06/12/2026
JUST THE MESSENGER: T1 NOT AUTOIMMUNE OR GENETIC
With T1D increasing 3% annually in the U.S. and 9% in some countries, a compassionate human is caught in a psychological dilemma... Do they discuss any of the hundreds of new studies showing environmental factors are linked to causing T1D, or do they remain silent, pretend those studies don't exist, and keep pushing the false narrative that, oh well, T1 just happens?
I can see how the choice between speaking out or remaining silent is difficult... On the one hand, remaining silent is psychologically comforting; let's not rock the boat. That way, we won't have to admit embarrassing mistakes. It won't infringe on the income many rely on for their beach houses and new car purchases.
On the other hand, that person can't erase the obvious, that turning a blind eye translates into increased suffering for thousands of children and T1 moms.
I'm fascinated how some can continue this facade. Maybe they aren't aware of the studies showing a young T1 child today has an 18-year loss in life expectancy - has guaranteed early onset vision loss and accelerated kidney, heart disease, and future mental illness. I guess that's easy to forget when focusing on monetary benefits.
Folks, the research community is in 100% agreement that environmental factors (from viruses to modern-day chemicals not present decades ago) interact with HLA genes, destroying beta cells faster than they can regenerate. This net loss of beta cells soon brings about T1D. Anyone who ignores this 100% majority research opinion (and there are many in the retail end of T1), I hope, has a very hard time sleeping at night.
NEW INSIGHT
Now here's where it gets interesting... So, about 85% of children with T1D have this unique HLA genetic marker. This may seem like a lot at first, and will make many people say - OK, this is proof T1 is genetic.
But hold on a sec... What they forget to tell you is that nearly 40% of the healthy U.S. population ALSO carries the same HLA risk-factor gene, and you know what? 99% of people with that gene NEVER, and I repeat, NEVER get T1D. So, only 1% of people with the HLA gene (actually less than 1%) get T1D, and 99% do not... Obviously, I think everyone can now agree, there is a lot more going on that brings about T1D, than just the presence of the gene. Agreed?
BRING IN THE SCIENTISTS
Six scientists from the University of North Carolina and the University of Colorado must have been reading the studies that free radicals can reduce insulin output, trigger Bax genes that cause beta-cell death, and increase autoimmunity down the road. This would lead to a new hypothesis:
Is there anything different in the blood of someone who gets T1D, months and years before T1 diagnosis, and before antibodies appear? The answer lies in DAISY.
THE DAISY STUDY
Ever hear of the DAISY study? Absolutely fascinating! It began in 1993 and screened 30,000 Denver newborn babies. They were looking for genetic and environmental risk factors for T1D. Eventually, they identified 2,542 children who did not have T1 diabetes, but were considered high risk because of family history or the presence of those HLA markers I mentioned earlier. These children were then followed for many years to see who developed T1D. During these follow-up years, children came into the hospital several times a year to provide blood samples. The blood was secured in a freezer so it could be used in later research by scientists.
WHAT THEY FOUND
The team of six scientists examined blood samples from children who never developed T1D and compared it to children who developed T1. They didn't just look at blood samples at the time of hospital diagnosis. The DAISY study allowed them to analyze blood samples months and years before T1 diagnosis, long before antibodies could even be measured. And what they found was a major breakthrough in my opinion, although it appears others would rather sweep this under the rug.
ANTIOXIDANT OVERLOAD
It turns out, abnormally high levels of antioxidants were discovered in the blood of children who later developed T1D. Antioxidants such as glutathione, superoxide dismutase, and catalase were much higher in the early blood samples of T1 children compared to blood samples from children who DID NOT develop T1D. Folks! This should be a major ah ha moment for all fo us!
IMPORTANT TO UNDERSTAND
Since high levels of antioxidants run PARALLEL with high levels of beta cell-killing free radicals, we have what many could call a smoking gun. But we have another problem, and a very big one at that..
WHERE DO FREE RADICALS COME FROM?
So, free radicals are actually natural. They are created inside your beta cells while making insulin 24/7. The most common free radical is known as Reactive Oxygen Species (ROS for short). And since a single beta cell is said to make 1 million insulin molecules per minute, a lot of free radicals are created, and a lot of antioxidants are needed to calm down those free radicals.
But don't worry, as long as your 3 Musketeer antioxidants keep working like tiny vacuum cleaners to clear out excess free radicals, everything is good... until it isn't.
OTHERS THEN CRASH THE PARTY
This is where Mother Nature must get very upset. Her smooth-running beta-cell Islet party that has worked without issues for thousands of years has now been thrown into complete chaos from uninvited guests.
Since the 20th century, it's no longer just free radicals being generated by beta cells making insulin or an occasional viral infection (Yes, viral infections create a lot of free radicals to kill a virus and could explain higher T1 after viral infections.)
Scientists are discovering a ton of free radicals are also produced after a child is exposed to vehicle exhaust, after eating food grown with pesticides, after an X-ray, after eating nitrates in meat, after exposure to petroleum fragrance chemicals, after exposure to disinfectants, after BPA teeth sealants in the dental office, or plastic chemicals in the home, etc., etc., etc. In other words, free radical chaos is hitting beta cells from every direction.
If our party crashers don't leave, free radicals continue to accumulate and eventually exceed the capacity of our vacuum cleaner antioxidants to keep them in check. This is referred to in the literature as "oxidative stress." When that red line is crossed, beta cells begin dying en masse, and we say hello to T1D.
A BIG HLA GENE DISCOVERY
I need to mention one more very important thing. Remember the HLA risk gene that is more frequent in T1D? There was a major discovery with that as well (which I'll discuss in detail soon). But here's a prelude...
While the gene is normally in an inactive state, sleeping and not displaying antigens that can cause autoimmunity (as seen in 99% of the normal population), something was discovered that can wake up that HLA sleeping giant, which then triggers autoimmunity. The gremlin responsible is... you guessed it.. FREE RADICALS.
Bottom line, if free radicals can be kept in check, the HLA gene can sleep peacefully. But if free radicals increase, boy do we have a problem, and HLA induced autoimmunity then really takes off.
There are many out there, worried to death you guys will see the new research that voids the decades of error-filled information they've been dispensing, while steadfast on ignoring the newer research themselves.
How long can this continue? Good question, but at some point, no amount of sleeping pills can numb the guilt at least a few of these people must be dealing with. We just need to keep reminding them of this rapidly growing new research, where acknowledgment of the environmental causes of T1D, would hands down, be the best cure for insomnia.
View study on free radical oxidative stress in early T1D
https://pmc.ncbi.nlm.nih.gov/articles/PMC5726913/
