Observations of symptoms leading to insulin resistance.

5 Aug - Visitor with headache

8 Aug - 3 Sep : Phantosmia starts

24 Aug : Acanthosis Nigricans

4 - 13 Sep : Calcium requirement & back crick

12 Sep : Rigors & fluey fever 37.9°C

17 Sep : Acanthosis Nigricans

1 - 3 Oct : Rigors & fluey fever 37.9°C

4 Oct : Reflux reaction to artichoke high in quercetin

6 Oct : Tingling peripheral nerves in legs, toes & cold numb calves

9 - 12 Oct : Achey muscles

13 -19 Oct : Cold numb calves & proteinuria (dark pee) & loss of optimism

20 Oct : Tingling toes

22 -26 Oct : Reflux / heartburn

This sequence of events suggests the onset of a diabetes 2 type condition as the consequence of an infection.

The most likely infectious agent is a covid variant and the implication is that covid activity interfered with ACEII receptor activity and left my body functioning on default RAS (Rennin Angiotensin System) because cleavage and processing of AngiotensinII to Angiotensin 1-7 has been obstructed.

This is a WIP and I will try to add interpretation and academic corroboration in due course.

Here for example is a report from a clinician. 

Sheela Magge, director of the Johns Hopkins Division of Pediatric Endocrinology and Diabetes, discusses the latest research regarding the rise of type 2 diabetes among youth during the COVID-19 pandemic. Experts used data from 24 clinics across the U.S. to track the sharp increase. in endocrinology and diabetes at Johns Hopkins.

https://www.youtube.com/watch?v=Uj7euxBx8_0&t=15s

Related paper https://www.jpeds.com/article/S0022-3476(22)00719-3/fulltext
"The Coronavirus Disease 2019 Pandemic is Associated with a Substantial Rise in Frequency and Severity of Presentation of Youth-Onset Type 2 Diabetes" Magge et al.

This is a sytematic review "Risk of incident diabetes after COVID-19 infection: A systematic review and meta-analysis" Lai et al. https://pmc.ncbi.nlm.nih.gov/articles/PMC9546784/

We found a 64 % greater risk (RR = 1.64, 95%CI: 1.51 to 1.79) of diabetes in patients with COVID-19 compared with non-COVID-19 controls, which could increase the number of diabetes events by 701 (558 more to 865 more) per 10,000 persons. We detected significant subgroup effects for type of diabetes and sex. Type 2 diabetes has a higher relative risk than type 1. Moreover, men may be at a higher risk of overall diabetes than women.

"COVID-19 and Diabetes: A Comprehensive Review of Angiotensin Converting Enzyme 2, Mutual Effects and Pharmacotherapy" Xie et al. https://pmc.ncbi.nlm.nih.gov/articles/PMC8639866/

Ang II acts on type 1 angiotensin receptor (AT1R), which increases blood pressure levels by inducing vasoconstriction and by increasing renal reabsorption of sodium as well as water. Moreover, Ang II promotes oxidative stress, inflammation and fibrosis (4). In addition to causing pulmonary edema and lung injury, it can also lead to insulin resistance, endothelial dysfunction and proteinuria. These effects of ACE-Ang II are directly opposite to those of ACE2-Ang- (1-7) signal transduction. ACE2 converts Ang II to Ang 1-7, which acts on Mas receptors and lowers blood pressure levels by mediating vasodilation, promoting renal sodium and water excretion. It suppresses inflammatory response and oxidative stress levels by producing nitric oxide (5). It also has anti-fibrosis, anti-proliferation and anti-thrombosis effects. Therefore, the classical ACE-Ang II-AT1R regulatory axis and ACE2-Ang1-7-MAS anti-regulatory axis can maintain homeostasis in vivo... 

 

After SARS-CoV-2 binds ACE2 receptors on the surface of alveolar epithelial cells, expressions of ACE2 in alveolar epithelial cells are down-regulated by internalization, shedding, viral replication and other mechanisms 

These papers support the idea that covid can increase likelihood of diabetes like symptoms, including insulin resistance, due to its affects on ACEII receptors.