I am so pleased - I may have just had Covid again

I have had a virus in the past few days. I had Covid in May 2020 (without a test, but it was not very nice) in 2021 (with a test). I have also had two vaccinations and some boosters (I have to some extent lost track). However, in the last few days I have had a virus which has lasted a week and involved some sniffles.

According to our national statistics body (the ONS) about 1/20 of the country are infected with Covid. Hence I think I have just had covid.

Why am I pleased?

I am pleased because I have now got a blood test (from yesterday) that demonstrates the effect of Covid on myself (which would be similar to other people, but without the weekly blood tests I would not have the information).

CRP going up from an unmeasureable figure to 5.13 mgl/L is an ideal demonstration of the impact on the immune system.

I am also pleased to see the drop in the CK Kinase and AST from stopping going to the gym.

The odd ones are transferrin and transferrin saturation dropping. I don’t understand those. I understand my albumin levels dropping because of a bit of intermittent fasting


You didn’t do a test, did you? So besides Covid it could be RSV or flu. Symptoms are similar. There’s a lot of RSV going around as well.

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I have not done a test this time. I don’t really mind what it is, what matters to me is that I have a blood test having had it so I can see the changes. It is probably Covid because it is very common in the UK this week.

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Hi John,

Covid is fascinating in regard to the inflammatory response. I’ve sadly treated a lot of cases. In general, for most individuals, now it is just a cold. I get exposed at least 10 times weekly and make sure I get regular exposures in the E.R. I’ve had it twice, neither time made me sick - last time was 2 days of sniffles.
Older individuals (65+) and those with multiple co-morbidities seem prone to have immune dysregulation and a significant inflammatory response, which can result in hypercoagulability and cardiac dysfunction.
I now see a modest number of people who had their health ruined by covid in the early days.
When it was alpha and delta, it was scary, as I’d see patients, often younger and rarely healthier than I was getting truly taken down by this illness.
Now, that is a rarity, and I’m admitting people who are already very unwell, who get covid and it tips them over the edge and they get admitted “with covid” - but they could have had any small insult on an already fragile situation and be unable to care for themselves due to weakness, or have minor decline in respiratory function that was already damaged.
We often see a leukopenia (low White Blood Cells), neutrophilia (which typically is associated with bacterial not viral infections), elevated CRP, elevated D-Dimer, often elevated Troponin (heart enzyme), also some elevated liver enzymes. It just depends on how unwell the person is. All of these things can be found in other significant viral illnesses - so there isn’t anything hugely unique with covid in this respect.
Hopefully this helps put a little perspective on this from someone who has cared for patients through this mess.


I have had quite a bit of leukopenia for some time. I think it results from my protocol. I have about 2.9E-9/l at the moment. I have not worried about that because my resistance to infection has been really good apart from this recent episode.

My CRP is normally below 0.15mg/L (which is lower than Bryan Johnson). That arises from the background SASP effect on IL-6 levels - which is good.

I am quite well, if currently mildly drunk, what was odd, however, was a transferrin saturation of 10.48, also my urate is lower than normal (which I am quite pleased with). Transferrin itself is quite low.

Still I am not complaining. I have been doing quite a bit of not eating much for dinner sort of intermittent fasting this week, but I am up for a binge (including binge drinking) tonight. I think eating less has driven down albumin.

I am in a good mood at getting a Hannum extrinsic epigenetic age friom Trudiagnostic of about 37 (I am 63). I think I understand the stickiness that results from the interplay of DNA methylation and histone acetylation. What I think happens is that methylation results from and causes a reduction in gene expression, but if you increase acetylation and hence transcription then that reduces methylation.

This does explain a lot of things about how things work.

I had Covid once for 6 days, it was mild and lasted 6 days - I didn’t discontinue rapamycin. Two other viral infections I had tested as neither Covid nor flu, so I assume it was either common cold or RSV. Both affected my biomarkers but not much.

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John - what are the things you are doing to maximize SASP effect apart from rapamycin? Are you doing any cyclic dasatinib with quercertin/fisetin or other measures, apart from optimizing diet and mix of fats?



I had two shots of the Pfizer Covid vaccine and one booster. I have never had Covid but the vaccine really did a number on me. Not planning to get another shot of the Covid vaccine anytime soon. In October I had this year’s flu shot with no reaction.
For now, I will just be getting my annual flu shots. Never had the flu in several decades.
IMO: I believe the side effects and consequences of the Covid vaccine are being underreported.


Not only that but I don’t know of one single person who has been vaccinated, that have not had COVID ( except you, first one I hear say had the vaccine and didn’t get Covid). To me that says the vaccine may not be effective, especially knowing the fact that the virus variant seems to change every couple months. Clearly it’s impossible for pharma to come up with the right vaccine for each variant. Why bother then if you’ll be taking the vaccine of last variant while the current one runs unabated lol


All variants have some parts in common - that’s why they still work for reducing the severity of the infection. The same is true for flu, shingles, etc. unfortunately there’s no 100% guarantee.


Its really minimising SASP rather than maximising it.

My working hypothesis is that a proportion of senescent cells are cells that are stuck in the process of differentiation through a shortage of nucleosolic acetyl-CoA caused in part by IL-10 reducing the expression of SLC25A1.

I have a protocol which is described on this thread: