La imagen es un video en el que se puede hacer clic.
estructura de edad de la población
https://youtu.be/2EvYU-HmsvI
Después de 7 años después de 2015, dedicado a tiempo completo al estudio del envejecimiento y al análisis profundo de la ciencia para desentrañar el empirismo y la erudición, estoy listo para anunciar que tengo una nueva teoría superior y una estrategia sólida para deshacerla. Sé que la parte de deshacer es correcta ya que está validada, aunque no empíricamente por la FDA, por autoaplicación y casi 1000 pacientes durante seis años por
Le creo solo por 1 razón, ha usado la receta en sí mismo y en pacientes (700-1000) durante seis años y tiene informes entusiastas (ahora tiene 78 años, comenzó con 72, se sintió bien después de 3 meses). Además de la autoaplicación, considera que los matemáticos y los informáticos, no los biólogos y los médicos, son mucho más adecuados para el envejecimiento. ¡Qué hallazgo milagroso para mí!
Todos los demás que no puedan demostrar que estoy equivocado, incluidos los tribunales, la policía, etc., y en particular los médicos, ¡váyanse al infierno! Lo pruebo yo mismo, aquí o en el extranjero. Continuaré con los médicos que me creen, para lanzar la terapia de envejecimiento en el lateral, con objetivos inmediatos de singularidad 1.0.
Mi teoría es la teoría composicional del envejecimiento: recopila varias teorías del envejecimiento como correctas al mismo tiempo, tal como lo prueban los relojes de ADNm, y refleja el envejecimiento de diferentes sistemas corporales, de 3 clases amplias que se programan de arriba hacia abajo para detener los efectos de mTOR , de abajo hacia arriba en torno a los factores de Yamanaka y la adversidad saludable como la restricción dietética, y la extensión de los telómeros basada en el uso de oxígeno hiperbárico intermitente. Creo en términos teóricos que los métodos mTOR de arriba hacia abajo y los métodos de Yamanaka de abajo hacia arriba se pueden reutilizar varias veces y tendrán una prioridad mucho mayor. La extensión de los telómeros rara vez será material.
Envejecimiento hiperfuncional: quién ordenó el envejecimiento humano (aparte de un dios jodido)
https://youtu.be/hyXH_m5a3NE
Comprender la evolución del envejecimiento en humanos: el envejecimiento es uno de los grandes logros de la biología. Entre vertebrados; peces, anfibios y reptiles tienen NS de senescencia insignificante. El problema con NS es que los animales pueden descubrir cómo vivir demasiado tiempo. Este es un problema en un mundo cambiante y dificulta la evolución de nuevos rasgos porque la cría y el acervo genético están entonces dominados por animales mayores y más grandes dentro de la especie, en particular los campeones de la cadena alimentaria. Este problema fue resuelto por los mamíferos recién llegados hace unos 180 millones de años. La solución fue matemática pura. Los animales crecían rápido, se reproducían durante algunas generaciones y luego morían. El efecto de poda de la muerte de animales mayores brindaría espacio para que la nueva generación prospere y tenga el potencial de introducir variaciones genéticas favorables. El problema era que los animales se habían vuelto demasiado buenos para descubrir cómo vivir mucho tiempo. La solución fue una píldora venenosa integrada en el código genético. Los animales con la píldora venenosa de repente comenzarían a envejecer y morirían. Los animales sin la píldora de veneno vivirían más tiempo y solo sufrirían una muerte estocástica o una muerte no relacionada con el envejecimiento. 180 millones de años después el ganador es claro. Todos los mamíferos terrestres eligieron la muerte senescente y programada. En el pasado, durante 180 millones de años, los peces, reptiles y anfibios se han mantenido insignificantemente senescentes y les ha ido razonablemente bien. Sin embargo, no han cambiado mucho; mientras que los mamíferos han hecho avances extraordinarios.
Comprender el envejecimiento es fácil si su campo son las matemáticas puras o los programas informáticos; sin embargo, parece casi imposible si su campo es la biología. Desafortunadamente, la teoría del envejecimiento fue desarrollada por biólogos y no por matemáticos o programadores informáticos, y el biólogo se equivocó por completo. Hoy en día, una teoría del envejecimiento está dominada por un campo que se autodenomina "Biología del envejecimiento". Su teoría es que el envejecimiento no tiene valor, ningún gen promueve el envejecimiento, y el envejecimiento en humanos es esencialmente lo mismo que envejecer en objetos inanimados, como un zapato viejo o un auto viejo. En resumen, la teoría del envejecimiento se fue por la madriguera del conejo.
Para entender el envejecimiento; compara un cocodrilo de 100 años con un humano de 100 años. El cocodrilo de 100 años es un animal extremadamente robusto; más grande y más fuerte que el cocodrilo de cincuenta años, sin mostrar signos de envejecimiento. Esto está en marcado contraste con un humano de cien años. Los mamíferos terrestres, incluidos los humanos, son animales senescentes, mientras que los reptiles, como los cocodrilos, muestran una senescencia insignificante NS.
La senescencia es un programa de muerte intencional que utiliza el envejecimiento programado. El plan es hacer que los mamíferos se deterioren y mueran. Esto crea más espacio para la nueva generación. La idea es que la nueva generación pueda tener nuevas mejoras genéticas y el objetivo del envejecimiento es eliminar a los animales más viejos para que sus genes no dominen el acervo genético. Todo es un gran plan para desarrollar mejoras genéticas. El plan es pura matemática. Animales sin mucho éxito en el desarrollo de mejoras genéticas a lo largo de los siglos.
population age structure https://youtu.be/2EvYU-HmsvI
After 7 years post, 2015 Full time devoted to the study of Aging and deep analysis of science to unpack empiricism and scholarship, I am ready to announce that I have a new latest superior theory and a solid strategy for its undoing. I know that the undo part is correct since it is validated, though not FDA-empirically, by self-application and almost 1000 patients over six years by
He is believed by me for just 1 reason, he has used the prescription on himself and patients (700-1000) for six years and has glowing reports ( He is now 78, started 72, felt good after 3 months). Other than self-application, he considers mathematicians and computer scientists, not biologists and doctors, far more suited to Aging! What a miraculous find for me!
Everyone else who can not prove me wrong, including courts, police, etc, and particularly doctors - go to hell! I try it on myself - here or abroad. I will continue with doctors who believe me, to launch aging therapy on the side, with immediate singularity1.0 objectives.
My theory is the compositional theory of Aging - collects various theories of aging as being right at the same time as tested by DNAm clocks, and reflects the aging of different body systems, from 3 broad classes being top-down programmed built around halting mTOR effects, bottom-up around Yamanaka factors and healthy adversity as dietary restriction, and telomere extension based using intermittent hyperbaric oxygen. I believe on theoretic grounds that top-down mTOR methods and bottom-up Yamanaka methods can be reused multiple times and will have much higher priority. Telomere extension will be rarely material.
Hyper function aging - Who ordered human aging (other than a fuckedup god)
https://youtu.be/hyXH_m5a3NE
Understanding the Evolution of Aging in Humans: Aging is one of the great accomplishments in Biology. Among vertebrates; fish, amphibians, and reptiles have negligible senescence NS. The problem with NS is animals can figure out how to live too long. This is a problem in a changing world and makes it difficult to evolve new traits because breeding and the genetic pool are then dominated by older and bigger animals within the species, particularly food chain champions. This problem was solved by the newly arrived mammals some 180 million years ago. The solution was pure mathematics. Animals would grow up fast, reproduce for a few generations and then die. The pruning effect of the death of older animals would provide space for the new generation to thrive and have the potential to introduce favorable genetic variations. The problem was animals had become too good at figuring out how to live a very long time. The solution was a poison pill built into the genetic code. The animals with the poison pill would suddenly start aging and die. The animals without the poison pill would live longer and only suffer stochastic death or non-aging-related death. 180 million years later the winner is clear. All terrestrial mammals chose senescent and programmed death. Over the past, 180 million years fish, reptiles, and amphibians have remained negligible senescent and done reasonably well. However, they have not changed very much; while mammals have made extraordinary advances.
Understanding aging is easy if your field is pure mathematics or computer programs; however, it seems to be nearly impossible if your field is Biology. Unfortunately, aging theory was developed by Biologist and not Mathematicians or Computer programmers and the Biologist got it totally wrong. Today, an aging theory is dominated by a field that calls itself, "Biology of Aging". Their theory is that aging has no value, no genes promote aging, and aging in humans is essentially the same as aging in inanimate objects, like an old shoe or an old car. In short, the aging theory went down a rabbit hole.
To understand aging; compare a 100-year-old crocodile with a 100-year-old human. The 100-year-old crocodile is an extremely robust animal; bigger and stronger than the fifty-year-old crocodile, showing no signs of aging. This is in sharp contrast to a hundred-year-old human. Terrestrial mammals, including humans, are senescent animals while reptiles, like crocodiles, show negligible senescence NS.
Senescence is an intentional death program using programmed aging. The plan is to make mammals deteriorate and die. This creates more space for the new generation. The idea is that the new generation may have new genetic improvements and the goal of aging is to remove the older animals so their genes do not dominate the genetic pool. It is all a grand plan to develop genetic improvements. The plan is pure mathematics. Animals not highly successful in the development of genetic improvements over the ages became extinct.
Aging is a way to give animals a relatively fixed life span and then prune them. Aging Is the secret to the success of terrestrial mammals. A poison pill in the plan for genetic improvement.
Forewarned is forearmed. Once you know your body is running an ancient genetic program to kill you; then you have a chance to turn off the death program. Successful anti-aging medicine is about the discovery of pro-aging programs and finding ways to block these programs. The chief culprit is mTOR, particularly mTOR2. All non-critical aging chemicals have an important role - even reducing the main aging has some effects and legacy effects that may not rise to critical but are still implicated in health decline. thus compositional aging means all factors need to be addressed, only duplicated effect producers can be ignored
What is science?
Ultimately. operable definition of science is scholarship constrained to empiricism alone. Pure objective empiricism is NOT science as a collection of chosen unrelated facts is pseudoscience! 99% of well-adjusted viewed intelligent engineers have zero offering in non-specialization orthogonal subjects. I know it well from watching my father who was number 1 in disaster topics but very poor in business subjects, most products, and politics.
A theory becomes science when it correctly predicts an easy-to-see orthogonal subject. As a computer scientist, I add a clever requirement to usual philosophical points, the predicted phenomenon must be a non-polynomial extrapolation to all data used. An interpolation point result can be obtained by standard numerical science methods.
Science must be refutable! It must be empirical. My claim to "LATEST NEW SUPERIOR THEORY and UNDO OF AGING" must be empirically established. Till then, it is a theory, better than all others with documented applications.
Why computer science?
I have no reason advanced by the Good doctor. I state things that are to difficult answer by biologists and chemical scientists. How can one answer completion questions? In other words, collect all methods that are likely to result in bio-age reversal and more important determine the consequences of repeated use of age reversal.
singularity?
For my purposes, I consider Singularity in 4 parts. Everyone is likely to undergo all of them,
Singularity1.0 is an extension of healthspan without the necessary increase in lifespan. There are many reasons for it including the reduction in the severity of chronic age-related chronic diseases and survival to singularity2.0 to enjoy their benefits. It has started, and singularity2.0 is expected to arrive by 2030.
Singularity2.0 is proven to increase a healthy lifespan. Since life-span increases, the singularity3.0 is the point to which the extension is needed. It is likely that singularity3.0 arrive by 2050. There are 8 years to singulrity2.0, all the methods needed are available in the non-proven form, and enough josh is available to reduce the costs of therapies for use by limited-corrupt or advanced states.
Critical to my thinking are societies like India. The fact that India was biological backwaters to 2 years back, but developed vaccines, their huge production, and distribution, speaks volumes about limited corruption, excellent politics, enormous intellectual energy, and advancing commerce. In India, we have, in mythology, the dream of a Ram-Rajya. I have no doubt in my mind that Modi-Yogi will lead to the first Modi-Yogi Rajya which provides the first life, free of the horrors of chronic diseases, and an extended healthy lifespan. There is no doubt in my mind that they will become as central to Indian culture as Ram-Rajya.
Singularity3.0 is expected in 2050. By definition, it will provide a healthy life extension of 1+ years per year for 500 years. You will still die from accidents and murder, but not from senescence. It is not too much to ask since there exist animals without senescence for this goal and trees that live 5000 years. That lifespan is possible for a normally not-unlucky careful person.
Singularity4.0 happens 500 years when brain-download becomes possible. Accident and crime deaths are eliminated then by brain download and redundancy safety. Assuming limited natural effects, one can live for trillions of years and roam the universe without travel boredom despite light-speed limits since traveling photons do not feel the path, and time increment is zero for them!
Singularity5.0 happens trillions of years later. Some smart Ph.D. theses will collectively lay the foundation for exiting the current universe and going anywhere in the multiverse.
Algorithms can solve a problem in top-down or bottom-up manners, like a manager or a scientist. The problem of aging can be understood by top-down hyperfunction, or bottom-up DNA fix errors reduction. From our viewpoint, a body is made up of trillions of identical cells specialized to current existence by folding and unfolds of the DNA.
As time passes, errors in DNA show up in mRNA or the cell even forgets what it is. Either case, it turns senescent and a source of further problems. Cells have other communications too, like commands from exosomes or secretions of hormones. These are in addition to blood-derived chemicals from near neighbors. The exosome makes the sender behave like a hormone production organ. Top-down E5 likely improves stem cells for building senescent cells using exosomes to restart youth-like stem cells frozen from lack of orders.
What is death?
Death is a cessation of function. It is easily understood by analogy with a car going to a destination. After the setup is done, the car goes into a freeway and can drive fast. Near the destination, it exits the freeway to normal speeds. But bio-systems do not reduce speed. The car travels normal roads at a bad speed and winds up dead in an accident. Meanwhile, the car rusts. In most cases, it is totaled. In rare cases, rust gets it eventually. we can draw multiple lines under the process of transport. Disruption can occur in transport due to one of many causes, each with a probability that is itself a function of time, For a car is totaled with about the same speed but rusting death becomes more probable with time. One proof is the nearly constant annual probability of death from all causes past 80.
Unlike Sirutin, AMPk, and igf-1, which reduce aging on a boost, mTOR increases aging and is boosted by every boost in technological evolution. All good modernities cause accelerated aging. They include better food, better communication, screened devices, time savers, you name any modernity and it increases aging, To improve aging, you must fast repeatedly, joint ice-water/steam bath, whole morning shirtless bare chest walk in snow mountain, etc. Healthy adversity is good.
What is hyperfunction solution - 6mg rapamycin every week once. Controls mTOR, has no FDA test yet, can't be wrong given Dr, Green, stupid for all without being his patient, can choose an MD by clicking on the link when there. I suggest boosting Sirutins and AMPk on the side and doing singularity1.0 also. All the other steps are from Dr. Sinclair and ensure health bottom up even as hyperfunction ensures mTOR!
Composition of methods?
There are many processes of Aging. They are all progressing in parallel. One can divide the aging undo methods into 3 classes -
1. small increment in lifespan but larger in healthspan. These include boosts. senolytics. Kennedy. Fahy.
2. some increments in lifespan but substantial healthspan, a limited small number of reuses. Senolytics. Sirtuin and AMPK boost.
#1 is good for singlarity1.0 #2 is good for singularity1/2, and #3 is good for singularity 1/2/3. Being healthy old requires lesser aging fixes, so start early in all methods.
At first view, undo aging and rejuvenation look the same. A very important distinction in my mind is the number of times the procedure work even though both deliver the fountain of youth. A technology delivering either must reduce your bio-age less than what you had before starting. It need not work a second time. or a small number of times. This is captured by my neologisms which attach a version number to rejuvenation to indication of upgraded definitely superior version.
Rejuvenation-1.0 only improves health span, life-extension is marginal. This may lead to next rejuvenation only in improved health span.
Rejuvenation-2.0 improves life-span, extend life-span, at least once. Life extension is seen in reduction of bio-age and increment in grimAge that measures expected demise interval. However the improvement may happen justice or small number of times.
Rejuvenation-3.0 allows significant number of reuses.
As a self-taught aging medicine expert, people do ask me real medicine questions. Rather than be a polite idiot, my response is always “outside my knowledge, here is some info, run it by a doctor, change doctor if different, changing till a doctor gives a persuading reason to disagree. This is because scientific American advice improves on all doctors!
How to Make Smart Decisions About COVID Risk-Benefit
Scientific American asks experts in medicine, risk assessment and other fields how to balance the risks of COVID with the benefits of visiting public indoor spaces
As COVID cases declined across the U.S. in recent months and mask mandates were lifted, more people returned to restaurants, concert halls and offices maskless. But the novel coronavirus’s Omicron subvariant BA.2—which caused another wave in Europe and China—and related variants threaten to reverse that progress here. Earlier this month dozens of attendees (including high-ranking government officials) tested positive for COVID after attending a dinner in Washington, D.C.The safest option, of course, is to continue avoiding crowded indoor activities. But there remains a lot of interest in safely enjoying bars, cafes and other higher-risk venues that offer the benefits of social interaction.
Scientific American asked experts in epidemiology, medicine, risk assessment and aerosol transmission for advice on how to decide which risks we are willing to take. These decisions are based on assessments of personal risk, community risk and exposure risk—and the steps one can take to take to mitigate them. Personal risk refers tothe danger of contracting COVID faced by an individual and the members of their household. Community risk is the current likelihood of encountering COVID among members of one’s community. And exposure risk accounts for the increased chances of catching COVID at a particular venue based on airflow characteristics of the space itself and other people’s behavior.
Here is what experts say about managing these risks while maintaining some of the benefits of public life.
How should a person factor personal risk for severe COVID into their decisions?
The number-one predictor of having a severe case of the disease is age, followed by the presence of comorbidities and immunocompromised status, according to Katelyn Jetelina, an epidemiologist who studies COVID risks at the University of Texas Health Science Center at Houston. Using data from the U.S. Centers for Disease Control and Prevention, she estimates that even vaccine-boosted people ages 50 to 64 are more than 10 times more likely to die from a severe breakthrough case than 18- to 49-year-olds with the same vaccination status. Donald Milton, a physician and clinical researcher who studies respiratory viruses at the University of Maryland, highlights recent research showing that, in households with a person who was infected with the Omicron variant (B.1.1.529) of the COVID-causing virus SARS-CoV-2, 43 to 64 percent of people became infected as well, depending on whether the initially infected person wasboosted, fully vaccinated or unvaccinated. Jetelina cautions that we also need to account for the personal risks of the people with whom we live in our own risk assessments.
In general, people should discuss personal COVID risk with their doctor; it depends, in part, on which medications they take. Ethan Craig, a rheumatologist at the University of Pennsylvania, cares for patients who are immunosuppressed because of disease or medication and studies COVID risks in that population. One such immunosuppressive drug, rituximab, “knocks out your ability to make antibodies against new viral exposures and impairs your ability to make a response to a vaccine,” he says. Craig adds that such patients usually take precautions of their own accord, such as wearing high-filtration N95 masks, and “if anything, I end up having to talk people down sometimes and be like ‘Look, it’s okay to go to the grocery store.’” For some people, however, even this amount of exposure could be considered an unacceptable risk.
How does the risk of dying from COVID compare to the risk of dying from other causes linked to common activities?
Jetelina estimates that, for people between the ages of 18 and 49 who are boosted, the risk of dying from COVID is roughly equal to the risk of dying when someone drives about 10,000 miles. COVID risk goes up substantially with age and with being unboosted or unvaccinated. Thanks to vaccines, infection-induced immunity, therapeutics, better care and other factors, the relative risk of dying from COVID if you catch it is now, broadly speaking, comparable to that of seasonal flu, Jetelina says—but importantly, because you are more likely to catch COVID than flu, the absolute risk remains much greater. Jetelina recommends COViD-Taser’s Relative Risk Tool, a resource funded by the National Science Foundation, that she helped to develop. It compares one’s risk of death from the disease to such risk posed by other activities, including driving. Although it is a research tool, Jetelina says she can “really trust the science and mathematics behind it.”
But Baruch Fischhoff, a professor of engineering and public policy at Carnegie Mellon University and an authority on how to communicate health risks, cautions against using risk-risk comparisons to make choices without fully considering benefits or unquantified risks. Employers may also misuse such comparisons to compel employees to accept certain risks on the job, which is not exactly a choice. Currently, risk calculators provide estimates based on retrospective data and may be unable to reliably weigh long-term complications of COVID.
How should one assess community risk?
There is no perfect way to measure community risk because it would take repeated random testing, so experts use other estimates: daily cases per 100,000 residents, test positivity rates and growth rates. Jetelina recommends using the New York Times’ tracker to look up community transmission for your county. She considers community risk high when there are more than 50 daily cases per 100,000 residents. When the risk is lower than that, Jetelina—a healthy, young boosted person—feels comfortable taking off her mask indoors. “I will say it’s taken a lot of time for me to be comfortable with that,” she says. “Once transmission rates of those indicators start increasing a bit, I’m putting my mask back on.” Others suggest an even lower risk threshold of 10 daily cases per 100,000 residents.
Daily city or county case counts are often an undercount because not everyone is getting tested and home test results are not always reported. As a work-around, health authorities use the “test positivity rate,” or “percent positive”—the percentage of COVID tests reported to public health authorities that were positive. If that number exceeds 5 percent, it is widely considered high risk for community transmission (provided the amount of testing in that area is adequate). But the community sample used to measure test positivity likely includes many people who seek out testing because they are currently experiencing COVID symptoms. So test positivity is typically higher than the infection rates among the people you might encounter in a cafe or grocery store, most of whom do not have any symptoms but could still be infectious.
Still, Robert M. Wachter, a professor and chair of the department of medicine at the University of California, San Francisco, says there is no test positivity threshold that separates “safe” from “not safe” because it also depends on other factors, such as whether the benefit outweighs the risk to you, personally, the number of people you will be exposed to, and the closeness and duration of exposure.
Because of these large uncertainties in test coverage, Gerardo Chowell, a professor of mathematical epidemiology at Georgia State University, prefers to look at the general trend in daily COVID cases, hospitalizations and deaths, or percent positive. “When the trend is going up, you’re seeing the transmission chains expand,” Chowell says. “That means that the reproduction number”—the expected number of secondary infections from each infected person—“must be greater than one. If it is increasing, that’s probably the time when [one has the] highest risk of acquiring COVID in a social setting without a mask,” he says.” Wachter points out that, where available, wastewater surveillance may also give an early indication of COVID trends.
What is known about exposure risk in different settings, such as bars or movie theaters?
Linsey Marr, a professor of civil and environmental engineering at Virginia Tech and one of the world’s leading experts on airborne transmission of viruses, says COVID risk in indoor spaces exists on a continuum. It is believed that reducing the amount of virus inhaled (i.e., the inhalation dose) makes infections less likely or illness less likely to be severe. Marr says one of the riskiest settings is an aerobic exercise studio: if somebody is infected, they are going to be exhaling more virus, and everyone else will be inhaling at a faster rate, too. Breathing heavily produces up to 10 times more aerosol particles that carry viruses than breathing normally, according to Richard Corsi, an expert on indoor air quality and dean of the College of Engineering at the University of California, Davis.
Marr says that talking in bars expels a similar number of respiratory particles as coughing, “so it’s like everyone’s in there coughing together.” Craig uses smoking as an analogy for aerosols exhaled during breathing and talking. In other words, “if a person was smoking in this place, would I be able to smell it?” he says. In movie theaters, there is risk of exposure from those seated immediately around you, but because of limited talking and, typically, a high ceiling, there is a lot more dilution of the air. So such a theater may be less risky than other crowded indoor venues. By that reasoning, museums, big-box retailers and grocery stores with high ceilings tend to be relatively safer as well.
Places with rapid rates of ventilation and filtration—such as some subways—are also much lower risk. The Bay Area Rapid Transport (BART) system in San Francisco Bay, for example, filters the air more than 50 times an hour with “virus-trapping MERV-14 air filters” inside each car. An Italian study of schools found that classrooms with ventilation systems that exchanged air six times per hour reduced infections by more than 80 percent, but many classrooms in the U.S. fail to meet this standard. Corsi characterized current public health recommendations of four to six air exchanges per hour as “a little bit anemic … we can do better.” He recommends owners or managers of crowded indoor spaces, such as classrooms, offices and bars, aim to filter or ventilate with fresh air at rates approaching 12 air exchanges per hour to reduce risks down to the level of an airborne isolation room in a hospital. Not all venues have the resources to do this, but the benefits increase with greater filtration rates, so the closer to this ideal, the better. In places with inadequate ventilation, consider bringing a portable high-efficiency particulate air (HEPA) purifier—or building your own using box fans and high-quality HVAC (heating, ventilating and air-conditioning) filters—to run nearby.
Although the virus is thought to be transmitted primarily through the air, there have been a few documented cases of surface transmission, so it remains a good idea to wash your hands frequently, Marr says.
How can one further reduce the risk of getting COVID from everyday activities?
Getting vaccinated and boosted protects against death, hospitalization and, to a lesser extent, catching and spreading the virus. To avoid infection, Wachter recommends wearing an N95 mask. He has observed that the risk of U.C.S.F. health care workers—himself included—getting infected from their patients while wearing a well-fitting N95 is extraordinarily low. These respirators get close to filtering all of the virus, but they do not filter 100 percent. And if an N95 does not form an airtight seal with your face, it may allow unfiltered air into your lungs. So it is essential to try out and select N95 models that fit and seal to your face without gaps.
What is the risk of taking your mask off in a restaurant or bar to take a sip or bite?
In the 1990s medical researcher Stanley Wiener, then at the University of Illinois College of Medicine, proposed that a person could use respirators to survive aerosolized biological attacks, taking it off briefly to consume food and drink. During the pandemic, many places have allowed masks (or N95 respirators) to be removed while actively eating and drinking. Removing an N95 momentarily for a bite or sip carries “some risk, but I think it’s pretty tiny if you’re exposed for three seconds,” Corsi says, unless an infected person is “right in your face ... and shedding a lot [of virus].” Provided community risk is low or trending downward, Chowell, too, feels comfortable briefly removing his respirator to eat or drink at a party.
What do we know so far about the risk of “long COVID”?
Ranu Dhillon, a physician at Brigham and Women’s Hospital in Boston, who advises governments on infectious disease outbreaks, says he is seeing some patients with “a constellation of different types of symptoms after acute COVID infection,” including young, boosted and relatively healthy people. Wachter cautions that some fraction of vaccinated individuals who get infected—which one study estimates to be around 5 percent and possibly higher—may continue to feel short of breath or fatigued or think less clearly than before. COVID may increase the risks of heart attack, stroke, brain abnormalities or the onset of diabetes. While there have been preliminary studies of the rates of long COVID, including risks of developing cardiovascular complications, Wachter says many of these involved unvaccinated people or infections with variants prior to Omicron. Provisionally, he likens these risks to 20 years of untreated high blood pressure or smoking and points out that one cannot know the risk of long COVID among vaccinated and boosted individuals until long-term studies have concluded, which will take years.
How can we balance these risks with the benefits of socializing and being with others?
According to Wachter, one of the most important factors in overall COVID risk is whether “the person next to me has it.” He acknowledges that if someone is both vaccinated and boosted, it is not irrational for that person to decide that the mental energy and angst of calculating risks and taking precautions is high enough—and the risks of getting sick or dying from COVID are low enough—that they will go back to “living like it’s 2019”—as people in many parts of the country already have. He still worries about the risk of long COVID, though. Milton says that many people “don’t want to wear masks forever” and that we should work to make our built environments better at stopping aerosol transmission. He says people also have to decide whether to wear a high-quality mask when they are around those at higher risk, such as the elderly or immunocompromised, or around other people in general, such as at a party. When community transmission is low, Chowell says he may feel comfortable removing his N95 at parties in some situations, such as to have a drink. “Then you find a way to still interact with people, and they smile back once in a while,” he adds.
Devabhaktuni Srikrishna is founder of Patient Knowhow, a Web site that aims to uncover reliable and easy-to-use information about disease prevention, transmission, causes and treatment. Follow him on Twitter @sri_srikrishna.
First time in my life that I find a massive bug in the thinking of 6 bio-professionals and doctors, writing in a peer reviewed publication with an absurd (to me) conclusion of hard limit on human life of 120-150 years.
Roughly, the paper proceeds to collect all relevant metrics into a vector called DOSI. It then applies Gompertz law to the values. Clearly, a component that diverges must exist.
Gompertz law is basic to life-insurance calculations. It enforces the observation that an exponential risk happens of death after 80. It is an old wrong law. The risk of death is constant per period afterwards, ie a linear risk after age 100. Even that is sufficient to enable the 120-150byear limit. But all the derivations are based on scientific observations absent interventions in centenarians. One immediately nullifies Gompertz law, nothing of it remains!
The Gompertz–Makeham law states that the human death rate is the sum of an age-independent component and an age-dependent component, which increases exponentially with age. In a protected environment where external causes of death are rare, the age-independent mortality component is often negligible.Wikipedia
THE GOMPERTZ-MAKEHAM LAW AND WHAT IT MEANS FOR LONGEVITY
by The Qyral Team
We all want the ability to live longer. Scientists have studied longevity for centuries, looking for the secret to delaying aging. However despite all their research, we still aren’t sure how long humans could live. Is there an upper limit to our lifespans? Or could we become immortal if we figure out the right factors that affect our longevity?
One of the models that researchers use to understand longevity is the Gompertz-Makeham Law of Mortality. This mathematical law helps predict how long a population will live. By looking at people who live beyond this law, we might be able to unlock the secrets of longevity.
The Gompertz-Makeham law says that the human death rate is the sum of an age-related component that increases exponentially, and an age-independent component.
So what does that mean? It’s basically a calculation of how likely we are to die in any given year. Two factors affect this risk. The first is age. As we get older, the chance of dying of an age-related condition increases. However it isn’t just old age that kills us. The second factor covers things like accidents, illnesses, and malnutrition that can affect anybody at any time.
The age-dependent factor is calculated using the Gompertz function. This is an equation named after the mathematician Benjamin Gompertz, who invented it. It was created to show the chances of death based on a person’s age. It was first used by life insurance companies to decide who to insure!
When Gompertz wrote the function, he calculated the chances of dying of an age-related factor were very low during childhood and young adulthood. Then through middle-adulthood and toward old age, the chances of dying of an age-related factor get higher and higher. But after a certain point, our risk factors level off.
Strangely, the very oldest people have a lower chance of dying of many age-related factors than people much younger than them do.
The other part of the Gompertz-Makeham law comes from William Makeham, another mathematician. He realized that the Gompertz function overlooked causes of death that weren’t related to aging. The Makeham term can be adjusted for different risks, including socio-economic and geo-political factors. Things like nutrition, accidents, and diseases. Between Gompertz’s function and Makeham’s addition, they created a model that can accurately predict mortality.
REDUCING THE MAKEHAM TERM
Researchers today know that the Gompertz-Makeham law is very effective at predicting human mortality between the ages of 30-80. The most variable factor of the law is the Makeham term — the factors unrelated to age that still affect longevity.
Before the 1950s, the human mortality rate was much higher. Advances in science, medicine, and sanitation have meant all countries now have lower mortality rates. For instance in 1800, there were 463 deaths for every 1000 live births in the U.S. By 1950, that had dropped to 40 deaths. Today, there are just 7 deaths per 1000 births.
As mortality rates improved, the Makeham term became less relevant to the Gompertz-Makeham law. Under controlled conditions, such as with lab mice, researchers found that the Gompertz function was incredibly accurate all on its own.
What does this mean? It suggests that there is a measurable link between aging and mortality. If we could remove all the other causes of death — accidents, diseases, poor nutrition, and so on — then we could predict our mortality based just on how old we are.
EXCEPTIONS TO THE GOMPERTZ-MAKEHAM LAW
We know the Gompertz function is accurate up to the age of 80. What happens after that time? And what can that tell us about longevity?
The key features of the function are the lower chances of death at the start and end of our lives. Dying of age-related causes before 30 is unlikely because many age-related diseases haven’t had time to appear yet. But it doesn’t make sense that the chances of dying from these diseases slow down in advanced old age.
Scientists call this the “late-life mortality deceleration theory.” This theory says that the very oldest people have a reduced risk of dying in any given year. It’s a controversial theory that not all scientists believe is true. However late-life mortality deceleration has been documented in other animals, especially insects.
Another theory is that our risk of death levels off after a certain point. Beyond approximately 100 years old, our chances of death in any given year are 50/50.
Because the Gompertz function is so accurate, it’s possible that the secret to our longevity lies in the people who live the longest. Why does the function stop working after the age of 80? What changes in people who reach that age? Why can they continue living for much longer? Researchers don’t know the answer to these questions, but there are many studies focusing on the secrets of extreme longevity.
FINAL THOUGHTS
The Gompertz-Makeham law is a reliable model for estimating human mortality throughout most of our lives. However since the 1950s, huge advances have been made in reducing age-independent causes of death. This has brought renewed attention to the age-dependent function of the law. Scientists are now researching ways to uncouple aging from mortality. If we can understand what about getting older causes our deaths, we could unlock the secret to our longevity and dramatically increas