A British government report has potentially lifted the lid on why Germany is pulling its citizens out of Portugal.
It is a report that answers the question yesterday by Portugal’s minister of foreign affairs Augusto Santos Silva: “Why are German authorities ignoring the Covid Digital Certificate?”
“People over the age of 50 who have been fully vaccinated are three times more likely to die from the Delta variant than those who haven’t received any vaccines” (this is a headline taken from Swiss online ‘uncut news’ yesterday).
The jabs can precipitate a ‘rare’ but deadly condition known as ADE (antibody dependent enhancement) which basically means that someone who might have naturally developed only a mild illness as a result of contracting Covid-19 could experience severe disease, lasting morbidity and even death as a result of having been vaccinated.
The British government report “SARS-CoV-2 variants of concern and variants under investigation” dated June 25 may explain it (click here).
Pages 13 and 14 explain that of the over-50s attending A&E as a result of contracting the Delta variant between February and June this year, 3,546 were fully-vaccinated (having received both jabs); 976 were unvaccinated.
Almost every organ had high levels, almost. Almost total infestation. Almost like someone injected it!
Boosters push and more explained at bottom.
“The first-ever postmortem study of a patient vaccinated against COVID-19 has revealed that viral RNA was found in every organ of the patient’s body, meaning that the vaccine is either ineffective or the coronavirus actually spreads faster in vaccinated individuals.”
Both. But more Latter. And more fatal. I already covered the jabbed dead versus normal. Jabbed are literally more likely to die from it. MSM is hiding this and going on about symptoms. Dead people have reduced symptoms, can confirm.
“A previously symptomless 86-year-old man received the first dose of the BNT162b2 mRNA COVID-19 vaccine. He died 4 weeks later from acute renal and respiratory failure. Although he did not present with any COVID-19-specific symptoms, he tested positive for SARS-CoV-2 before he died. Spike protein (S1) antigen-binding showed significant levels for immunoglobulin (Ig) G, while nucleocapsid IgG/IgM was not elicited. Acute bronchopneumonia and tubular failure were assigned as the cause of death at autopsy;
however, we did not observe any characteristic morphological features of COVID-19.
Postmortem molecular mapping by real-time polymerase chain reaction revealed relevant SARS-CoV-2 cycle threshold values in all organs examined (oropharynx, olfactory mucosa, trachea, lungs, heart, kidney and cerebrum) except for the liver and olfactory bulb. These results might suggest that the first vaccination induces immunogenicity but not sterile immunity.”
So to save 86 year-olds, for like, six months, we need to damage all young adults and children? Fucking locusts. Are the Bad Boomers in power pushing this a Biblical plague? Maybe the jab itself is more Boomer Doomer than the wild virus.
It makes sense the liver would be clear because the liver’s function is clearing that shit but finding it in the heart? Goner. Dead man walking. Kidney? Suggests liver moved it there. Cerebrum? Yep, zombie.
Maybe the liver pushed it out of the liver, and back into the bloodstream, infecting the brain? Old people and some heavily disease-burdened (like STDs) have thin blood brain barrier.
The cerebrum or telencephalon is the largest part of the brain containing the cerebral cortex, as well as several subcortical structures, including the hippocampus, basal ganglia, and olfactory bulb. In the human brain, the cerebrum is the uppermost region of the central nervous system.Wikipedia
All we need is psychosis and they’re literal zombies. Maybe the psychotic break happens later, once it’s really stewed in the brain juices for a while. It’s written off as dementia in old people so may already be happening. Maybe they get a form of terminal agitation in addition. I do actually know my stuff. When it’s in the basal ganglia you are absolutely screwed. That’s motor control. It’s in the hippocampus possibly explaining the terminally stupid decision to get a second one. It’s damaging memory then, which suggests senility symptoms oncoming. I wonder if it’s more likely to kill small or large amygdala people faster. Likely smaller.
What is the overall effect of this death stick? Advanced cellular senescence? Meaning the average age of death would be those with least lifespan left, presently seen, but that will just keep getting younger and younger and younger. Logan’s Run modRNA mod? So a basic model we assume their remainder lifespan is cut in half. Does this help pension plans and national debt? Well assuming 80 is lifespan (slightly shorter in men, who are dying faster from this…) then a 60yo would die at 70, a 50yo would die at 65, a 40yo at 60, a 30yo at 55, a 25yo at ~50. a 20yo at <50, a 10yo at 45 a 5yo at 40 … etc. Down to school age.
Nobody would die before 35 except anomalies. Do we see this? Why try to deny those unless pattern?
Anomalous deaths would be acute advanced senescence. Intention may be largely chronic. They can blame global warming.
So, yes. That’s very neat. A lot of younger fertile people getting it would die around menopause/manopause. Hence, perfect economic efficiency is achieved. The aging (genetic void) population dies off as soon as reproduction is achieved. We’d need at least ten years to see if average lifespan has gone down (80 to 70). Assuming this simple model. Younger Boomers and Gen Xers are the ones to watch. A reversal of lifespan is unprecedented. This is the slowest kill model and explains the push until 2023*. We’ll begin to notice by then en masse. This is why new techs need a decade PLUS of human trials. They look at lifespan.
*MPs love the book Nudge. Has the NHS guaranteed treatment for genomic ‘vaccine’ damage? No. Nobody is talking about this. Experimental subjects are considered consenting adults, so may not be eligible for NHS treatment.
Add in a sterilising effect especially in men, STD transmission, and the guidestones would be about right.
If that basic of the most basic models is correct, then the kids currently injected will die shortly after their feckless parentals. Remember, saving the NHS also means fewer old people burdening it like lampreys. They could come out later and thank you for your willing participation, since you did technically save the NHS – by dying younger. Experiments are permitted to legally deceive you, so long as they debrief you. In 2023.
By accelerating aging population, that’s very eugenic technically but deeply wrong re family. Surplus of orphans. Pedo paradise. Adult IQ would be higher (and GDP shoot up) since the morons would’ve happily skipped along for the euthanasia, children in tow.
The average age is 80-something now because they have no remainder, so it becomes weeks, not years. It fits.
And there’s no known time limit on shedding those synthetic SPs, secondhand smoke-like. At a certain uptake, society may be fumigating itself. Birth rates already have tanked. We may need a leper colony. They could be lifelong biohazards. They could easily test their exhalation at different points post-experimental injections. PE majors have a tube you breathe into, they could easily do it. The fact they don’t means they know the result would make them hated. Could be like the Island 2005 film.
The basal ganglia are a group of subcortical nuclei, meaning groups of neurons that lie below the cerebral cortex. The basal ganglia is comprised of the striatum, which consists of the caudate nucleus and the putamen, the globus pallidus, the subthalamic nucleus, and the substantia nigra The basal ganglia are primarily associated with motor control, since motor disorders, such as Parkinson’s or Huntington’s diseases stem from dysfunction of neurons within the basal ganglia. For voluntary motor behavior, the basal ganglia are involved in the initiation or suppression of behavior and can regulate movement through modulating activity in the thalamus and cortex. In addition to motor control, the basal ganglia also communicate with non-motor regions of the cerebral cortex and play a role in other behaviors such as emotional and cognitive processing.
If it retarded them, I doubt any of us would notice.
An earlier coronavirus vaccine paper: why boosters and well, all of this really
Vaccines against infectious bronchitis of chickens (Gallus gallus domesticus) have arguably been the most successful, and certainly the most widely used, of vaccines for diseases caused by coronaviruses, the others being against bovine, canine, feline and porcine coronaviruses. Infectious bronchitis virus (IBV), together with the genetically related coronaviruses of turkey (Meleagris gallopovo) and ring-necked pheasant (Phasianus colchicus), is a group 3 coronavirus, severe acute respiratory syndrome (SARS) coronavirus being tentatively in group 4, the other known mammalian coronaviruses being in groups 1 and 2. IBV replicates not only in respiratory tissues (including the nose, trachea, lungs and airsacs, causing respiratory disease), but also in the kidney (associated with minor or major nephritis), oviduct, and in many parts of the alimentary tract–the oesophagus, proventriculus, duodenum, jejunum, bursa of Fabricius, caecal tonsils (near the distal end of the tract), rectum and cloaca (the common opening for release of eggs and faeces), usually without clinical effects. The virus can persist, being re-excreted at the onset of egg laying (4 to 5 months of age), believed to be a consequence of the stress of coming into lay. Genetic lines of chickens differ in the extent to which IBV causes mortality in chicks, and in respect of clearance of the virus after the acute phase. Live attenuated (by passage in chicken embryonated eggs) IBV strains were introduced as vaccines in the 1950s, followed a couple of decades later by inactivated vaccines for boosting protection in egg-laying birds. Live vaccines are usually applied to meat-type chickens at 1 day of age. In experimental situations this can result in sterile immunity when challenged by virulent homologous virus. Although 100% of chickens may be protected (against clinical signs and loss of ciliary activity in trachea), sometimes 10% of vaccinated chicks do not respond with a protective immune response. Protection is short lived, the start of the decline being apparent 9 weeks after vaccination with vaccines based on highly attenuated strains. IBV exists as scores of serotypes (defined by the neutralization test), cross-protection often being poor. Consequently, chickens may be re-vaccinated, with the same or another serotype, two or three weeks later. Single applications of inactivated virus has generally led to protection of <50% of chickens. Two applications have led to 90 to 100% protection in some reports, but remaining below 50% in others. In practice in the field, inactivated vaccines are used in laying birds that have previously been primed with two or three live attenuated virus vaccinations. This increases protection of the laying birds against egg production losses and induces a sustained level of serum antibody, which is passed to progeny. The large spike glycoprotein (S) comprises a carboxy-terminal S2 subunit (approximately 625 amino acid residues), which anchors S in the virus envelope, and an amino-terminal S1 subunit (approximately 520 residues), believed to largely form the distal bulbous part of S. The S1 subunit (purified from IBV virus, expressed using baculovirus or expressed in birds from a fowlpoxvirus vector) induced virus neutralizing antibody. Although protective immune responses were induced, multiple inoculations were required and the percentage of protected chickens was too low (<50%) for commercial application. Remarkably, expression of S1 in birds using a non-pathogenic fowl adenovirus vector induced protection in 90% and 100% of chickens in two experiments. Differences of as little as 5% between the S1 sequences can result in poor cross-protection. Differences in S1 of 2 to 3% (10 to 15 amino acids) can change serotype, suggesting that a small number of epitopes are immunodominant with respect to neutralizing antibody. Initial studies of the role of the IBV nucleocapsid protein (N) in immunity suggested that immunization with bacterially expressed N, while not inducing protection directly, improved the induction of protection by a subsequent inoculation with inactivated IBV. In another study, two intramuscular immunizations of a plasmid expressing N induced protective immunity. The basis of immunity to IBV is not well understood.
Serum antibody levels do not correlate with protection, although local antibody is believed to play a role.
Adoptive transfer of IBV-infection-induced alphabeta T cells bearing CD8 antigen protected chicks from challenge infection. In conclusion, live attenuated IBV vaccines induce good, although short–lived, protection against homologous challenge, although a minority of individuals may respond poorly. Inactivated IBV vaccines are insufficiently efficacious when applied only once and in the absence of priming by live vaccine. Two applications of inactivated IBV are much more efficacious, although this is not a commercially viable proposition in the poultry industry.
However, the cost and logistics of multiple application of a SARS inactivated vaccine would be more acceptable for the protection of human populations, especially if limited to targeted groups (e.g. health care workers and high-risk contacts). Application of a SARS vaccine is perhaps best limited to a minimal number of targeted individuals who can be monitored, as some vaccinated persons might, if infected by SARS coronavirus, become asymptomatic excretors of virus, thereby posing a risk to non-vaccinated people.
Looking further into the future, the high efficacy of the fowl adenovirus vector expressing the IBV S1 subunit provides optimism for a live SARS vaccine, if that were deemed to be necessary, with the possibility of including the N protein gene.
“cardiometabolic clinical correlates related to total testosterone (TT), free testosterone (fT), androstenedione (ASD), dehydroepiandrosterone-sulfate (DHEAS), estrone (E1), estradiol (E2), and sex hormone-binding globulin (SHBG).
Results: Waist circumference and BMI (β-coefficient: -0.03; 95% CI: -0.04; 0.03) were inversely related to SHBG, and BMI was positively related to TT (β-coefficient: 0.005; 95% CI: 0.001; 0.009), fT, E1, and E2. Smoking was positively related to TT (β-coefficient: 0.04; 95% CI: 0.01; 0.06), ASD, and fT. Systolic blood pressure (TT: β-coefficient: 0.002; 95% CI: 0.001; 0.003), hypertension (TT: β-coefficient: 0.05; 95% CI: 0.003; 0.11), low-density lipoprotein (LDL) cholesterol (TT: β-coefficient: 0.02; 95% CI: 0.01; 0.05), and total cholesterol (TT: β-coefficient: -0.03; 95% CI: 0.01; 0.05) were positively related to TT and ASD. Finally, type 2 diabetes mellitus (T2DM), and metabolic syndrome (MetS) were positively related to fT, but inversely related to SHBG.
Conclusions: Our population-based study, with sex hormone concentrations measured by liquid chromatography tandem mass spectrometry, revealed associations between clinical correlates including waist circumference, smoking, cohabitation, systolic blood pressure, cholesterol, and MetS with sex hormones. Thus, sex hormones and SHBG may play a role in the cardiovascular risk profile of women.”
Both obesity and anxiety symptomatology were separately associated with the same sex hormone alteration in premenopausal women: higher total testosterone level (0.97 ± 0.50 in obese vs. 0.86 ± 0.49 nmol/L in normal-weight women, p = 0.026 and 1.04 ± 0.59 in women with vs. 0.88 ± 0.49 nmol/L in women without anxiety symptomatology, p = 0.023). However, women with anxiety symptomatology had non-significantly higher estradiol levels than women without anxiety symptomatology (548.0 ± 507.6 vs. 426.2 ± 474.0 pmol/L), whereas obesity was associated with lower estradiol levels compared with those in normal-weight group (332.7 ± 386.5 vs. 470.8 ± 616.0 pmol/L). Women with anxiety symptomatology had also significantly higher testosterone and estradiol composition (p = 0.006). No associations of sex hormone levels and BMI with anxiety symptomatology in postmenopausal women were found.
Conclusions: Although both obesity and anxiety symptomatology were separately associated with higher testosterone level, there was an opposite impact of anxiety and obesity on estradiol levels in premenopausal women. We did not find an evidence that the sex hormone alterations related to obesity are playing a significant role in anxiety symptomatology in premenopausal women. This could be the explanation why we did not find an association between obesity and anxiety. In postmenopausal women, other mechanisms seem to work than in the premenopausal group.
Regional fat distribution (RFD) has been associated with metabolic derangements in populations with obesity. For example, upper body fat patterning is associated with higher levels of free testosterone (FT) and lower levels of sex-hormone binding globulin (SHBG). We sought to determine the extent to which this relationship was true in a healthy (i.e., non-obese) female population and whether RFD influenced androgen responses to resistance exercise. This study examined the effects of RFD on total testosterone (TT), FT, and SHBG responses to an acute resistance exercise test (ARET) among 47 women (22+/-3 years; 165+/-6 cm; 62+/-8 kg; 25+/-5%BF; 23+/-3 BMI). RFD was characterized by 3 separate indices: waist-to-hip ratio (WHR), ratio of upper arm fat to mid-thigh fat assessed with magnetic resonance imaging (MRI ratio), and ratio of subscapular to triceps ratio (SB/TRi ratio). Skinfolds were measured for the triceps, chest, subscapular, mid-axillary, suprailaic, abdomen, and thigh regions. The ARET consisted of 6 sets of 10 RM squats separated by 2-min rest periods. Blood was obtained pre- and post- ARET. TT, FT, and SHBG concentrations were determined by radioimmunoassay. Subjects were divided into tertiles from the indices of RFD, and statistical analyses were performed by an ANOVA with repeated measures (RFD and exercise as main effects). Significant (p < or = .05) increases following the AHRET were observed for TT (approximately 25%), FT (approximately 25%), and SHBG (4%). With multiple regression analysis, anthropometric measures significantly predicted pre- concentrations of FT, post-concentrations of TT, and pre-concentrations of SHBG. The SB/TRi and MRI ratios but not the WHR, were discriminant for hormonal concentrations among the tertiles. In young, healthy women, resistance exercise can induce transient increases in testosterone, and anthropometric markers of adiposity correlate with testosterone concentrations.
So exercise will boost a woman’s natural T. If they already have high T….
If their BMI is higher for their size, they already have high T comparatively. If they already have it racially… probably not good.
Compared to the decline in E2 concentrations, androgen concentrations declined minimally over the MT. T (β 9.180, p < 0.0001) and E1 (β 11.365, p < 0.0001) were higher in Whites than in AAs, while elevations in DHEAS (β 28.80, p = 0.061) and A4 (β 0.2556, p = 0.052) were borderline. Log-transformed E2 was similar between Whites and AAs (β 0.0764, p = 0.272). Body mass index (BMI) was not significantly associated with concentrations of androgens or E1 over time.
so black and white is off the hook
This report suggests that the declines in E2 during the 4 years before and after the FMP are accompanied by minimal changes in DHEAS, A4, T, and E1. There are modest differences between Whites and AAs and minimal differences by BMI.
During a median follow up of 6.3 years, 45 patients relapsed. Testosterone levels significantly increased across BMI categories (p = 0.001). Both circulating testosterone and BMI were positively associated with disease free survival (p = 0.005 and p = 0.021, respectively). A significant interaction was found between testosterone and BMI (p = 0.006). For normal-weight women, testosterone concentration around median (0.403 ng/mL) or third quartile (0.532 ng/mL) showed a high significant HR of relapse (5.52; 95% CI:1.65–18.49 and 4.55; 95% CI:1.09–18.98, respectively). Overweight patients showed increased HR at increasing testosterone levels, reaching a significant high HR (4.68; 95% CI:1.39–15.70) for testosterone values of 0.782 ng/mL (95th percentile). For obese patients HR decreased (not significantly) at increased testosterone concentrations, explaining the interaction between testosterone levels and BMI categories.
In ER-positive postmenopausal breast cancer patients, high testosterone levels are associated with worse prognosis in normal-weight and overweight women, whereas in obese seems to be associated with a better outcome. Although the results require further validation, they suggest that assessment of circulating testosterone and BMI could help to identify postmenopausal ER-positive patients at higher risk of relapse and potentially open new therapeutic strategies.
High T isn’t good, even in normal weight women. Water is wet.
“The findings of this study suggest high plasma levels of testosterone could play a role in the pathogenesis of type 2 diabetes among women,” Jon Jarløv Rasmussen, MD, PhD, a specialist registrar and postdoctoral researcher in the department of endocrinology at Rigshospitalet in Copenhagen, Denmark, told Healio. “The incidence of type 2 diabetes was rather low in the study, but the results implicate that screening for type 2 diabetes among women with higher plasma levels of testosterone may be beneficial, even among women who are young and without established comorbidities, such as polycystic ovary syndrome.”
In a retrospective study, Rasmussen and colleagues analyzed data from 8,876 healthy women (mean age, 38.5 years) who provided blood samples to measure plasma testosterone, dehydroepiandrosterone-sulfate (DHEAS), dihydrotestosterone (DHT) and sex hormone-binding globulin (SHBG) between January 2007 and December 2015. Researchers analyzed androgens using tandem liquid-chromatography mass spectrometry. Researchers used Poisson regression models to calculate incidence rate ratios for developing type 2 diabetes during a median follow-up of 8.1 years, stratified by androgen quartiles.
‘Normal weight’ women can get Type 2. Since Asians have higher T from higher BMI (against the white norm), they’ll be more likely to get it. This also explains the gestational diabetes common in Asian women, especially if the baby is mixed.
Nationwide, as many as 1 in 4 people who have diabetes don’t know they have it. But for Asian Americans, that number is much higher—1 in 2, the highest of all ethnic/racial groups. Why aren’t more getting diagnosed?
Weebs do not mention this. If your apparent rationale for avoiding fat white women is avoiding the Diabeetus genes, Asian is then categorically the worst racial group to mix with.
1 in 2, flip a coin, rice cooker.
I bet it’s higher in the women due to sweet tooth, so likely worse.
But people of Asian descent have less muscle and more fat than other groups and often develop diabetes at a younger age and lower weight. That extra body fat tends to be in the belly (visceral fat). This isn’t the “inch you can pinch,” the fat stored just under the skin. Visceral fat is out of sight, wrapped around organs deep in the body. You can’t tell how much visceral fat someone has by looking at them.
I didn’t call them skinny-fat to be mean, they really are!
Visceral fat is also sometimes known as “active” fat because it drives certain processes in the body that can increase the risk for heart disease, stroke, and other serious health conditions. Everybody has some visceral fat, but having too much is a major risk factor for developing type 2 diabetes.
….But BMI doesn’t catch Asian Americans in the normal weight range (18.5 to 24.9) who may very well have too much visceral fat and be at risk for type 2 diabetes. Researchers are now suggesting that people of Asian heritage get tested if their BMI is 23 or greater. Type 2 diabetes can be prevented or delayed, but only if people know they’re at risk and can take action!
They need a totally different (lower) testing standard, but they’re just like us, guys! Nay, SUPERIOR!
The same volume food in a smaller body, this isn’t hard to figure out. They’re not white women, eating like us makes them FAT.
Pregnant South Asian women carry a higher risk for developing gestational diabetes, a condition that’s dangerous for both mother and child. Between 2 and 10 percent of all pregnancies each year are complicated by gestational diabetes
2-10% in which demographic? Sounds like all? I bet it’s higher in certain ones, isn’t it?
Under risk factors is basically – be non-white
Being of Hispanic, Native American, African-American, Asian-American or Pacific Islander descent.
Women who have had gestational diabetes have a 20 to 50 percent chance of developing diabetes in the 5 to 10 years following pregnancy.
Our data indicate that although the historical or clinical risk factors for GDM are valid in Asians, using risk factors alone to select such patients for testing for GDM is inadequate. Many Asian women who develop GDM have no risk factors at all.
When Natural Selection hates you so much… maybe give it up?
r-types have higher numbers of issues like this, that would be fatal under natural law
They don’t ‘choose’ to stop at 1-2 kids, it isn’t ‘culture’, it’s fear (see below).
To avoid overlooking significant numbers of women with GDM, one may lower the specificity of the criteria, but this requires that the majority of patients be tested.
wow, that bad
Logistically, it is much simpler to conduct universal screening for all Asian women in Western countries, rather than to apply selective testing in order to spare a small percentage of women from being tested. Therefore, our findings strongly support recommendations for universal screening for GDM in pregnant women of Asian origin in Western countries. However, in places where the incidence of GDM is low, such as in some developing countries, the selection of patients for testing by the risk factors may be reasonable.
Introduction:Asian women have a higher prevalence of gestational diabetes mellitus than women of other races/ethnicities. We aimed to compare the prevalence of gestational diabetes among Asian American women to other racial/ethnic groups and explore whether the higher occurrence of the disorder among Asian women can be explained by acculturation.
Clearly I am making this all up to feel better, right guys?
Among the 5,562 women studied, the weighted prevalence of gestational diabetes was 15.5% among Asian American women, followed by 9.0% among non-Hispanic black women, 10.7% among Hispanic women, and 7.9% among non-Hispanic white women.
15.5% v. 7.9%
Diabetes at DOUBLE the rate of whites!
but they’re just like us
2.44x the risk
and that’s controlled, independently
Compared with non-Hispanic white women, Asian women had 2.44 (95% confidence interval [CI], 1.81–3.29; P < .001) times the odds of having gestational diabetes, independent of maternal age, education, marital status, income, prenatal care adequacy, prepregnancy BMI, and physical activity. Acculturation was negatively associated with having gestational diabetes (odds ratio [OR] = 0.93; 95% CI, 0.86–0.99) and explained 15.9% (95% CI, 11.38%–25.08%; P < .001) of the association between Asian race and the condition.
About 85% genetic. Great odds.
We found that Asian race was an independent risk factor for gestational diabetes, and higher acculturation may play a protective role against it in Asian American women.
What is already known about this topic?
Asian women have a higher prevalence of gestational diabetes mellitus than women of other races. However, little data exist on why prevalence is highest among Asian women.
I sense genetics.
If they’re having unnatural babies (too large for their race, mixed) supported by modern medicine, they’d be more likely to die anyway, right? Medicine can only do so much. Weaker genes die a la Darwin.
The biggest r-select factor would be risk of death while breeding, that would be the surest thing. The genes trying to extinct themselves.
Does this data exist? Also for the neonates?
YOU BET IT DOES.
Let’s see the weebs explain away these studies. They’ll probably just ignore me… again.
Pregnancy related mortality can be defined as death of the mother during pregnancy, delivery, or within one year postpartum. While 700 pregnancy-related deaths occur each year, 2/3 of these deaths are considered to be preventable.
Modern medicine, dysgenic again.
Overall pregnancy related mortality in the United States occurs at an average rate of 17.2 deaths per 100,000 live births. However, that number jumps to 43.5/100,000 for non-Hispanic Black women and decreases to 12.7/100,000 for non-Hispanic white women and 11/100,000 for Hispanic women.
No data listed for Asian, odd?
For mothers of all backgrounds, leading causes of death include cardiovascular conditions, hemorrhage, and infection. However, for non-Hispanic Black women, leading causes of death include cardiovascular conditions in addition to cardiomyopathy, pre-eclampsia, and eclampsia (hypertensive disorders).
Non-Hispanic Black women are also significantly more likely to have a severe maternal morbidity (SMM) event at the time of delivery. For every maternal death there are 70 cases of SMM events that are considered “near misses.” These events can have long-term or short-term consequences to a woman’s health. Over the past 20 years, cases of SMM have increased by over 200%, while cases disproportionately affect Black women. One study found Black women experienced SMM at a rate 2.1 times greater than that of white women.
To better understand and address these disparities, researchers suggest providers increase screening for social determinants of health. Levels of stress, trauma, food insecurity, neighborhood violence, and access to prenatal care are all factors that may contribute to the disparities and warrant further investigation.
Although most maternal deaths result from cardiovascular and hypertensive disorders, researchers found Asian/Pacific Island women exhibit the highest prevalence of gestational diabetes, which can increase pregnancy complications, at 14.8%.
One study presented in the session focused on behavioral interventions and protective factors among women with gestational diabetes. A Kaiser Permanente analysis of women in northern California found Black women have a lower prevalence of gestational diabetes when compared with Asian Indian, Filipina, Southeast Asian and Chinese women. White women had the lowest rates of the disease overall.
Screening for postpartum diabetes is recommended to all women within 4 to 12 weeks postpartum. However, rates of screening vary among women with different racial and ethnic backgrounds, suggesting tailored strategies to reduce risk and improve healthcare behaviors may be effective.
Racial medicine, openly.
An additional study explored how racial and ethnic disparities impact severe neonatal morbidities, specifically among very preterm children (born <32 weeks of gestation). Preterm birth has been associated with several health conditions developing later in life, including diabetes.
Presenter Teresa Janevic, PhD, defined race as “linked to phenotype and /or ancestry that indexes one’s location on the US social hierarchy of socially constructed groupings (i.e., races) that has been based primarily on skin color.”
genes aren’t social
Africans in Africa also have the same ‘risk’ as one in America. No magic dirt.
In contrast, Janevic defined ethnicity as “tied to race and used both to distinguish diverse populations and to establish personal or group identity, usually based on shared culture or beliefs.”
Culture? Belief? Believe your way out of diabetes. I’ll wait.
In a population-based retrospective cohort analysis using hospital discharge data linked with vital statistics at birth and death records, researchers determined Black infants were at the highest risk of dying within less than 28 days after discharge, or suffering neonatal morbidities in the time between birth and discharge. Black infants were followed by Hispanic infants, while white and Asian infants had similar low risks.
We’ll see about that.
Of the 39 New York City hospitals included in the study, researchers found a 6-fold difference in risk of combined mortality and morbidity outcomes. “Black infants were at twice the risk of being at a hospital that has risk-adjusted high rates of combined mortality and morbidity,” Janevic noted, while Hispanic infants had a 1.5 increased risk to receive care from one of these hospitals. “Hospital quality where women of color deliver likely contributes to these disparities,” she concluded.
Like schools, it depends on the IQ of the people working there.
Another investigation detailed how environmental factors and population level exposures impact disparities in preterm birth and infant mortality. “Non-Hispanic Black infants compared with non-Hispanic white infants have twice the risk of death in the first year,” explained presenter Heather Burris, MD. “This is particularly striking because Black infants just make up 15% of all births in the United States but are counting for 29% of all deaths.”
Among causes of infant death, preterm birth and low birth weight related death, along with pregnancy complications, account for the highest racial and ethnic disparities between non-Hispanic Black and white infants. Black infants are also significantly more likely to be born preterm than white infants.
an r-factor unless twins
Researchers note genetics and education level have very little impact in accounting for disparities in preterm birth. Although women with higher education tend to have lower preterm birth rates, Black women who graduated from college have a higher risk of preterm birth than white women who dropped out of high school.
I’m so glad white people already survived multiple genetic purges in our history.
Through analyzing delivery data and creating models based on air pollution severity in Philadelphia, Pennsylvania, investigators discovered air pollution is associated with spontaneous preterm birth. Data also show Black Americans experience consistently higher exposure to air pollutants, measured in fine particulate matter (PM)2.5.
An additional analysis between preterm birth and nationwide neighborhood deprivation index (encompassing income below the poverty level, vacant homes, education levels, among other factors) found that Black women experience neighborhood deprivation exposure at almost 2 standard deviations (SDs) higher than white women in Philadelphia.
Overall, Black women are 4 times more likely to live in a neighborhood with high violent crime and high air pollution than white women. “When we look at preterm birthweights, we can see that it is women living in these high-high neighborhoods that have the highest risk of preterm birth,” Burris said. However, these associations were consistent regardless of race.
They gestate for less time than whites, this is known. Africans in Africa do it.
Now we’ve established some things. An r-study in Asian women.
Increased Perinatal Morbidity and Mortality Among Asian American and Pacific Islander Women in the United States
Background: Asian American/Pacific Islanders (AAPIs) are the fastest-growing racial group in the United States.
America is now owned by Asia, demographically.
Despite a higher socioeconomic status, AAPI women experience higher rates of maternal morbidity and mortality.
can’t pay your way out of r-genes
if controlled for SES, aka $, their data would be even worse
Methods: Using the National Inpatient Sample, we performed a retrospective cohort analysis of women who were hospitalized for delivery from 2002 to 2013. The primary outcome variable was inpatient mortality rate, and the presence of severe maternal morbidities was estimated using the Bateman Comorbidity Index, a validated tool for predicting obstetric morbidity.
Results: AAPI women presenting for delivery between 2003 and 2012 were older, more likely to reside in a zip code in the top quartile of annual income, be privately insured than Caucasian women,
where’s Asian privilege?
and less likely to have a higher Bateman Comorbidity Index. However, AAPI women had a higher likelihood of postpartum hemorrhage (3.4% vs 2.7%, P < .001), uterine atony, severe perineal lacerations, and severe maternal morbidities. Procedures such as transfusion, hysterectomy,
So they could have one kid and die, have one kid and have that die, OR have one kid and then their organs all removed – so no more kids?
Yes clearly our biological superiors, right weebs? Totally not rationalising a fetish, are we?
I wonder why one child was law? They don’t have a culture of many kids because they’re too r-select to survive without modern medicine. Wake up. They pretend 1-2 is a choice and that’s why they mock and envy large white families (3+ standard) like the Amish. They envy us that ability. They would die.
and mechanical ventilation were also more common in AAPI women.
Calling it – Mother Nature is anti-Asian.
Furthermore, AAPI women had a higher mortality rate that persisted despite adjustment for an apparently higher income and comorbidities (odds ratio 1.72, 95% confidence interval: 1.14-2.59, P = .01).
Conclusions: Despite having a higher socioeconomic status, AAPI women had higher rates of maternal mortality during hospitalization for delivery. This increase persisted even after adjustment for factors known to affect peripartum outcomes. Further investigation is needed to better clarify the causes of racial differences in maternal morbidity and mortality.
Results: A total of 360,370 women with postpartum hemorrhage from 2012 to 2014 were included in this analysis. Risk for severe morbidity was significantly higher among non-Hispanic black women (26.6%) than non-Hispanic white, Hispanic, or Asian or Pacific Islander women (20.7%, 22.5%, and 21.4%, respectively, P < .01).
The white is 20%, Asian is 21%.
And these are the fattest white people, like, ever.
White and Asian bolded-
For non-Hispanic black compared with non-Hispanic white, Hispanic, and Asian or Pacific Islander women risk was higher for disseminated intravascular coagulation (8.4% vs 7.1%, 6.8%, and 6.8%, respectively, P < .01) and transfusion (19.4% vs 13.9%, 16.1%, and 15.8%, respectively, P < .01). Black women were also more likely than non-Hispanic white women to undergo hysterectomy (2.4% vs 1.9%, P < .01), although Asian or Pacific Islander women were at highest risk (2.9%). Adjusting for comorbidity, black women remained at higher risk for severe morbidity (P < .01). Risk for death for non-Hispanic black women was significantly higher than for nonblack women (121.8 per 100,000 deliveries, 95% confidence interval, 94.7-156.8 vs 24.1 per 100,000 deliveries, 95% confidence interval, 19.2-30.2, respectively, P < .01).
The weebs either did 1. no research (typical gammas) or 2. they’re delusional.
Almost double the risk of hysterectomy, roughly.An additional 52% risk over white women, minimum, in just this study.
What’s the point of being married to them, at that point? Their baby machine is broken.
Non-Hispanic black (black) and non-Hispanic American Indian/Alaska Native (AI/AN) women experienced higher PRMRs (40.8 and 29.7, respectively) than all other racial/ethnic populations (white PRMR was 12.7, Asian/ Pacific Islander PRMR was 13.5 and Hispanic PRMR was 11.5). This was 3.2 and 2.3 times higher than the PRMR for white women – and the gap widened among older age groups.
Notably, we found that, when aggregated, the top cause of death among Asian Americans is cancer. However, when disaggregated, there is wide variation in the leading cause of death. For instance, for Asian Indians, nearly twice as many men die of heart disease (31 percent), compared to cancer (18 percent). In contrast, for Koreans, the opposite is true — the death rate for cancer (34 percent) is much higher than the death rate for heart disease (19 percent).
Remember the breast cancer and Asian BMI/testosterone stuff?
Research led by the University of Birmingham has found that increased levels of hormones including testosterone could cause a brain condition that can lead to blindness in women.
We are all jealous of your waifu, yes.
Idiopathic Intracranial Hypertension—also known as IIH—is caused by high pressure in the brain with consequences from blindness to incapacitating daily long-term headaches. IIH was originally identified over 100 years ago yet the cause of the condition has remained unknown although there has been much speculation about why more than 95 per cent of total incidence is in women with obesity.
And Asians, they’re 1/2 obese in America!
They then compared the results with the levels observed in women with obesity of the same age and body mass index (BMI), as well as a cohort of women with polycystic ovary syndrome (PCOS).
PCOS is far more common in Asians. Look it up.
Most notable were the high levels of the androgen ‘testosterone’ found in the blood in IIH women. Crucially, levels of androgens were uniquely increased in the brain fluid (CSF) of women with IIH. When the researchers, analysed human choroidal plexus tissue, which is the site in the brain where CSF is produced, they confirmed that androgens could increase the rate of CSF secretion, a potential driver for increased brain pressure.
Results: We found that the South Asian women presented at a younger age for the management of sub-fertility. An extended stimulation phase and Caucasian ethnicity showed an inverse correlation with the number of oocytes retrieved in the PCOS subgroup. Caucasian ethnicity was associated with a higher fertilization rate however increase in body mass index (BMI) and the laboratory technique of IVF appeared to have a negative impact on fertilization rates in the PCOS subgroup. Commencing down regulation on day 1 of the cycles was negatively associated with fertilization rates in the tubal group. In terms of clinical pregnancy rates, the Caucasian PCOS had a 2.5 times (95% CI: 1.25-5) higher chance of an ongoing clinical pregnancy as compared with their Asian counterpart. Also, a unit increase in the basal FSH concentration reduced the odds of pregnancy by 18.6% (95% CI: 1.8-32.6%) in the PCOS group.
Conclusions: The Asian PCOS have a greater sensitivity to gonadotropin stimulation with lower fertilization and ongoing clinical pregnancy rates as compared with their Caucasian counterparts.
The ethnicity of women undergoing fertility treatments like IVF can affect the rate of successful live births, according to new research. After adjusting for certain factors including age of patient at time of treatment, cause of female or male infertility, and type of treatment, the study found that White Irish, South Asian Indian, South Asian Bangladeshi, South Asian Pakistani, Black African, and Other Asian women had a significantly lower odds of a live birth than White British women.
White women, still winning. Thank God for the Ice Age.
Overall, studies have shown higher testosterone levels in women and lower levels in men are related to incident diabetes. The major risk factors contributing to diabetes are biochemical, environmental, sedentary lifestyle, socioeconomic status and genetic factors. All of them together or independently are responsible for the development of the DM.  Besides, certain studies show Impaired Glucose Tolerance (IGT) is more common in females than males independent of age. 
We found a high prevalence of GDM among the Asian population. Asian women with common risk factors especially among those with history of previous GDM, congenital anomalies or macrosomia should receive additional attention from physician as high-risk cases for GDM in pregnancy.
Body mass index (BMI) was a very strong negative predictor of body attractiveness ratings, similar to previous findings. Zero-order associations between women’s mean hormone concentrations and mean attractiveness ratings were not significant; however, after controlling for BMI, attractiveness ratings were independently and positively associated with both estradiol and testosterone concentrations. Discussion focuses on the implications of these findings for whether attractiveness assessment mechanisms are specialized for the detection of cues of differential fecundity in young women’s bodies.
High T = ugly!
Did I mention water is wet? Can they seriously accuse of cherry picking? I’m not even looking hard.
Previously covered WHR, use search bar. Asians lose. Even black women do better.
Asians have way more T as a race than Europeans, get over it. Historically, we considered them savages, less civilized, for that reason. How is this surprising? Do you think we colonised India for fun? It’s obvious in the broad manjaws, duh. Marquardt covered this. Anyone can do a replication study, but I suggest you include the women too, so it isn’t just a sexual effect but race.
From a blog “East Asians were found to have the highest average total plasma testosterone (5,673 ρg/mL) followed by Africans (5,442 ρg/mL) and then Europeans (4,992 ρg/mL). Given that the sample size for Africans is smaller (N < 10,000), their relative position may change with more data. Nonetheless, the claim that East Asians have the least testosterone is not supported by scientific data. “
Yeah, fake redpills who think T = manly, good thing. It’s just a hormone.
“There is no way of accurately determining free testosterone. Even if there was, this would also be irrelevant since bio-availability is prime. Since race realists use total serum testosterone, why is this an issue?”
true, it’s just applying the same standard
Culturally, gang rape is more normal in Asia than Africa. This is why. You don’t get African Taharrush, really. Asia has Eve Teasing and the like. Trust me, you don’t want this.
“Mass sexual assault is the collective sexual assault of women, and sometimes children, in public by groups of unrelated men. Typically acting under the protective cover of large gatherings, victims have reported being groped, stripped, beaten, bitten, penetrated and raped.”
As for the contention that there are no studies indicating a 10% difference between East Asians and Europeans, I did find one age controlled study where the Chinese sample had 8.8% more total T, 11.4% more bio-available T and 12% more free T than the European sample. The Japanese sample had 10.5%, 5.1% and 6.7% more than Europeans respectively [Wu et al. 1995]. Wonder if race realists discuss this study, or perhaps they are too busy in celebratory dance around the Korean/Swede campfire?
They’re not really redpill. I believe data even if I dislike it. Asians have high T as a race. Get over it.
High T can also dovetail with lower national IQs e.g. India, so…. why want this? Low IQ nations have more crime.
Additionally, this recent study shows HK Chinese having some 3% more bio-available T than US Europeans.
Lol, he’s right. But T isn’t a good thing. It’s just a hormone, in men or women.
Being a race realists seems to be a length engagement with delusion, fantasy and ‘scientific’ homo-erotica.
Not here, son. I believe the T-data. Penis size generally correlates to racial height (in white men), not really T. Forum bros are wrong again. Penis stuff is sexual selection, aka chosen by women.
There was a similar increase in the positive effect of penis size on attractiveness with a more masculine body shape (i.e., greater shoulder-to-hip ratio). Surprisingly, larger penis size and greater height had almost equivalent positive effects on male attractiveness. Our results support the hypothesis that female mate choice could have driven the evolution of larger penises in humans. More broadly, our results show that precopulatory sexual selection can play a role in the evolution of genital traits.
It was concluded that all penile measurements are interrelated to each other; the height and weight also the other body measurements that are related to the penile measurements in less than 50%. It seems that the penile measurements are polygenic traits and are under multifactorial influences.
There are racial differences in associations of hormone levels with age and BMI in late reproductive age women. Further study is needed to replicate these findings and to determine the relationships of these hormonal associations with menopausal symptoms
Obesity is an important factor in hormone dynamics independent of age, race and smoking in mid-life women, although the mechanisms remain unclear.
From “A Study of the Correlation of Some Sex Hormone with Obesity in Women with Secondary Infertility” (google it)
Infertility is the inability to conceive a child for more than one year. The present study indicates
that the obesity associated with infertility. The aim of the study to determine follicle stimulating
hormone, luteinizing hormone, testosterone hormone and prolactin levels. and cholesterol and
triglyceride concentration in 2nd inferetid women. This study was carried out at kamal al-samaarai
hospital the data were collected from 95 secondary infertilial women were age between 16-45 years old and grouped them in to obese (n = 46) and non obese(n = 49). There was no significant difference between the two groups (p <0.05).Body mass index in Infertile obese women is slightly higher than non obese Infertile women which is statistically significant (P<0.001). However LH,
TSH, cholesterol and triglyceride concentration in obese infertile women is significantly higher than
non obese infertile women (p >0.05).The BMI was correlated positively with triglyceride in obese
group while BMI was positive correlation highly significant with cholesterol in non obese group.
Regression analysis revealed obese to be strongly associated with observed infertility. The elevated
prolactin values in secondary infertile women clearly shows that there is a mechanism operating at
the anterior pituitary level which shows an abnormal distribution of FSH and LH which may further
explain the abnormal delay ovum maturation. This study also indicates obese associated with
infertile more than non obese women.
“suggesting the second copy offers a protective effect.”
known for decades
how many blues would you want to build a house? fewer or more?
“which could point to pathways for extending life” not for men it’s like anything genetic, the people in a stronger position just win harder
HBD hates men? lol no
Imagine if immortality was possible but only for women?
Because it might be so.
Maybe doppel genes are required for it. We dunno.
Women existed in the genetic record prior to men, men are the mutants of the species. As abnormal, they’d be likelier to die. It isn’t personal, narcs.
Women can self-fertilise, men aren’t technically needed. Our cells can mutate into sperm, it’s biologically possible. The cell types that can mutate are called polar bodies.
“The idea that a second copy of the same sex chromosome is protective has been around for a while, supported by the observation that in mammals – where females have two of the same sex chromosomes – males tend to have shorter lifespans. In birds, males live longer on average and have two Z chromosomes, while females have one Z and one W chromosome.”
God hates men? Would explain the proclivity to violence and why in Genesis Adam was told he needs a woman. One woman.
He did not tell women they need a man.
Any claim to that effect adds to the Word and is un-Christian.
“The results reveal that individuals with two of the same sex chromosomes live 17.6% longer, on average, than those with either two different sex chromosomes or just one sex chromosome.
The team say the findings back a theory known as the “unguarded X hypothesis”. In human cells, sex chromosome combinations are generally either XY (male) or XX (female). In females only one X chromosome is activated at random in each cell.
As a result, a harmful mutation in one of the female’s X chromosomes will not affect all cells, and hence its impact can be masked. By contrast, as males only have one X chromosome, any harmful mutations it contains are far more likely to be exposed.”
Part of genetic load. Maybe why men defend their mother so?
In degenerate times, even more men would die. This explains male interest in politics, which will influence their own epigenetics in society. Good conditions/rules – more likely to survive.
“The team found that in species where males have two of the same sex chromosomes, these males live on average 7.1% longer than females. However, in species where the sex chromosome pattern is the other way around, such as humans, females live 20.9% longer on average than males.”
“But there are also other possibilities as to why the longevity gaps differ in size, including that oestrogen appears to protect the ends of chromosomes from being damaged – a process linked to ageing.”
Oestrogen also protects the brain from stress.
T-takers are literally killing themselves.
“For instance, owl monkey males live longer than females and the males play a big role in infant care in that species,” he said, noting such males have two different sex chromosomes.”
I have noted anecdotally that responsible K-type men outlive r-types of the same birth year, who often succumb to young (40-60yo) heart attacks and strokes, suddenly. If anyone has a study about r/K health outcomes in men esp. mortality, please link?
We know the children of monogamous men fare better.
I said you can’t pretend to be K, since it’s in your DNA.
Early cancer in r-types can easily be attributed to their microbiome being overloaded with STDs.
“However, the period of ‘youth’ in medieval England, before the achievement of full social adulthood, may have extended well past physical adolescence, and the age of 25 years is often used as the cut-off point.14″
Louder for the pedos at the back.
“but for most medieval young women physical adulthood did not equate to social adulthood.16″
“Instead, puberty may have marked the beginning of the phase of ‘maidenhood’ rather than adulthood.17”
We now call it teenagehood but I prefer that name for women.
“Lifestyle changes for the teenager, in particular the onset of formal work, may have marked a further step away from childhood, particularly if this involved a move away from the parental home. That the 14th-century poll tax was levied on all those aged 14 years and above suggests that young women were expected to be earning their own money by this age.18“
HA. Yeah, the guys who say women should sit at home all day twiddling their thumbs waiting to marry are 1. wrong and 2. have put too much stock in middle-class novelist Austen.
“Although exact numbers are impossible to calculate, it is clear from the documentary evidence that a significant proportion of young women migrated to urban centres such as London and York to obtain employment, most commonly a service position.19″
Exactly like today:
“This move would have been a dramatic, and potentially a traumatic, change in lifestyle for young women. Although it may have brought greater freedom and responsibility, it does not seem to have conferred full adult status; there is evidence that young women in service were always viewed as ‘girls’ regardless of their age, just as young men were not viewed as full adults before the completion of an apprenticeship contract.20″
So they didn’t marry for money, they were already economically independent.
If you actually read history and here, forensics.
“in reality, marriage at such a young age was largely restricted to the nobility, with the average age at marriage in the general population estimated at 20–25 years,22
and perhaps even later following the Black Death.23
This would provide a very late age of achievement of ‘adulthood’ by modern standards. However, although marriage was very much the expected path a significant minority of women — perhaps around 15% — never married.24″
Who is dumb enough to have never looked this up?
I keep seeing Americans who make sweeping fictional statements about what ‘we’ Europeans did and it’s like… no. That’s never happened. Citation? Statistics? They are liars. Even in their revenge fantasies of ‘oppressing’ women from work (oh joy, welfare on the backs of random men? can’t win, can we?) then they assume all women would marry off (literally never happened in human history), all women are fertile and their children all magically survive (LOL) and that all men want to marry and got to choose who (LOL no). The economy also needs young workers, part of the immigrant problem is caused by not allowing teens to work.
They’re in bloody La La Land.
Extended maturation is K-selected, the men and women were tougher as a result.
Just realised my grandmothers might be in here.
Almost certainly. Yeah, don’t lie about my nana/s.
“Alongside these dramatic but infrequent events, most young medieval females would have experienced everyday hardships and hazards.”
” The average femoral diaphysis length recorded for the medieval 14-year-old females (354 mm) is closest to that recorded by Maresh for 20th-century 10-year-olds (348 mm). The average figures for medieval 15- and 16-year-old females (365 mm and 366 mm respectively) are still lower than for 20th-century 11-year-olds (367 mm). These data suggest that growth in medieval England fell well below modern standards, perhaps reflecting the lower standard of living medieval children would have experienced.”
If it was that hard on the girls, you don’t wanna go back to that, guys.
“It does not necessarily follow that medieval women were considerably shorter than their modern counterparts. When compared to dental formation, epiphyseal fusion in the female adolescent skeletons from our sample was delayed by two to three years in comparison to modern standards, allowing them to ‘catch-up’ their growth during the pubertal growth spurt.27 This pattern of extended growth appears to have been common in the medieval period;”
The English are tough.
” Only very slight differences in stature were noted between the women of Lincolnshire, London and Gloucester, although the London females had greater diversity in adult height.”
“This may suggest that girls who experienced poorer conditions for childhood and adolescent growth were more likely to die around or before the age of 25 years.”
K-selection. Stunted or shorter women likelier to die. Same with men.
“It has been suggested that female height may have suffered in comparison to male height in medieval Europe due to preferential feeding and care of male children,33causing greater sexual dimorphism in growth and final stature between the sexes. By comparison, the average stature of young men at our sites (156 individuals) was 169.5 cm (5 ft 7 in). This may simply be the result of sexual dimorphism as such comparisons are similar for modern western populations, and therefore does not support the hypothesis that girls experienced poorer nutrition and living standards than boys.”
K-types invest well in all offspring.
“According to these indicators, it appears that all of the individuals studied had entered the pubertal growth spurt by the age of 14 years. In the modern western world girls tend to begin puberty around the age of 10 years,37 and so this result would fit with modern expectations. “
Puberty begins then takes a few years, 14-18/19 matches what I read elsewhere about menarche (posted here).
The ‘modern’ data is skewed by non-whites, especially Asians and Africans, with much lower menarches.
The African is nine, measured in America, as I recall.
“More information can be gained from examining the epiphyseal fusion of the hand phalanges, a process known to occur during the deceleration phase of the pubertal growth spurt, and correlated with first menstruation in modern females. Although the age at which this event occurred varied in our sample just as among modern girls, fusion appears to have occurred most frequently between 15 and 17 years (Fig 2). At 14 years, only 36% of girls display fusing or fused hand phalangeal epiphyses, but by 17 years this figure has risen to 84%.”
Still not 100%, K-types have a later range of menarche.
“A second skeletal event known to be associated with first menstruation, the ossification of the iliac crest of the ilium, was also only found in girls aged at 15 years or over. Interestingly, this is roughly in line with the average age at menarche suggested by the few available documentary sources.38An average age at menarche of between 15 and 16 years would be much later than the modern British average of just under 13 years.39In addition to their shorter stature, this finding adds weight to the argument that environmental factors such a deficient diet and disease were having a negative impact on medieval female growth and development. Interestingly, however, this average age at menarche is below the age of 17 years recorded for mid-19th century females,40indicating that urban conditions were not as detrimental as those experienced during rapid industrialisation.”
The female body takes YEARS to develop, periods often occur too early to carry a child to term. Hollywood lies, because it’s full of creeps.
Men shouldn’t be discussing a reproductive system they cannot understand.
“The evidence for medieval England, however, shows a delay in the achievement of this milestone, which appears to have fallen between 17 and 18 years for most girls, based on 247 individuals with this bone surviving (Fig 3). Complete fusion of the iliac crest of the ilium, which signals the end of pelvic growth, was only seen in a minority of women aged below 20 years, based on the 277 individuals “
They’re K-types, it isn’t a delay, it’s NORMAL. Modern people are aberrant.
17-18 periods stabilize (this takes years, I have spoken to doctors about it).
The pelvis keeps growing to carry and support a child though, only when this is done (about 21, spinal plate fusion) is the woman actually sexually mature with a low risk of still birth, miscarriage or death.
Modern medicine is allowing a lot of non-white thots to survive a process Nature is telling them is fatal. Do not confuse that with Nature’s approval.
“These data suggest that puberty was extended into the very late teens for young medieval women, pushing back the timing of achievement of full physical adulthood. This extended period of physical adolescence indicates that living standards for young medieval women, at least in the urban and small town environments, were considerably poorer than those of modern British adolescents. Some variation between the sites was noted, with pubertal development most advanced in the small town of Barton-upon-Humber, and most delayed in the urban hospital cemetery of St Mary Spital, London. This presumably reflects the harsher living conditions experienced by the girls living and working in London.”
Nah, hard work and low fat diet. Treating the women like men will delay them more.
“It is believed that the demographic changes caused by the Black Death may have led to increased opportunities for many women to migrate and work.43
Although less documentary evidence is available for women than for men, there is evidence for female servants much younger than 12 years in urban households,44and some migration may have occurred at a very young age. Although legislation was passed to regulate the minimum age for apprentices — 13 years in the early 14th century, rising to 16 years by the 15th century — apprenticeships were rarely available for girls, and no such legal minimum age existed for servants or casual workers. The available evidence suggests that girls started formal work away from home at a younger age than boys.45“
This concept of female laziness is really American.
” a degree of personal freedom; the latter is perhaps most clearly indicated by the large number of migrant women recorded as making ‘merchet’ payments for the right to choose their own marriage partner.46 On the other hand, moving away from home, particularly to a town or city, could bring with it new challenges and hazards, such as sexual predation, mistreatment, injury and disease.”
Americans are so wrong it hurts.
” this result indicates that much greater numbers of women living and dying in London were actually suffering from tuberculosis.”
“Again, the numbers are too small for statistical analysis, but this may provide further evidence for girls having a more indoor lifestyle than boys in the medieval period.”
Forcing women to sit at home is literally bad for their health.
We aren’t mole people.
On the whole, the women actually had it harder than men.
“There can be little doubt that this extensive workload was exhausting for many women, but osteological study can provide further direct evidence for the impact that this had on young women’s bodies.
A wide range of trauma has been recorded on the skeletons of young medieval women, including fractures of the upper limb and finger bones, cranium and ribs, lower limbs and feet.57 However, the prevalence of fractures of each type is lower than among males, suggesting that girls were exposed to (or exposed themselves to) fewer risks of injury than boys.”
We hadn’t evolved for that labour, men did.
“It is notable that, of the 48 cases of trauma reported in the grey and published literature, cranial, rib and jaw injuries, suggestive of interpersonal violence, only started to appear in women aged 17–25 years, comprising 18.6% of the 43 fractures for this age group. This suggests that the risk of violence rose as girls turned into young women, perhaps reflecting domestic violence after marriage.58″
That would explain the death rate. Stress and fractures – no healthy baby.
“There is one area of the skeleton where young women seem to have suffered virtually the same frequency of fractures as young men, the vertebral column. By far the highest prevalence rate for vertebral fractures (4.7%, n = 9) was found at St Mary Spital suggesting that female workers in the capital, or at least the poor workers buried in this hospital cemetery, were undertaking the activities most likely to cause spinal injury. The majority of these fractures were compression fractures, often caused by falls from a height, although avulsion and hyperflexion injuries were also present.59“
The men sitting at a desk in an apprenticeship had it easy.
“Schmorl’s nodes are common, often asymptomatic, depressions caused by herniation of the nucleus pulposus on the superior and inferior surfaces of the vertebral bodies. Their aetiology is complex, although spinal trauma caused by vigorous activity and flexion and extension of the spine is most commonly associated with their formation.60 The age of their occurrence is not clear, but they generally appear before the age of 18 years.61Plomp et al argued that males are more susceptible to these lesions due to the size and shape of their vertebrae.62 In our study, medieval women had a higher prevalence of the lesions). Analysis of the location of Schmorl’s nodes on the vertebrae revealed that the lumbar vertebrae were affected far more often among women, and the central thoracic vertebrae among men. This mirrors vertebral fractures where in the women all of the fractures occurred in the lower thoracic and lumbar vertebrae, while in young men the central thoracic vertebrae were affected. This may suggest different activities; strain on the lumbar vertebrae, in particular, may be caused by bending and lifting.63″
aka back breaking labour, which could cause…
“Further evidence for stress being placed on the spines of young medieval women is provided by cases of spondylolysis. This describes the partial separation of the inferior facets on the neural arch from the vertebral body, usually between the ages of 10–12 years. The condition results from microtrauma in low grade stress on the lower back due to bending and lifting strains, or a fall from a height,64 but may have an underlying congenital cause. This injury was present in 4.4% of the female skeletons examined. This is higher than the prevalence of this condition found by the authors among young medieval males (2.9%), although the numbers involved were too small for statistical analysis. Again, the area involved is the lumbar region of the vertebral column. In addition, three young women, two aged at around 21 years and one at 22–25 years, display early degenerative joint disease of the vertebral column.”
Forcing women into labour like that kills them, reminder.
“What emerges from the osteological evidence is that the workload of many young medieval women appears to have been literally backbreaking, and these early injuries may be expected to have led to significant back problems and pain in later life. It seems likely that these early spinal problems were caused primarily by carrying heavy loads at a time when the spine was still forming and vulnerable. Research from the grey and published literature reveals that rates of spinal injury were higher in urban than rural women65 and suggests that the workload of the young migrant women in service was harder than that of the young women who remained in the country or in small towns with their families. For example, the prevalence of vertebral fractures, spondylolysis and Schmorl’s nodes was lowest at Barton-upon-Humber, a wealthy small town.66″
Marriage, Sexual Activity and Childbirth
There is considerable evidence to suggest that marriage was a defining moment in the medieval female life course, marking the transition into true social adulthood.67 It is notable, however, that there was a significant gap between the legal age at marriage (12 years) and the average age at marriage (20–25 years even before the Black Death) in medieval England.68 The new analysis of pubertal development in medieval England discussed above suggests that the average age at menarche was 15–16 years. Full fertility, in terms of the likelihood of conception, carrying a healthy pregnancy to term and surviving childbirth, would only have followed several years after menarche with the completion of pelvic growth,69 which in our medieval sample appears to have been rare before the age of 19 years.
aka what I already typed, dammit
The fact that many young medieval women would not have been fertile before their 20s may be one reason for the relatively late average age of marriage during this period.70 It also suggests that marriage at the legal minimum age of 12 years would rarely have been fruitful, and any pregnancy that did ensue would have carried significant risks for the mother. We know of several medieval legal cases of the marriage of young girls where the ‘physical readiness for marriage’ of the girl in question was debated.71
This don’t go to college because you get periods thing from America is pig ignorant on female anatomy.
There is evidence to suggest, however, that the majority of cases of marriage before 15 years were confined to the nobility.72Today, girls of higher socio-economic status, with a considerably better standard of life, mature earlier than average. For example, high caste girls in 20th-century India have an average age at menarche over a year younger than low caste girls.73The average age at menarche for noble girls in medieval England may therefore have been younger than the average age of 15–16 years described above.
more r-selected by men, explains eventual decadence and homosexuality rates, especially in the French
Even so, a pregnancy before the completion of pelvic development would have been dangerous; a famous example of this is provided by Margaret Beaufort, who appears to have been rendered sterile by a difficult first birth (of the future king Henry VII) at the age of just 13 years.74 An understanding of these risks is demonstrated by several contemporary authors,75 and was reflected in the Jewish rule that contraception (banned by Christian teaching) could be used to prevent pregnancy if the bride were too young to safely bear a child.767
The guys trying to force women to reproduce young would ironically render their own wife sterile via their stupidity. Good riddance. The Lord works in mysterious ways.
In theory, marriage coincided with sexual initiation for young women, and if the Church’s remonstrations to remain celibate until marriage were universally followed, it would indicate a relatively late age of sexual initiation. In reality, premarital sex among betrothed couples seems to have been common,77
that links to this study, no, they weren’t slutty
and sex with other partners, in not all cases consensual, was far from rare.
Are you really counting rape?
Evidence for this is provided by the erratic enforcement of ‘legerwite’ or ‘leyrwite’ fines on serf women who engaged in premarital sex.78
What about the men.
Premarital sex is thought to have been particularly common among young girls and women living away from home, for example in service roles, due to the greater freedom and availability of partners as well as the risk of sexual predation or pimping from employers.79The sexual exploitation of girls in service appears to have been a frequent problem based on the legal record,80 and many young women must have lost their virginity in these circumstances. The extensive focus of many writers on admonishing young women to stay celibate until marriage may be taken as further evidence that premarital sex was seen (at least for women) as a significant societal problem.
Rape isn’t sleeping around, WTF.
Pedophiles raping virgins don’t really count as premarital sex, a choice, does it?
Two aspects of osteological analysis may shed light on sexual activity among young medieval women. The first is a sexually transmitted disease. Venereal syphilis, a treponemal disease, affects the skeleton in its tertiary stage, causing distinctive skeletal lesions.81From the end of the 15th century, syphilis is believed to have been endemic in urban areas of England, although recent work has suggested that it may have been present at a much earlier date.82
Men spread that, sailors caught that. Your point?
If a virgin woman married a man with it, she’d get it. That can happen after marriage.
These female authors really want to present all women throughout history as sluts. Cui bono?
Among the 14–25 year old female individuals examined, four probable cases of treponemal disease were recorded, based on the presence of characteristic gummatous lesions in the cranium or long bones.83 Three of these were found in the young women from London (Fig 5), and one was found in York, at St Helen-on-the-Walls. One further case is known from Blackfriars, Gloucester;84no cases were identified in the rural or small town sites consulted in the wider survey. The two youngest women to show signs of treponemal disease were aged at just 16 years. It is difficult to rule out congenital syphilis in these cases, as the presentation of the two conditions can be very similar, although none of these skeletons display the typical dental deformations of congenital syphilis.
So their fathers were sluts, so?
If the disease is the venereal form of treponemal disease, or syphilis, this would suggest the girls were very young when first infected. Syphilis generally takes several years to cause such destruction in the skeleton.85 Although the number of cases recorded is small, given that only 10–20% of individuals with tertiary syphilis experience skeletal involvement, and that skeletal lesions take several years to develop,86 it seems likely that much greater numbers of young women were affected by this disease.
To imply they wanted to be raped by syphilitic men is a bridge too far though.
The spread of sexually transmitted diseases such as syphilis was exacerbated by the problem of prostitution in medieval towns and cities. Karras argues that regulations of the Guilds limited women’s access to the normal labour market, forcing them to turn to prostitution out of necessity.87
Assuming that was a mistake.
There is little direct evidence that apprentices were procured as prostitutes, but one extant record from London City and Ecclesiastical Court (ad 1423) attests that one Alison Boston took apprentices who she hired out for the ‘horrible vice of lechery’.88 There are also accounts of men taking young girls (invenculae) to the London stews and selling them as prostitutes, suggesting the types of danger faced by young unskilled immigrant women. Goldberg89 cites the famous references from medieval York in ad 1482 that place prostitutes within the legal realm of ‘lepers’ and pigs in the hazards they caused for the local population.
She does not discuss the age at which women may have turned to prostitution, but suggests widows and daughters of labourers, known as ‘spinsters’ and ‘seamstresses’ (sempsters), needed to work several jobs to make ends meet, including petty theft, illegal ale retailing and prostitution. Goldberg argues that although full-time, ‘professional’ prostitutes were rare, many women were forced into occasional prostitution in hard times.90
also why we have the welfare state
This would have been a particular risk for a migrant girl away from the safety of her family.91 Although it is impossible to state that any of the young medieval women examined were forced into this profession, this must be considered in the cases where possible syphilis is recorded.
No shit, nobody would choose that. The excuses these women make for rape are appalling.
A second consequence of sexual activity, pregnancy, may also in exceptional circumstances be visible in the archaeological record. In total, eight cases of young women buried with fetuses in utero have been recorded from medieval cemetery contexts. These burials represent ‘obstetric catastrophes’ with the death of both mother and child in late pregnancy or childbirth. Although there was a Christian injunction in place in medieval England for infants to be removed from their mother’s womb before burial,92 this does not appear to have been rigorously obeyed.
Yeah, who wouldn’t choose to die like that? I guess they were all just happy sluts, huh Mizz Feminist?
All of the individuals buried with a fetus in utero in medieval cemeteries have an estimated age at death of around 20 years or over, and thus none represent particularly young ‘teenage’ pregnancies.
Because they rarely got pregnant. Look at the evidence.
This may support the idea that in the medieval period teenage girls were not falling pregnant, as first pregnancies are often seen as the most hazardous.93
May? It’s anatomical.
It also fits with the known late pattern of marriage in this society. However, it is by no means certain that all of these women were married. The two examples from St Mary Spital may have represented extramarital pregnancies as the hospital was known to accept unmarried women in pregnancy or childbirth.94 It may be significant that neither of these women received an individual grave or any grave ornamentation. In contrast, the elaborate nature of one young mother’s burial at Barton-upon-Humber, in a coffin within the church and with a cloth of gold artefact,95 surely indicates that this woman was married and held a position of substantial social standing.
Clearly, their situation was a choice.
Given the high mortality rate of women in childbirth in the medieval period revealed by documentary sources,96sit is clear that these rare burials represent a dramatic under-estimation of the real levels of maternal mortality. In many cases, the churches prohibition on burying fetuses in utero may have been observed. In a large proportion of births, too, the child may have been saved, leaving little clue as to the cause of death of the mother.
But doctors (when sane) will elect to save the mother because she can have countless children later but an orphan baby is already financially a goner. Remember this, America.
The period of social adolescence for young medieval women seems to have been an important life stage, encompassing the growth to full physical adulthood and fertility, the adoption of adult working roles and, for most young women, the move from legal dependence on a father to legal dependence on a husband, with perhaps a few brief years of relative independence in between. The comparative absence of young women from documentary sources means that osteological information plays a vital role in our understanding of this group, and it can reveal a great deal about the way in which medieval girls grew into women, the living conditions they enjoyed or endured, the work they did and the health problems they faced.
Many of the conclusions drawn from osteological analysis of this group articulate with and illuminate the documentary evidence. The average age at which full fertility appears to have been achieved, around 20 years, is substantially later than in modern England, but ties in well with the known average age at marriage in this society. The greater susceptibility of young women to respiratory infections, from the relatively benign maxillary sinusitis to the deadly serious tuberculosis, chimes with the picture drawn from documentary sources of an indoor lifestyle for women, close to the smoky fire, and of the cramped living conditions that helped to spread disease. The backbreaking work clearly undertaken by many young women paints a clearer physical picture of their daily lives than that provided by documentary sources alone, and the development of signs of venereal disease in very young women hints at the problem of girls being driven to prostitution in England’s medieval cities.
Gang rape, we still have it. They are driven to it, slave-driven.
Trans fats—on their way to being largely phased out of food—had the most significant adverse impact on health. Every 2% higher intake of trans fat was associated with a 16% higher chance of premature death during the study period.
That’s a big deal.
Higher consumption of saturated fats was also linked with greater mortality risk. When compared with the same number of calories from carbohydrate, every 5% increase in saturated fat intake was associated with an 8% higher risk of overall mortality.
That’s practically insignificant proportionally, especially since the method painstakingly avoid citing animal source or non-animal sourced fats. Too vague.
Conversely, intake of high amounts of unsaturated fats—both polyunsaturated and monounsaturated—was associated with between 11% and 19% lower overall mortality compared with the same number of calories from carbohydrates.
You cannot compare to sick Americans as your control population. No.
They don’t want people learning how to be really healthy. It would show up on their data more. You need half a century of plant propaganda to convince people our declining health is good for us.
Among the polyunsaturated fats, both omega-6, found in most plant oils, and omega-3 fatty acids, found in fish and soy and canola oils, were associated with lower risk of premature death.
The Western diet is toxic purely because there’s too much omega 6, a deadly excess.
The lifespan of India also suggests avoiding animal products is…. ill-advised.
People who replaced saturated fats with carbohydrates had only slightly lower mortality risk.
eat your GMO grains, you’ll live longer
“Our study shows the importance of eliminating trans fat and replacing saturated fat with unsaturated fats, including both omega-6 and omega-3 polyunsaturated fatty acids. In practice, this can be achieved by replacing animal fats with a variety of liquid vegetable oils,” said senior author Frank Hu, professor of nutrition and epidemiology at Harvard Chan School and professor of medicine at Harvard Medical School.
An Asian at Chan school.
Looking as Asia’s meat consumption, you are lying.
As of June 18 of this year, trans fats have been officially banned from all manufactured foods.
Research in the 1990s found a strong link between trans fats, also known as “partially hydrogenated oil,” and heart disease.
You are what you eat.
In addition, more and more studies are finding that trans fats cause cellular destruction in the brain and can adversely impact hormone production, memory and increase inflammation by suppressing the production of Omega-3 fatty acids.
Actively suppresses omega 3.
Now, our brains do need fat to function. In fact, the brain relies on natural, healthy fats to maintain cell membranes, keep brain inflammation at bay and transport fat soluble vitamins such as vitamin A, D, E and K. Focus on getting your daily doses of fat from olive oil, coconut oil, nuts, seeds and avocado.
A study of almost 3000 people in 2017 reported a link between artificial sugar consumption and an increased risk of stroke and dementia. In the study, those participants that reported having just one diet beverage a day were three times more likely to develop dementia or suffer from a stroke. Although more research is needed, the findings are alarming.
Aspartame, one of the most commonly used artificial sweeteners in foods and beverages, has also been shown to cause neurodegeneration, mood imbalances and potentially cause brain cells to kill themselves. Instead of artificial sweeteners, use small amounts of natural sugar, such as raw honey, pure maple syrup or dates.
Yeah it also tastes like death.
A literal neurotoxin.
A study of 550 men and women over 30 years published in The BMJ found that even moderate drinking, which they defined as about 6-9 drinks a week, can damage the brain, including hippocampal atrophy.
Anyone that has had a few drinks knows that alcohol can impair judgement, balance, speech and even memory. Many studies have shown that long term heavy drinking can create serious and persistent changes in brain function that include mental confusion, eye nerve paralysis and difficulty with muscle coordination.
Drunkenness is just a form of brain damage that becomes more persistent with chronic alcoholism.
Until they never ‘sober up’ – clear the toxin, ever again.
Let the brain shrinkage vegans eat their fake flesh.
Trans fatty acids (TFA) are produced either by hydrogenation of unsaturated oils or by biohydrogenation in the stomach of ruminant animals. Vanaspati ghee and margarine have high contents of TFA. A number of studies have shown an association of TFA consumption and increased risk of cardiovascular disease (CVD). This increased risk is because TFA increase the ratio of LDL cholesterol to HDL cholesterol. Food and Agriculture Organization of the United Nations and World Health Organization have come up with the recommendation that the contents of TFA in human dietary fat should be reduced to less than 4%. There is high prevalence of CVD in Pakistan. High consumption of vanaspati ghee which contains 14.2-34.3% of TFA could be one of the factors for this increased burden of CVD in Pakistan. Consumption of dietary fat low in TFA would be helpful in reducing the risk of CVD in South Asia. Denmark by banning the sale of food items with TFA has brought down the number of deaths due to coronary heart disease by nearly 50% over a period of 20 years. Public awareness about the adverse effects of TFA on human health would be extremely important. Media can play a very effective role in educating the masses and advocating the policy for the sale of only low TFA food items.
A third pattern characterized by high trans fat was associated with less favorable cognitive function and less total cerebral brain volume.
Participants with higher plasma trans fat scores had worse cognitive function overall (memory, attention, language, processing speed, and global).
Each 1-SD increase in the trans fat score associated with a 0.30-SD decrease in global cognitive score.
You sure showed us!
They’re literally retarding themselves.
The high trans fat pattern was consistently associated with worse cognitive performance and less TCBV. Linolelaidic acid is predominantly found in bakery foods such as cookies, doughnuts, cakes, pastries, and pies.27
I’d rather eat a donut than fake oozing flesh.
These foods are often prepared with hydrogenated vegetable oils to allow for a long shelf life. Higher trans fatty acid intake increases cardiovascular risk, systemic inflammation, and endothelial dysfunction, all of which may explain an association with cognition.37,38 Unfortunately, very few studies have assessed trans fat and risk for cognitive decline.26
Big Food funding PACs?
Simple, scan vegan brains and see if they’re atrophied.
Trans fat may aggravate cognitive function independently and jointly through interaction with other dietary factors.e11 Trans fat may displace DHA in neuronal membranes, but apparently does not impact the neuropathologic Alzheimer hallmarks in mice.39The consistency of the association of plasma trans fat with poorer cognitive function and more brain atrophy suggests neurologic consequences in humans, but these findings need to be confirmed.
The European Food Safety Authority issued a report last year warning consumers about the high levels of potentially carcinogenic contaminants in palm oil (an ingredient used in Kit Kat Bars, Nutella, and Cheez-Its, among other treats) when refined at temperatures above 392°F.
With caveats inherent for ecologic, nutrient disappearance analyses, a healthy dietary allowance for n-3 LCFAs for current US diets was estimated at 3.5 g/d for a 2000-kcal diet. This allowance for n-3 LCFAs can likely be reduced to one-tenth of that amount by consuming fewer n-6 fats.
Stop blaming women and ‘sexism’, we aren’t omnipotent gene meddlers.
Also, genetic proof of a male wall. LOL. An explanation to why so many middle-aged men suddenly look like lesbians.
[coughs in Bruce Jenner]
And there’s no way to reverse it, before the snake oil salesmen jump up with a solution that, if it worked, would make them a billionaire.
Popping pills to get out of laziness is what lefties do.
Bold for the lazy.
“Using new tools to analyze genetic variations that accumulate with age, we can help explain how sporadic diseases like cancer or Alzheimer’s manifest,” says first author Jan Dumanski.
One such postzygotic mutation found in the cells of biological males is the loss of the Y chromosome in a degree of blood cells. Loss of Y occurs in up to 17 percent of men and is more likely to be found in older men and men who smoke. This study expands on the idea that loss of Y, already a known risk factor for cancer (10.1038/ng.2966), could be a predictive biomarker for a wider range of poor health outcomes, specifically Alzheimer’s. Why loss of Y can be linked to an increased risk for disease remains unclear, but the authors speculate it has to do with reduced immune system performance.
They should look at age groups of men.
The researchers looked at over 3,000 men to ascertain whether there was any predictive association between loss of Y in blood cells and Alzheimer’s disease. The participants came from three long-term studies that could provide regular blood samples: the European Alzheimer’s Disease Initiative, the Uppsala Longitudinal Study of Adult Men, and the Prospective Investigation of the Vasculature in Uppsala Seniors. Across the datasets, those with the highest fraction of blood cells without a Y chromosome were consistently more likely to be diagnosed with Alzheimer’s.
….Really more of an outcome of poor genetic health….
Did you test for aluminium?
Attempt chelation therapy?
Yeah, fuck the easy solution, blame the Y chromosome.
Like women don’t get it.
“Having loss of Y is not 100 percent predictive that you will have either cancer or Alzheimer’s,” Forsberg says, adding that there were men in the study who had the mutation and lived with no symptoms well into their 90s.
Were their fathers older or younger?
If paternal age is a factor in ANYTHING, it’s a risk factor for this.
Male chromosome plus mutation. Come on.
Men think they can fool women but white hairs on a ballsack don’t lie.
“But in the future, loss of Y in blood cells can become a new biomarker for disease risk and perhaps evaluation can make a difference in detecting and treating problems early.”
Forsberg, Dumanski, and colleagues will next investigate the effect of loss of Y in larger cohorts and explore in greater detail how it confers risk for specific types of cancers and disease. They also plan to look at the cellular changes caused by loss of Y and how it affects different types of blood cells.The researchers looked at over 3,000 men to ascertain whether there was any predictive association between loss of Y in blood cells and Alzheimer’s disease. The participants came from three long-term studies that could provide regular blood samples: the European Alzheimer’s Disease Initiative, the Uppsala Longitudinal Study of Adult Men, and the Prospective Investigation of the Vasculature in Uppsala Seniors. Across the datasets, those with the highest fraction of blood cells without a Y chromosome were consistently more likely to be diagnosed with Alzheimer’s.”
Should look at heart disease, primary killer of American males.
But that’s none of my business.
If men aged well, they wouldn’t need to be on supplements.
Young men on supplements is just sad, like young women getting plastic surgery.
There’s no room to move. If you can’t be all that young, what are they going to do?
Our society treats aging like cancer, it’s ridiculous Boomer youth cult propaganda to sell them supplements like detox tea and testosterone ball rub. You can’t fool mother nature.
When they actually hit middle-age, they won’t be able to keep up with that crap anyway.
Imagine most of your shallow friends disappearing because you dropped the massive timesink of gym addiction.
The Ken Doll homoerotic gym attention bros look sad after about 40.
Plus bodybuilder types know there are two types of muscle: appearance and strength. Guess which one they all go for?
The one that instantly converts to stubborn fat if they so much as look at a complex carbohydrate past 30.
The Johnny Bravo look is actually, industry secret, physically weak.
In a fight, any martial artist will tell you the bulk limits their range of motion like a fatty anyway.
All men need is a healthy range of light muscle, which women prefer but don’t require any supplement sales.
Light muscle also provides cognitive benefits with no musculoskeletal downsides, including sag and joint pain. Bruce Lee could take a Henry Cavill any day of the week.
With the T&A they have a woman’s hourglass in profile, they gay.
A study that tried to find positive (pro-veg) differences had arbitrary, strict age limits and time exclusions. https://academic.oup.com/ajcn/article/70/3/516s/4714974 “There were no significant differences between vegetarians and nonvegetarians in mortality from cerebrovascular disease, stomach cancer, colorectal cancer, lung cancer, breast cancer, prostate cancer, or all other causes combined.”
Logically, if meat consumption caused colon cancer, that is impossible.
Pro-vegan paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4073139/
“Non-vegetarian diets were compared to vegetarian dietary patterns (i.e., vegan and lacto-ovo-vegetarian) on selected health outcomes.” Why not compare vegetarian to vegan? “Males experience greater health benefits than females. Limited prospective data is available on vegetarian diets and body weight change.”
Don’t bother studying that, though.
“Large randomized intervention trials on the effects of vegetarian diet patterns on neurological and cognitive functions, obesity, diabetes, and other cardiovascular outcomes are warranted to make meaningful recommendations.” …useless.
Vegetarian, vegan diets and multiple health outcomes: A systematic review with meta-analysis of observational studies
There appears to be a confound e.g. not drinking. Claim:
“This comprehensive meta-analysis reports a significant protective effect of a vegetarian diet versus the incidence and/or mortality from ischemic heart disease (−25%) and incidence from total cancer (−8%). Vegan diet conferred a significant reduced risk (−15%) of incidence from total cancer.”
DATA: (they hope we won’t look at)
“With regard to prospective cohort studies, the analysis showed a significant reduced risk of incidence and/or mortality from ischemic heart disease (RR 0.75; 95% CI, 0.68 to 0.82) and incidence of total cancer (RR 0.92; 95% CI 0.87 to 0.98) but not of total cardiovascular and cerebrovascular diseases, all-cause mortality and mortality from cancer. No significant association was evidenced when specific types of cancer were analyzed.”
Clear as mud.
You’re literally more likely to DIE on this diet but they claim “protective”.
Vegans – putting the DIE in DIET.
“The analysis conducted among vegans reported significant association with the risk of incidence from total cancer (RR 0.85; 95% CI, 0.75 to 0.95), despite obtained only in a limited number of studies.”