Blood Sugar and Post-Meal Spikes

If you have ever watched a continuous glucose monitor after a bowl of white rice, you have seen the thing this article is about: a steep climb over thirty to sixty minutes, a peak, then a slide back down that sometimes overshoots. That climb is the postprandial glucose excursion — the post-meal spike.

White mulberry leaf does one thing, and it does it to that curve. It is worth understanding exactly what “one thing” means, because the honest version is both more impressive and more limited than the marketing version.

Why the Spike Is Its Own Problem
The Enzymes: Where the Last Cut Happens
How DNJ Blocks Them
What a Blunted Curve Actually Looks Like
The Human Trials, One at a Time
What Happened When They Looked Past One Meal
The Results That Were Negative
Timing Is Not a Refinement — It Is the Intervention
What It Does Not Do
Who This Might Actually Suit
Cautions
Key Research Papers
Connections

Why the Spike Is Its Own Problem

For decades, diabetes care measured two things: fasting glucose and HbA1c. Both are averages of a sort — fasting glucose is a single point taken at the calmest moment of the day, and HbA1c is a rolling three-month average written into your red blood cells. Neither one sees the shape of the day.

Two people can have identical HbA1c values and completely different days. One runs a flat 6.5 mmol/L (117 mg/dL) most of the time. The other sits lower at baseline and hits 12 mmol/L (216 mg/dL) three times a day after meals. The averages match; the experience does not, and there is reasonable evidence that the peaks matter in their own right.

Why the peaks might matter:

Glucose variability stresses blood vessels acutely. A postprandial surge transiently increases oxidative stress and impairs endothelial function. Some of that is measurable within an hour.
Impaired glucose tolerance is defined by the spike, not the fast. The 2-hour value on an oral glucose tolerance test is what separates normal from impaired — and impaired glucose tolerance is where progression to diabetes happens.
The subjective version is real too. The heavy, foggy, sleepy hour after a large carbohydrate meal, and the shaky, hungry crash that sometimes follows, track the shape of the curve rather than its average.

Which is to say: an intervention that only flattens peaks and does nothing to your fasting glucose is not a trivial intervention. It is a narrow one. Those are different criticisms.

The Enzymes: Where the Last Cut Happens

Almost no carbohydrate is absorbed in the form you eat it. Bread, rice, pasta and potato are chains of glucose. Table sugar is a two-unit molecule — glucose bonded to fructose. Milk sugar is glucose bonded to galactose. None of these can cross the intestinal lining. They have to be reduced to single sugars first.

Digestion of starch happens in three stages:

Salivary amylase in the mouth makes a start on starch chains — which is why a cracker turns sweet if you hold it long enough.
Pancreatic amylase in the small intestine does the bulk of the chopping, leaving short fragments: maltose, maltotriose and branched “limit dextrins.”
Brush-border α-glucosidases perform the final cut.

That third stage is the target. The brush border is the densely fringed surface of the cells lining the small intestine — microvilli packed so tightly that a square millimetre of gut carries an enormous absorptive area, with digestive enzymes anchored directly into the membrane. Two enzyme complexes do most of the work:

Sucrase-isomaltase — splits sucrose (table sugar) into glucose and fructose, and handles the branch points in starch.
Maltase-glucoamylase — trims glucose units off the ends of the short starch fragments.

The design is elegant: the sugar is liberated within nanometres of the transporter that will carry it into the cell. There is essentially no delay between cutting and absorbing. That efficiency is exactly why a refined-carbohydrate meal produces such a fast rise, and it is also why interfering at this step is such a leveraged intervention. Block the last cut and the whole downstream cascade slows.

How DNJ Blocks Them

1-Deoxynojirimycin is what chemists call an iminosugar or azasugar. Take a glucose molecule. Its six-membered ring contains five carbons and one oxygen. Replace that ring oxygen with a nitrogen, and remove one hydroxyl group. That is DNJ. It is glucose with a different atom at the hinge.

The enzyme cannot tell the difference at the moment of binding — the shape and the hydroxyl pattern are close enough. But two things then go wrong from the enzyme’s point of view:

The nitrogen is protonated at gut pH, so it carries a positive charge. Glycoside-cleaving enzymes work through a transition state in which the sugar carbon develops exactly that kind of positive character, and the active site is built to stabilise it. DNJ therefore mimics not the substrate but the transition state — and enzymes bind transition states orders of magnitude more tightly than they bind substrates.
There is no bond to cut. DNJ is not a disaccharide. The enzyme grips it and has nothing to do.

The result is a tight, competitive, reversible block. Nothing is destroyed; the enzyme is simply occupied. This is a key machined to fit the lock, with the tip fused solid: it goes in, it will not turn, and while it sits there no real key can be used.

Three licensed drugs work on exactly this enzyme. Acarbose is a pseudo-tetrasaccharide originally isolated from Actinoplanes bacteria. Voglibose is a valiolamine derivative used mainly in Japan. And miglitol is an N-hydroxyethyl derivative of DNJ — the mulberry molecule with a small chemical handle added to improve its absorption. This is not an analogy. The pharmaceutical is the plant compound, modified.

That shared identity is why mulberry leaf sits on firmer ground than most botanical hypoglycaemics, and why its side effects and interactions are predictable rather than speculative. You do not have to guess what happens when you inhibit intestinal α-glucosidase in a human being. It has been done in tens of thousands of people, under a drug licence, for forty years.

What a Blunted Curve Actually Looks Like

The measure researchers use is the incremental area under the curve (iAUC): draw the glucose trace for two hours after a meal, subtract the baseline, and measure the area of the hump. It captures both how high the peak went and how long it stayed up.

The cleanest human numbers come from a randomised, double-blind, crossover study run at Oxford Brookes University in the UK. Thirty-seven normoglycaemic adults, aged 19 to 59 with BMI between 20 and 30, each took a placebo and three doses of a standardised mulberry leaf extract alongside 50 g of maltodextrin. Against placebo, the incremental area under the glucose curve fell by:

6.1 percent at half dose (not statistically significant, p = 0.316)
14.0 percent at the normal dose (p = 0.022)
22.0 percent at double dose (p < 0.001)

Insulin fell in the same stepwise pattern. Two things are worth pulling out. First, this is a genuine dose-response relationship — more extract, more effect, with the lowest dose failing to reach significance. Dose-response is one of the strongest signals that an effect is real rather than noise. Second, these were people without diabetes, which means the mechanism does not require impaired glucose handling to show up.

A 14 to 22 percent reduction in the area under the curve is meaningful but not dramatic. It is a smaller, later, gentler hump. It is not a flat line.

The mechanism, observed rather than inferred

The most satisfying study in this literature is also one of the smallest. A group at the Minneapolis VA gave participants — adults with type 2 diabetes and control subjects — 75 g of sucrose with or without mulberry leaf extract, and measured two things: blood glucose, and breath hydrogen.

Breath hydrogen is the trick. Human cells produce no hydrogen gas. Colonic bacteria produce plenty of it when they ferment carbohydrate, and a fraction diffuses into the blood and is exhaled. A rise in breath hydrogen after a meal is direct evidence that carbohydrate reached the colon undigested. In that trial, glucose came down and breath hydrogen went up — the two halves of the mechanism observed simultaneously in the same people.

The same laboratory quantified it in a companion study of a black, green and mulberry tea extract, comparing hydrogen output against a known non-absorbable sugar. Their estimate: the extract caused roughly 25 percent of the carbohydrate load to be malabsorbed. Notably, the same extract did not cause fat malabsorption, despite in-vitro claims about pancreatic lipase inhibition — a useful reminder that test-tube activity does not automatically appear in people.

The Human Trials, One at a Time

Mulberry leaf has more human data than most herbs on this site. The trials are small, but there are several of them, they were done by independent groups in Japan, Korea, Thailand, the United Kingdom, the United States and Iran, and they point the same way.

The dose-finding work (Japan, 2007)

A Japanese group set out to answer two questions: how much DNJ is actually in mulberry leaf, and how much do you need? They found that commercial mulberry products carried about 0.1 percent DNJ — too little to expect much — and that DNJ concentrated in young leaves from the top of the branch, harvested in summer. Optimising harvest and drying for the cultivar Morus alba var. Shin-ichinose, they produced a food-grade powder at 1.5 percent DNJ.

Healthy volunteers then took 0, 0.4, 0.8 or 1.2 g of that powder — corresponding to 0, 6, 12 and 18 mg of DNJ — followed by 50 g of sucrose, with plasma glucose and insulin measured for three hours. Suppression of the postprandial rise followed the dose.

Those three numbers — 6, 12, 18 mg — have anchored the field ever since, and they are far more useful to a consumer than any milligram figure for extract weight.

Impaired glucose metabolism (Japan, 2011)

A follow-up paper reported two studies. Study 1 was a randomised, double-blind crossover in 12 people with fasting plasma glucose of 100–140 mg/dL, given extract containing 3, 6 or 9 mg DNJ or placebo before a challenge of 200 g of boiled white rice — a real food, not a sugar solution. Post-challenge glycaemia was attenuated in a dose-dependent way (p = 0.006 for the group-by-time interaction).

Study 2 ran 12 weeks in 76 people with fasting glucose 110–140 mg/dL, taking 6 mg DNJ three times daily. The result is instructive and is covered in the negative-results section below.

Prediabetes (Korea, 2015)

A randomised, double-blind, placebo-controlled trial in 36 subjects with impaired fasting glucose gave 5 g/day of mulberry leaf aqueous extract for four weeks, then repeated a carbohydrate challenge. The postprandial glucose response was attenuated, most clearly at 30 and 60 minutes (p = 0.003 and 0.033). Insulin and C-peptide responses fell too, and the incremental area under the insulin curve was significantly lower than placebo.

The insulin result matters. If mulberry leaf lowered glucose by squeezing more insulin out of the pancreas, insulin would go up. It goes down — consistent with less glucose arriving in the first place, which is what the mechanism predicts.

Normoglycaemic adults (United Kingdom, 2017)

The 37-person Oxford Brookes crossover described above, using the proprietary standardised extract sold as Reducose. It is the best-designed acute study in the set: randomised, double-blind, repeat-measure crossover with an explicit dose ladder and a report of gastrointestinal tolerability.

Type 2 diabetes (United States, 2017)

The Mul-DM pilot randomised 24 patients with type 2 diabetes on stable oral therapy to 1,000 mg standardised mulberry leaf extract three times daily with meals, or placebo, for three months, after a two-week placebo run-in. Seventeen completed. Post-meal self-monitored glucose fell 16.1 percent from baseline and 18.2 percent versus placebo (both p < 0.05).

The rest of this trial belongs in the negative section.

Obesity and borderline diabetes (Thailand, 2020)

A two-part study. First a dose-finding arm in healthy adults on the same 0/6/12/18 mg DNJ ladder with a sucrose solution, which concluded that 12 mg of DNJ was the minimum effective dose. Then a 12-week randomised trial in obese people with borderline diabetes taking 12 mg mulberry DNJ three times daily.

Against their own baseline, participants’ fasting plasma glucose fell by 3.86 ± 5.99 mg/dL (p = 0.002) and HbA1c by 0.11 ± 0.22 percentage points (p = 0.011). Insulin resistance tended to improve but missed significance (p = 0.057). Look closely at those numbers: the standard deviations are larger than the means. These are small effects with wide scatter.

Type 2 diabetes, metabolic markers (Iran, 2022)

A randomised, double-blind, placebo-controlled trial in 60 patients with type 2 diabetes taking 300 mg Morus alba extract twice daily for 12 weeks. Compared with placebo, the extract group had lower insulin (p = 0.026), lower malondialdehyde — a marker of oxidative stress (p < 0.001) — and higher HDL cholesterol (p = 0.001). Other metabolic markers did not change. Note that a twice-daily schedule cannot cover three meals, which is a design mismatch with the mechanism.

What Happened When They Looked Past One Meal

Acute studies are easy: give the extract, give the sugar, draw blood for two hours. The harder question is whether repeatedly flattening spikes changes anything measurable over months.

The best pooled answer comes from a 2023 systematic review and meta-analysis of 12 clinical trials covering 615 participants. Across those trials, mulberry leaf or its extract produced statistically significant reductions in:

Fasting blood glucose: −0.47 mmol/L (about −8.5 mg/dL)
HbA1c: −2.92 mmol/mol (roughly −0.27 percentage points in the older DCCT units)
Fasting plasma insulin: −0.58 µIU/mL

Subgroup analysis suggested longer supplementation (eight weeks or more) worked better, and that people with baseline fasting glucose above 6.1 mmol/L responded more than healthy people did.

How should you read that? Cautiously, in both directions. The effects are real in pooled data and consistently in the right direction. They are also small. An HbA1c drop of about a quarter of a percentage point is at the edge of clinical relevance — less than most single diabetes medications, and less than a serious change in diet or activity typically achieves. Twelve trials with 615 people between them is a modest evidence base, and small-trial literatures are the ones most vulnerable to publication bias, because a null result in 20 people is easy not to publish.

There is also a mechanistic puzzle worth naming. Why would an intestinal enzyme blocker lower fasting glucose at all? There is no carbohydrate in the gut when you are fasting. Several explanations are plausible — less glucose toxicity over time improving beta-cell function, changes in the gut microbiome and its short-chain fatty acid output, effects of the leaf’s flavonoids independent of DNJ — but none is established in humans. Treat the fasting-glucose finding as an observation in search of an explanation.

The Results That Were Negative

A page that hides the failures is not worth reading. Here are the ones that matter.

Twelve weeks did not move fasting glucose, HbA1c or glycated albumin

In the Japanese 12-week study of 76 people, the extract group showed a clear rise in 1,5-anhydroglucitol — a blood marker that goes up when postprandial spikes get smaller, and a sensitive index of exactly the thing mulberry leaf is supposed to do (p < 0.001 for the group-by-time interaction). But there were no differences between groups in fasting plasma glucose, HbA1c or glycated albumin.

That is a coherent and honest result: the drug did what it does — smoothed post-meal excursions — and did not do what it was never mechanistically going to do.

The pilot in type 2 diabetes did not beat placebo on HbA1c

In the 24-person Mul-DM study, HbA1c fell from 7.30 to 6.94 percent in the mulberry group — but that did not reach significance (p = 0.079), and there was no difference in HbA1c between mulberry and placebo. There was also no effect on weight, fasting glucose or blood pressure.

And one safety signal deserves attention rather than burial: serum creatinine rose about 15 percent in the mulberry group compared with both baseline and placebo (p < 0.05). In a 17-person pilot, a single lab change of that size can be chance, dehydration from loose stools, or a real effect — there is no way to tell from one small study. It has not been replicated, and it has not been refuted. If you have reduced kidney function, this is worth mentioning to your doctor before starting.

Glucose tolerance did not improve in the Thai trial

Twelve weeks of 12 mg DNJ three times daily produced small within-group falls in fasting glucose and HbA1c, but improvement in glucose tolerance was not observed, and the insulin resistance change missed significance.

The design weaknesses across the field

Small samples. Twelve, 23, 24, 36, 37, 60, 76 people. No large trial exists.
Short duration. Most acute studies last hours. The longest are 12 weeks.
Different products. Whole leaf powder, aqueous extract, DNJ-enriched powder and proprietary standardised extracts are not interchangeable, yet they are all called “mulberry leaf.”
Surrogate endpoints only. Every outcome is a laboratory number. Nobody has shown mulberry leaf prevents a single complication of diabetes, because nobody has run a trial that could.
Industry involvement. Several of the better-designed studies used a specific commercial extract. That does not invalidate them; it does mean independent replication matters.

Timing Is Not a Refinement — It Is the Intervention

Every trial above dosed mulberry leaf with the carbohydrate. Not before bed, not with a morning supplement stack, not on an empty stomach.

The reason is structural. The enzyme is anchored in the intestinal wall and the substrate is your meal. If DNJ is not physically present in the small intestine at the same moment as the carbohydrate, there is nothing for it to block. Human pharmacokinetic work shows DNJ is absorbed and cleared — it does not linger in the gut waiting.

The practical rule: take it at the start of the meal, ideally with the first few bites, or in the five to ten minutes before. A capsule taken an hour after eating has mostly missed its window. A capsule taken with a meal that contains no starch or sugar has nothing to do.

This is also why mulberry leaf cannot “build up” and why there is no loading phase. It is closer to a digestive enzyme than to a vitamin. Full practical detail is in How to Take It: Timing and Side Effects.

What It Does Not Do

Because the mechanism here is genuinely good, it is especially important to mark the boundary.

It is not a treatment for diabetes. No trial has shown mulberry leaf controls diabetes, prevents complications, or substitutes for metformin, a GLP-1 agonist, an SGLT2 inhibitor or insulin. Even acarbose — the licensed pharmaceutical version of the same mechanism — is a second- or third-line adjunct that lowers HbA1c modestly.
It does not cancel a meal. Carbohydrate is delayed, not deleted. Most of it is still absorbed, just further down the gut and later in the afternoon. This is not permission to eat differently.
It does not cause hypoglycaemia by itself. Slowing the breakdown of incoming carbohydrate cannot push glucose below baseline. It can, however, contribute to hypoglycaemia caused by other drugs.
It does not produce weight loss. No good human evidence supports this, and the theory is weak.
It does not replace the things that actually work. Reducing refined carbohydrate, walking for ten minutes after meals, eating protein and vegetables before starch, sleeping properly, and treating diabetes with proven medication all move the glucose curve more than mulberry leaf does.

Who This Might Actually Suit

A fair reading of the evidence suggests mulberry leaf is a reasonable option for a fairly specific person:

Someone with prediabetes or borderline glucose who is already changing diet and activity and wants an additional, low-risk, mechanistically sensible nudge on the meals that are hardest to avoid.
Someone whose problem is specifically post-meal spikes — often visible on a continuous glucose monitor — rather than a high fasting number.
Someone with a fixed carbohydrate-heavy meal they cannot easily change: a rice-based cuisine, a work canteen, a family meal.

And it suits some people badly:

Anyone hoping to replace prescribed diabetes medication.
Anyone with inflammatory bowel disease, an IBS flare, or a history of bowel obstruction — the mechanism deliberately sends carbohydrate to the colon.
Anyone unwilling to take something three times a day with meals. Once-daily dosing does not fit the mechanism.
Anyone whose fasting glucose is the problem. This is the wrong tool.

Cautions

⚠ Prescription α-glucosidase inhibitors — acarbose, miglitol, voglibose. Mulberry leaf hits the identical enzyme. Stacking them is additive in effect and in gastrointestinal side effects, which can become severe. Do not combine without your prescriber’s involvement.
⚠ Insulin, sulfonylureas and glinides. Mulberry leaf will not cause a hypo on its own, but it lowers the glucose curve your doses were titrated against. Monitor more closely when starting, and tell your prescriber — dose adjustment may be needed.
⚠ Treating a hypo while taking it. Hypoglycaemia occurring on an α-glucosidase inhibitor must be treated with pure glucose — dextrose tablets or gel — not juice, sweets, milk or table sugar. The whole point of the mechanism is that sucrose is broken down slowly, so the usual rescue foods will not work fast enough. This is standard advice for anyone on acarbose or miglitol and it transfers directly. Carry glucose tablets.
Gastrointestinal effects — bloating, wind, rumbling, cramping and loose stools — are common, dose-dependent, worst at the start, and usually settle over one to two weeks. In one Thai study using leaf tablets three times daily, 26 percent reported mild diarrhoea.
Kidney function. A single small pilot found a 15 percent rise in serum creatinine. Unreplicated, but worth mentioning to your doctor if your kidney function is already reduced.
Pregnancy, breastfeeding and children. Concentrated extracts have not been studied. Avoid.
Surgery. Stop at least two weeks before a scheduled operation.
Product variability. DNJ content varies severalfold between products at the same stated milligram dose. Prefer products that state milligrams of DNJ per serving.

Key Research Papers

Every identifier below was verified live against NCBI E-utilities — title, first author, journal and year all had to match before a PMID was printed. Study type is labelled.

Acute postprandial trials in humans

Mudra M, Ercan-Fang N, Zhong L, Furne J, Levitt M. Influence of mulberry leaf extract on the blood glucose and breath hydrogen response to ingestion of 75 g sucrose by type 2 diabetic and control subjects. Diabetes Care. 2007;30(5):1272–1274. Human.
Kimura T, Nakagawa K, Kubota H, Kojima Y, et al. Food-grade mulberry powder enriched with 1-deoxynojirimycin suppresses the elevation of postprandial blood glucose in humans. Journal of Agricultural and Food Chemistry. 2007;55(14):5869–5874. Human, dose-ranging (0/6/12/18 mg DNJ).
Lown M, Fuller R, Lightowler H, Fraser A, et al. Mulberry-extract improves glucose tolerance and decreases insulin concentrations in normoglycaemic adults: results of a randomised double-blind placebo-controlled study. PLoS ONE. 2017;12(2):e0172239. Human, n = 37, crossover.
Kim JY, Ok HM, Kim J, Park SW, et al. Mulberry leaf extract improves postprandial glucose response in prediabetic subjects: a randomized, double-blind placebo-controlled trial. Journal of Medicinal Food. 2015;18(3):306–313. Human, n = 36.

Longer trials and pooled analysis

Asai A, Nakagawa K, Higuchi O, Kimura T, et al. Effect of mulberry leaf extract with enriched 1-deoxynojirimycin content on postprandial glycemic control in subjects with impaired glucose metabolism. Journal of Diabetes Investigation. 2011;2(4):318–323. Human, n = 12 acute and n = 76 over 12 weeks. Postprandial control improved; fasting glucose and HbA1c did not.
Riche DM, Riche KD, East HE, Barrett EK, et al. Impact of mulberry leaf extract on type 2 diabetes (Mul-DM): a randomized, placebo-controlled pilot study. Complementary Therapies in Medicine. 2017;32:105–108. Human, n = 24. No HbA1c advantage over placebo; creatinine rose 15 percent.
Thaipitakwong T, Supasyndh O, Rasmi Y, Aramwit P. A randomized controlled study of dose-finding, efficacy, and safety of mulberry leaves on glycemic profiles in obese persons with borderline diabetes. Complementary Therapies in Medicine. 2020;49:102292. Human. 12 mg DNJ = minimum effective dose; glucose tolerance unchanged at 12 weeks.
Taghizadeh M, Mohammad Zadeh A, Asemi Z, Farrokhnezhad AH, et al. Morus alba leaf extract affects metabolic profiles, biomarkers of inflammation and oxidative stress in patients with type 2 diabetes mellitus: a double-blind clinical trial. Clinical Nutrition ESPEN. 2022;49:68–73. Human, n = 60.
Cui W, Luo K, Xiao Q, Sun Z, et al. Effect of mulberry leaf or mulberry leaf extract on glycemic traits: a systematic review and meta-analysis. Food & Function. 2023;14(3):1277–1289. Meta-analysis, 12 trials, 615 participants.

Mechanism, malabsorption and pharmacokinetics

Zhong L, Furne JK, Levitt MD. An extract of black, green, and mulberry teas causes malabsorption of carbohydrate but not of triacylglycerol in healthy volunteers. American Journal of Clinical Nutrition. 2006;84(3):551–555. Human. ~25 percent of carbohydrate malabsorbed; no fat malabsorption.
Nakagawa K, Kubota H, Tsuzuki T, Kariya J, et al. Validation of an ion trap tandem mass spectrometric analysis of mulberry 1-deoxynojirimycin in human plasma: application to pharmacokinetic studies. Bioscience, Biotechnology, and Biochemistry. 2008;72(8):2210–2213. Human pharmacokinetics.
Kim JY, Kwon HJ, Jung JY, Kwon HY, et al. Comparison of absorption of 1-deoxynojirimycin from mulberry water extract in rats. Journal of Agricultural and Food Chemistry. 2010;58(11):6666–6671. Animal.
Yatsunami K, Ichida M, Onodera S. The relationship between 1-deoxynojirimycin content and alpha-glucosidase inhibitory activity in leaves of 276 mulberry cultivars (Morus spp.) in Kyoto, Japan. Journal of Natural Medicines. 2008;62(1):63–66. Analytical.
Hu TG, Wen P, Shen WZ, Liu F, et al. Effect of 1-deoxynojirimycin isolated from mulberry leaves on glucose metabolism and gut microbiota in a streptozotocin-induced diabetic mouse model. Journal of Natural Products. 2019;82(8):2189–2200. Animal.

The drug class, for comparison

Chiasson JL, Josse RG, Gomis R, Hanefeld M, et al. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. The Lancet. 2002;359(9323):2072–2077. Human, n = 1,429.
Van de Laar FA, Lucassen PL, Akkermans RP, Van de Lisdonk EH, et al. Alpha-glucosidase inhibitors for type 2 diabetes mellitus. Cochrane Database of Systematic Reviews. 2005;(2):CD003639. Systematic review, 41 trials.
Van de Laar FA, Lucassen PL, Akkermans RP, Van de Lisdonk EH, et al. Alpha-glucosidase inhibitors for people with impaired glucose tolerance or impaired fasting blood glucose. Cochrane Database of Systematic Reviews. 2006;(4):CD005061. Systematic review.

Live PubMed Searches

Connections

All Herbs
White Mulberry Leaf Benefits — the hub, with the evidence map and the whole citation set.
How to Take It: Timing and Side Effects — dosing by DNJ, titration, interactions, hypo rescue.
Cholesterol and Cardiovascular — whether flattening spikes buys anything for the heart.
Traditional Use and the Silk Road — why the tree makes DNJ in the first place.
White Mulberry Leaf (Morus alba) — botany, names, forms and the full cautions list.
Type 2 Diabetes — the condition this herb is most often reached for.
Gymnema — a different blood-sugar herb with a different mechanism.
Bitter Melon — another Asian plant used for glucose, with weaker mechanistic footing.
Berberine — works on AMPK and the liver, not on gut enzymes.

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