Mark78L

This is a nonsensical response that lacks meaning or context - odd coming from a 'biology expert'. A phase 3 longitudinal study is designed over several years to establish the long-term side effects of a drug or vaccine - or have you forgotten this? Yes here you go: this is from the FDA website (the link is below the quote, which is on page 11) "The number of participants in the current clinical development program is too small to detect any potential risks of myocarditis associated with vaccination. Long-term safety of COVID-19 vaccine in participants 5 to <12 years of age will be studied in 5 post-authorization safety studies, including a 5-year follow-up study to evaluate long term sequelae of post-vaccination myocarditis/pericarditis." https://www.fda.gov/media/153409/download See my previous response regarding a nonsensical comment and context in terms of phase 3 studies looking at long term safety data.

You're view is based on a major misconception: That you can expedite long-term safety testing by simply throwing money and people at the experiment - you can't. The aim of long-term safety testing is to establish safety over, say 3 years, because some long-term side-effects only manifest themselves after a number of years, as may be the case with infertility. For instance, recently Pfizer highlighted there was insufficient data on the myocarditis risk to young children with their covid vaccine, and to fully understand this risk these children would need to be monitored for 5 years. It doesn't matter whether you throw 10,000 people or 1 million people in to a 4 month trial, the data you get will only be for 4 months - adverse effects may not be seen for 2 years in all of these subjects - you cannot expedite human metabolism and latent reactions - time is a standard metric you cannot 'speed up', hence why clinical trials can take up to 10 years, or 6 years minimum. Your analogy presents many fallacies where you conflate a constant (time to reach a destination / time it takes to get long term safety data) with the ability to speed up that constant (police escort in a traffic jam / adding more people and money can speed up time). A better travel analogy would be: In 1066 it would take you 5 days to travel between London and Birmingham by horse on your own (the horse being the fastest mode or transport at the time). Throwing 500 more horse riders at the journey will not make you or anyone else get there any quicker - on average it will still take 5 days. The limiting factor is the fitness of the horse, you may be able to tweak the weight the horse carries (speed of developing a vaccine), but by and large you are restricted by the constant of time and the metabolic requirements of the horse that cannot be changed regardless of money and people thrown at it (this represents the metabolic constant of humans, you cannot increase this rate to reduce the reaction time of the vaccine trial). What exactly is the red herring you are referring to? You haven't rebutted any of my points. In the quote of Arete she does not deal with long-term safety trial data. Please show me the many 'other vaccines' you claim don't have any long term data. The recent Ebola vaccine was rushed through and safety corners were cut, but this still took 6 years to produce. Your claim doesn't appear to have merit. The long-term safety data is usually part of the clinical trial - hence why the PfizerCovid vaccine is still in its trial phase and won't finish till March 2023 - they are actively collating the long-term data because sufficient time has not yet passed to show any long-term data - how then, can it be claimed to be safe, when by Pfizers own admission, through the way in which the trial has been set up (standard trial requirements), the long-term safety part of the trial is still underway? ..."it"... what exactly are you referring to? What is "it" in reference to various vaccines with different efficacy and disease threat ratios?

"Should vaccines be mandated for NHS staff?" I think that entirely depends upon the threat posed by a disease and the safety and efficacy profile of the vaccine. A vaccine proven to be effective at protecting others as well as the recipient, that has a very good safety profile with long term safety data to support it, is very different from an experimental vaccine that does not protect others, has no long-term safety data and has questionable efficacy to boot, and especially where the full trial data has not been released or normal clinical trial protocol followed. The latter example should clearly not be mandatory especially if natural immunity is being ignored - a mandatory vaccine for someone already immune poses a heightened risk to the recipient with little to no benefit for others while ignoring the robust protection a doctor or nurse may have already acquired.

The somatic mutation theory (SMT) is being called into question. After 60 years it has failed to elucidate the specific mutations allegedly required to induce tumour development and cancer progression and fails to explain the vast majority of hallmarks as defined by Hanahan and Weinberg in their 'next generation' update: '...despite 65 years of research on the mutation theory, there is still no proof for even one set of mutations that is able to convert a normal cell to a cancer cell.' https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115917/ '‘...mutations are increasingly being questioned as the causal event in the origin of the vast majority of cancers as clinical data show little support for this theory.’ https://pubmed.ncbi.nlm.nih.gov/27160408/ Is cancer caused by something other than the DNA mutations stipulated by the SMT? Have we misunderstood cancer and is it time to consider different theories?

You're conclusion is based on the assumption that random mutations have resulted in a selective bias where key genes are less prone to mutation, and that his explains the study's uncharacteristic results. This is pure speculation on your part. What is the factor that confers protection to specific genes and not others from random mutation? Even your conclusion contradicts the status quo, that random mutations define evolution, because you are admitting that, actually, those mutations are not random across the genome, but are instead focused on particular genes that provide a benefit - which indicates a level of conscious input in accordance with external stiumli, and focused protection on the most important survival genes. How can specific genes develop more robust protection compared with other genes around them? All nDNA genes are made from the same substrates, are subject to the same insults, and are repaired by the same mechanisms. How, for instance, can random free radical damage have a preference over which DNA genes are damaged and mutated? Contradictory to make such a bold statement as fact when in the same sentence you highlight the elephant in the room - "we do not understand the concept of consciousness"... and yet you're adamant that consciousness does not play a role, when you admit this concept is not understood. Thanks, but doesn't accidental imply consciousness? If something occurs accidentally then it is in opposition to the intention of something (the mutation occurred against the will of the organism, by accident) Intention requires consciousness.

Why do you need the word 'conscious' to be present in order to draw that conclusion? The study found that evolutionary mutations weren't random and appeared to be focused. While the word conscious wasn't used, the implied interpretation is there. The progression of science and relevant discoveries require a detachment from "literal thinking". The results of the study challenge the random evolutionary model, what other explanation can there be for focused mutational changes that aren't random? Surely any inquisitive mind would be open to this concept given the data here? Here's another quote from the study: "Our discovery yields a new account of the forces driving patterns of natural variation, challenging a long-standing paradigm regarding the randomness of mutation and inspiring future directions for theoretical and practical research on mutation in biology and evolution."

What did you think of the Nature study I linked to at the beginning of the thread? That study provides the "case for mutations being a conscious occurrence in response to stimuli". You must have missed it.

To Bufofrog (I think I'm restricted due to this being my first day of responding for a long time) If brain cells are not operating on any conscious level, then how does consciousness arise from them? Is consciousness not simply the ability to store information and recall that information? Are you saying cells do not store information and cannot recall said information? Yes there is... (I didn't realise this discussion malarchy could be so simple)....;)

You don't think that cells are operating on any conscious level?

Why not random change - because advancements in science are rarely made by agreeing with the status quo. And there is a case for mutations being a conscious occurrence in response to stimuli. Why not a conscious adaption? Below is the conclusion drawn from the study I shared, which opens the possibility of mutations being a conscious adaption...why would we not consider it? "We conclude that epigenome-associated mutation bias2 reduces the occurrence of deleterious mutations in Arabidopsis, challenging the prevailing paradigm that mutation is a directionless force in evolution."

In support of Jay's enquiry: https://www.nature.com/articles/s41586-021-04269-6 This paper highlights the mutational bias generated by epigenetic stimuli associated with the plant Arabidopsis thaliana, which indicates that mutational evolution is not random, but a conscious response to improve survival on the part of the organism. To use a crude example - indigenous people who live at altitude have developed a mutation that increases their ability to operate more effectively in low oxygen environments. Was this a random mutation that then led these people to colonize areas of high altitude (the mutation drove their behaviour), or, while living at altitude for extended periods did their genes adapt to the environment to improve their chances of survival? (the mutation was a direct response to environmental cues aimed at improving survival). The former equates to a random mutation, the latter a conscious adaption by the organism (mutation) in response to local conditions and the need to out-compete other organisms for survival. The latter makes more sense to me. We can't discuss evolution without considering consciousness. I would argue that mutations in genes that confer an advantage are primarily a conscious response to stimuli at the cellular level, or at a level of crosstalk between cells, mitochondria and the microbiome of larger organisms that all work symbiotically to, again, enhance their survival.

Hi all. Does anyone know of any studies that confirm the virulence of fungi in connection with human cell interactions - in particular, is there any evidence confirming that human fungal pathogens directly manipulate the sonic hedgehog pathway in order to facilitate disease within human cells?