Excess deaths in Britain and the Diabetes question

And elsewhere

Earlier yesterday a piece of news went viral pretty fast, this was the piece I was working on before the AIDS paper caught my attention.

Silent crisis of soaring excess deaths gripping Britain is only tip of the iceberg

Britain is in the grip of a new silent health crisis.

For 14 of the past 15 weeks, England and Wales have averaged around 1,000 extra deaths each week, none of which are due to Covid.
Prof Robert Dingwall, of Nottingham Trent University, a former government adviser during the pandemic, said: “The picture seems very consistent with what some of us were suggesting from the beginning.

“We are beginning to see the deaths that result from delay and deferment of treatment for other conditions, like cancer and heart disease, and from those associated with poverty and deprivation.

“These come through more slowly – if cancer is not treated promptly, patients don't die immediately but do die in greater numbers more quickly than would otherwise be the case.”

The Government has admitted that the majority of the excess deaths appear to be from »»»»»circulatory issues and diabetes««««« – long-term, chronic conditions that can be fatal without adequate care.

Such conditions were also likely to have been exacerbated by lockdowns and work-from-home edicts that increased sedentary lifestyles and alcohol intake at a time when Britain was already facing historic levels of obesity and heart disease.

Post-pandemic excess death is nothing new, in fact, it is not even a “hot take” anymore, but a widely accepted fact, the argument lies in the cause. In fact, the entire media establishment went pretty hard on the “Sudden Adult Death Syndrome” which isn’t actually a thing before 2021. As excess death keep increasing year over year in countries with a high rate of vaccination with Spike-centric platforms, we will see an increasing argument that it was in fact, not the vaccines, maybe the virus, or something else, graph readers will subscribe to such developments towards postponing screening and all else.

It is not the point of this piece to discuss the intricacies of pushing BS, it is however to bring attention to one of the world’s biggest “disease” creators and accelerators of our modern times. And one SARS-CoV-2 is best friends with.

Diabetes.

Very early on 2020, I was already witnessing an abnormal uptick in glucose-related conditions, especially after a SARS-CoV-2 infection, which led me to the hepatic rabbit hole. I spent most of 2021 going down the metabolic pathways to attempt to understand how/why this was happening, you could find dozens of tweets of me stating precisely that. Here is one of the “classics”.

John Paul @ThingsHiddenn

Increase in hepatic and pancreatic cancers. Lymphomas, colorectal cancer too. Diabetes type 1 and 2, thyroid issues. Neurodegeneration. Congestive heart failure. Massive increase in pulmonary arterial hypertension. Perpetual infections. Posting the receipts for when SHTF.

Also here on Substack, I got many pieces that intertwine poor glycemic control, diabetes, and most of the bad outcomes and the many pathways this disease uses to cause damage and inflammation. To the point, it can affect even the immune response to vaccination. So to bring the point home on how this increase in diabetes and circulatory problems are either cause or further accelerated by the virus, here are a few data points.

Type 1 diabetes incidence increased during the COVID-19 pandemic years 2020-2021 in Czechia

The COVID-19 pandemic was associated with a notable upward inflection of the type 1 diabetes incidence curve; the early months of the first lockdown were however hallmarked by a significant dip in new diabetes diagnoses. Long-term observation will show whether the increased incidence originated only from accelerating an advanced preclinical Stage 2 to overt diabetes, or whether the pandemic triggered new cases of islet autoimmunity.

Risks and burdens of incident diabetes in long COVID: a cohort study

In the post-acute phase, we report increased risks and 12-month burdens of incident diabetes and antihyperglycaemic use in people with COVID-19 compared with a contemporary control group of people who were enrolled during the same period and had not contracted SARS-CoV-2, and a historical control group from a pre-pandemic era. Post-acute COVID-19 care should involve identification and management of diabetes.

The Incidence of Diabetes Among 2,777,768 Veterans With and Without Recent SARS-CoV-2 Infection

SARS-CoV-2 is associated with higher risk of incident diabetes in men but not in women even after greater surveillance related to hospitalization is accounted for.

Long-term cardiovascular outcomes of COVID-19

Our results provide evidence that the risk and 1-year burden of cardiovascular disease in survivors of acute COVID-19 are substantial.

There are two real mechanisms for both types of diabetes to happen after a Covid infection.

Indirect and Direct Effects of SARS-CoV-2 on Human Pancreatic Islets

Pathology of the pancreas from deceased hyperglycemic patients who had COVID-19 revealed mild lymphocytic infiltration of pancreatic islets and pancreatic lymph nodes. Moreover, SARS-CoV-2–specific viral RNA, along with the presence of several immature insulin granules or proinsulin, was detected in postmortem pancreatic tissues, suggestive of β-cell–altered proinsulin processing, as well as β-cell degeneration and hyperstimulation. These data demonstrate that SARS-CoV-2 may negatively affect human pancreatic islet function and survival by creating inflammatory conditions, possibly with a direct tropism, which may in turn lead to metabolic abnormalities observed in patients with COVID-19.

Several emerging clinical reports have described an increased incidence of patients with new-onset hyperglycemia associated with acute COVID-19 (20) or onset within a few weeks from recovery of the disease (21)
To our knowledge, this is the first report showing the coexistence of an exaggerated peripheral inflammation and a direct tropism of SARS-CoV-2 virus, which together may drive β-cell dysfunction/damage. Our data suggest that a dysregulation of cytokines and a proinflammatory environment may synergistically act in concert with pancreatic localization of SARS-CoV-2 to promote abnormal glycometabolic control.

Unless someone wants me to break down the entire paper, which is rather complex and many will get lost in the middle, the summary is simple.

The authors decided to finally test one of the biggest debates among clinicians and researchers since the pandemic went full throttle, does SARS-CoV-2 attack the liver (human pancreatic islets). The islets are small patches of tissue in the pancreas that consists of 3 different types of cells. The most common, and arguably the most important for some would be the Beta Cells, the ones that produce insulin, a major hormone with systemic effects in the body.

One of the hallmarks of Type 1 Diabetes in that the body itself attacks the islets among other mechanisms and Type 2 where your body is resistant to insulin, leading to more secretion, toxicity, and faster cell death of said cells.

The authors describe a state where the body produces excessive inflammation elsewhere and direct tropism (meaning the virus does enter the liver and may cause direct damage, which in their opinions and clinical evidence will show anyone paying attention that this is the case, leading to Beta Cells damage. It is a two-for-one.

“Ok by your own explanation this would explain Type 2, not the autoimmune type.”

Molecular Mimicry between SARS-CoV-2 and Human Endocrinocytes: A Prerequisite of Post-COVID Endocrine Autoimmunity

SARS-CoV-2/COVID and Type 1 Diabetes Mellitus: An immunoinformatics approach

Immunoinformatics data suggest a potential pathogenic link between DM1 and SARS-CoV-2/COVID. Thus, by means of molecular mimicking we check that sequences similarity among SARS-CoV-2/COVID and human insulin and human glutamic acid decarboxylase-65 may lead to production of an immune cross-response to self-antigens, with breakage of self-tolerance that can trigger DM1

After reading all this, do you still think the virus didn’t play ANY role ? Or it is the driving culprit ? Also for the vaccine aficionado, there are many published clinical cases of vaccine-induced diabetes, of both types.

A friend recently said we came full circle with all the current published papers proving many of the observations and all else made by a handful of people. And indeed, we came full circle.

Because the molecular mimicry aspect of it all is still one of the most damning aspects of this disease, and with every new infection some are rolling the dice. The mimicry also plays a role in the Tryptophan and Kynurenine aspects of this, therefore the bioenergetics too, but this one I will cover later on.

Plagued by Design II

For full disclosure, many other countries are now experiencing excess deaths in the thousands every other week, with the “boosted” accounting for a large portion of the deaths. Now you understand why I am adamant about a low carbohydrate diet, besides all the other motives ?

And the excess deaths barely started, wait until someone with a functional brain and not being bad at math takes into account dynamic variables such as all the other diseases SARS-CoV-2 sets off. Something I wrote to a couple of friends, I will leave it here, publicly.

Why would you need to create 20 different bioweapons if just one will do the job of 20 and much more ?

If my next piece has BMO in the title and you don’t want to get mildly depressed with the states of other things (energy, logistics, food), you might want to skip that one. We also came full circle in that regard…

Massive appreciation to all supporters here and on Kofi !!!