Subject: GLP-1s and Slowed Gastric Emptying Part 2: What About Nutrient Absorption?
From: Derek from Research Radar <[email-masked]>
To: [email-masked]
Date: Sat, 25 Apr 2026 19:54:50 +0000
List-Id: <derekpruski.substack.com>

View this post on the web at https://derekpruski.substack.com/p/glp-1s-and-slowed-gastric-emptying-4ec

After the first post on medication absorption, a lot of you asked the natural follow-up question: what about food? What about nutrients? If gastric emptying is slowed dramatically, are we actually absorbing more from our meals because food sits in the stomach longer? Or is something else going on?
There’s a popular claim floating around that slowed gastric emptying means “you digest your food better” — and like most popular claims, it’s partially true, partially misleading, and worth unpacking properly.
Let’s walk through it.
The Mechanism Recap
Quick refresher from Part 1: GLP-1 receptor agonists slow gastric emptying by reducing antral contractility, increasing pyloric tone, and dampening the migrating motor complex. Food sits in the stomach longer. The release of chyme into the small intestine becomes slower and more gradual.
The intuitive leap people make is: longer time in the stomach equals more breakdown equals better absorption downstream. Sounds reasonable. Reality is more nuanced.
What Actually Happens to Nutrient Absorption
Here’s the key distinction — gastric emptying and nutrient absorption are two different processes happening in two different places.
The stomach’s main jobs are mechanical breakdown and acid/pepsin denaturation of proteins. The actual absorption of macronutrients and most micronutrients happens in the small intestine. So slowing the stomach doesn’t directly mean “more absorption” — it means food is being released into the small intestine on a delayed, smoothed-out timeline.
What the literature actually shows for GLP-1 users:
Macronutrient absorption is largely preserved. Protein, carbs, fats — the small intestine still absorbs them effectively. Total caloric absorption from a given meal isn’t meaningfully reduced. The curve is just stretched out.
Postprandial glucose excursions are blunted. This is one of the most well-documented effects. Because carbs trickle into the small intestine more slowly, blood glucose rises more gradually. This is part of how GLP-1s improve glycemic control — not by blocking carb absorption, but by smoothing the delivery.
Gastric digestion of protein may be more thorough. This is the kernel of truth in the “you digest better” claim. With food sitting in acidic gastric conditions longer, protein denaturation by pepsin has more time to occur. Whether this translates to meaningfully better downstream amino acid absorption is less clear in the human data, but mechanistically it’s plausible.
Fat digestion timing shifts. Fats normally slow gastric emptying on their own as a feedback signal. On a GLP-1, that signal is layered on top of an already-slowed system. Fat-heavy meals can sit particularly long, which is part of why high-fat meals tend to produce the worst GI side effects on these protocols.
Specific Nutrient Issues That Have Popped Up
This is where the rubber meets the road. Across the broader GLP-1 user base — both clinical and community-reported — certain nutrient deficiencies and suboptimal labs have shown up consistently enough that they’re worth flagging individually.
Protein and lean mass loss. This is the big one. Studies on semaglutide weight loss have shown that 25–40% of total weight lost can come from lean mass when protein intake and resistance training aren’t prioritized. The mechanism isn’t a protein absorption problem — it’s that users are eating dramatically less total protein because appetite is suppressed across the board. Combined with reduced training stimulus from low-energy availability, the body has every reason to drop muscle. This is the most consistent and most preventable issue on GLP-1 protocols.
B12 (cobalamin). Showed up early in GLP-1 literature and continues to be reported. B12 absorption requires intrinsic factor produced by gastric parietal cells, and the absorption itself happens in the terminal ileum. Reduced overall food intake plus altered gastric environment can produce suboptimal B12 status over months on protocol. Symptoms can be vague — fatigue, brain fog, neuropathy in worse cases. Worth checking on bloodwork.
Iron. Iron absorption in the duodenum is dependent on gastric acid for solubilization, particularly for non-heme iron from plant sources. GLP-1s appear to reduce gastric acid output in some users, and combined with reduced red meat intake (which is common because protein-heavy meals often feel the worst), iron status can drift downward. Women with menstrual losses are at particular risk here.
Magnesium. Often shows up as cramping, restless legs, sleep disturbances, or muscle twitches. Multifactorial — reduced food intake, increased GI losses (especially during dose escalation when GI side effects are worst), and the fact that magnesium is one of the most common borderline-low nutrients in the general population even before adding a GLP-1.
Potassium and sodium. Electrolyte disturbances are common, especially during dose escalation. Reduced food intake means reduced potassium intake (most people get the majority of their potassium from food, not supplements), and reduced sodium intake combined with any GI losses can produce real symptoms — lightheadedness on standing, fatigue, headaches, muscle weakness. The “GLP-1 keto flu” people describe in the first weeks is largely an electrolyte story.
Vitamin D. Not necessarily an absorption issue — more an intake issue, since vitamin D-rich foods (fatty fish, fortified dairy, eggs) often drop out of the diet when appetite tanks. Pre-existing low vitamin D in the population gets worse, not better, on protocol.
Calcium. Calcium absorption depends on gastric acid for solubility and on adequate vitamin D status. Both can shift on GLP-1 protocols. Long-term concern is bone density, particularly in users on extended protocols who are also losing weight rapidly — bone mass loss has been documented alongside lean mass loss in some semaglutide and tirzepatide studies.
Thiamine (B1). Less commonly discussed but worth mentioning. Thiamine has limited body stores (only 2–3 weeks worth) and requires consistent intake. Cases of thiamine deficiency have been reported in patients on GLP-1s with significant intake reduction or persistent vomiting during dose escalation. The clinical presentation can include neurological symptoms and is one of the more serious nutrient issues that’s emerged.
Hydration / fluid balance. Not a nutrient per se, but worth grouping here. Reduced food intake means reduced incidental water intake (food carries more water than people realize). Combined with reduced thirst signaling that some users report, dehydration is one of the most common practical issues — and it amplifies a lot of the other symptoms above.
The Pattern Behind All of This
Notice the through-line — most of these issues aren’t actually about altered absorption from slowed gastric emptying. They’re about dramatically reduced intake, layered on top of slightly altered absorption conditions, layered on top of pre-existing borderline status in the general population.
The reduced intake piece is doing the heavy lifting. If someone’s eating 40% less food across the board, they’re getting 40% less of everything in that food. That’s not an absorption problem — that’s an intake problem. But the two get conflated constantly.
So Is It True That You “Digest Better”?
Partially. The longer gastric residence time does likely improve mechanical and chemical breakdown of food, particularly proteins. That’s the legitimate kernel.
What it doesn’t mean is that you’re extracting more total nutrition from less food. The math on caloric and macro absorption doesn’t really change. What changes is the kinetics — same total nutrition, delivered on a stretched-out curve.
The Practical Takeaway
A few things worth keeping in mind on a GLP-1 protocol:
Protein intake matters more, not less. Because total food intake drops significantly for most users, and because muscle preservation depends on hitting adequate protein, the protein piece becomes proportionally more important. Slower gastric emptying doesn’t fix an underdose — it just changes the timing of an adequate one.
Hydration and electrolytes need attention. Reduced food intake means reduced incidental fluid and electrolyte intake. This is one of the more common practical issues users run into, and it shows up early.
Micronutrient density matters. When total volume drops, every meal needs to do more nutritional work. This is where multivitamin or targeted supplementation conversations come up, and where bloodwork on longer protocols actually starts to earn its keep — particularly for B12, iron, vitamin D, and magnesium.
Resistance training is non-negotiable for lean mass. The lean mass loss data on GLP-1s is the most consistent finding across studies. Adequate protein plus actual training stimulus is the only thing that meaningfully shifts that curve.
Don’t interpret slower digestion as “better digestion” in a way that lets you eat less and call it equivalent. It’s not. The math on total nutrition still has to work out. The GLP-1 changes the curve, not the conservation of mass.
The framing from Part 1 applies here too: slower does not mean less, but it also doesn’t mean more. The kinetics shift; the totals mostly don’t. Where things actually go wrong on GLP-1 protocols isn’t usually absorption — it’s the dramatic reduction in intake that gets ignored because the appetite suppression is doing its job.
Pay attention to what you’re putting in. Slowed gastric emptying is doing interesting things to the timing, but it can’t manufacture nutrition out of food that isn’t there.
This article is for research and educational purposes only. The compounds and protocols discussed are intended for in vitro and laboratory research use. Nothing in this article constitutes medical advice, clinical guidance, or recommendations for human consumption.

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