More than you probably think. T-1, T-2, LADA, and MODY are the big four, while also…
4000 years ago, healers in ancient Greece, India, and China knew about diabetes. They noticed that sufferers had sweet-smelling pee, so the Greeks named it diabetes (conveying or siphoning) mellitus (honey).
Diabetes is an insulin problem. When our insulin isn’t working right, our cells struggle to get the nourishment that our bloodstream has carried to them. Parts of us starve, while other parts build up such toxic levels of sugar that our kidneys say, “yikes—better shovel this stuff outa here.”
In the fifth century, doctors figured out that two “opposite looking” kinds of people were diabetics. But it wasn’t until 1936 that the bodaciously named Sir Harold Percival Himsworth figured out why.
Big picture, there’s two ways to have an insulin problem: not having enough insulin—OR—having plenty of insulin which struggles to do its job. Back in Sir Harold’s day this was a revolutionary insight.
These two types came to be called:
Type-1. Why do people run out of insulin? Friendly fire, sadly. We mistake our own body for the enemy, and attack ourselves. Running-out-of-insulin diabetes is an auto-immune disease. Diabetics aren’t alone in this: the American Autoimmune-Related Diseases Association (AARDA) lists over a hundred auto-immune diseases, including Multiple sclerosis, Lupus, and several forms of arthritis. The reasons our bodies decide to attack ourselves, and whether and how we can wave the white flag and get ourselves to cease and desist, is still largely a medical mystery.
Type-2. Why does insulin sometimes lose power? Our bodies can become resistant to insulin. Picture living with a teenager whose music, already not to your taste, keeps getting louder and louder. First you try earplugs, then acoustic tiles, and finally you begin thumbing brochures with pictures of palm trees. When insulin is too high too long, cells can become insulin-resistant. At a physical level, the ‘locks’ on the cell wall where the insulin ‘key’ needs to fit get gummed up, broken, or disappeared.
LADA. In the 1980s, type 1.5 was discovered. Scientists are still bickering about what to call us. Many call us LADA, Latent Auto-immune Diabetes of Adults, (although LADA is not latent, and not always in adults. Cute sense of humor!) LADA is like type-1 played at lower RPMs or ‘type-1 mellow.’ LADA is friendly-fire (auto-immune), but it’s a meadow path—rather than a cliff—down to the river of no-insulin, perhaps offering opportunities for prolonging the descent.
MODY. Maturity Onset Diabetes of the Young—wait, what? Another awkward name for another important form of diabetes. MODY is not auto-immune; it is caused by any one of several gene variations which reduce insulin production. Genetic testing shows which of the 14 (at last count) genetic variants is at work, and which treatment is recommended.
T-1, T-2, LADA and MODY are the big four. And as scientists digger deeper into genetics and antibodies, and keep parsing things out more finely, diabetics can be split into ever-finer sub-types. There’s more and more and more, all hopping through the frothy waves and scrambling to the shore (as Lewis Carroll’s walrus told his carpenter).
Many view diabetes as a spectrum, with type-1 at one end and type-2 at the other, and many kinds of “diabetweeners” in between types 1 and 2.
Scientists now believe that LADA is the most common form of auto-immune diabetes, more common than type-1 [1][2][3]. Yet too many of us are still misdiagnosed. As one scientific article lamented, right in the title: “Latent Autoimmune Diabetes in Adults Should Be Less Latent.” [4]
The good news is: us. We can spread the word, and help misdiagnosed LADAs learn which disease they actually have. I am forever grateful to the friend who helped me discover that LADA existed.
A simple GAD[5]-antibody test shows if we are LADA[6]. As more LADAs are correctly diagnosed, the subtleties of our LADA ‘flavor’ of diabetes will become better and better understood. Helping each other, we help ourselves.
[1] Laugesen E, Østergaard JA, Leslie RD. Latent autoimmune diabetes of the adult: current knowledge and uncertainty. Diabet Med. 2015;32(7):843-852.
[2] Liu B, Xiang Y, Liu Z, Zhou Z. Past, present and future of latent autoimmune diabetes in adults. Diabetes Metab Res Rev. 2020;36(1):e3205.
[3] O’Neal KS, Johnson JL, Panak RL. Recognizing and Appropriately Treating Latent Autoimmune Diabetes in Adults. Diabetes spectrum: a publication of the American Diabetes Association vol. 29,4 (2016): 249-252.
[4] Fourlanos S, Dotta F, Greenbaum CJ, et al. Latent autoimmune diabetes in adults (LADA) should be less latent. Diabetologia. 2005;48(11):2206-2212.
[5] glutamic acid decarboxylase
[6] Felman, A with Prelipcean M, MD. How do GAD antibodies affect diabetes? Medical News Today. March 25, 2019. www.medicalnewstoday.com/articles/313764
