For the narcissists like me, also helps hair growth.
Distribution of proteoglycans during the hair growth cycle in human skin
The involvement of proteoglycans in hair growth has been recognized through the observation of increased hair growth in diseases such as the mucopolysaccharidoses and pre-tibial myxedema, which involve an increase in skin proteoglycan content. In an attempt to understand this, we have examined the distribution of chondroitin 6 sulphate (C6S), unsulphated chondroitin (COS), dermatan sulphate (DS), and heparan sulphate proteoglycans (HSPG) in frozen tissue sections of normal scalp by immunostaining. Results show that during anagen, the thick connective tissue sheath around the follicle strains strongly for C6S, COS, and DS. COS is uniquely associated with this region and is not found beneath the epidermis or infundibular epithelium. HSPG is, however, localized in the basement membrane zone adjacent to the outer root sheath. In addition, all of these proteoglycans are localized in the dermal papilla. In mid-catagen, we observed significant loss of C6S and COS staining from both the dermal papilla and the connective tissue sheath, but no decrease in staining for HSPG. In late catagen, very little staining of C6S and COS was observed. In early anagen, we observed that C6S was again present in the connective tissue sheath and dermal papilla; however, COS staining appeared to be weaker and less closely associated with the follicle. HSPG staining was observed in early anagen in a pattern very similar to that found for other basement membrane components. Results for DS were not obtained for catagen or early anagen. These results provide further evidence that hair growth is associated with the presence of chondroitinproteoglycans in the follicle environment and that the cessation of growth is associated with their removal. Further studies are underway to characterize the relationship between hair growth and proteoglycans.
three decades ago they knew this
If you get hair loss issues despite that, try a B complex and iron. Maybe with biotin. Women get knock-on problems from excess blood loss (including childbirth) and our collective hivemind research suggests that works. If the problem is thickness, bamboo. It contains silica. These are Woman Inc Secrets. Share with care.
One problem of oestrogen dominance in men is excess copper in the body. It tanks your T. Get a blood test and also check for iron and zinc. Post-partum women are usually iodine-deficient. If you really don’t have the other issues, check that, especially if you donate blood. Among many reasons women should be able to describe blood loss without grown men having a hissy fit.
I would’ve guessed September due to schools and universities. Then there’s the magic bean branding of Poison AZ is worse than Poison PF. The illusion of choice.
So hypothetically we can sue the companies for damage from spike protein shedding, since we didn’t consent to take it into our body. Like trespassing, biochemically.
So good for you, the military in Australia is apparently using ‘task forces’ with the police to hold people down and inject them (chemical rape). I’ve asked for public videos I can link to about this, yet to see anything but it would make sense why Youtube suddenly suspended Sky News Australia. Why now?
Design and Analysis of Shedding Studies for Virus or Bacteria-Based Gene Therapy and Oncolytic Products Guidance for Industry
No pretending they didn’t know, this paper is six years old.
I’ve yet to see any proven limit to the shedding. Rumour has it they may stop after 2-4 weeks post each injection but this is unlikely. We know people have been producing spikes some 5 months later, so I’d wager eternal production that tapers off. This could be a straight AIDs.
See sections VI and also page 15.
“Shedding of such products may be intermittent and unpredictable”.
“higher potential for recombination or reversion in the patient, the shedding pattern and/or what is shed may change”
They’re supposed to already know, among other things:
“The duration of shedding, including the first and last day of shedding, and the peak period(s)”
Page 16 notes they need to study:
“• Whether the shed product was determined to be infectious.”
Watch the cop out:
“Because transmission to untreated individuals is an extremely low probability event,”
that is opinion, not fact
the point of science is checking
“monitoring such individuals for transmission is usually not required during the clinical
development of a product. However, if there is a potential for transmission, additional”
like a gain of function spike? That potential?
“data will be needed to assess that possibility; in which case, we recommend that sponsors
consult with OCTGT in connection with developing a monitoring plan.”
Monitoring. Not stopping. That’s it. And it’s probably why some of them were given placebo and saline. The shedding group?
“Conclusions The risk of miscarriage varies greatly with maternal age, shows a strong pattern of recurrence, and is also increased after some adverse pregnancy outcomes. Miscarriage and other pregnancy complications might share underlying causes, which could be biological conditions or unmeasured common risk factors.”
That’s important, write that down.
aka if you go Third World and force women to start breeding too early, they’ll be more likely to miscarry healthy children in future. Mother Nature hates r-types.
“Results There were 421 201 pregnancies during the study period. The risk of miscarriage was lowest in women aged 25-29 (10%), and rose rapidly after age 30, reaching 53% in women aged 45 and over. There was a strong recurrence risk of miscarriage, with age adjusted odds ratios of 1.54 (95% confidence interval 1.48 to 1.60) after one miscarriage, 2.21 (2.03 to 2.41) after two, and 3.97 (3.29 to 4.78) after three consecutive miscarriages. The risk of miscarriage was modestly increased if the previous birth ended in a preterm delivery (adjusted odds ratio 1.22, 95% confidence interval 1.12 to 1.29), stillbirth (1.30, 1.11 to 1.53), caesarean section (1.16, 1.12 to 1.21), or if the woman had gestational diabetes in the previous pregnancy (1.19, 1.05 to 1.36). The risk of miscarriage was slightly higher in women who themselves had been small for gestational age (1.08, 1.04 to 1.13).”
LOWEST of all ranges in the mid-late 20s, which, per The World We Have Lost, happens to be the age our wiser medieval ancestors commonly married and commenced reproduction. Almost like they didn’t want their wife to die?
You can’t expect modern medicine to bail you out of degeneracy.
And forcing a woman to start “too early” (really before the pelvic growth plates fuse at 21) makes it more likely your later heirs will be miscarried too. No blaming the woman for your own impatience.
All those described factors sound r-selected, especially the C-section, which doctors shouldn’t be forcing women into for convenience. These are your future kids they’re risking.
This study isn’t precise enough because they try to dodge the teen death issue but here
“Figure 3 shows the age related risk of spontaneous abortion stratified by parity status and number of previous spontaneous abortions. The association between spontaneous abortion and age was similar in all strata, although the level increased with increasing number of previous spontaneous abortions.”
Similar. It isn’t a huge difference by age alone like you falsely claim, stop being dumb. However….
if we look at marriage survival against IQ (linked to years ago) and cross-reference the J-curve beneath, delayed motherhood (sufficient time to educate) is healthiest for society in terms of infant survival and marital longevity. Divorce is lower in high IQ women, who tend to marry later, which we can lump into the No Shit category.
Fridge horror: The early marriage of the poor CAUSED a lot of their baby deaths! aka The Oven Ain’t Done Yet!
Pedos reee but nature hates them to breed. They’re extreme r.
“The incidence of spontaneous abortion varied according to a woman’s parity and number of spontaneous abortions in the preceding 10 years; among women aged 25-29 years spontaneous abortion occurred in 8.9% of nulliparous women and 9.3% of parous women without a history of spontaneous abortion, in 12.4% and 11.8% of those with a history of one spontaneous abortion, and in 22.7% and 17.7% of those with a history of two spontaneous abortions. After three or more spontaneous abortions, the proportion of pregnancies ending in spontaneous abortion increased to 44.6% in nulliparous women and 35.4% in parous women.”
Personal history and then family history are more important than age. Men need to get this through their thick skull. This is like the IQ and beauty versus popularity and personality divide. A man who praises his wife’s ‘nice’ personality is admitting her ugliness. She isn’t docile, she doesn’t respect you. If we plan to outlive a man, what does his opinion matter? ‘Nice’ is a quality of puppies, not a viable sexual partner. Your level is the best woman you can get – and keep. Men forget the second part. Cheating on a great wife to lose her is stupid.
Widows were hot commodities because they had proven fertility. Especially great if their husband was stoned to death for adultery, so she’ll be quite young.
Do you want to bet on the horse that has won races or never raced?
If marrying a woman at the proper time, with no personal fertility history, ask about the oldest aunt of theirs who had kids.
Ideally, you’d hear 40s for a firstborn. Those are top-tier genes, especially if the child was perfectly healthy. No genetic load. Miscarriages are common though (about 10% under ideal conditions) and hard to tell early on so it isn’t an exact science. It’s odds, it’s probability. So it isn’t so much age, it’s familial genetic load of mutations compounded by time, it only seems like age. The mutations already in their DNA (and higher in men because sperm constantly need to renew) simply become more of what they already are.
The IVF people do not want normie people to discover the simple ways to ensure better fertility health, they’d go out of business if we had a simple eugenic questionnaire prior to marriage e.g. period frequency. Also, miscarriage is actually good if very early because print error kids get expensive. That’s a sign the body is doing what it should, miscarriages aren’t all created equal, only most are bad.
In future we could probably devise a spiteful mutant test prior to marriage. Very Gattaca. On second thought, that might actually be what the test was. Ks approve.
Obviously with age the mutants (only one parent need be) become more apparent, and this also determines things like aging facial bone structure too, but it isn’t CAUSED by age, it’s their genome!
Age is not the true variable, the confound is mutation burden in your DNA (inc germline). Age can estimate on a population level but I implore you, on an individual one, speak to the family for same-sex history up to cousin level, there’s a reason doctors ask about it! It allows them to adjust their predictions without prejudice.
In general women have less abortions young because 1. it counts the healthiest time to breed, the twenties, which conceals the brief increase in the teens, 2. white women conceal the worse stats for non-white women while still a technical majority and 3. they’d have less time to experience anything, there’s been less time alive. This assumes they’re even having sex. Age is a poor metric. Ask about Aunt Meryl with the four kids after 30. You may strike gold and the woman has twins in the family.
Miscarriage is a J-curve by age, NOT linear. Younger is not automatically better, learn maths dudebros.
Then we isolate the J-curve with no history:
Gee, why don’t the socialists encouraging teen pregnancies tell you this in Sex Ed class?
For my next trick, because I’m that bitch, compare the teen miscarriage line to other young women? [young being prior to middle-age, for women approx 40s]
It’s data from 1,221,546 pregnancy outcomes in a white country.
The mid-30s miscarriage risk is the same for that woman as a teen with the same history.
It’s a deeper 20s scoop if both example women had a miscarriage history of one.
Data doesn’t care about your deviance, pedos.
Mother Nature hates you. So those data-ignorant “dusty egg” jokes of mothers in their 30s should logically be applied to ‘teen whore’ types too. If you were being logical, which we all know you aren’t. Teen mothers (and fathers) also tend to have lower IQ, which suggests spiteful mutant. The data lines up perfectly.
They don’t really ‘believe’ in starting prematurely, it’s their life history strategy talking.
They feel a need to breed immediately because they know they’d likely miscarry if they waited like a K-type. Suck it?
“In women with no history of spontaneous abortions we found a slightly lower overall risk of spontaneous abortion among nulliparous women than parous women (10.0% v 11.6%). This tendency was found in all strata of age except for women aged 40-44 years. “
Again, actual women’s middle age. You’d expect that. The system is shutting up shop.
It’s slightly better to have had NO abortions than ONE. Duh? I think women would agree. So if that one spontaneous abortion would be likelier in the teens, should a fertility-oriented high IQ society encourage teen pregnancy?
The answer is clearly no.
And the Middle Ages Western Europeans were smarter than current America.
And you wonder why the white birth rate is so, so low.
“Among women with a history of spontaneous abortion, the reverse tendency was observed; in general, nulliparous women had a higher age specific risk than did parous women (fig (fig33).”
Stop getting this wrong. We need to avoid spontaneous abortions (miscarriages) to increase the birth rate. You can’t throw conceptions at the wall to see what sticks.
That’s a male perspective on women’s bodies and it’s demonstrably, mathematically wrong.
Not to mention stressful on the longsuffering wife.
Teens (biological children) have a higher pregnancy risk than adult, mature mothers:
“Under the assumption that only 80% of women with abortions in recognised pregnancies were hospitalised the risk of spontaneous abortion would be: 12-19 years, 13.3%; 20-24, 11.1%; 25-29, 11.9%; 30-34, 15.0%; 35-39, 24.6%; 40-44, 51.0%; and 45 or more, 93.4%.” that’s :-
Minor: 13.3% natural abortions
20s: 11.5% natural abortions
30s: 19.8% natural abortions (average, more variation)
40s: basically at least half. You’d need top tier DNA to survive that.
So stop lying, pedos. Call yourself hebe all you like, a POS by any other name.
This doesn’t factor in the mental trauma of giving birth, PTSD is quite common, discounting obvious cases like episiotomies without cause and C-sections with no pain relief. It happens.
Obviously, traumatising your teenage girls will put them off breeding altogether.
Then what happens to your precious ego birth rate?
The teen ectopic pregnancy rate also peaks in the teens comparable to a near-thirty year old.
DAT J-shape curve.
You mad, pedos?
Wait, there’s more!
Now onto stillbirths:
The rate for minors (teens) peaks at the same level as women in their late 30s.
That’s gotta hurt.
Good luck with your scientism though.I’m sure 1M+ white births are lying.
DAT 20s dip:
and it’s fractions of a percent, hardly apocalyptic is it? They’re such special snowflakes with the bloody victim complex.
“The association between maternal age and stillbirth showed a J-shaped curve, but the effect of age was less than for spontaneous abortions and ectopic pregnancies (fig (fig5).5). When restricting the analysis to nulliparous women, we found an identical pattern, although the level was slightly higher. The proportion of stillbirths was substantially increased in teenage pregnancies and was at the same level as for the 35-39 year age group. The incidence of stillbirth was unchanged during the study period.”
I’d also like to see a subdivision of dead babies risk in teen/minor mothers by aged daddy. Maybe next time. I covered paternal age generally beforehand anyway.
It’s funny that the paper writers still try to make it about age though. Nice try. Miscarriage is the biggest factor in future fertility according to their actual data, age is more important for niche risk of ectopic and stillbirth, but less so. And most importantly, NONE OF THIS IS LINEAR. NONE OF IT. The curve is a J. Redpills read the data. I don’t care what the researchers claim to get gibs, read the data itself. It is a non sequitur to claim older = worse outcomes and also a non sequitur to claim younger = better outcomes when the data doesn’t show that, it blatantly shows the opposite, a kind of Goldilocks effect in the 20s.
To put this all on increasing age is false reasoning, as shown, it’s increasing mutant burden. Age is a vector of genetic load, not the cause. Like – Being in a car is a vector of drunk driving, it isn’t the alcohol!
But they wanna get cited so…. they’ll twist their own data. Or try? God forbid anything be genetic, even reproduction!
nb “The increase in risk of ectopic pregnancies in teenage women is most likely caused by pelvic inflammatory disease.”
Teenagers are not women but k. And that’s wrong. The female human reproductive system takes time to fully develop. r/K explains this. Inflammation takes years, it’s literally impossible to blame that or 20s would be still higher.
“The risk of stillbirth was found to be high among teenagers, as previously reported.24 This may be a result of unfavourable social and behavioural conditions among pregnant teenagers, although a biological explanation cannot be excluded. The risk of stillbirth among women aged more than 35 years was increased but to a lesser extent….”
Our study shows an important increase in the risk of spontaneous abortion and other types of fetal loss among women aged more than 40 years”
Middle-age, then? Duh? The body’s aborting print errors like it should?
Yeah because like I said about the r/K system starting up, it also takes years to wind down?
Why aren’t you getting this?
“increase is already considerable among those in their 30s.”
no it isn’t data varies too much in that decade so you cannot accurately comment
“This increase is observed irrespective of a woman’s reproductive history.”
but that’s the bigger effect size? it’s the objectively more important factor?
Can’t hurt feels or lose those IVF shekels, huh?
The effect is still there but that’s a curious omission of scale.
“For society, such findings would indicate that tendencies to postpone pregnancy increase the overall incidence of fetal loss and possibly the costs of health care.”
ooooh they’re pushing teen pregnancies
“overall” POPULATION is not filial risk (personal risk)
filial risk is genetic, kin based
socialists shouldn’t be allowed to science
postponing in a K-select manner is MATURING
higher actual birth rate, higher maternal safety, higher child survival
healthier children! higher IQs!
WHAT IS THE DOWNSIDE
= fewer r-types, I weep!
“these factors are highly correlated” = NOT CAUSATION
for the reproductive equation, you must include the age of BOTH parents at conception
That’s the genetic equation of causation. Single parents are not up for discussion here, they didn’t impregnate themselves?!!
12-19 (minor/teen) pregnancies, not aborted: 51,132.
That’s a huge dataset of adverse pregnancy outcomes. How will the hebes recover?
According to a study that examined how informed consent is given to COVID-19 vaccine trial participants, disclosure forms fail to inform volunteers that the vaccine might make them susceptible to more severe disease if they’re exposed to the virus.
The study,1 “Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Disease,” published in the International Journal of Clinical Practice, October 28, 2020, points out that “COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were not vaccinated.”
They don’t want a control group showing them up.
“Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the development and testing of these vaccines suggest a serious mechanistic concern: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralizing antibodies), be they composed of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE),” the paper states.
“This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-19 vaccine trials that adequate patient comprehension of this risk is unlikely to occur, obviating truly informed consent by subjects in these trials.
The specific and significant COVID-19 risk of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, as well as those being recruited for the trials and future patients after vaccine approval, in order to meet the medical ethics standard of patient comprehension for informed consent.”
As noted by the authors of that International Journal of Clinical Practice paper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious concern: The vaccines have a tendency to trigger antibody-dependent enhancement.
HERE WE GO HERE WE GO HERE WE GO
What exactly does that mean? In a nutshell, it means that rather than enhance your immunity against the infection, the vaccine actually enhances the virus’ ability to enter and infect your cells, resulting in more severe disease than had you not been vaccinated.2
This is the exact opposite of what a vaccine is supposed to do, and a significant problem that has been pointed out from the very beginning of this push for a COVID-19 vaccine. The 2003 review paper “Antibody-Dependent Enhancement of Virus Infection and Disease” explains it this way:3
“In general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of ways. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This activity is known as antibody-dependent enhancement (ADE) of virus infection.
The ADE of virus infection is a phenomenon in which virus-specific antibodies enhance the entry of virus, and in some cases the replication of virus, into monocytes/macrophages and granulocytic cells through interaction with Fc and/or complement receptors.
This phenomenon has been reported in vitro and in vivo for viruses representing numerous families and genera of public health and veterinary importance. These viruses share some common features such as preferential replication in macrophages, ability to establish persistence, and antigenic diversity. For some viruses, ADE of infection has become a great concern to disease control by vaccination.”
Recently bought some nice funeral outfits for myself, so that’s nice…. hope I don’t need them. Pray. Literally.
Of those, the four best vaccine candidates were then given to ferrets, which are the closest analogue to human lung infections. In the video below, which is a select outtake from my full interview, Kennedy explains what happened next. While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, once they were challenged with the wild virus, they all became severely ill and died.
ALL OF THEM DIED
But what about humans, I hear you ask?
“They tested it on I think about 35 children, and the same thing happened,” Kennedy said. “The children developed a champion antibody response — robust, durable. It looked perfect [but when] the children were exposed to the wild virus, they all became sick. Two of them died. They abandoned the vaccine. It was a big embarrassment to FDA and NIH.”
Instead of preventing viral infection, binding antibodies trigger an abnormal immune response known as “paradoxical immune enhancement.” Another way to look at this is your immune system is actually backfiring and not functioning to protect you but actually making you worse.
In an April 2020 Twitter thread,6The Immunologist noted: “While developing vaccines … and considering immunity passports, we must first understand the complex role of antibodies in SARS, MERS and COVID-19.” He goes on to list several coronavirus vaccine studies that have raised concerns about ADE.
In other words, if the vaccine does not result in a robust response in neutralizing antibodies, you might be at risk for more severe lung disease if you’re infected with the virus.
And here’s an important point: COVID-19 vaccines are NOT designed to prevent infection. As detailed in “How COVID-19 Vaccine Trials Are Rigged,” a “successful” vaccine merely needs to reduce the severity of the symptoms. They’re not even looking at reducing infection, hospitalization or death rates.
NHS data: lol nope
This could end up being important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also caused by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually be at increased risk for severe COVID-19 after vaccination, and only those who have already recovered from a bout of COVID-19 would be protected against severe illness by the vaccine.
On top of all of these concerns, there’s evidence showing the elderly — who are most vulnerable to severe COVID-19 — are also the most vulnerable to ADE. Preliminary research findings14 posted on the preprint server medRxiv at the end of March 2020 reported that middle-aged and elderly COVID-19 patients have far higher levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.
DS: Looks kinda convenient for the depopulation people, dunnit?
Ironically, the data17,18,19 we now have no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the age of 60.20 If you’re under the age of 40, your risk of dying from COVID-19 is just 0.01%, meaning you have a 99.99% chance of surviving the infection. And you could improve that to 99.999% if you’re metabolically flexible and vitamin D replete.
To circle back to where we started, participants in current COVID-19 vaccine trials are not being told of this risk — that by getting the vaccine they may end up with more severe COVID-19 once they’re infected with the virus.
In closing, consider what this PNAS news feature states about the risk of vaccine-induced immune enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offer the most:21
[since the 60s, they knew]
Some animals or people who received the vaccine and were later exposed to the virus developed more severe disease than those who had not been vaccinated. The vaccine-primed immune system, in certain cases, seemed to launch a shoddy response to the natural infection …
This immune backfiring, or so-called immune enhancement, may manifest in different ways such as antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to aid infection; or cell-based enhancement, a category that includes allergic inflammation caused by Th2 immunopathology. In some cases, the enhancement processes might overlap …
Some researchers argue that although ADE has received the most attention to date, it is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-19, given what is known about the epidemiology of the virus and its behavior in the human body.
‘There is the potential for ADE, but the bigger problem is probably Th2 immunopathology,’ says Ralph Baric, an epidemiologist and expert in coronaviruses … at the University of North Carolina at Chapel Hill.
In previous studies of SARS, aged mice were found to have particularly high risks of life-threatening Th2 immunopathology … in which a faulty T cell response triggers allergic inflammation, and poorly functional antibodies that form immune complexes, activating the complement system and potentially damaging the airways.”
VAERS data released today by the CDC showed a total of 491,218 reports of adverse events from all age groups following COVID vaccines, including 11,405 deaths and 48,385 serious injuries between Dec. 14, 2020 and July 16, 2021.
Data released today by the Centers for Disease Control and Prevention (CDC) included a total of almost 500,000 reports of injuries and deaths, across all age groups, following COVID vaccines — an increase of 27,761 compared with the previous week.
Comment: Historically, any other medication capable of inflicting this much damage would have been taken off the market and blacklisted by now. To continue to push this agenda onto children, the most vulnerable in society, is nothing short of evil.
Chris Whitty, England’s Chief Medical Officer, has warned that we may have to lock down again within weeks if hospital admissions continue to rise. Professor Neil Ferguson has said we could be facing a “significant flu epidemic” in the coming months because the lockdowns so successfully suppressed it last winter that the NHS risks being overwhelmed now.
DS: good excuse for ADE, TIS BUT THE FLU
“We couldn’t get away with it in Europe, we thought,” said Neil Ferguson, referring to the imprisonment of healthy people in their homes in China in February, 2020, “and then Italy did it. And we realised we could.”
If we don’t make use of our freedoms, if we don’t again leave our homes when we want, meet up with whoever we choose and move around masked as we will, we’ll be telling the government they can reimpose restrictions whenever their chronically mismanaged NHS is under strain. Which is every winter, forever.
When Matt Hancock announced the rollout of the vaccine programme, he claimed we could “cry freedom” when the most vulnerable groups in our society had been vaccinated. With two-thirds of the adult population now double jabbed, we’ve long passed that milestone.
DS: imagine in this year of our Lord, expecting an honest politician. Then it truly is the ACoofalypse.
If they stopped testing for covid, swab PCR tests ramped up to 35-40 cycles with maybe 50% false positives, and people go to hospital for other things like a sprained ankle or car accident, no covid symptoms, get PCR test oh and another official covid case to go crazy about despite covid deaths in UK near record lows. Get rid of covid testing and this whole thing disappears.
BOYCOTT EVERYTHING….. Save some cash.
It’s a doorway into your system for what is yet to come. This one is just to crack the door open and lay a foundation.
A restaurant in Huntington Beach, California is requiring that patrons show proof they’re unvaccinated before they can receive service.
The report comes amid a Tuesday admission by the Biden administration that vaccinated people can still contract and transmit COVID – while the Daily Mail reported last week that one fully-vaccinated Australian man infected at least 60 people in a single weekend.
DS: there’s the purpose.
I realize this restaurant is probably making a political statement, but the irony is that they are also making a good medical choice. The vaccinated are dangerous to themselves and others.
That won’t be what happens. It’ll be like the SARS mRNA vaccines these things were based on, where, in clinical trials, 400 out of 2500 participants were diagnosed with massive terminal cancer throughout their bodies, 18 months later. I bought the medical white papers showing all this stuff that “they” don’t want you to know, but it’s there for anybody who cares to dig deep enough, and shell out a few bucks here and there. I’ve been having “I Am Legend” style nightmares about this every night for months.
If you are not free to make your own medical choices the rest of life is obviously meaningless.
No multi-year trials (what if three years from now the human landscape resembles the opening of I am Legend?)
Keep those viral shedding compliant hoi polloi away from the critical thinking population that will survive this attempted extermination
Since we know now that a vaxed person is actually a super spreader then it’s high time for the Fema camps to come online and take over.
DS: I do sense a twist.
It’d be a great way of getting the obedient drones out of the way that can be replaced with robots.
The r-type smugly bragging about killing people legally.
‘Honestly, I have no idea how many people I infected, I came into contact with so many it could be hundreds,’ he told Daily Mail Australia.
‘Everyone in Australia is complaining [about lockdowns]? At least the government is protecting people.’
LOL natural slaves
Those who chose to not vaccinate clearly have not read any history of the past 500 years. At one time London was having a pandemic every ten years. Pandemics exist to increase the quality of human beings and mother nature is smarter than the rest of us. They have been expecting a pandemic since the last one in 1918. 20-40 million died and that was when less travel but the soldiers after the first world war brought it home with them.
Spanish Flu caused the vaccinated to drop dead, actually. Hence the young age of death.
“It might sound strange, but its true, this remedy has been passed around the feminist community since the 70’s, appearing in many grassroots publications, some of which are cited here. There are also numerous reports of women using it successfully from this era, I’ve heard many stories, but never saw any kind of documentation, which isn’t surprising in a time, where a woman’s right to choose an abortion and have access to safe legal abortion services was just being won.”
Great for ye olde days of gang rape though. Useful if the Red Army comes around town. Abortion does make sense where continuing would kill the mother so there is an ethical grey area e.g. ectopic. I acknowledge that. We also must know what kills a baby so all mothers know to AVOID it. This is why keeping women ignorant leaves them vulnerable to such evil. Parts of nature hate us. Wiccans are imbeciles.
This is why I don’t supplement liposomal Vitamin C, as I suggested for OLDER people.
“The scientists who conducted the research, Samborskaia and Ferdman came to the conclusion that high doses of Ascorbic Acid appeared to increase estrogen levels which contributed to the interruption of an otherwise normal pregnancy. 20 women who approached doctors requesting an abortion participated in the study. Research was conducted by ob/gyn L.I. Ivanyuta. The women ranged from 20 to 40 years of age. The article does not say if a positive pregnancy test was obtained from the participating women. We also don’t know how much ascorbic acid the women were given. They did however measure estrogen levels before and after treatment with ascorbic acid, finding that estrogen levels were higher after taking the ascorbic acid. Of the 20 women, 16 began menstrual type bleeding within 1 to 3 days from administration of ascorbic acid.”
It makes giving kids lemonade real sinister. Mountain Dew, Sunny D, the works.
“Vitamin C works to produce an unfavorable climate within the uterus so that the egg does not implant, or if implantation has already occurred, Vitamin C can weaken the fertilized ovum’s grip on the uterine wall. Possibly by stimulating estrogen, and interfering with progesterone. This also makes it useful as an emergency contraceptive, when taken before implantation occurs on the 6th day following ovulation. The hormone, progesterone is essential for pregnancy, its function is to prepare a nourishing bed for the fertilized egg, if there is not enough progesterone the uterus becomes less supportive to the egg. Which is desirable when the goal is to end pregnancy.”
Progesterone means pro-gestation. Anything that reduces that and/or increases oestrogen causes miscarriage, including xenoestrogens. BPA also causes genetic defects inc. Downs, and can cause abnormal egg development in a female fetus, which can go on to experience many miscarriages (modern rates?) and Downs children themselves.
Also NO parsley. Yes, it kill babies. Viva Italia some other time. Can be used to induce labour, ironically.
History will view the use of xenos as pure evil*. I think endometriosis is caused by it, like a poisoning. Explains the miscarriage common to it. Most common cause of infertility in women. Pure progesterone creams hard to come by, easier to patent a toxic variety close enough. Even pure creams can include preservatives that are oestrogenic! Vegan love of vit C may cause vegan menopause, imho. Xenos also cause premature puberty in girls as young as ONE, especially seen in high-estro skin products used by American blacks and not found in African ones. Xenos (including hops in beer**) also cause a small penis and breast development in boys/men. This shit should be BANNED forever in all skincare vehicles (10x more potent, bypassing liver filter). The amount required (parts per billion) is rarely tested for but maintains estrogenic effect at this level. Parabens were disused in some products due to this. Others like SLS and phthalates also. It isn’t hype, it’s killing men/women hormonally and babies silently. A silent killer in shampoo, lotion, food etc. No wonder American rates of miscarriage are so high. Test ALL skin products for endocrine disruption, especially those that break down into it (XENOS), in rats. Xenos can bio-accumulate for decades in the body (heard of DDT?) and stay for decades too. I share this hoping people won’t abuse the info.
*file under Molech
**how Anglos have gotten softer and softer and softer… literally and morally.
Synthetic perfume is also a xeno. Sorry. I’m sad about it too. They’re aiming this at teen girls and boys, who get fat. And in the case of girls, look sexual. The boys look twinkish. I’m sure the traffickers love that.
They blame kids for being fat when they’re hormonally drugged from seemingly everywhere. They cannot lose weight! The environment is too polluted!
Phyto-estrogen can bind protectively and reduce the capacity of xeno to attach. This is limited. It’s less potent but still oestrogenic and thus reduces progesterone. Can detox from the body in a matter of days since it’s natural.
A recent report published in JAMA Network Open revealed that in an analysis 38 semen samples from COVID-19 patients, 6 (four at the acute stage of infection and, alarmingly, two who were recovering) tested positive for the virus by RT-PCR.1 Importantly, at this point, we have no idea whether the actual virus was viable and infectious. Nevertheless, the possibility that this coronavirus could have a pathophysiological impact on the testes was suggested by additional data indicating that active COVID-19 infection dramatically reduced the testosterone-to-LH ratio, suggesting a significant impact on the responsiveness of Leydig cells to LH stimulation.2 In many ways, we should not be surprised by these observations because the blood-testes barrier is known to offer little defense against viral invasion, given the wide range of pathogenic viruses (HIV, hepatitis, mumps, papilloma) that are known to be capable of damaging the testes and rendering the host infertile.
Furthermore, the spike protein that gives the COVID-19 virus its corona is known to target ACE2 (angiotensin-converting enzyme 2), which is highly expressed by several cell types in the testes including Leydig cells, Sertoli cells, and the germ line. As a result of these factors, several opinion pieces have been published already, raising the possibility of testicular damage and infertility consequent to COVID-19 infection.2–4
However, it is also possible that the virus could gain access to male germ cells once they leave the testes, either in the epididymis or following ejaculation. In this Opinion Article, I shall be focusing on this post-testicular route of infection pointing out, for the first time, that the mature spermatozoon has all of the machinery needed to bind this virus, fuse with it, and even achieve reverse transcription of the viral RNA into proviral DNA. Such considerations raise the possibility that spermatozoa could act as potential vectors of this highly infectious disease. This happens in insects5—why not us?
The other side of COVID-19 pandemic: Effects on male fertility
RECONCILE ABOVE WITH
The outbreak of novel coronavirus disease 2019 (COVID-19) has become a major pandemic threat worldwide. According to the existing clinical data, this virus not only causes respiratory diseases and affects the lungs but also induces histopathological or functional changes in various organs like the testis and also the male genital tract. The renin-angiotensin system (RAS), also ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2.
Because the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases. As the COVID-19 pandemic has affected the male genital system in direct or indirect ways and showed a negative impact on male reproduction, this paper focuses on the possible mechanisms underlying the damage caused by COVID-19 to the testis and also other components of the male genital tract.
SO THE SPIKE PROTEIN ALONE TARGETS ACE2, FOUND IN THE BALLS, LIKE URINE* (*THAT PART WAS A JOKE)
and they wanna force all young men to get it
college age men too
and all young women
when other papers cite it might act like an STD?
The male genital system presents high ACE 2 expression therefore, it will be highly important to investigate and clarify the relationship between COVID-19 and the male genital tract.
I’m not even a man but I can feel my lady balls shrink reading that.
If we look at the mechanisms of these changes caused by SARS-CoV-2 in the testis, as mentioned above, this virus uses ACE 2 for entry into the cells through its surface spike (S) proteins. S proteins have two subunits, S1 and S2, which are responsible for receptor recognition and membrane fusion. Studies have shown that SARS-CoV-2 enters into the host cell through the binding of its C-terminal domain of the S1 subunit to ACE 2. Additionally, some studies have reported that the level of autophagy receptor SQSTM1/p62 in SARS-CoV-2 infected cells has increased, suggesting a decrease in autophagy flux.
So, SARS-CoV-2 itself or via ACE 2 can directly induce or inhibit the autophagy pathway to achieve virus survival.
As a result, SARS-CoV-2 may cause male reproductive disorders by regulating the level of autophagy in male germ cells.4 On the contrary, another hypothesis is that testis degeneration in the COVID-19 cases is attributed to an increase in testicular temperature as an indirect effect of the inflammation.5
Do the jabs cause inflammation?
Can spike proteins microwave your balls? Do they nuke your little swimmers?
BUT WAIT. THERE’S MORE.
Another molecule effective at entering the cell of the SARS-CoV-2 is host proteases like transmembrane serine protease 2 (TMPRSS2), which cleaves the viral S protein to induce a conformational change that allows to a fusion of the virus and host cell membranes.34 TMPRSS2 is the key molecule for the successful infection process.35
This protease is more expressed in human tissues than ACE 2; co-expression of ACE 2 and TMPRSS2 has been shown in the testis, endometrium, and placenta. Researchers investigated the coexpression of these two molecules in the testis and accordingly, they found that ACE 2 is predominantly expressed in myoid cells, spermatogonia, Leydig, and Sertoli cells, while TMPRSS2 is expressed in spermatogonia and (elongated) spermatids of the testicular tissue34 (Figure 3).
I warned you about endometriosis-like function. Maybe naturally having endo is protection?
It’s lifelong inflammation. Kinda like cancer. You literally have to cut the tissues out.
Like Fight Club, they’d have to take your balls.
Shocked men aren’t more protective of their bollocks and demanding ONE safety study.
ModRNA has owners. Repossession is plausible, legally.
“Recent studies have reported that SARS-CoV-2 is easily found in human bodily fluids.35 The presence of a virus in a semen sample is still a topic of discussion and research due to the small number of studies. For example, two different studies have analyzed SARS-CoV-2 presence in semen samples and according to these studies, SARS-CoV-2 (+) semen samples were found in two patients from 23 cured patients and four patients from 15 patients in the acute phase. Another study reported that SARS-CoV-2 was not detected in the semen samples of 34 COVID-19 patients.31“
“It is also known that the prostate gland secretes prostate fluid, one of the main seminal components, and muscles of the gland help in pushing the seminal fluid through the urethra during ejaculation.31 The critical point is that, as we mentioned above, a small percentage of the prostate hillock and club cells express ACE 220 and also TMPRSS2 is highly expressed by the epithelium of the human prostate;37 so it is more likely to get SARS-CoV-2 infection, which may affect its secretions.31
These mechanisms could explain the SARS-CoV-2 (+) semen samples of the studies.23“
“If the presence of the virus in semen is definitively proved by studies, assisted reproduction techniques will also be affected. For instance, testing all male patients like HIV or Hepatitis B/C cases, and using appropriate sperm washing techniques, or paying extra attention to sperm freezing for COVID-19 positive patients.35“
“Like SARS-CoV-2, most viruses enter the human body through nasal and oral routes, and viral particles may break the blood-brain barrier.” but don’t worry about shedding?
“It has been reported that the brain cells (glial cells and neurons) also express ACE 2 receptors, making them a possible target to induce neuronal death for SARS-CoV-2. Importantly, the central nervous system plays a critical role in endocrine control and spermatogenesis.31
The Hypothalamic-Pituitary-Gonadal Axis (HPGa) exerts a vital role in reproduction; in other words, HPGa can inhibit the body’s reproductive functions via hormones.31, 38“
We have our mechanism for sterility, people.
Gonadotropin-releasing hormone (GnRH) expressing neurons from the hypothalamus secretes GnRH and it activates the release of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland. A low level of GnRH causes a decrease in FSH and LH, resulting in impaired function of the Sertoli and Leydig cells.31 Ma et al.39 showed that COVID-19 patients had significantly higher serum LH levels but decreased testosterone/LH and FSH levels than healthy men, suggesting potential hypogonadism. Taken together, patients with COVID-19 have been found to present a reduced testosterone/LH ratio, indicating possible subclinical damage to male gonadal function.5 Additionally, activation of the HPGa and subsequent alterations in hormone concentrations play a critical role in poor sperm quality.38
Therefore, besides its direct effects on testis, SARS-CoV-2 may affect fertility indirectly via the central nervous system.31
Like a remote control, for your balls.
In conclusion, all preliminary findings mentioned above suggest that the COVID-19 pandemic affects the male genital system in direct or indirect ways and shows a negative impact on male reproductive health, inducing spermatogenic failure. Additional studies are necessary to answer all the questions and further investigations are warranted, but ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2. As the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases.
The pandemic caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to several hypotheses of functional alteration of different organs. The direct influence of this virus on the male urogenital organs is still to be evaluated. However some hypotheses can already be made, especially in the andrological field, for the biological similarity of the SARS-CoV and SARS-CoV2. As well as SARS-CoV, SARS CoV-2 uses the ‘Angiotensin Converting Enzyme-2’ (ACE2) as a receptor to enter human cells. It was found that ACE2, Angiotensin (1-7) and its MAS receptors are present, over in the lung, also in the testicles, in particular in Leydig and Sertoli cells. A first hypothesis is that the virus could enter the testicle and lead to alterations in testicular functionality. A second hypothesis is that the binding of the virus to the ACE2 receptor, could cause an excess of ACE2 and give rise to a typical inflammatory response. The inflammatory cells could interfere with the function of Leydig and Sertoli cells. Both hypotheses should be evaluated and confirmed, in order to possibly monitor fertility in patients COVID-19+.
Specific genes relating to male fertility have already been found e.g.
Male infertility is a rising problem around the world. Often the cause of male infertility is unclear, and this hampers diagnosis and treatment. Spermatogenesis is a complex process under sophisticated regulation by many testis-specific genes. Here, we report the testis-specific gene 1700102P08Rik is conserved in both the human and mouse and highly expressed in spermatocytes. To investigate the role of 1700102P08Rik in male fertility, knockout mice were generated by CRISPR-Cas9. 1700102P08Rik knockout male mice were infertile with smaller testis and epididymis, but female knockout mice retained normal fertility. Spermatogenesis in the 1700102P08Rik knockout male mouse was arrested at the spermatocyte stage, and no sperm were found in the epididymis. The deletion of 1700102P08Rik causes apoptosis in the testis but did not affect the serum concentration of testosterone, luteinizing hormone, and follicle-stimulating hormone or the synapsis and recombination of homologous chromosomes. We also found that 1700102P08Rik is downregulated in spermatocyte arrest in men.
Together, these results indicate that the 1700102P08Rik gene is essential for spermatogenesis and its dysfunction leads to male infertility.
As the incidence and severity of SARS-CoV-2 are reported to be higher in males than females, Shastri et al. performed a study to determine the time to viral clearance after infection in a total of 68 individuals (48 males and 20 females) with median age of 37 years (Shastri et al., 2020).
They observed that females were able to achieve viral clearance significantly earlier than males.
Furthermore, a serial follow-up evaluation of three families with both male and female patients demonstrated that female members of the same household cleared the SARS-CoV-2 infection earlier in each family (Shastri et al., 2020). In order to determine the reason for delayed clearance in males, they also checked the expression of ACE2 in tissue-specific repositories.
It was found that testicular tissues were one of the tissues showing ACE2 expression in 3 independent RNA expression databases (Human Protein Atlas, FAMTOM5 and GETx). Interestingly, the ovarian tissue showed very low expression of ACE2 (Shastri et al., 2020).
Impact of COVID-19 and other viruses on reproductive health
They admit the male HPV link I posted about previously.
Male infertility is linked to some viral infections including human papillomavirus (HPV), herpes simplex viruses (HSV) and human immunodeficiency viruses (HIVs). Almost nothing is known about severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) effect on fertility. The possible risk factors of coronavirus disease 2019 (COVID-19) infection on fertility comes from the abundance of angiotensin-Converting Enzyme-2 (ACE2), receptor entry of the virus, on testes, a reduction in important sex hormone ratios and COVID-19-associated fever. Recent studies have shown a gender difference for COVID-19 rates and comorbidity. In this review, we will discuss the potential effect of COVID-19 on male fertility and talk about what needs to be done by the scientific community to tackle our limited understanding of the disease. On the other side, we will focus on what is known so far about the risk of COVID-19 on pregnancy, neonatal health and the vertical transfer of the virus between mothers and their neonates. Finally, because reproduction is a human right and infertility is considered a health disease, we will discuss how assisted reproductive clinics can cope with the pandemic and what guidelines they should follow to minimise the risk of viral transmission.
Remember, viral entry via SPs cause inflammation that might cause sterility? WELL-
Virus entry begins when the virus surface enzyme called Spike (S) glycoprotein binds to the angiotensin-converting enzyme 2 (ACE2) located on the host cell membrane (Hoffmann et al., 2020; Wang et al., 2020). S protein contains two different domain regions: S1 and S2, each one has its own role in virus entry. S1 domain is the part that binds directly to the host ACE2 receptor while the S2 domain helps the virus to fuse with the target cell membrane using its functional elements (Glowacka et al., 2011; Hoffmann et al., 2020). This process is also mediated by a Transmembrane Serine Protease 2 (TMPRSS2) located on the surface of the target cell membrane used for the priming of the S protein causing the virus entry (Hoffmann et al., 2020; Shen, Mao, Wu, Tanaka, & Zhang, 2017; Wang et al., 2020).
When the fusion of the virus with the target cell membrane occurs, the virus releases its genome and using the host cell organelles to replicates its RNA and releases new mature virion to target other cells (Boopathi, Poma, & Kolandaivel, 2020; Jiang, Hillyer, & Du, 2020) Figure 1.
wait wait wait the wild virus replicates its RNA too?
minor flex –
3.1 Human papillomavirus (HPV) and its impact on male fertility
Human papillomavirus (HPV) is a non-enveloped DNA virus and sexually transmitted worldwide. In some cases, it causes either warts or precancerous lesions (Ljubojevic & Skerlev, 2014). More than 170 HPV types have been identified and completely sequenced (Chouhy, Bolatti, Pérez, & Giri, 2013). Recent studies suggest that HPV infection affects male fertility. In cases of idiopathic asthenozoospermia, HPV DNA was observed in the sperm cells of infertile patients (Foresta et al., 2010; Lee, Huang, King, & Chan, 2002) confirming its role of infertility. Strong association between HPV infection and impairment of sperm parameters, especially a reduction in sperm motility and concentration, was observed in HPV-infected men (Garolla et al., 2012; Jeršovienė, Gudlevičienė, Rimienė, & Butkauskas, 2019). Garolla and coworkers (Garolla et al., 2012) reported that HPV can bind to the head of a spermatozoon and impair sperm motility in men. Certain sperm DNA exons undergo apoptotic fragmentation on HPV-infected men suggesting that HPV types degrade different exons of important genes (Lee et al., 2002). Collectively, these evidences suggest that HPV plays a role in male factor infertility.
3.2 Herpes simplex viruses (HSVs) and their impact on male fertility
Herpes simplex viruses (HSVs) are enveloped DNA viruses of the family Herpesviridae. HSVs include two distinct viruses HSV-1 and HSV-2 (Whitley & Roizman, 2017). HSVs are sexually transmitted and targets reproductive system. HSV-1 causes oral and, occasionally, genital sores while HSV-2 is common cause of genital herpes which may lead to infertility problems in both males and females. HSV DNA was detected in semen from about 50% asymptomatic infertile males (Amirjannati et al., 2014; Bezold et al., 2007; Monavari et al., 2013; Neofytou, Sourvinos, Asmarianaki, Spandidos, & Makrigiannakis, 2009). A strong association of HSV infection and low sperm count, poor motility, and increased apoptotic cells were reported (Monavari et al., 2013). Haematospermia and a lower seminal volume and abnormal viscosity were found in HSV-2-infected males which indicate prostate dysfunction (Kurscheidt et al., 2018). Bezold et al. (2007) reported significantly reduced sperm concentration and motility as well as reduced citrate concentrations and neutral α-glucosidase in HSV-infected males, suggested impaired epididymal and prostate function.
The manwhore diseases are listed alongside HIV, lol. The wages of sin is death, in men as well as women. How will PUAs recover? They won’t. God Willing.
The concern show that SARS-CoV-2 may affect male reproductive organ and thus results in male infertility stems from several observations. Early studies both in China and Italy showed that males are more susceptible to COVID-19 compared to females (Guan et al., 2020; Livingston & Bucher, 2020).
A recent large cohort observational study from United Kingdom featuring around 20 thousands COVID-19 patients reported that males represented 60% of cases and considered the male sex as one of the risk factors for COVID-19 (Docherty et al., 2020).
DS: MRAs: crickets
More alarming is the result of a new systematic review—included 48 recently published articles and 16 databases—where it found that men are more likely to suffer or to die from the complications of COVID-19 compared to women (Serge, Vandromme, & Charlotte, 2020).
DS: suffer or die? Binary?
Large proportion of these vulnerable males is in their childbearing age, and thus their reproductive ability can be affected.
Finally, like influenza, COVID-19 patients suffer from fever, which may affect sperm production. It was reported that febrile illnesses had an impact on semen parameters (Sergerie, Mieusset, Croute, Daudin, & Bujan, 2007). Total sperm count and motility percentage were reduced significantly at days 15, 37 after fever episode before going back to normal after several weeks (Sergerie et al., 2007). Increase of sperm DNA fragmentation index and alteration in the nuclear protein composition of ejaculated spermatozoon were reported after fever episode (Evenson, Jost, Corzett, & Balhorn, 2000).
Different viruses use different routes to enter into the host cells. SARS-CoV-2 uses the same ACE2 receptor used by its cousin, the SARS-CoV virus, with the help of TMPRSS2 (see Figure 1). Single cell expression analysis has detected the expression of ACE2 RNA not only in the lung epithelial cells, but also in several other organs, among them are the kidneys and the bladder (Fan et al., 2020; Lin et al., 2020; Tipnis et al., 2000). Protein expression analysis also confirmed the presence of ACE2 protein in multiple tissues (Hamming et al., 2004).
Interestingly, the highest expression of ACE2 was found in the testes (Fan et al., 2020). The high expression of the ACE2 receptor in the testes raises a concern that the SARS-CoV-2 has the route to enter some if not all testicular cells and thus could cause damage.
To further analyse the types of testicular cells vulnerable for SARS-CoV viruses, Wang et al. studied single-celled ACE2 expression in the human testes (Wang & Xu, 2020). They found that ACE2 is mainly expressed in spermatogonia, leyding and Sertoli cell, while spermatocytes and spermatids had very low expression (Wang & Xu, 2020). Interestingly, TMPRSS2 expression is similar to ACE2, where TMPRSS2 was also enriched in spermatogonia and spermatids. It has been also shown that ACE2 positive spermatogonia cells express genes that are important for virus reproduction and transmission, while ACE2 positive leyding and Sertoli cells express genes that are required for cell–cell junctions and immunity.
Collectively, these results highlight the risk of COVID-19 on testicular cells and on the spermatogenesis process.
The only direct evidence for the effect of COVID-19 on male reproductive function comes from a study where sex hormones namely testosterone (T), luteinising hormone (LH) and follicle-stimulating hormone (FSH) among others were compared between COVID-19 patients and healthy controls. While the T level was not different between the two groups, the ratio of T to LH and the ratio of FSH to LH were significantly decreased in COVID-19 patients (Ma et al., 2020).
This might be the first direct evidence for the influence of COVID-19 on testicles’ ability to produce sex hormones; however, the results of this study should be followed by a more direct analysis of the seminal fluid of COVID-19 patients to evaluate the effect—if any—on sperm count, volume, morphology or motility. It has been reported that SARS-CoV causes orchitis in addition to other complications (Xu et al., 2006), so it is also possible that SARS-CoV-2 may cause the same complication in males.
Y NO DO THIS ON JABBEES?
And it may kill pregnant women only:
Pregnant women have been shown to be at high risk of comorbidity and mortality related to influenza infections (Rasmussen, Jamieson, & Bresee, 2008; Rasmussen, Jamieson, & Uyeki, 2012). The previous SARS infection showed that pregnant women had higher fatality rate (25%) compared to the general population (10%; Wong et al., 2004). With the rise of numbers of pregnant women and children affected by COVID-19, it is worth to know if pregnant women are a high-risk group for COVID-19 death or increased hospitalisation and also to evaluate the risk of vertical transfer either from the mother to the foetus or from the neonates to the mother.
Neonatal health is another important concern in the COVID-19-infected mothers. In a study from Wuhan, 33 neonates were born to mothers with COVID-19, and no health complications were reported except for shortness in breath in four cases (Zeng et al., 2020). Other studies, including less number of cases, did not report any neonatal health issues except for low birthweight (<2,500 g) and premature delivery (Cao et al., 2020; Chen & Lou, 2020). Two other studies from China and Iran reported two neonatal deaths out of 19 cases studied (Hantoushzadeh et al., 2020; Zhu, Wang, et al., 2020). No cases of miscarriages have been reported in the first trimester of COVID-19 pregnancies. Overall, it seems that neonates delivered by COVID-19 pregnant mothers have no increased risk of clinical complications compared to normal pregnancies and some of the reported neonatal complications could be related to mothers’ overall health status rather than a consequence of COVID-19 infection.
Then why jab them?
The risk of vertical transfer of SARS-CoV-2 between the mother and the foetus is possible knowing that the ACE2 receptor is expressed in the placenta and uterus (Levy et al., 2008); however, most published data do not support this predication as most neonates born for mothers affected by COVID-19 tested negative (Chen et al., 2020; Liu et al., 2020; Yu et al., 2020). A few studies have reported a vertical transfer of SARS-CoV-2 from the mother to the neonates (Hantoushzadeh et al., 2020; Yu et al., 2020), but these studies should be carefully interpreted as they occur less frequently and possibly resulted because of the neonatal exposure to SARS-CoV-2 after delivery.
One way to get you on the hook financially is reproductive tech.
Risk of ovarian hyperstimulation syndrome should be taken very seriously during COVID-19 pandemic crisis and all guidelines clearly stated that reproductive endocrinologists should adopt gonadotropin-releasing hormone (GnRH) antagonist as a default protocol for ovarian stimulation with GnRH-agonist trigger to minimise the risk of ovarian hyperstimulation syndrome (OHSS), hospital admissions and intensive care unit (ICU) occupancy (ASRM; Carugno et al., 2020; ESHRE; JSF).
Isn’t that an endometriosis fertility treatment? Odd. So you’re saying it works?
Many health issues related to COVID-19 have been addressed in this review. Pregnancy and maternal health have been discussed. Many reports have evidences against a direct link between COVID-19 and maternal death. Neonates born to a COVID-19 mothers are not at increased risk of adverse health consequence compared to the ones born for COVID-19-unaffected mothers, and the possibility of viral vertical transfer has not been confirmed. Large cohort studies should be followed to confirm these results; additionally, first-trimester COVID-19 cases should be included and be evaluated for the risk of miscarriages.
The gender difference in COVID-19 incidence, comorbidity and death rates—males are at higher risk—requires prompt actions to understand the source of difference biologically and behaviourally. Viral infection by HPV, HSV, HIVs, HBV, HCV and MuV challenges reproductive health and can be considered as a risk factor for male infertility. These viruses have been detected in semen and can impair testicular function. Some viruses such as HIV, MuV and SARS-CoV are associated with orchitis resulting in male infertility, so it would be interesting to study if SARS-CoV-2 can cause the same problem. Because many males at childbearing age are affected by COVID-19, the high expression of ACE2 receptor in the testes and the association of COVID-19 with fever; a multidimensional andrological translational research project was suggested (Salonia et al., 2020). This project aims to develop international collaboration for data registry, hormonal studies and genomic studies to better understand the sex difference for COVID-19 health-related consequences.
re the endo treatment
GnRH agonists are a group of drugs that have been used to treat women with endometriosis for over 20 years . They are modified versions of a naturally occurring hormone known as gonadotropin releasing hormone, which helps to control the menstrual cycle.
At present, the usual length of treatment with a GnRH agonist is 3–6 months. However, in Germany, 12 months treatment with add-back therapy (5 mg of norethisterone per day) has been approved, and other countries may do the same in the future.
The SARS-CoV-2 spike protein disrupts the cooperative function of human cardiac pericytes – endothelial cells through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease
paper DECEMBER 2020
AKA they KNEW
(they knew and they pushed it on you – and your kids, soon!)
Findings We show, for the first time, that the recombinant S protein alone elicits functional alterations in cardiac PCs. This was documented as: (1) increased migration, (2) reduced ability to support EC network formation on Matrigel, (3) secretion of pro-inflammatory molecules typically involved in the cytokine storm, and (4) production of pro-apoptotic factors responsible for EC death. Furthermore, the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in cardiac PCs.
Accordingly, the neutralization of CD147, using a blocking antibody, prevented the activation of ERK1/2 and partially rescued the PC function in the presence of the S protein.
SO do they permit this treatment to their loyal pets?
I think you’ll find the storms fully operational by the time flu season arrives. AKA Coof Coof Part Two. Satanist humour is killing everyone scared enough of death to get guinea pigged. Great way to sort wheat from chaff actually.
Interpretation Our findings suggest the new, intriguing hypothesis that the S protein may elicit vascular cell dysfunction, potentially amplifying, or perpetuating, the damage caused by the whole coronavirus. This mechanism may have clinical and therapeutic implication.
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.
“We have documented the pharmacokinetics and biodistribution of lipidots, synthetic 55-nm-diameter lipid nanoemulsions with potential applications for diagnostics and drug delivery. After intravenous injection in healthy mice, lipidots are stable in blood and taken up preferentially in liver, adrenals, and ovaries, where they release their lipidic cargo. Lipidots depict an original biodistribution, not previously reported for other inorganic or organic nanoparticles, toward organs involved in steroid hormone synthesis and storage (adrenals and ovaries) and localize to precise sites in these organs, suggesting potential applications for imaging and drug delivery.”
A friend suggested the Pfizer one may be ‘safe’ because rich areas are buying it. That was Boomers avoiding the heart effects reported from AZ, possibly to push them to the others, none of them are safe. Potassium is also used in lethal injections, to stop the heart. It’s in Pfizer. Talk about red herring. Watch deaths from heart disease in, say, the next three years.
In this country, they don’t give you even the illusion of choice, it’s largely based on age and supposed availability. There is no safe one.
The lipids preferentially allow the modRNA to ‘slip into the cell’ of those organs, as the enclosed PDF plainly states.
nb The effects described in Malice or Mistake? in the brain are prion–like, they needn’t be actual prions.
In this study, this study, and this study, it was found that people who were extroverts, outgoing and social had more D2 receptors in their brain (this is an oversimplification of the results. Link is provided for more detailed read.
It has been shown through the science of addiction and fMRI scans that the brain chemistry of the porn addict mimics the brain chemistry of addicts with other forms of addiction. These brain chemistry are characterized by hypofrontality (memory and cognitive impairment) and largely reduced number of D2 Receptors.
Actually, hypofrontality is a nice way of saying retardation since it refers to incomplete development or function. That’s literally what a retard is, the word meaning slow in French.
So they are literally retarding themselves, the wankers.
COMMENTS: First study to show that drug use causes a decline in dopamine (D2) receptors. Important because addicts have a low number of such receptors, which may contribute to addiction. Also shows that receptors can bounce back, but rate is highly variable and not related to baseline D2 receptors.