Diabetes, not me


Well-Known Member
FWIIW... here is the reference I was looking for wrt the effect of previous meals

"the “lentil effect,” or the ability of lentil consumption to blunt the sugar spike of foods consumed hours later at a subsequent meal.34 Lentils are so rich in prebiotics that they create a feast for your friendly flora, which in turn feed you right back with beneficial compounds, such as propionate, that relax your stomach and slow the rate at which sugars are absorbed into your system.35. Chickpeas and other legumes were found to have a similar influence, and so this phenomenon was later renamed the “second-meal effect.”36"


First time at the rodeo.

Risk for Newly Diagnosed Diabetes >30 Days After SARS-CoV-2 Infection Among Persons Aged <18 years — United States, March 1, 2020–June 28, 2021
Early Release / January 7, 2022 / 71

Catherine E. Barrett, PhD1,2; Alain K. Koyama, ScD1,2; Pablo Alvarez, MPH1; Wilson Chow1; Elizabeth A. Lundeen, PhD1,2; Cria G. Perrine, PhD1; Meda E. Pavkov, MD, PhD2; Deborah B. Rolka, MS2; Jennifer L. Wiltz, MD1; Lara Bull-Otterson, PhD1; Simone Gray, PhD1; Tegan K. Boehmer, PhD1; Adi V. Gundlapalli, MD1; David A. Siegel, MD1; Lyudmyla Kompaniyets, PhD1; Alyson B. Goodman, MD1; Barbara E. Mahon, MD1; Robert V. Tauxe, MD1; Karen Remley, MD1; Sharon Saydah, PhD1 (View author affiliations)
View suggested citation
What is already known about this topic?
SARS-CoV-2 infection is associated with worsening of diabetes symptoms, and persons with diabetes are at increased risk for severe COVID-19. SARS-CoV-2 infection might also induce newly diagnosed diabetes.
What is added by this report?
Persons aged <18 years with COVID-19 were more likely to receive a new diabetes diagnosis >30 days after infection than were those without COVID-19 and those with prepandemic acute respiratory infections. Non–SARS-CoV-2 respiratory infection was not associated with an increased risk for diabetes.
What are the implications for public health practice?
The increased diabetes risk among persons aged <18 years following COVID-19 highlights the importance of COVID-19 prevention strategies in this age group, including vaccination for all eligible persons and chronic disease prevention and treatment.

New diabetes diagnoses were 166% (IQVIA) and 31% (HealthVerity) more likely to occur among patients with COVID-19 than among those without COVID-19 during the pandemic and 116% more likely to occur among those with COVID-19 than among those with ARI during the prepandemic period. Non–SARS-CoV-2 respiratory infection was not associated with diabetes. These findings are consistent with previous research demonstrating an association between SARS-CoV-2 infection and diabetes in adults (47). The inclusion of only patients aged <18 years with a health care encounter possibly related to COVID-19 in the non–COVID-19 HealthVerity group could account for the lower magnitude of increased diabetes risk in this group compared with risk in the IQVIA group. In addition, patients without COVID-19 in HealthVerity had higher hospitalization rates than did those in IQVIA, suggesting more severe disease at the index encounter in the HealthVerity comparison group.
The observed association between diabetes and COVID-19 might be attributed to the effects of SARS-CoV-2 infection on organ systems involved in diabetes risk. COVID-19 might lead to diabetes through direct attack of pancreatic cells expressing angiotensin converting enzyme 2 receptors, through stress hyperglycemia resulting from the cytokine storm and alterations in glucose metabolism caused by infection, or through precipitation of prediabetes to diabetes (8). A percentage of these new diabetes cases likely occurred in persons with prediabetes, which occurs in one in five adolescents in the United States.†††† Steroid treatment during hospitalization might lead to transient hyperglycemia; however, only 1.5%–2.2% of diabetes codes were for drug- or chemical-induced diabetes, with the majority of codes being for type 1 or type 2 diabetes. Alternatively, COVID-19 might have indirectly increased diabetes risk through pandemic-associated increases in body mass index,§§§§ a risk factor for both serious COVID-19 illness and diabetes. Future studies addressing the role of comorbidities and increases in body mass index in post–COVID-19 diabetes are warranted. Although this study can provide information on the risk for diabetes following SARS-CoV-2 infection, additional data are needed to understand underlying pathogenic mechanisms, either those caused by SARS-CoV-2 infection itself or resulting from treatments, and whether a COVID-19–associated diabetes diagnosis is transient or leads to a chronic condition.
Evidence of increased pediatric type 1 diabetes has been reported during the COVID-19 pandemic (1,2). Among persons aged <18 years with COVID-19 and new diabetes diagnoses in this study, nearly one half had DKA at or around the time of diagnosis. This number was higher than that in comparison groups, and higher than previous reports of DKA among incident type 1 diabetes cases before the pandemic (28%) (9). Increased frequency of DKA at time of diagnosis of type 1 diabetes during the pandemic has previously been reported and was thought to be due to delayed care-seeking for diabetes (3). However, the observed association of increased risk for diabetes diagnosis following SARS-CoV-2 infection would not be explained solely by delayed care. COVID-19 has disproportionately affected racial/ethnic minority groups, and those aged <18 years in these groups are also at increased risk for type 2 diabetes (10). An association between COVID-19 and new pediatric diabetes diagnoses might disproportionately affect racial/ethnic minority groups. Race/ethnicity data were unavailable in the present data sets; however, future studies should address racial and ethnic disparities in COVID-19 and diabetes, and whether persons aged <18 years who are at risk for COVID-19 are also those at risk for delaying medical care.
Health care providers should screen for diabetes symptoms in persons aged < 18 years with a history of SARS-CoV-2 infection. These symptoms can include frequent urination, increased thirst, increased hunger, weight loss, tiredness or fatigue, stomach pain, and nausea or vomiting.¶¶¶¶
The findings in this report are subject to at least four limitations. First, the definition of diabetes might have low specificity because it used a single ICD-10-CM code, did not include laboratory data at the time of diagnosis, and could not reliably distinguish between type 1 and type 2 diabetes. Second, patients infected with SARS-CoV-2 without a COVID-19 diagnosis or documented positive test result might be misclassified as not having COVID-19. Third, the present analyses lacked information on covariates that could have affected the association between COVID-19 and incident diabetes, including prediabetes, race/ethnicity, and obesity status. Finally, estimated associations are only representative of persons aged <18 years seeking care included in these commercial claims databases and not of pediatric populations with SARS-CoV-2 infection without commercial health insurance or who do not seek health care.
These data suggest an increased risk for diabetes among persons aged <18 years with COVID-19, which is supported by independent studies in adults (47). These findings underscore the importance of COVID-19 prevention among all age groups, including vaccination for all eligible children and adolescents, and chronic disease prevention and treatment. Public health messages highlighting the risks associated with COVID-19 among the pediatric population are especially important to inform clinicians and parents about possible sequelae of COVID-19. SARS-CoV-2 infection might lead to type 1 or type 2 diabetes through complex and differing mechanisms. Partner agencies and clinicians in the field should be aware of long-term consequences and monitor persons aged <18 years in the months following a SARS-CoV-2 infection for new diabetes onset. Long-term follow-up studies of COVID-19 are warranted to further define the potential association between COVID-19 and increased diabetes risk among those in this age group.


Well-Known Member
Re..,"The observed association between diabetes and COVID-19 might be attributed to the effects of SARS-CoV-2 infection"

In an autoimmune disease some of the immunity cells slip through the tests to protect against acting against our own organs. There must also be a defect in the cellular protein (MHC) that presents antigens to immune cells. This slip is bad, but not disasterous because the immune cells must be activated at the "infection " site, if not activated they just sit around in the lymph nodes waiting for a inflammatory signal to call them to action at the proper place....

The problem arises when an opertunistic infection hits the organ that contains a protein segment an immune cell recognizes. The immune cell arrives, called by the various inflammatory signals, recognizes the protein segment it tags as bad, and commences to destroy the organ producing it.

Sars covid 2 is just one example of an opportunistic infection setting off a chain off destruction in those who are unfortunately disposed to it

Here's an excerpt from how the immune system works that explains it in greater detail

"The latest thinking is that for autoimmunity to occur, at least three conditions must be met. First, an individual must express MHC molecules that efficiently present a peptide derived from the target self antigen. This means that the MHC molecules you inherit can play a major role in determining your susceptibility to autoimmune disease. For example, only about 0.2% of the U.S. population suffers from juvenile diabetes, yet for Caucasian Americans who inherit two particular versions of class II MHC genes, the probability of contracting this autoimmune disease is increased about 20-fold.

"The second requirement for autoimmunity is that the affected person must produce T and, in some cases, B cells which have receptors that recognize a self antigen. Because TCRs and BCRs are made by a mix-and-match strategy, the repertoire of receptors that one individual expresses will be different from that of every other human, and will change with time as lymphocytes die and are replaced. Even the collections of TCRs and BCRs expressed by identical twins will be different. Therefore, it is largely by chance that a person will produce lymphocytes whose receptors recognize a particular self antigen.

"So for autoimmune disease to occur, a person must have MHC molecules that can present a self antigen, and lymphocytes with receptors that can recognize the self antigen – but this is not enough. There also must be environmental factors that lead to the breakdown of the tolerance mechanisms which are designed to eliminate self-reactive lymphocytes. For years, physicians have noticed that autoimmune diseases frequently follow bacterial or viral infections, and immunologists believe that microbial attack may be one of the key environmental factors that triggers autoimmune disease. Now clearly, a viral or bacterial infection cannot be the whole story, because for most people, these infections do not result in autoimmunity. However, in conjunction with a genetic predisposition (e.g., the type of MHC molecules inherited) and lymphocytes with potentially self-reactive receptors, a microbial infection may be the “last straw” that leads to autoimmune disease.


Bad Cop
This is a very complicated explanation of a problem that may be this complicated, but for a long time, it has been understood that there was a correlation between infection with Coxsackie B virus and type 1 diabetes, and that perhaps a viral protein coincidentally had an epitope (a 3-D surface structure caused by how the protein folds) that mimicked a protein on pancreatic islet beta cells, and that antibodies generated to bind to the viral protein and signal other parts of the immune system to eliminate the virus, cross-reacted with the beta cell protein, and the immune system then killed those cells.



Well-Known Member
I'll summarize the autoimmune perspective from how the immune system works

1) you have the bad luck to inherit a gene or genes for a molecule that displays your own protein segment from a particular organ (MHC)

2) you have more bad luck that the surface receptors on your adaptive immune cells happen to hit on just that protein segment in their combinatorial shuffle to protect you against everything

3) your luck reaches rock bottom when you get an environmental or biological insult to just that organ that, when inflammed, calls those immune cells to just the place they can do the most harm....

I don't know if all autoimmune diseases fall into this pattern, the discussion builds on the observation that your adaptive immune system has strong protections against acting against yourself.

For example, DianaCox's reference indicates the root problem is a similarity between viral antigen and self protein. What makes it more complicated is the immune system has a multifactor authentication system that prevents it from acting against self. From what we know of the immune response the pancreatic cell would have to present the self protein segment on an MHC. The immune cell locks onto the presented antigen that set off intra cellular processes that lead to apoptosis ( hard to avoid sounding complicated).

That said... it does have the characteristic of at least two factor authentication. The antibodies attach to the similar self protein and mark it for death ( either by macrophage or killer T cell or simple obstruction of function). What differs from the HISW description is, in general, ther is no need for antigen similarity. The errors in step 1 an 2 are sufficient to set you up for problems

FWIIW...I have a niece that developed Lupus after a severe auto accident that swelled her up from hip to throat. I always wondered how mechanical insult could lead to an autoimmune disease... now I understand a little better
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First time at the rodeo.
And now, a friend just sent me this link:

The demyelinating neurodegenerative disease multiple sclerosis (MS) is a complication of infection by the Epstein-Barr virus (EBV), suggests a new study published in Science by researchers at Harvard Medical School.

The breakthrough findings, powered by a gargantuan dataset taken from two decades of US military personnel, represent the culmination of years of circumstantial evidence showing links between EBV, an endemic and latent infection found in up to 95% of the population, and the onset of MS.

MS – a complication of viral infection
“The key finding is that MS is a complication of infection with EBV,” says study senior author Alberto Ascherio, a professor of epidemiology and nutrition at Harvard’s T.H. Chan School of Public Health. MS has been considered for many years an autoimmune disease of unknown etiology. I think this study establishes that this immune process that leads to brain damage is driven by infection with EBV.”

The link between MS and EBV has been suspected for many years, without any killer study able to establish a solid causal link. While the great majority of healthy adults show prior EBV infection, the number rises even further for MS patients – 99.5% of this group test positive. Ascherio says that this new study firmly establishes that connection. “It was quite striking how black and white the results are. I think the results are very solid and leave very little doubt [about the causal link],” he says.

What is EBV?
The Epstein-Barr virus (EBV) is a herpesvirus that causes the childhood disease infectious mononucleosis. Primarily transmitting through saliva, it persists as a latent infection in human B-cells.

Efforts to establish causal confirmation of previous studies hinting at a MS-EBV link have, until now, faced a major challenge. With so many people infected with EBV by even early adulthood, producing a sample population substantial enough to find EBV-negative individuals that would then go on to develop MS would require a unique study design with an unprecedented sample size.

“There is no comparable population in the world”
Ascherio and his team found that exceptional sample in the records of the Department of Defense Serum Repository (DoDSR). All active US military personnel are required to submit a blood serum sample at the start and then after every two years of service. Primarily designed to detect HIV, the DoDSR has built up to a vast cornucopia of biological data made up of over 62 million serum samples taken from over 10 million individuals.

“There is no comparable population in the world,” says Ascherio. Using it, his team were then able to identify personnel that showed antibodies against EBV, an indicator of infection, at the time of their first sample donation. In a demonstration of the ubiquitous nature of EBV, just 5.3% of the individuals examined were uninfected. Separately, they looked for individuals that developed MS during their service period, noting 801 such cases that had EBV status records.

800 of 801 MS cases occurred in individuals who had previously tested positive for EBV. 35 of those individuals had tested negative upon their first donation, and all but one then became positive (a process called seroconversion) prior to their MS symptoms emerging, corresponding to a 97% seroconversion rate. By contrast, just 57% of an initially EBV-negative control population who didn’t later develop MS showed seroconversion. Becoming EBV-positive resulted in a 32-fold increased risk of later developing MS as opposed to remaining EBV-negative. The next-strongest known risk factor for MS is having a set of genes that encode for proteins found of the surface of certain immune cells. People with a particular set of these immune cells, who have a homozygous genotype for the HLA-DR15 allele, have a threefold increased risk of MS.

Put simply, apart from one case, every single MS patient documented in the study became EBV-positive prior to their symptoms developing. The median time from seroconversion to MS diagnosis was 7.5 years, with a wide range seen from 2 to 15 years.

Ruling out confounders
In the absence of a randomized controlled trial, the gold-standard for assessing cause and effect in disease onset, it was possible that the team’s findings could be explained by a confounding variable or by reverse causation. To rule these out, the team conducted further analysis of the serum data.

Could there be another factor that simply increased the risk of both getting EBV and MS? The huge risk factor associated with EBV made that unlikely, but Ascherio’s team examined antibodies against cytomegalovirus, another saliva-borne virus that has also infected most of the world’s population, to serve as a negative control. Individuals who were CMV-negative at their first sample showed no increased risk of MS if they later became CMV-positive. CMV positivity was actually associated with a lower risk of MS.

MS is thought to have a long prodromal phase, meaning the disease could affect the immune system years before symptom onset and diagnosis. Could the EBV-MS relationship be reversed? Perhaps people who have MS but don’t yet show symptoms are more likely to develop an infection such as EBV. To rule this out, Ascherio’s team looked at 30 MS patients, and 30 healthy controls. They used a search tool called VirScan that enables the detection of any antibody raised against any protein in any of the ~200 viruses known to infect humans. The only virus to show significantly increased presence in MS cases was EBV.

These findings could potentially reshape the direction of MS research. But EBV cannot be the whole story. The study suggests that EBV seropositivity is necessary to develop MS, but it is clearly not sufficient, or the disease would affect 95% of the world’s population, as opposed to only the few million cases of MS thought to exist worldwide.

Genetic factors
It is likely that genetic and environmental factors instead contribute to the disease onset, meaning that once an individual has been infected with EBV, their own unique genotype and phenotype will go on to determine whether they will later develop MS. A companion perspectives piece published in the same issue of Science by Stanford University’s William H. Robinson and Lawrence Steinman suggested that molecular mimicry may be involved. This would imply that immune cells targeting EBV are accidentally attacking the protective myelin sheath around axons, leading to the neurodegeneration and motor symptoms of MS. Supporting this theory, prior study has identified EBV-infected B cells in the brains of MS patients.

One final question from Ascherio’s data concerns the lone EBV-negative MS patient in the study. The paper’s discussion section identifies infection in between sampling or failure to seroconvert as potential explanations, but another reason, Ascherio suggests, may be due to the limitations of diagnosis.

“Before the polio vaccine, say 99% of poliomyelitis cases were caused by the polio virus, but, unless you define the disease based on the infectious agent, for any disease, there will be occasional cases that are not caused by that that agent,” says Ascherio. For example, acute flaccid paralysis – which was virtually eradicated after the success of the polio vaccination program, still is seen in rare cases. “There is no reason,” says Ascherio, “that MS should be an exception, because, even if MS is a complication of EBV infection, when you describe the disease clinically and radiologically, there will always be an occasional case that is due to something else.”

Can we eradicate MS?
Interest will now also move to the prospect of developing vaccines and antivirals against EBV with the aim of eradicating MS. No vaccine currently exists, but Ascherio says its development is realistic. The more interesting treatment option now, he points out, could be adapted from immunosuppressive therapy. Currently, he says, the most effective treatment is anti-CD20 immunotherapy. “This depletes the B cells,” says Ascherio, “in which EBV establishes infection. Most likely, the reason the anti-CD20 is so effective is because by getting rid of the cells, we also get rid of the virus, at least temporarily.”

A more effective treatment, he says, could instead target EBV directly with antivirals, while leaving the B cells unharmed. Again, those treatments do not yet exist. But now, says Ascherio, research at least knows the questions it wants to ask, rather than dealing with MS’s previously unknown etiology. “Once you establish the causal connection, I think that it's a question of providing sufficient rationale for research on antivirals, specifically for EBV, that could help the 2.8 million people with MS in the world,” Ascherio concludes.


Bjornevik, K, Cortese, M, Healy, BC, et al. Longitudinal analysis reveals high prevalence of Epstein-Barr Virus associated with multiple sclerosis. Science. 2022. doi: 10.1126/science.abj8222


Well-Known Member
The anti-virus mode of action, once cells are infected, is induced apoptosis. I wonder if the demyelination is apoptosis gone wrong, or a more direct effect of the viral infection.

Both the viruses you mention are a plague to young adults. I think their other disease symptom is mono...


Staff member
They’ve know for decades that viral illnesses triggered type 1 diabetes in kids, why is it so shocking that the Covid virus would do that as well.

My oldest stepdaughter, now approaching 40, was 12 when both she and her younger sister got the flu. Younger one was fine, older one developed type 1. Why one and not both, who knows. Luck of the genetic draw. But if the generic flu can do that, why not Covid. The medical community should not be so shocked.


Well-Known Member
Re "Why one and not both, who knows"

Maybe the bit about the random combinatorial form of antigen receptors in immune cells .. Item 2 below

Three things have to happen :

  1. defect in antigen presenting molecule (genetics)
  2. an immune cell that, by random shuffling, just happens to see a self protein as an antigen ( bad luck)
  3. an insult to the organ with that protein ( e.g. the virus)
Item 2 is why even identical twins do not get the same auto immune disease