Anyone try the Stelo or Lingo yet? Are they both good enough?
I ask because I haven’t been able to get a libre 3 for over a month, so I might give up and just order one of those while I wait for the issue to be resolved.
Yes, I tried the Lingo, twice, absolute garbage, off by 30-40 points when I validated it against vein test at UCLA. Absurd readings at all times, and the app is trash as well. Like a moron I bought the $249 6 sensor version and now 4 of them are sitting in a drawer. But that’s just my experience, yours may be different.
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WOW, that is shocking. Do you assume the RX version (freestyle libre 3) is equally crappola?
And would you guess dexcom’s stelo is better?
Are you guessing this is an issue of the OTC versions not being as robust? Or an Abbott issue?
I realize you don’t know, but your guess is better than mine!
I’m afraid my guess is no better. Re: libre 3 - theoretically libre 3 should be better than the lingo, because the lingo uses the libre 2 sensor which is less accurate than the libre 3. However the accuracy differences between these two sensors are pretty modest, and if you have inaccuracies on the order of 30-40 points, that’s just noise.
I have not used the dexcom product, but reports seem to indicate they are fairly similar when it comes to accuracy. There are other considerations, like price, size, quality of attachment and app, all of which seem to slightly favor the lingo (which is why I picked it), but that’s on paper, individual preferences are key, and also on paper the app for lingo is better, but as I experienced it, it’s complete garbage, where almost none of the features actually work… big on promises, sh|t on delivery.
I don’t know, I’m completely disenchanted with my CGM experience so far. But then again a ton of people use them, and are happy, at least with the Rx versions. I must say, I am stunned by the apparent low expectations of many users, where they just accept what to me would be shockingly bad error margins - my fingerprick monitor has an 8% error margin (validated at a UCLA vein reading), which I think is not great, but what seems acceptable in the CGM world is just mindboggling… I cannot see any value in readings so wide of the mark - may as well make random guesses and you’ll be more accurate. I don’t get it.
But that’s just me. It’s possible that my interstitial glucose levels are very nonstandard and deviate from serum by many more SDs than in the general population. Or I got two bum sensors in a row. I guess I could try again at some point, but I’m not in a hurry. Bottom line, I’m an N=1, and your experience might be very different, so I can’t really tell you what to pick. What I would definitely recommend is always validating it against a good fingerprick monitor, otherwise you really don’t know what you’re getting. Good luck!
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FYI, You can get 15% off Lingo with code THANKFUL15 (for 2- and 4-week plans). Offer ends 12/3/24.
There is another code: FREAKONOMICS for 10% off. I’m not sure if there is an expiration date for this one.
I’ve been using Lingo since early September and I learned a lot from using it. If anyone wants to try it, I recommend the 4-week plan because 2 weeks is not enough time.
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Speaking of CGMs, here is a short clip about using them to verify that taking a little vinegar before a high-carb meal like pizza really does lower glucose spike (and normally these spikes last a long time):
It’s a recording by this guy, posted to a different channel:
He does lots of n=1 tests of the effect of different foods on his blood glucose.
Anyways, it seems that this single test result showed positive benefits. Of course he would have to do many more tests with and without vinegar to know if it’s having much effect.
There is a new “Reverse Aging Revolution” video that claims vinegar lowers blood sugar by 40%:
Incidentally, Novos chews contains a nice blend of things: Apple Cider Vinegar (Acetic Acid), Trehalose, Nattokinase, Rutin, Lutein, Zeaxanthin, and Inulin.
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Vinegar (Acetic Acid) as a Metabolic Postbiotic
I. Executive Summary
The provided transcript posits vinegar (acetic acid) as a functional “postbiotic” supplement with significant potential for metabolic regulation, specifically in the context of Type 2 Diabetes (T2D) and pre-diabetes. The core thesis centers on the ability of acetic acid to flatten postprandial glucose spikes by approximately 40% when consumed alongside starch-heavy meals. This mechanism is attributed to two primary factors: the inhibition of carbohydrate-digesting enzymes (disaccharidases) and the slowing of gastric emptying. Beyond acute glycemic control, the speaker argues for systemic benefits, including reductions in Hemoglobin A1C (HbA1c), fasting glucose, and potentially improved lipid profiles (triglycerides/cholesterol).
From a clinical analyst perspective, the classification of vinegar as a “postbiotic” is technically accurate; acetic acid is a primary short-chain fatty acid (SCFA) typically produced by the fermentation of dietary fiber by the gut microbiome. By ingesting vinegar directly, a user effectively bypasses the requisite microbial fermentation phase, delivering the metabolite directly to the systemic circulation.
Current clinical data (2022–2026) largely supports the glycemic claims, though the magnitude of effect in broader meta-analyses is more conservative (20–30%) compared to the 40% figure cited. The evidence for cardiovascular benefits (blood pressure and lipids) remains secondary and less robust than the glycemic data. Emerging research into the “gut-brain axis” suggests a potential role for acetic acid in modulating mood via metabolic pathways, though this remains in the experimental tier due to small sample sizes and specific study contexts.
The primary translational gap exists in the delivery format. While liquid vinegar is effective, its impact on tooth enamel and esophageal tissue necessitates strict dilution protocols. Furthermore, the “interference” with gastric emptying may contraindicate use in patients with gastroparesis. Overall, acetic acid represents a low-cost, high-leverage tool for metabolic optimization, provided it is utilized as a tactical adjunct to—rather than a substitute for—foundational nutritional strategies.
II. Insight Bullets
- Postbiotic Bypass: Vinegar functions as a direct delivery system for acetic acid, a key SCFA that normally requires fiber fermentation.
- Enzyme Inhibition: Acetic acid interferes with disaccharidases (sucrase, maltase) in the small intestine, slowing starch-to-glucose conversion.
- Gastric Deceleration: Acetic acid delays the rate at which food leaves the stomach, naturally smoothing the glucose entry curve.
- Glycemic Attenuation: Clinical evidence confirms a 20–30% reduction in post-meal glucose spikes in insulin-resistant populations.
- HbA1c Modulation: Consistent use (8–12 weeks) is associated with statistically significant reductions in long-term glycemic markers.
- AMPK Activation: Preliminary data suggests acetic acid may activate the AMPK pathway, potentially increasing fatty acid oxidation.
- Insulin Sensitivity: Acute ingestion improves tissue sensitivity to insulin, aiding in glucose clearance.
- Lipid Profiles: Minor but consistent reductions in triglycerides and LDL cholesterol are observed in diabetic cohorts.
- Mood Correlation: Emerging RCTs suggest a reduction in depression symptoms, potentially linked to altered urinary metabolites and metabolic signaling.
- Weight Management: Weight loss effects are statistically significant but clinically modest (approx. 2–4 lbs over 12 weeks).
- Protocol Specificity: Optimal timing is 15–20 minutes before a meal or with the “first bites” of a starch-containing meal.
- Dose Response: The standard clinical dose is 15–30 ml (1–2 tablespoons) diluted in at least 8 oz of water.
- Safety Threshold: Acetic acid concentration is strictly regulated due to potential toxicity at high levels (glacial acetic acid).
- Enamel Risk: Undiluted vinegar or high-frequency exposure can lead to permanent dental erosion.
- Gastroparesis Warning: Individuals with delayed gastric emptying (common in long-term T2D) may see worsened symptoms.
- Satiety Mechanism: Some weight loss may be secondary to mild nausea or the “fullness” feeling from delayed emptying.
- Metformin Synergy: Some studies indicate vinegar may potentiate the glucose-lowering effects of Metformin.
- Liquid vs. Pill: Current data suggests liquid vinegar is more effective than most encapsulated or gummy versions.
- Gummy Caveat: Most vinegar gummies contain added sugars that may negate the metabolic benefits of the acetic acid.
III. Adversarial Claims & Evidence Table
| Claim from Video | Speaker’s Evidence | Scientific Reality (Current Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| 40% reduction in postprandial glucose. | Internal/Published Study. | Meta-analyses show a 20-30% reduction in insulin-resistant subjects. Wander et al., 2026 | Level A | Plausible (High) |
| Vinegar lowers HbA1c and fasting glucose. | Meta-analyses (5+ studies). | Confirmed: Significant reductions in A1C and fasting glucose over 3 months. ResearchGate, 2026 | Level A | Strong Support |
| Vinegar acts as a “Postbiotic”. | Biological Definition. | Correct. Acetic acid is a validated short-chain fatty acid (SCFA) metabolite. [Cell Host & Microbe, etc.] | Level E/B | Strong Support |
| Vinegar reduces depression symptoms. | Recent Research (Current focus). | 4-week RCT (n=27) showed reduction in depression scores vs placebo. Examine/NCT05698381, 2024 | Level B | Speculative |
| Reduces blood pressure/cholesterol. | Mentioned as “appearing to.” | Significant for Lipids (TG/LDL); blood pressure data is largely animal-based or low-power human trials. ResearchGate, 2026 | Level C | Plausible (Moderate) |
IV. Actionable Protocol (Prioritized)
High Confidence Tier (Metabolic Optimization)
- Dose: 1 tablespoon (15 ml) of organic Apple Cider Vinegar (ACV) or White Vinegar.
- Dilution: Must be diluted in 8–10 oz of water to prevent esophageal burns and enamel erosion. Use a straw to further minimize dental contact.
- Timing: 10–20 minutes before a meal containing >30g of complex carbohydrates (starch).
- Frequency: Up to twice daily (before the two largest starch-containing meals).
Experimental Tier (Mood & Lipid Support)
- Consistency: Daily ingestion for a minimum of 4–8 weeks is required to observe shifts in lipid markers or mood states.
- Context: Use during periods of high metabolic stress or as part of a gut-health focused “postbiotic” stack.
Red Flag Zone (Safety Warnings)
- Gastroparesis: Do not use if diagnosed with delayed gastric emptying or severe GERD.
- Undiluted Intake: Never consume “shots” of vinegar without water.
- Potassium Monitoring: Excessive use may contribute to hypokalemia (low potassium).
- Gummies/Capsules: Avoid products with >2g added sugar per serving; efficacy of capsules is generally inferior to liquid.
V. Technical Mechanism Breakdown
The physiological impact of acetic acid is driven by several distinct molecular pathways:
- Disaccharidase Inhibition: Acetic acid competitively inhibits the activity of alpha-glucosidase and other disaccharidases in the intestinal brush border. This prevents the rapid hydrolysis of starches and disaccharides into monosaccharides, thereby slowing glucose absorption.
- Gastric Emptying Rate (GER): Acetic acid appears to modulate the rate of gastric emptying, likely through the stimulation of osmoreceptors or by influencing the release of gastrointestinal hormones like GLP-1. This ensures a “slow-drip” of nutrients into the duodenum.
- AMPK Pathway: Acetic acid is converted to acetyl-CoA, which can increase the AMP/ATP ratio, triggering the activation of Adenosine Monophosphate-activated Protein Kinase (AMPK). This serves as a metabolic master switch that promotes glucose uptake in muscles and inhibits fatty acid synthesis in the liver.
- SCFAs and the Gut-Brain Axis: As a short-chain fatty acid, acetic acid can cross the blood-brain barrier via monocarboxylate transporters. Once in the CNS, it may influence hypothalamic signaling related to appetite and potentially impact neurotransmitter metabolites (e.g., 3-hexenedioic acid), though the direct link to serotonin remains unverified.
- Glycogen Synthesis: Acetic acid may promote the upregulation of GLUT4 transporters and glycogen synthase, shifting the fate of ingested glucose toward storage in muscle tissue rather than remaining in the bloodstream.
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Something that occurs to me is that, since part of how apple cider vinegar (and other vinegar) prevents glucose spikes is partly down to its inhibition of starch breakdown in the small intestines, after you eat some starchy food (say an hour after taking apple cider vinegar), more of it than usual should make its way to the colon where it can be fermented. So, it should cause more butyrate to be produced than one would normally expect.
I posed this to Google search, and this is what it said:
Your hypothesis is scientifically plausible and aligns with the mechanism of action for vinegar in metabolic health. By inhibiting starch-digesting enzymes (like amylase), apple cider vinegar (ACV) does indeed reduce the amount of starch broken down into glucose in the small intestine. This results in more starch passing into the large intestine, where it can be fermented by gut microbiota to produce short-chain fatty acids (SCFAs), including butyrate
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I double checked this (out of curiosity) using Claude Opus 4.7. Here is its response:
From Claude:
The reasoning is plausible in direction but probably modest in magnitude, and there’s a wrinkle worth flagging in the premise itself.
The closest “clean” version of this experiment in humans is actually acarbose, the α-glucosidase inhibitor used in type 2 diabetes. Acarbose works by exactly the mechanism you’re describing — it prevents complete hydrolysis of starch and disaccharides in the small intestine, more carbohydrate reaches the colon, and the colonic microbiota ferments it. The downstream effects are well-documented: acarbose meaningfully shifts the gut microbiome toward butyrate-producers (Faecalibacterium, Roseburia, Bifidobacterium, various Lachnospiraceae), raises fecal and portal-vein SCFA concentrations, and increases butyrate specifically. So the principle — “inhibit upper-GI starch digestion → more colonic butyrate” — is real.
The wrinkle is that with vinegar, enzyme inhibition is only one of several mechanisms, and probably not the dominant one. Acetic acid does inhibit disaccharidases (sucrase, maltase) and to a lesser extent salivary/pancreatic amylase in vitro, but the effect size in vivo is small compared to acarbose. The larger contributor to vinegar’s blunted glucose curve is delayed gastric emptying, and a slower gastric emptying simply spreads absorption over time — the starch still gets fully digested and absorbed in the small intestine, it just trickles in. That portion of the effect would not result in extra substrate reaching the colon. So if you partition vinegar’s glucose-blunting effect, only the fraction attributable to true enzyme inhibition (probably the minority) would plausibly translate into more colonic fermentation.
There’s also a separate, more direct route to butyrate from vinegar that doesn’t depend on starch malabsorption at all: acetate cross-feeding. Many butyrate-producing Firmicutes (notably via the butyryl-CoA:acetate CoA-transferase pathway) use luminal acetate as a co-substrate to make butyrate. The catch is that the vast majority of ingested acetate is absorbed in the stomach and upper small intestine, so how much actually reaches the colonic microbiota is uncertain and probably small at typical vinegar doses (~15–30 mL).
Direct human evidence that ACV raises colonic or fecal butyrate is thin. Most of the microbiome-and-vinegar work is in rodents, where vinegar and acetate supplementation have been shown to alter microbial composition and increase SCFAs, but extrapolation to humans at culinary doses is shaky. I don’t know of a well-controlled human trial that has measured stool or breath markers of colonic fermentation (e.g., breath H₂/CH₄, fecal SCFA profile) after chronic ACV with a starchy meal — that would be the experiment to settle it.
So: directionally yes, but expect the effect to be a small fraction of what something like acarbose produces, and most of vinegar’s glucose effect is doing something different (slowing absorption) that doesn’t generate extra fermentable substrate. If your underlying goal is to boost colonic butyrate, resistant starch (cooled cooked potatoes/rice, green banana flour, high-amylose maize) or a fiber like wheat bran or psyllium is a much more direct lever than vinegar.
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Verry interesting. I learned something about acarbose from thet. Perhaps part (not all) of its lifespan-extending effect in mice is due to that, the increase of butyrate production.