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I have spent more than 25 years watching food sensitivities show up in places nobody expects: migraines, joint pain, eczema, bloating, brain fog. Blood sugar belongs on that list too. Other practitioners who use MRT have reported glucose improvements in their clients, and people with diabetes have described the same thing after LEAP. So when I wore a continuous glucose monitor before my MRT test and again after following my LEAP eating plan, I was looking for a change. The difference turned out to be hard to ignore.
This post walks through my actual glucose data, the science connecting food reactions to inflammation and insulin resistance, and, just as important, what my results do and do not prove. If you have been doing everything “right” and your blood sugar still will not cooperate, this may be the missing piece worth testing.
What my CGM showed before and after MRT
I wore a Lingo biosensor, an over-the-counter continuous glucose monitor, before I did my Mediator Release Test (MRT) and again after I had been following my LEAP protocol for [timeframe]. Lingo assigns each glucose spike a score based on how high it climbs and how long it lasts, which makes it easy to compare days.
| Measure | Before MRT (late April/May 2025) | After LEAP |
|---|---|---|
| Daily average glucose | 100 mg/dL | About 80 mg/dL on a typical day |
| Lingo spike scores logged | 13, 20, 22 (April 29); 15, 13 (May 1) | 6, 3, 7, 4 |
| Highest readings on the days shown | Above 170 mg/dL, twice in one evening | Under 100 mg/dL all day |
| Peak after the same portion of rice | 187 mg/dL | 148 mg/dL (September 22, 2026) |
| Peak after 2 Medjool dates | 163 mg/dL | 115 mg/dL |

Two things stand out to me. First, my daily average dropped by about 20 mg/dL, from 100 to a fairly consistent 80. A daily average of 100 is not alarming by conventional standards, but it sat right at the upper edge of where I want a non-diabetic adult to live. Second, and more telling, the spikes changed shape. Before MRT, I had jagged climbs past 170 mg/dL that took a couple of hours to settle. After LEAP, a midnight snack of goat cheese and oat crackers scored a 6, and carrots scored a 3.
I am still eating carbohydrates. My typical carb intake is under 125 grams a day, and I have not eaten a high-carb diet in more than a decade. That stayed the same before and after MRT. What changed was which foods I eat, not how many carbs I eat. That is exactly why I think this is worth writing about.
Same foods, same portions, before and after
The comparisons I find most convincing are the simplest ones: the same food, in the same amount, before and after. Rice gave me my highest spike before MRT, at 187 mg/dL. After following my LEAP plan, the exact same portion peaked at 148 mg/dL. Two Medjool dates, a naturally sweet whole food many people assume is a safe snack, took me to 163 mg/dL before MRT. After LEAP, the same two dates peaked at 115 mg/dL.

That is a 39 mg/dL lower peak for rice and a 48 mg/dL lower peak for dates, from identical carbohydrate loads. Both foods still raised my blood sugar, as any starch or fruit will, and rice still nudged a little above the 140 mg/dL mark. But the dates now stay well below it, and my body handled both noticeably better. When the food and the amount stay the same and the response changes, the difference points to something about how my body is processing glucose, and reduced inflammation is the most likely explanation I can see.
Why a food sensitivity could show up on a glucose monitor
MRT measures how your white blood cells respond to foods and food chemicals. When a reactive food triggers them, they release chemical mediators such as histamine, prostaglandins, leukotrienes, and cytokines. That is the same inflammatory machinery that drives symptoms like headaches, gut pain, and joint aches. You can read the full breakdown in my complete guide to MRT testing and the LEAP method.
Here is where it connects to blood sugar. Inflammatory cytokines interfere with insulin signaling. In a landmark 1993 study, researchers showed that the cytokine TNF-alpha plays a direct role in obesity-linked insulin resistance, and blocking it improved insulin sensitivity in animals. Decades of research since have confirmed that chronic, low-grade inflammation is one of the central drivers of insulin resistance and type 2 diabetes.
The numbers behind that are striking. In the Women’s Health Study, researchers followed more than 27,000 healthy middle-aged women for four years. Women with the highest levels of C-reactive protein (CRP), a standard blood marker of inflammation, had about four times the risk of developing type 2 diabetes compared with women with the lowest levels, even after accounting for weight, family history, smoking, exercise, alcohol, and hormone therapy. More broadly, a 2019 review in Nature Medicine linked systemic chronic inflammation to the diseases that together cause most disability and death worldwide, including heart disease, cancer, diabetes, kidney disease, fatty liver disease, and autoimmune conditions, and it named poor diet and psychological stress among its drivers. These studies show that inflammation predicts disease risk; they do not show that food sensitivities are the source of it. That is the question personal testing can help answer. If you want to know where your own inflammation stands, a high-sensitivity CRP test is available on my functional labs page.
The gut matters here too. When the intestinal barrier is compromised, bacterial fragments called lipopolysaccharides (LPS) can enter the bloodstream. A 2007 study in Diabetes found that raising LPS levels in mice was enough to trigger inflammation, weight gain, and insulin resistance, a process the researchers called metabolic endotoxemia. Many of my clients with food sensitivities also have gut barrier problems, and the two feed each other.
Finally, inflammation is a physiological stressor. Stress hormones like cortisol tell your liver to release stored glucose. If you have ever seen your glucose climb on a CGM without eating anything, stress hormones are a common reason. I cover that side of the story in depth in my book, Cortisol Fix, including the gut-cortisol connection and how I use MRT alongside other food sensitivity tests.
Healthy foods don’t spike everyone the same way
One of the most important nutrition studies of the last decade came out of the Weizmann Institute in 2015. Researchers fed 800 people standardized meals and tracked their glucose continuously. The same food produced wildly different responses from person to person. Some people spiked on bread and not on bananas; others did the opposite.
A 2018 Stanford study added another layer. Using CGMs on people who did not have diabetes, researchers found that many of them regularly reached glucose levels in the prediabetic and even diabetic range after meals. Standard fasting glucose and A1c tests missed this completely.
Together, these studies explain why generic “low glycemic” food lists fail so many people. Your response to a food depends on your microbiome, your sleep, your stress, and, in my clinical experience, whether that food provokes your immune system. This is why I say test, not guess.
Food sensitivities are one piece of the blood sugar puzzle
Removing my reactive foods made a real difference, but it is not the only thing that shapes my glucose. Other factors contribute a lot, and my CGM shows them clearly.
Protein is the biggest one. Eating protein alongside carbohydrates has always blunted my glucose response, and since following LEAP, that effect is even stronger. Protein slows how quickly food leaves your stomach and changes the hormone signals that help your body handle glucose, so the same carbs enter your bloodstream more gradually.
Carbs on their own are a different story. When I eat carbohydrates without protein or fat, my glucose rises faster, and sometimes it overshoots in the other direction. A quick rise can trigger a larger insulin release than you need, and your blood sugar can then dip too low a couple of hours later. That has happened to me, and it is one reason a dip below 70 mg/dL sometimes follows a spike on a CGM graph.
So if you are experimenting with your own glucose, pair your carbs with protein, and look at the whole curve, not just the peak. Food sensitivities, meal composition, sleep, stress, and activity all work together.
What my results do and don’t prove
I want to be straightforward here, because blood sugar is too important for hype.
- This is one person’s data. I am a sample size of one. Apart from the rice and date comparisons, my before and after days involved different meals, and even with those, sleep, activity, and what I ate earlier in the day can all shift a glucose response.
- Consumer CGMs have a margin of error, and individual sensors vary. Small differences on a single day should not be overinterpreted.
- MRT is not a diabetes test. It does not measure glucose or insulin, and no clinical trial has yet studied MRT-guided diets for blood sugar. The published research on MRT so far focuses mainly on digestive symptoms, including a 2017 randomized trial in people with irritable bowel syndrome.
- Other changes may have contributed. Removing reactive foods often changes overall eating patterns, and that alone can shift glucose, although my total carbohydrate intake stayed about the same.
What I can say is that the pattern I saw in myself matches what the inflammation research predicts. It also matches what other practitioners and people with diabetes have reported after LEAP, which is why I went in expecting a change. Those reports are observations, not controlled studies, and my data adds one more observation rather than proof. My personal MRT story started with symptoms, and tracking my glucose let me check whether those reports held true for me.
How I would use a CGM and MRT together
If you want to find out whether food sensitivities are affecting your own blood sugar, here is the approach I use:
- Get a baseline. Wear a CGM for a full sensor cycle while eating normally, and log your meals, sleep, and stress. Note your daily average and your biggest spikes.
- Test your reactive foods. An MRT panel measures your reactions to 170 foods and food chemicals, including “healthy” foods you would never suspect.
- Follow a LEAP plan built around your safe foods. You start with your lowest-reactive foods and expand in phases, so you are not guessing.
- Wear a second CGM and compare. Look at the same measures as your baseline: daily average, spike height, and how long spikes last.
- Reintroduce foods one at a time. Watch both your symptoms and your glucose curve for each new food.
A quick note on how I read MRT results, because it matters for how fast inflammation comes down. Each food on an MRT report gets a number. Foods under 1.5 are your safest, least reactive foods. Foods in the 1.6 to 1.9 range are not reactive per se, but they are less safe and more inflammatory for you than foods under 1.5. To bring inflammation down faster, I have clients leave out those 1.6 to 1.9 foods for the first 11 days, along with their reactive foods. After day 11, we add the 1.6 to 1.9 foods back one at a time, one new food each day, so you can see exactly how your body responds to each one.
Food sensitivity testing through my practice is not a self-checkout purchase. I review your history first to make sure MRT is the right tool for you. If you would also like baseline labs such as fasting insulin, A1c, or inflammatory markers, you can find them on my functional labs page.
A note on safety. If you take insulin, a sulfonylurea, or any other glucose-lowering medication, talk to your prescriber before changing your diet. Reducing inflammatory foods can lower your glucose, and your dose may need adjusting to prevent low blood sugar. Elimination diets also are not the right fit for anyone with a history of disordered eating or during pregnancy without close professional guidance. Lingo is designed for adults who are not on insulin and is not meant to diagnose or manage diabetes.
Frequently asked questions
Can food sensitivities cause high blood sugar?
Food sensitivities are not a recognized cause of diabetes, but they can contribute to inflammation, and inflammation is a well-documented driver of insulin resistance. In my own continuous glucose monitor data, removing my reactive foods coincided with a lower daily average and much smaller spikes.
Is MRT testing a blood sugar test?
No. MRT (Mediator Release Test) measures how white blood cells react to foods and food chemicals. It does not measure glucose or diagnose diabetes. I use it to identify reactive foods, then use a glucose monitor to see how my body responds after those foods are removed.
Can a CGM tell me which foods I’m sensitive to?
Not reliably on its own. A CGM shows your glucose response, but a spike can come from carbohydrate load, stress, poor sleep, or exercise timing as well as an inflammatory food. I pair CGM data with MRT results so I’m testing, not guessing.
Should I stop my diabetes medication if my glucose improves?
No. Never change or stop a glucose-lowering medication on your own. If you remove inflammatory foods and your numbers improve, talk with your prescriber, because doses may need to be adjusted to prevent low blood sugar.
The bottom line
My blood sugar did not improve because I cut carbs. The same bowl of rice that once sent me to 187 mg/dL now peaks at 148, and two Medjool dates dropped from 163 to 115. That changed after I stopped eating the foods my immune system was reacting to. The science linking inflammation to insulin resistance is strong. The direct research on food sensitivities and glucose is still young. That is exactly the gap a CGM and an MRT test can help you fill for your own body.
If your glucose is creeping up despite a clean diet, reach out about MRT testing and let’s find out what your body is really responding to. #TheHealthyRD
References
- Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science. 1993;259(5091):87-91. doi:10.1126/science.7678183
- Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006;116(7):1793-1801. doi:10.1172/JCI29069
- Cani PD, Amar J, Iglesias MA, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761-1772. doi:10.2337/db06-1491
- Zeevi D, Korem T, Zmora N, et al. Personalized nutrition by prediction of glycemic responses. Cell. 2015;163(5):1079-1094. doi:10.1016/j.cell.2015.11.001
- Hall H, Perelman D, Breschi A, et al. Glucotypes reveal new patterns of glucose dysregulation. PLoS Biol. 2018;16(7):e2005143. doi:10.1371/journal.pbio.2005143
- Ali A, Weiss TR, McKee D, et al. Efficacy of individualised diets in patients with irritable bowel syndrome: a randomised controlled trial. BMJ Open Gastroenterol. 2017;4(1):e000164. doi:10.1136/bmjgast-2017-000164
- Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA. 2001;286(3):327-334. doi:10.1001/jama.286.3.327
- Furman D, Campisi J, Verdin E, et al. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019;25(12):1822-1832. doi:10.1038/s41591-019-0675-0
