AWAN Clinic

04/08/2026

-IR provides a practical surrogate estimate of insulin resistance using fasting glucose and insulin:
HOMA-IR = [Fasting Insulin (µU/mL) × Fasting Glucose (mmol/L)] ÷ 22.5
HOMA-IR = [Fasting Insulin (µU/mL) × Fasting Glucose (mg/dL)] ÷ 405
While not a replacement for the euglycemic clamp, HOMA-IR remains one of the most widely used tools in clinical research and metabolic risk assessment.
Matthews DR, et al. Diabetologia. 1985;28:412-419.

21/07/2026

Casual exercise

19/07/2026

The incretin system - the hormonal communication network between your intestine, pancreas, and brain - is one of the most clinically significant biological systems in Type 2 diabetes, and it is the system that the most widely prescribed new class of diabetes medications is designed to target. Understanding it naturally reveals why specific dietary choices produce such powerful effects on blood sugar.

Incretins are hormones released from specialized cells lining the small intestinal wall in direct response to food arriving in the gut. The two primary incretins are GLP-1 (glucagon-like peptide-1) produced by L-cells, and GIP (glucose-dependent insulinotropic polypeptide) produced by K-cells. Together they are responsible for approximately 50 to 70% of the insulin secreted after eating - a phenomenon called the incretin effect. This means that more than half of your post-meal insulin response originates not from your pancreas detecting blood glucose directly, but from your gut detecting food and pre-signaling the pancreas to prepare an insulin response.

GLP-1 simultaneously suppresses glucagon release from alpha cells - preventing the inappropriate glucagon surge that compounds post-meal hyperglycemia in Type 2 diabetes. It slows gastric emptying - reducing the rate at which glucose enters the bloodstream from the intestine. And it signals the brain's hypothalamus and brainstem to reduce appetite and increase satiety - providing a coordinated meal-termination signal across three organ systems simultaneously.

In Type 2 diabetes an incretin defect is well documented - GLP-1 release from L-cells is significantly reduced, and the remaining GLP-1 is more rapidly degraded by the DPP-4 enzyme. This incretin deficiency explains approximately 30% of post-meal hyperglycemia in established Type 2 diabetes and is the biological basis for an entire medication class - GLP-1 receptor agonists mimic GLP-1, while DPP-4 inhibitors prevent its degradation.

Dietary fiber is the most powerful natural GLP-1 stimulant available. L-cells detect fiber fermentation products from gut bacteria - particularly short-chain fatty acids — and respond with dramatically increased GLP-1 release. Research has confirmed that 35 grams of daily dietary fiber raises natural GLP-1 levels by 23% - producing clinically meaningful improvements in the incretin effect without pharmaceutical intervention.

Key takeaway: Your gut is a hormone factory for blood sugar management. Feeding it fiber is activating the same hormonal system your diabetes medication targets - naturally and simultaneously.

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📌 RESOURCES
— GLP-1 and Incretin System Research: pubmed.ncbi.nlm.nih.gov — search "incretin effect Type 2 diabetes GLP-1"
— American Diabetes Association — Incretin Therapies: diabetesjournals.org/care
— Endocrine Society — GLP-1 Biology: endocrine.org/patient-engagement/endocrine-library

19/07/2026

What does indicate?

C-peptide is a marker used to assess pancreatic beta-cell function and determine the type of diabetes. Here's what different levels typically indicate:

- Low C-peptide levels (≤0.20 nmol/L, as correctly pointed out, not mmol/L) often suggest Type 1 Diabetes (T1D), where the body's immune system attacks and destroys insulin-producing beta cells.
- High C-peptide levels (≥0.30 nmol/L or higher) typically indicate Type 2 Diabetes (T2D), where the body either resists insulin or doesn't produce enough.

C-peptide levels help clinicians differentiate between T1D and T2D, guiding treatment decisions and insulin therapy.

10/07/2026

A rapid remission clinical trial published in Cell Metabolism in 2024 has produced findings that are significantly compressing the timeline previously assumed necessary for meaningful Type 2 diabetes reversal - demonstrating metabolic normalization in a matter of weeks rather than months under specific dietary conditions.

The trial enrolled 57 adults with Type 2 diabetes of less than 6 years duration - a population chosen specifically to maximize the potential for beta cell recovery. Participants were randomized to either a very low calorie diet of 800 calories daily for 12 weeks using total diet replacement meal plans, or standard diabetes management guidelines.

At the 12-week primary endpoint, 61% of participants in the very low calorie diet group had achieved HbA1c below 6.5% without diabetes medication - meeting the formal definition of Type 2 diabetes remission. More remarkably the timeline of metabolic recovery was mapped in unprecedented detail through weekly testing.

Liver fat began measurably reducing within 7 days of dietary intervention - before any significant weight loss had occurred. Fasting blood glucose began normalizing within 2 weeks. Hepatic insulin sensitivity was measurably restored within 3 weeks. First-phase insulin secretion from beta cells - the most critical functional marker and the last to recover in previous studies - showed measurable improvement at the 4-week mark in responders, earlier than any previous trial had documented.

The researchers identified a specific biomarker - liver fat percentage measured by MRI - that predicted remission success at week 2 of intervention with 84% accuracy. Participants who showed greater than 30% reduction in liver fat by day 14 had a 91% probability of achieving remission at week 12. This finding opens the possibility of early personalized prediction of dietary intervention response - potentially transforming how rapid remission protocols are targeted to the patients most likely to benefit.

Always consult your doctor before making changes to your diet or treatment plan.
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📌 RESOURCES
— Cell Metabolism — Rapid Remission Research: cell.com/cell-metabolism
— DiRECT Trial — Diabetes Remission: thelancet.com
— Diabetes UK — Remission Information: diabetes.org.uk/about-us/research/our-research-projects/remission

Impactful basic and clinical metabolic research addressing the molecular mechanisms underlying physiological homeostasis and what goes awry in disease.

03/07/2026

Two people can carry the same weight, the same insulin resistance, and the same fasting glucose, and still find that the diet which most improves their metabolic health runs in opposite directions, because what separates them is not how resistant they are but which organ the resistance sits in.

A Dutch team ran what precision nutrition rarely gets: a randomized controlled trial. They took 242 adults with overweight or obesity, measured whether each person's insulin resistance was concentrated in muscle or in the liver using an oral glucose tolerance test, then assigned them for twelve weeks to one of two diets, a high-monounsaturated-fat diet or a low-fat diet high in protein and fiber, arranged so that one group's pairing was the mirror image of the other's. The pre-registered primary outcome, a measure of how well the pancreas compensates for insulin resistance, did not improve in either arrangement.

The arrangement in which the muscle-insulin-resistant people ate the low-fat, high-protein, high-fiber diet and the liver-insulin-resistant people ate the high-monounsaturated-fat diet produced greater improvements in insulin sensitivity, blood glucose control, triglycerides, and C-reactive protein than the opposite arrangement. Same two diets, same twelve weeks, the same degree of insulin resistance at baseline. The only thing that differed was whether each person's diet was matched to the tissue driving their resistance, and that matching alone separated the two groups on markers that track long-term cardiometabolic risk.

Insulin resistance is usually treated as a single condition, but it is not distributed evenly. In some people the defect sits mainly in skeletal muscle, where insulin normally drives glucose out of the blood and into the tissue; in others it sits mainly in the liver, where insulin normally restrains glucose output and fat production. These can be measurably different states, separable by the pattern of glucose and insulin across an oral glucose tolerance test, and recent work shows they carry distinct plasma protein signatures rather than being two names for the same problem. Because muscle and liver handle carbohydrate and fat differently, it is biologically reasonable that the macronutrient mix which helps one is not the mix that helps the other, though this trial demonstrates the pattern more clearly than it explains the precise reason.

Several things keep this a proof of concept:

The pre-registered primary endpoint was null, so the positive results all come from secondary and exploratory analyses, which carry less weight and a higher chance of a false positive. It is a single twelve-week trial in adults with a body mass index between 25 and 40, so it says nothing about lean or older people, or about effects that take longer than three months to surface. Several of the authors are employed by nutrition companies, including a dairy company and companies that sell the kinds of fats and proteins the diets emphasized, which does not invalidate the work but is worth naming. And the phenotyping depends on an oral glucose tolerance test with timed blood draws, which is not something most people or most clinics do, so the path from this finding to an individual's plate is not yet built.

What the evidence supports is that where insulin resistance sits, in muscle or in the liver, appears to change which macronutrient pattern improves a person's cardiometabolic markers, and that treating insulin resistance as one uniform condition may be leaving some of that improvement unclaimed. What it does not support is any specific personalized-nutrition product or test sold on the promise of a diet tailored to your biology, because the primary outcome was null, the effect lives in secondary markers, and no one has yet shown that this matching changes hard outcomes like diabetes or cardiovascular events. The practical reframe is still worth stating: the personalized-nutrition industry is built on the premise that your biology should set your diet, and this is one of the few randomized trials to test a real, measurable version of that premise rather than a genetic or microbiome readout of uncertain meaning. The open question is whether matching diet to insulin-resistance phenotype changes anything a person can feel or that lengthens a life, or whether it is a real but small metabolic signal that will never justify the testing required to act on it.

Trouwborst et al., Cell Metabolism 2023
Abdul-Ghani et al., Diabetes Care 2007
Kemper et al., J Clin Endocrinol Metab 2026

01/07/2026

01/07/2026

01/07/2026

23/06/2026

Newer Antihypertensive Agents for Resistant Hypertension

Aprocitentan

• First novel oral antihypertensive mechanism approved in decades
• Dual endothelin receptor antagonist
– Blocks ET-A and ET-B receptors
• Add-on therapy for resistant/uncontrolled hypertension

• Adverse effects:
– Fluid retention/edema
– Anemia
– Possible liver-related concerns

Baxdrostat

• First-in-class aldosterone synthase inhibitor
• Reduces aldosterone production
• Add-on option for uncontrolled/resistant hypertension
• Significant BP reduction shown in trials

• Potential adverse effects:
– Hyperkalemia

Widaplik

• Single-pill combination:
– Telmisartan + amlodipine + indapamide
• Improves adherence and simplifies treatment
• Not a new mechanism of action