25% of diabetics have the insulin-deficient type – 62% of them have <30 ng/mL Vitamin D

Exploratory Analysis of Type 2 Diabetes Mellitus Metabolic Phenotypes and Their Association With Vitamin D Status in Primary Care Patients

Diabetes, Obesity and Metabolism, 2026, https://doi.org/10.1111/dom.71275

Liliane Viana Pires, Matheus Menezes-Santos, Andréa Costa Goes, Heitor Siqueira Ribeiro, Luana Ferreira Alves, Beatriz Cruz dos Santos, Jéssyca Teles Barreto, Roberta Cristina Vieira Meneses, Ana Mara de Oliveira e Silva, Ana Hermínia Andrade e Silva, Sadraque Eneas de Figueiredo Lucena BRAZIL

Summary by Claude - August, 2026

Type 2 diabetes is not one disease. This cross-sectional study of 178 primary-care patients in Sergipe, Brazil sorted them into the four clusters proposed by Ahlqvist in 2018, then looked at vitamin D in each.

How the 178 patients split:

Severe insulin-deficient (SIDD-like): 25.1% – the group of interest here
Severe insulin-resistant (SIRD-like): 19.6%
Mild obesity-related (MOD-like): 26.8%
Mild age-related (MARD-like): 28.5%

The insulin-deficient quarter was the worst off on nearly every measure: youngest at diagnosis (42 years), highest HbA1c (10.1%), lowest beta-cell function, highest fasting glucose (216 mg/dL), and by far the most insulin use (37.8% vs 2.9%–10%).

Vitamin D findings: 62.2% of the insulin-deficient group were under 30 ng/mL, versus 31.2% of the mild obesity group. After adjusting for sex, age and education, the insulin-deficient group had 3.68X higher odds of being under 30 ng/mL than the mild age-related group (95% CI 1.34–10.56, p=0.013). Grouping all four into severe vs mild, median 25(OH)D was 28.6 vs 32.4 ng/mL (p=0.027). Female sex independently raised the odds 2.63X.

What this does not show: no supplementation, no doses, no follow-up — cross-sectional only, so causation runs either way (the authors say the relationship "is likely bidirectional," noting hyperglycemia itself suppresses CYP2R1/CYP27B1 and boosts CYP24A1). Across all four groups as a continuous variable, vitamin D missed significance (p=0.066); only the severe/mild regrouping and the SIDD-vs-MARD contrast reached it. The insulin-resistant group, though labeled severe, showed no association (OR 1.21, p=0.692). Sun exposure was not measured, and n=178 is small for a four-way split. Note also that this is a tropical cohort at 10°S with year-round sun — median levels were near 30 ng/mL even in the worst group, so a temperate population would start much lower.

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Followup question to Claude AI:

I am used to Diabetics having insulin resistance. Do those with severe insulin resistance need more? All the time, some of the time, more often during the day, or higher doses?

Answer

Your intuition matches the popular picture of type 2 diabetes, but this paper is a good illustration of why it breaks down. In this cohort the severe insulin-resistant group used the least insulin of all four: 2.9%, versus 37.8% in the insulin-deficient group and about 10% in the two mild groups.

This is because resistance and injected insulin address different problems.

Insulin resistance means the tissues need more insulin to move a given amount of glucose. That demand can be met from inside as long as the pancreas can keep up, and in the SIRD group it clearly was: HOMA-B of 145.9, the highest of the four clusters and roughly double the MARD group. That is compensatory hyperinsulinemia — the beta cells running hot to overcome the resistance. The result was good numbers on paper: HbA1c 6.0% and fasting glucose 101 mg/dL, the best in the study. No reason for a prescription.

The SIDD group is the mirror image. HOMA-B of 30, HbA1c 10.1%, fasting glucose 216. The beta cells have failed, so the insulin has to come from a syringe. That is what drives the 37.8%.

So to your four options: higher doses, not more often.
When an insulin-resistant person does eventually need insulin — and they usually do, since the compensation is not permanent — the characteristic pattern is large total daily doses, sometimes several times what a lean insulin-deficient patient needs, because each unit accomplishes less. The insulin-deficient patient needs relatively modest amounts but needs them reliably and timed to meals, because there is no endogenous supply underneath to smooth things out.

The paper's own discussion sketches the trajectory: the insulin-resistant profile "preserves compensatory hyperinsulinemia, allowing years of maintained glucose tolerance before β-cell failure occurs." Resistance buys time. Deficiency is what ends it.

This cohort's SIRD group had unusually good glycemic control, which the authors flag as a departure from other studies where SIRD carries high complication risk, especially kidney disease.

The separation here was not clean: HOMA-IR was elevated in the SIDD group too (3.2, actually the highest), so "insulin-deficient" in this sample meant deficient and resistant. That muddies the contrast somewhat.

25% of diabetics have the insulin-deficient type – 62% of them have <30 ng/mL Vitamin D

Exploratory Analysis of Type 2 Diabetes Mellitus Metabolic Phenotypes and Their Association With Vitamin D Status in Primary Care Patients

Followup question to Claude AI:

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