyroidism