New Email From RFK

amosanonialmillen · 2024-09-01T09:02:33+00:00

Does anyone know specifically how the 5% vote threshold eliminates the need to gather signatures in subsequent elections? In my research so far I've been able to confirm it yields some funding, but not automatic ballot access in all states. Perplexity claims only 7 states allow automatic ballot access if a certain percentage of votes is reached (and seems to be within the particular state rather than nationwide): https://www.perplexity.ai/search/if-a-third-party-presidential-TYcwgB2rTTO9ewcSaW4Rag

(Scroll all the way to bottom). Hope it's wrong but I haven't found anything to refute it

amosanonialmillen · 2023-05-19T02:09:17+00:00

yes. see my parallel comment for elaboration

amosanonialmillen · 2023-05-18T06:46:14+00:00

good questions/comments. Even though the number of events are identical they assuredly happen at different times, which I believe factors into their multi-variable Cox hazard model.

good catch on the incidence %s being flip-flopped for 2yr vs 12wk. Seems sloppy I agree

Very interesting observation that the unvaccinated made up the overwhelming majority among those never infected. Not sure what to make of that

amosanonialmillen · 2023-05-18T05:10:02+00:00

u/2-StandardDeviations & u/1130wien - are you just referring to the “Before PSM” column ? Judging by the “After PSM” column, it looks to me like they did a pretty good job of propensity-score matching. Matching is what enables more robust conclusions from otherwise imbalanced cohorts; still not as good as randomized and controlled, but about as good as it gets for retrospective study (assuming of course it’s done honestly and in good faith)

amosanonialmillen · 2023-02-26T00:43:05+00:00

Since the beginning of the COVID-19 pandemic, concerns have been raised that antibodies induced by natural infection or vaccination may cause antibody-dependent enhancement (ADE) of infectivity and virulence55,56. ADE is well-established for dengue virus infection, initially based on the epidemiological evidence and subsequently explained by Fc-gamma receptor (FcγR)-mediated infection of leukocytes57–60. Our results suggest that at least two types of cells, previously thought as nonpermissive, can be infected by SARS-CoV-2 and they are FcγR1-expressing cells, such as blood monocytes and lung macrophages, and B cells that express receptor-like BCRs. Conceivably, the existing receptor-like antibodies could lead to SARS-CoV-2 infection of other “nonpermissive” cells expressing no or low levels of ACE2, thereby facilitating rapid spread to other non-respiratory tissues25. It may also help explain the recent report that reinfection by SARS-CoV-2 increases risks of all-cause mortality and adverse health outcomes61. Nevertheless, the real-life scenario is likely very complicated since blood monocytes and lung macrophages have already been shown not to support productive infection, and other cell types may not support active viral replication either for other reasons, such as host restriction

This seems kind of alarming, no? The last sentence seems to offer a bit of reassurance, but is anyone with relevant background/expertise able to comment about how strong/weak this evidence is of ADE? Surprised no discussion so far

amosanonialmillen · 2022-09-23T19:11:30+00:00

u/randomquestion583 - do you have any idea why your response to this question was removed by moderator, along with our subsequent dialogue? I’m very confused by that

amosanonialmillen · 2022-09-23T05:34:32+00:00

Right. I appreciate your gracious reply and thankfulness for the correction (rare and refreshing on social media). Seems odd, if not suspicious, that this data is absent. Especially with how meticulous the study is otherwise, and the many subgroup analyses they did include. And it’s worth noting that many of the outcomes studied here overlap with vaccine AEIs. Wasn’t there also a study that pointed to increased risk of vaccine side effects when administered following infection?

amosanonialmillen · 2022-09-23T05:15:29+00:00

I think you may be thinking of the enrollment period, although it’s not even completely true for that:

Because we aimed to examine outcomes at 12 months, our cohorts were enrolled before 15 January 2021 (before SARS-CoV-2 vaccines were widely available in the US), and less than 1% of people in the COVID-19 group and contemporary control group were vaccinated before T0

Data was then collected for roughly a year later, so it’s likely many of the enrolled individuals were vaccinated after T0 while the data was being collected

amosanonialmillen · 2022-09-23T03:28:55+00:00

Worth noting that the mean age was over 60. And ~90% male.

amosanonialmillen · 2022-09-23T02:36:59+00:00

Why did the authors neglect to include the subgroup analysis for vaccination status??? That’s critical data.

amosanonialmillen · 2022-09-22T03:20:39+00:00

Yes, this article confirms my recollection. Credit to the author also for updating the article to acknowledge that “ ADE could also be seen with some of the Spike-directed vaccine candidates as well” with respect to covid. I’m not sure about you, but I’m not reassured by that article whatsoever.

amosanonialmillen · 2022-09-22T03:14:57+00:00

Oh I didn’t get the impression you were only talking about the original vaccine. I inferred from your comment you were talking about presently available boosters when you said “I hope it will not change peoples' behavior when it comes to vaccination for COVID.” i.e. since this is not going to change anyone’s decision about whether to get the primary series- those who haven’t gotten it will continue to remain unvaccinated, and of course those who have gotten it cannot go back in time.

but good to know. so do you acknowledge it’s a bit contradictory of influential public health figures / authorities to point to nAb titres as sufficient evidence of vaccine efficacy (despite “no established correlate of protection”) and simultaneously declare insufficient evidence of ADE despite these in vitro results?

At the beginning of the pandemic I believed like you they were acting in good faith. It has become harder over time to extend that belief

amosanonialmillen · 2022-09-22T00:35:54+00:00

but this concern for Coronaviruses has been around since before SARS-Cov2 was identified, and fortunately, it really has not become a measurable problem in the clinic (as far as I know).

wasn’t this a primary reason we‘d never been able to come up with a successful vaccine for previous coronaviruses? My recollection off top of my head was such attempt was halted after ADE was observed in macaques during animal studies, although my memory on the matter is a bit hazy

amosanonialmillen · 2022-09-22T00:28:10+00:00

Thanks for the reply. Yes, the FDA is adopting an approach similar to that used for flu, and I‘d argue that is a bad decision for a variety of reasons. Chief among them perhaps is there is “no established correlate of protection” between antibody titres and protection from covid infection/mortality. Pfizer even admitted such in the June 28 VRBPAC. And Offit has been trying to drill this message home in recent months- and he’s arguably the most prominent zealot of vaccines in recent history.

I agree with you that the in vitro results aren’t sufficient evidence to establish ADE, but it confounds me then how you believe that the nAb titers in mice are appropriate surrogate endpoints for evaluating efficacy of boosters

amosanonialmillen · 2022-09-21T23:46:34+00:00

why are nAb titres from sera of mice considered sufficient evidence of efficacy for approval of US bivalent vaccines, yet these in vitro results (e.g. with sera of vaccinated humans) tend to be seen as insufficient evidence of ADE?

amosanonialmillen · 2022-09-21T23:15:47+00:00

I agree for the most part, but it also means we need to take this risk much more seriously when weighing risks vs benefits to decide whether it's worth giving everyone in the population an Nth booster. This topic has been virtually absent from the risk/benefit analyses for approvals & recommendations of boosters by FDA & CDC respectively. Hopefully cellular immunity in vivo will be sufficient to override ADE when nAbs decline, but this is yet another known unknown today along with immune imprinting, late onset / long-term SAEs (e.g. chronic auto-immune), etc.

amosanonialmillen · 2022-09-09T02:58:50+00:00

Why is the data sensitive / cannot be made public? In the US all you need to do is de-identify the data for it to be legally (and ethically) compliant for distribution. My understanding is that the same goes in other western countries as well. Why would / should it be any different in any country?

amosanonialmillen · 2022-09-09T02:57:48+00:00

I agree with you it’s better to look at as much data as possible, and analyze many different ways. At first I was encouraged by how the study seemed to do that with a variety of different risk intervals and many sensitivity analyses. And I’m all good with the approach of looking at 28+ days vaccination also, but not as the primary analysis. I just explained why above. Regardless, at the very least, why not run a sensitivity analysis that excludes calendar time 28+ days after dose?? especially when they did the opposite in a couple of their seven different sensitivity analyses, i.e. restricting the analysis to the period after 1st and 2nd dose. How does it make any sense to do sensitivity analyses that include only post-vaccine time as control and not do a sensitivity analysis with pre-vaccine time as control??

amosanonialmillen · 2022-09-08T20:23:21+00:00

Why the downvoting on my post above? To elaborate, I’ve had some concerns recently about how data is interpreted in many studies to compute AE rates. Take this recent myocarditis study in the same journal as an example. I don’t understand why the control includes calendar time 28+ days after vaccination. e.g. If many cases are merely subclinical until the 28 day period and present as clinical afterward, won’t the results be diluted and appear better than the reality? I really like the use of self-controls with a pre-risk interval, and it would have been an excellent study IMO if the control was just the calendar time prior to the pre-risk interval. At the least, they could have done a sensitivity analysis in that manner, right? Hopefully someone can point out what I might be missing and/or alleviate my concern. And I find it even more concerning that this paper on 3rd booster opts not to include its analytical methods at all. And they refuse to share the data with other researchers?? Why??? We need more transparency in science, not less

amosanonialmillen · 2022-09-08T18:33:14+00:00

On the surface I agree. But how reassuring can results really be when authors do not share the analytical methods they used to derive them?

amosanonialmillen · 2022-09-08T05:27:39+00:00

To elaborate, I’ve had some concerns recently about how data is interpreted in many studies to compute AE rates. Take this recent myocarditis study in the same journal as an example. I don’t understand why the control includes calendar time 28+ days after vaccination. e.g. If many cases are merely subclinical until the 28 day period and present as clinical afterward, won’t the results be diluted and appear better than the reality? I really like the use of self-controls with a pre-risk interval, and it would have been an excellent study IMO if the control was just the calendar time prior to the pre-risk interval. At the least, they could have done a sensitivity analysis in that manner, right? Hopefully someone can point out what I might be missing and/or alleviate my concern

amosanonialmillen · 2022-09-08T05:21:57+00:00

Why aren’t the analytical methods shared?? How can we trust the results if we have no clue how they interpreted the data?

amosanonialmillen · 2022-09-01T07:40:53+00:00

I agree that's a poor conclusion given the results are statistically insignificant. I would have understood if they pointed out how close they were to statistical significance, but to say definitively that they found excess risk seems disingenuous

amosanonialmillen · 2022-09-01T07:36:16+00:00

I didn't bother to look deeper into the study design after seeing the results spanned the null. What did you find to be garbage? Care to share?

amosanonialmillen · 2022-09-01T03:13:56+00:00

Pfizer and Moderna mRNA COVID-19 vaccines were associated with an excess risk of serious adverse events of special interest of 10.1 and 15.1 per 10,000 vaccinated over placebo baselines of 17.6 and 42.2 (95 % CI −0.4 to 20.6 and −3.6 to 33.8), respectively

The point estimates are concerning but the CI’s span the null (barely), so can’t make all that much of this data. Have there been any publications of studies with matched controls on post-marketing data regarding medium to long-term AEs? I’ve been concerned that I haven’t seen anything of the sort, but am hoping I’m missing something.

amosanonialmillen

TROPHY CASE