“If one member suffers, all the members suffer with it.” — 1 Corinthians 12:26
When the Body Forgets Its Own: Type One Diabetes as an Autoimmune Condition
This week I want to talk about type one diabetes, and I want to start by naming it plainly for what it is. Type one diabetes is an autoimmune condition. It shows up in the pancreas and it’s managed through blood sugar, so it gets filed away as a pancreas problem or a sugar problem. But the pancreas is where the damage lands. It isn’t where the story starts.
Some of you are living with this yourselves. Some of you are raising a child with it, or you watched a grown son or daughter get the diagnosis at nineteen or twenty-five, or you were told in your forties that what you thought was type two is actually the slower adult form of type one. Wherever you’re standing with it, this article is for you. I’m not here to talk you out of anything your body needs to stay alive. I’m here to ask the question that almost never gets asked after diagnosis, which is why the immune system turned on the body in the first place, and what we can do with our terrain about it.
What Makes Type One Autoimmune
This isn’t a new idea, and it isn’t a fringe one. In 1974 a group of researchers in London found antibodies against islet cells, the small hormone-making clusters in the pancreas where the beta cells live, circulating in the blood of people with type one diabetes. That finding reframed the whole disease. Before it, type one was understood as a pancreas that stopped working. After it, the question became why the body was making weapons against its own tissue.
In the fifty years since, the case has only gotten stronger, and it rests on three pillars.
The first is genetic.
The strongest inherited risk for type one sits in the HLA genes, the part of our DNA that teaches the immune system how to tell self from not-self. Certain versions of these genes, the ones known as DR3-DQ2 and DR4-DQ8, show up again and again in people who develop type one. Those are immune genes, not pancreas genes. That alone tells you where to look.
The second is the autoantibodies.
Before diagnosis ever happens, often years before, the blood starts showing antibodies aimed at specific parts of the beta cell: insulin itself, an enzyme called GAD65, a protein called IA-2, and a zinc transporter called ZnT8. Nearly everyone newly diagnosed carries at least one of them. When children in long-term studies developed two or more, the large majority went on to develop diabetes within fifteen years. The attack is measurable long before blood sugar ever tips over.
The third is what’s been seen in the tissue.
As far back as 1965, a pathologist studying the pancreases of children who had died shortly after diagnosis found immune cells packed into and around the islets. That infiltration has a name, insulitis, and it has been confirmed many times since. The immune cells were right there in the tissue, doing the dismantling.
Put those three together and the picture is clear. The beta cells aren’t wearing out on their own. They’re being taken apart by an immune response that has lost track of what belongs to the body. That puts type one diabetes in the same broad family as Hashimoto’s, coeliac, and rheumatoid arthritis. Different target, same misdirection.
Why It Rarely Travels Alone
Once you see type one this way, something that confuses a lot of families starts to make sense. It tends to bring company. Autoimmune thyroid disease shows up in a large share of people with type one, somewhere between one in five and one in three depending on the study. Coeliac disease runs several times higher than in the general population. Autoimmune gastritis, the kind that quietly steals B12 absorption, along with Addison’s and vitiligo, all cluster here too.
If type one were only a pancreas problem, that pattern wouldn’t exist. It exists because the underlying drive, an immune system in a reactive and confused posture, doesn’t stay politely in one organ. When I work with someone who has type one, I’m never only thinking about the pancreas. I’m thinking about the thyroid, the stomach lining, the small intestine, and the whole terrain that set the stage.
Genes Are Not the Whole Story
Here’s the part that gives me so much hope. Genes matter, but they aren’t destiny. When one identical twin develops type one, the other twin, carrying exactly the same DNA, often does not. Long-term twin studies land somewhere around half, climbing over a lifetime but never reaching all. And new cases have been rising for decades, around three to four percent a year across Europe, far faster than any gene pool can change. Something in how we’re living is tipping susceptible people over the edge.
The research keeps pointing to the same places we already work in: the gut lining, the microbiome, early life, viral infections, sunlight and vitamin D, and stress. That’s terrain. And terrain is something we can tend.
The ARP Question: Why Did the Immune System Turn?
The conventional model does one thing very well, which is replace the insulin the body can no longer make. That keeps people alive, and I thank God for it. But it manages the fallout. It doesn’t ask why the immune system went to war in the first place, and it doesn’t ask what’s keeping the war going.
That’s the work we do here. It sits in four places, and none of them will be new to you.
Restoring the gut barrier.
The lining of the small intestine is a single layer of cells, and it’s meant to decide carefully what gets into the body and what doesn’t. When it loosens, fragments of food proteins, bacterial pieces, and endotoxin slip through and meet the immune system directly, and the immune system reacts. In type one this isn’t theoretical. Researchers have found increased intestinal permeability in people with type one before clinical onset, and elevated zonulin, the protein that opens the junctions between gut cells, both in people with type one and in relatives who were still in the early antibody stages.
Gluten is worth naming here, because it’s one of the strongest known triggers of zonulin release and because coeliac and type one travel together so often. For most people with type one, taking gluten out is one of the kindest things they can do for their gut. Then we rebuild. Bone broth, gelatin, and collagen for glycine. Well-cooked meats and good animal fats. Low-antinutrient plants cooked soft. Space between meals so the lining can do its repair work. If you’ve done a GI-MAP, look at your zonulin, secretory IgA, and calprotectin, because together they’ll tell you how inflamed and leaky that barrier is and how much work there is to do.
Feeding the microbiome.
Your gut microbes are in constant conversation with your immune system, and they’re one of the main ways it learns calm. Certain bacteria ferment fibre into short-chain fatty acids, especially butyrate, and butyrate helps the body make regulatory T cells, the immune cells whose whole job is to tell the rest of the immune system to stand down. In the largest study ever done of children at genetic risk for type one, the children who stayed well carried more of the microbial genes that make those short-chain fatty acids. In another group of at-risk children, microbial diversity dropped in the months before diagnosis. And in animal work, diets that delivered acetate and butyrate to the gut protected against type one altogether.
There’s a study I think about often. Finland and the Russian side of Karelia sit right next to each other and share much of the same genetic background, yet they have one of the widest gaps in autoimmune disease anywhere in the world. The Finnish children, living cleaner and more modern lives, had gut bacteria whose signals were weaker at training the immune system. The children with more contact with farms, animals, and soil carried microbes that taught their immune systems better. That’s microbes as medicine, and it’s living soil.
So we feed these helpers. Traditionally fermented foods like sauerkraut, kefir, and yogurt if dairy is tolerated. Time outside with your hands in the dirt. Animals. The low-antinutrient plants your gut can handle. And where something is there that shouldn’t be, like overgrowth, parasites, or H. pylori, we clear it, because pathogen load keeps the immune system on high alert. Enteroviruses in particular have been tied to the start of islet autoimmunity, with long-lasting enterovirus infections in the gut showing up in children who went on to develop antibodies. A strong gut terrain is part of how the body meets those infections without the immune system losing its bearings.
Calming the nervous system.
A body that lives in threat mode keeps its immune system in a reactive posture. Stress hormones and sympathetic signalling change how immune cells behave, and over time the body gets worse at telling a real threat from a harmless one. The vagus nerve works the other direction. It runs a pathway researchers have named the inflammatory reflex, where calm vagal signalling tells the immune system to turn inflammation down.
This shows up in type one research too. A large Swedish study following thousands of children from birth found that those who had lived through a serious life event, a death in the family, a divorce, a frightening illness, had roughly three times the risk of developing type one. I don’t share that to put more weight on anyone. I share it because it means nervous system work isn’t a side project. It’s immune work. Morning light, a steady daily rhythm, Gregorian chant or baroque music playing in the kitchen, time in nature, being held by the people who love you, and prayer that lets you lay down what you’ve been carrying. All of that speaks directly to the immune system.
And to the parents of a newly diagnosed child, the diagnosis itself is a serious life event for the whole household. Tending your own nervous system is part of tending your child’s.
Supporting the mitochondria.
This one gets less attention than it deserves. Beta cells are some of the hardest-working cells in the body, and they’re built with surprisingly little antioxidant protection. Compared with liver cells, they carry very low levels of the enzymes that clean up oxidative stress. So when the body is inflamed, undernourished, short on sleep, or pushed around by blood sugar swings, the beta cells feel it first.
Here’s why that matters for autoimmunity. When beta cells are under that kind of energy strain, their protein-making machinery gets stressed and starts producing altered proteins, including hybrid pieces of insulin fused to other fragments the body was never taught to recognise. The immune system sees those unfamiliar shapes and flags them as foreign. A cell under strain, in other words, starts to look like a threat. Supporting mitochondrial function is how we help those cells look like themselves again.
That means sunlight on bare skin, especially in the morning. Vitamin D, from the sun when you can get it and supplemented when you can’t. In one Finnish study that followed over ten thousand babies, the ones given regular vitamin D in their first year had about an eighty percent lower risk of type one later on. It means grounding, dark nights, and real sleep. And it means deep nourishment. Zinc matters here more than people realise, because beta cells hold some of the highest zinc levels in the body to package their insulin, and ZnT8, the zinc transporter, is one of the very proteins the immune system targets. Oysters, red meat, and liver bring in zinc, selenium, B vitamins, and CoQ10 in the forms our ancestors ate them.
Where Blood Sugar and Ketosis Fit
Insulin isn’t optional in type one, and nothing in this protocol replaces it. Everything I’m describing stands beside it.
What steadier blood sugar does is lower the oxidative strain on whatever beta cells remain, and on the blood vessels, nerves, eyes, and kidneys too. Many people with type one do beautifully with lower-carbohydrate, animal-based meals, because a smaller carbohydrate load needs a smaller insulin dose, and smaller doses mean fewer highs and fewer lows. There’s real experience behind this, including a survey of hundreds of children and adults with type one eating very low carbohydrate who reported excellent blood sugar control with low rates of complications.
If ketosis is part of your protocol, the key distinction is between nutritional ketosis, which is a gentle and steady state, and diabetic ketoacidosis, which is an emergency that happens when there isn’t enough insulin in the body. They are not the same thing. With type one, lowering carbohydrates always goes hand in hand with adjusting insulin alongside whoever helps you manage it, checking ketones as well as glucose, and never skipping basal insulin because you’ve eaten less. Go slowly. Your body will tell you how it’s doing.
What About the Beta Cells That Are Left?
I want to be clear about what this work does and doesn’t do. It isn’t going to hand you back beta cells that are already gone. What it does is address the autoimmune drive underneath, so the body isn’t continuing the attack on whatever remains, and isn’t going on to build the cascade of thyroid, gut, and stomach autoimmunity that so often follows.
And there is often more remaining than people were once told. When researchers studied people who had lived with type one for fifty years or more, a large number of them were still making small amounts of their own insulin, and some still had beta cells that responded to a meal. Many people newly diagnosed also go through a stretch, often called the honeymoon, when the pancreas is still producing a meaningful amount. Every bit of that is worth protecting. Holding on to some of your own insulin production is linked with steadier blood sugar and fewer complications, and calming the terrain is how we protect it.
For Families
If type one is in your family, the terrain work is for everyone in the house, not only the person with the diagnosis. Brothers, sisters, and children of someone with type one carry a higher risk, and antibody screening now exists that can pick up the early stages years before blood sugar changes. Whether or not you choose that testing, the ground you stand on is the same: a well-sealed gut, a well-fed microbiome, sunlight and vitamin D, living soil, a peaceful home, and deep nourishment.
For babies and little ones, that starts with the microbiome they’re born into, breast milk when it’s possible, time outdoors, and a mother’s calm presence. None of this has to be perfect. Every small piece of it counts.
Remembering Who You Are
Saint Paul wrote to the church in Corinth about the body, how the eye cannot say to the hand that it has no need of it, and how if one member suffers, all the members suffer with it. He was talking about the Church, but he chose the body as his picture because the body is made to hold its members together in care. Autoimmunity is what it looks like when the body forgets that. It loses track of its own and starts treating a part of itself as an enemy.
I think that’s why this work feels so much like remembering to me. We aren’t forcing the immune system into submission. We’re giving it back the conditions it needs to recognise what belongs: the sealed gut, the old microbial friends, the sun, the rhythm, the peace, the nourishment. The mass remembering of how to be human includes the body remembering itself.
And please hear this. You are not your diagnosis. You are not a pancreas that failed, or a number on a meter, or the sum of your insulin doses. The psalmist tells us we are fearfully and wonderfully made, and that is still true of a body that’s struggling. Saint Irenaeus wrote that the glory of God is man fully alive. That aliveness is still yours, alongside the insulin, alongside the carb counting, alongside the hard nights.
Go gently. Seal the gut. Feed the microbes. Get in the sun. Rest your nervous system. Nourish your cells. Lean on your community and let them lean on you, and bring all of it before the Lord. The body was made to know itself, and it can learn to remember.
I am so proud of you and love you all!
References
G.F. Bottazzo, A. Florin-Christensen, and D. Doniach. “Islet-cell antibodies in diabetes mellitus with autoimmune polyendocrine deficiencies.” The Lancet, 1974 — first identification of islet cell antibodies.
Willy Gepts. “Pathologic anatomy of the pancreas in juvenile diabetes mellitus.” Diabetes, 1965 — insulitis in children who died near diagnosis.
Anette-G. Ziegler et al. “Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children.” JAMA, 2013.
Janet Wenzlau et al. “The cation efflux transporter ZnT8 (Slc30A8) is a major autoantigen in human type 1 diabetes.” PNAS, 2007.
Maria Redondo et al. Twin concordance studies in type 1 diabetes. Diabetologia, 2001; New England Journal of Medicine, 2008.
Christopher Patterson et al. “Incidence trends for childhood type 1 diabetes in Europe during 1989–2003.” The Lancet, 2009.
George Kahaly and Martin Hansen. “Type 1 diabetes associated autoimmunity.” Autoimmunity Reviews, 2016 — thyroid, coeliac, gastric, adrenal, and skin autoimmunity alongside type one.
Emanuele Bosi et al. “Increased intestinal permeability precedes clinical onset of type 1 diabetes.” Diabetologia, 2006.
Anna Sapone et al. “Zonulin upregulation is associated with increased gut permeability in subjects with type 1 diabetes and their relatives.” Diabetes, 2006.
Tommi Vatanen et al. “The human gut microbiome in early-onset type 1 diabetes from the TEDDY study.” Nature, 2018.
Aleksandar Kostic et al. “The dynamics of the human infant gut microbiome in development and in progression toward type 1 diabetes.” Cell Host & Microbe, 2015.
Tommi Vatanen et al. “Variation in microbiome LPS immunogenicity contributes to autoimmunity in humans.” Cell, 2016 — the Finland, Estonia, and Russian Karelia comparison.
Eliana Mariño et al. “Gut microbial metabolites limit the frequency of autoimmune T cells and protect against type 1 diabetes.” Nature Immunology, 2017.
Yukihiro Furusawa et al. “Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells.” Nature, 2013.
Kendra Vehik et al. “Prospective virome analyses in young children at increased genetic risk for type 1 diabetes.” Nature Medicine, 2019 — prolonged enterovirus B shedding and islet autoimmunity.
Kevin Tracey. “The inflammatory reflex.” Nature, 2002.
Maria Nygren et al. “Experience of a serious life event increases the risk for childhood type 1 diabetes: the ABIS population-based prospective cohort study.” Diabetologia, 2015.
Markus Tiedge, Sigurd Lenzen et al. “Relation between antioxidant enzyme gene expression and antioxidative defence status of insulin-producing cells.” Diabetes, 1997.
Thomas Delong et al. “Pathogenic CD4 T cells in type 1 diabetes recognise epitopes formed by peptide fusion.” Science, 2016 — hybrid insulin peptides from stressed beta cells.
Elina Hyppönen et al. “Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study.” The Lancet, 2001.
Hillary Keenan et al. “Residual insulin production and pancreatic β-cell turnover after 50 years of diabetes: Joslin Medalist Study.” Diabetes, 2010.
Belinda Lennerz et al. “Management of type 1 diabetes with a very low–carbohydrate diet.” Pediatrics, 2018.
Richard K. Bernstein. Dr. Bernstein’s Diabetes Solution. Little, Brown, 2011.
1 Corinthians 12:12–26; Psalm 139:14.
St. Irenaeus of Lyons. Against Heresies, Book IV — “The glory of God is man fully alive.”
Ancestral Regeneration Protocol — Gut Barrier, Microbes as Medicine, Nervous System, and Mitochondrial Support pillars.