It seems that after resetting the State count by over 10,000 the Trolls of Trenton have now reconfigured the web site removing the data of the data and forcing a complex process to obtain each county. There must be some wizard who wants to obfuscate something.
The State numbers are declining but continually changes make obtaining data nearly impossible. Most likely they gave the job to some politically connected tyro whose understanding of epidemiological data is below zero.
We keep hearing about the "science" and COVID. I propose a few questions. I ask for the answers and the experimental basis for the answer as available in a peer reviewed professional journal of some repute. Here we go:
What is the cause of COVID-19 infections?
How does the virus attack and propagate in a patient?
How does the virus spread?
Can a patient be asymptomatic?
What are the sequellae from the infection?
What are the demographics for infection and mortality?
What are the autoimmune responses from infection?
What are the autoimmune responses from the vaccine?
If ACE2 receptor is entry point of virus, is there then differences in ACE2 making some more or less vulnerable?
Are the differences in receptor genes related to ethnicity and if so how does this affect virulence?
How long is an infected person contagious?
How high an Ab titer is there post vaccination?
How long is protection from the virus post vaccination?
How broad is the protection of the vaccination in terms of variants?
If a vaccinated person is exposed to the virus, does the virus invade that person?
If the virus invades a vaccinated person, is it limited to the nasopharynx at 94F and remain inactive or does it spread to the lungs at 98.6 F and become active?
Does the expulsion of inactive 94F virions from a vaccinated person have a significant potential for viral infection of unvaccinated?
If a vaccinated person has inactive 94F virions in nasopharynx, how long do they survive there?
If the exposure to the virus is a result of an infected person spreading active virions 98.6F via aerosols, what are the spatio-temporal dynamics of such a spread? Statistically?
What dominates the distance factor for virion spread: individual aspiration, viscosity of the environment, buoyancy?
What are the effects of temperature, humidity, air flow on rate of spread amongst non-infected individuals from an infected person?
"Trust me" is not science. Ex cathedra statements are not science. Experimental and in situ measurements are. So let's have them!
New Jersey Stats on COVID have always been noisy, But the past few days they have been unstable. On Monday they reported a total of 865,895 cases. On Tuesday they reported 865,700 cases. That is an increase. OK
But on Sunday they reported 874,895 cases. That is a drop of about 10,000 cases in a single day! There of course is no explanation. Counties randomly showed similar drops between Sunday and Monday.
Perhaps an explanation is warranted? Ya think!
UPDATE: The Trolls in Trenton provided an explanation.
Ending April and things appear to be getting better. It is important to note that NJ is the second highest incidence per PoP per day of all states. We will examine this a bit. We begin with the normalized incidence. It seems to be leveling off but that is still a bad sign. We are now well above 50% immune.
http:// The CDC published a set of recommendations for vaccinated people in JAMA. They note:
In addition, preliminary but rapidly increasing evidence suggests that fully vaccinated people likely pose little risk of transmission to unvaccinated people. Studies from the US, UK, and Israel found that 2 doses of Pfizer-BioNTech or Moderna vaccines were 86% to 92% effective against asymptomatic and symptomatic SARS-CoV-2 infection. More specifically, studies from Israel demonstrated that the Pfizer-BioNTech COVID-19 vaccine was 90% effective against asymptomatic infection, and vaccinated people who developed COVID-19 had a substantially lower viral load than unvaccinated people. Viral load has been identified as a key driver of transmission and this observation may indicate reduced transmissibility. Collectively, these findings demonstrate that vaccination has the potential to substantially reduce the COVID-19 disease burden in the US.
OK, so the vaccines work. But where is the data. The CDC and the Government in general treats us mushrooms as the story goes, keep using the dark and feed us with, well you know. Science demands data, full open, readily accessible, analyzable etc. We cannot seem to get that from the CDC. The FDA seems to be open but not the CDC and Mother Doom.
They continue:
A growing body of evidence suggests that fully vaccinated people are less likely to have asymptomatic infection and potentially less likely to transmit SARS-CoV-2 to others. However, further investigation is ongoing.
Modeling studies suggest that preventive measures such as mask use and social distancing will continue to be important during vaccine implementation. However, there are ways to take a balanced approached by allowing vaccinated people to resume some lower-risk activities.
Taking steps toward relaxing certain measures for vaccinated persons may help improve COVID-19 vaccine acceptance and uptake.
The risks of SARS-CoV-2 infection in fully vaccinated people cannot be completely eliminated as long as there is continued community transmission of the virus. Vaccinated people could potentially still get COVID-19 and spread it to others. However, the benefits of relaxing some measures, such as quarantine requirements, and reducing social isolation may outweigh the residual risk of fully vaccinated people becoming ill with COVID-19 or transmitting the virus to others
Where is this "body of evidence"? Why cannot we see and examine it. Models do not work. So stop with the models. They fail in every dimension. This is not some Issac Asimov tale. There is no Harry Seldin.
Read the above carefully. It appears that they cannot get their stories straight.
The facts are that we really do not know all there is as to transmission and resistance. If a vaccinated person is exposed, we think that as the virus moves to the lungs the immune system will kill it. However that in the upper passage may linger in a small amount for perhaps a short period of time. We think. But the data does not exist.
Overall we must have full and open data sources. The CDC could have data sets readily accessible and lists of peer reviewed reports asserting the bases for their claims. Regrettably they do not.
As an update, I returned to the CDC web site in search of real scientific evidence regarding mask usage and vaccinated individuals. The best I could find was a note based in data from 2002 thru May 2020. There was no data demonstrating the current pandemic. What one does not epidemiologically is that there are "clusters" in towns which dominate the infection rates. New Jersey is ranked second in infections per PoP. But drilling down one sees just a few places which dominate that density. So why not call them out and solve the problem. That was done almost 200 years ago with cholera in London drinking water. It may even be a set of Typhoid Mary carriers, but whatever, go find it and drive it to zero. It is this lack of Public Health competence, Local and Federal, which is now the driver!
The NY Times provided a zero evidenced based article on the use of masks. Now let's review the points:
First the author states:
If you stop to have an extended conversation with someone who isn’t vaccinated, masks are recommended. Even outdoors, your risk of breathing someone else’s air increases the longer and closer you stand to them. One of the few documented cases of outdoor transmission happened in China early in the pandemic, when a 27-year-old man stopped to chat outside with a friend who had just returned from Wuhan, where the virus originated. Seven days later, he had his first symptoms of Covid-19.
One must be truly indoctrinated to believe this Wuhan reference. It is baseless and sourced from a highly unreliable basis. And there is no scientific basis in some peer reviewed journal detailing this effect. It is at best anecdotal and at worst propaganda.
Now let's see where we are:
1. 50% of the population now has immunity. Great!
2. Allegedly, and I use this even cautiously, the virus spreads by aerosols. I worked on aerosols some 55 years ago and was a bit of a specialist. Just what is an aerosol? It is a small particle that is less dense than air and has some initial velocity and is in a cloud. It floats and moves. But just how far? It depends. If you are some academic seeking fame you take a flash photo spitting out a mouth full of aerosolized liquid to get an impressive shot. Science? No, just PR. Frankly the science is still out.
3. Let's remember how the virus operates. If I am immunized then I cannot get the infection, my immune system stops it. However I may carry the virus in an inactivated state in my nasopharynx. The virus is dormant there at 94F because it needs 98F to get active. Thus if I were to cough or sneeze or shout I putatively could spread the virus. Thus if I were in a large room perhaps I could be a spreader. But there are a lot of ifs. Frankly we still do not really know.
4. Models just do not work. The author notes:
To understand just how low the risk of outdoor transmission is, researchers in Italy used mathematical models to calculate the amount of time it would take for a person to become infected outdoors in Milan. They imagined a grim scenario in which 10 percent of the population was infected with Covid-19. Their calculations showed that if a person avoided crowds, it would take, on average, 31.5 days of continuous outdoor exposure to inhale a dose of virus sufficient to transmit infection.
I think by this time we should have no faith in models. Remember the University of London one where half the world died! The author concludes with:
assistant professor of epidemiology at the Yale School of Public Health, said he recently was with a group of parents, including many vaccinated physicians, who met in a New Haven park to celebrate a child’s first birthday. “We’re all just standing around, everybody was masked, and then we started asking, ‘When’s the time we can be outside and take off our masks?’” Dr. ... said. “If people are vaccinated and you’re outdoors, masks are probably superfluous at this point.”
This should read: We really do not know! If I am vaccinated I am allegedly safe. If you are not, shame on you. It is kind of like seat belts. Not the mask, the vaccine.
This is not science, it is social control.
We have just posted a Report on the use of metformin in Prostate Cancer. This is an update from an earlier 2015 Report.
Prostate cancer is a complex disorder and it also very heterogeneous. It is the most significant male cancer with a moderate mortality rate of about 25%. However, this mortality rate is quite confusing since genomic differences, demographic differences and even psychographic differences come into play. Namely there is a small group who have genetic variants which result in an aggressive disease. Second there are demographic groups who defer any testing until it is often too late. The cancer generally is slow growing, unlike ovarian or pancreatic cancer, and thus is properly attended to can be handled with minimal consequence. The problem often is getting the patients tested and followed.
In 2015 we produced a report discussing the research regarding metformin and statins in dealing with prostate cancer (PCa)[1]. This was one of several early reports addressing the use of metformin. In a sense it was an incidental observation. However, in the years since then a significant number of results have been provided further strengthening the utility of metformin before and after a PCa diagnosis.
There has been a great deal of progress in the past ten years in dealing with PCa. The chart below is from Beltram (as modified) and represents the multiplicity of therapeutics available. This chart presents the current general understanding on how to treat PCa.
As the disease progresses there are tools available to slow
and hopefully inhibit the process, even after metastasis and androgen resistance occurs.
Cancer has a complicated and intertwined ecosystem that initiates and supports it. It is not just the genetic disruptions alone that engender its overall aggressiveness. We lay out some of these below.
1. Genomic[2]: This is the internal disruption of normal homeostasis in a cell's status. Generally the focus has been on this element and the therapeutic approach has also been focused in disrupting this process.
2. MET, Mesenchymal Epithelial Transition[3]: Cancer cells lose their location specificity and not only proliferate but lose their basic location anchoring. For example, we see melanocytes moving from the basal layer upwards and then downwards. The same happens in PCa with basal and luminal interactions.
3. TME, Tumor micro-environment[4]: The environment surrounding cancer cells often is protective. The TME is a complex of a large set of these protective elements.
4. TAM, Tumor associated macrophages: Macrophages generally are the garbage collectors in the body. M1 macrophages perform a positive task even addressing cancer cells. However, M2 macrophages may exert a protective function for cancer cell clusters.
5. TAF, Tumor associated fibroblasts: We have discussed this at length elsewhere.
6. Metabolic[5], Epigenetic[6], miRNAs etc?: Cancer cells have a complex metabolic interaction and this is typified by Warburg processes. In addition, epigenetic issues such as methylation and acetylation have been shown to play a significant role as well. We also have such factors a miRNAs which play a role.
Thus it is essential that when providing a therapeutic we
address all of these elements. For example in immunotherapy we generally face
two obstacles. First is the TME and affiliated elements blocking cell attack.
Second, and this seems to be more critical as it is addressed, that
immunotherapy is used as an adjuvant. Namely it is used ex post facto to other
treatments, such as surgery or radiation. Recent studies indicate that if used
as a neo-adjuvant, namely when tumor burden is higher, it may be significantly
better having been trained on a larger tumor set.
Now for the topic of this note. Metformin is a classic
therapeutic for Type 2 Diabetes, T2D. As Zhao et al have noted:
Complex I, AMPK, mTOR, and mGPD have all
been suggested as molecular targets mediating the antitumor activities of biguanides. Consistent with
Complex I serving as a main target, biguanides preferentially target
subpopulations of slower-growing cancer cells that are more reliant on OXPHOS for
survival, creating therapeutic opportunities for the combination of biguanides
with drugs that act on rapidly cycling populations to
exert greater tumor clearance. Targeting compensatory metabolic pathways needed for cancer cells to survive metabolic
disruptions may also improve biguanide efficacy in combination.
In addition, biguanides exert effects on the TIME, with the potential
to influence the immune recognition and elimination of the tumor.
Interestingly, biguanides can also affect host pathophysiology by modulating
the gut microbiota, raising the possibility that biguanides may indirectly
impact patient response to cancer therapies.
Therefore, it is unknown whether biguanides affect direct targets in cancer cells, the tumor microenvironment, or
commensal microbiota, bearing in mind that none of these putative effects are
mutually exclusive. Finally, the pharmacodynamic properties of phenformin suggest that it may be preferred over
metformin for applications in cancer therapy, as
metformin has shown limited efficacy in recent clinical trials possibly due to its
more limited pharmacodynamic properties. While the toxicity profile of phenformin
is not ideal as a longterm maintenance therapy for type 2 diabetes patients, it
is well within the limits for treating cancer.
The incorporation of preclinical and clinical studies of
biguanides, including novel
derivatives, will help to elucidate biomarkers that predict therapeutic
efficacy, define proper patient
cohorts with sensitivity to biguanides, and guide clinical trials of both mono-
and combination therapies in cancer
Whitman et al have also noted:
Since epidemiological studies first demonstrated a
potential positive effect of metformin in reducing cancer incidence and mortality, there has been an
increased interest in not only better understanding metformin’s mechanisms of
action but also in exploring its potential anti-cancer effects. In this review,
we aim to summarise the current evidence exploring a role for metformin in
prostate cancer therapy. Preclinical studies have
demonstrated a number of antineoplastic biological effects via a range of
molecular mechanisms.
Data from retrospective epidemiological studies in prostate cancer has been mixed; however, there are several
clinical trials currently underway evaluating metformin’s role as an
anti-cancer agent. Early studies have shown benefits of metformin to inhibit
cancer cell proliferation and improve metabolic syndrome in prostate cancer patients receiving
androgen deprivation therapy (ADT). Summary While the
body of evidence to support a role for metformin in prostate cancer therapy is
rapidly growing, there is still insufficient data from randomised trials, which
are currently still ongoing. However, evidence so far suggests metformin could
be a useful adjuvant agent, particularly in patients on ADT
Thus, there appears to be significant potential for the use
of metformin as part of an overall therapeutic regime.
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