Cabbage Glucosinolates and Sulforaphane

Table of Contents

1. What Glucosinolates Actually Are
2. Myrosinase: The Enzyme in the Other Compartment
3. Which Ones Cabbage Actually Contains
4. Why Chopping and Resting Matters
5. What Cooking Does — and How to Cook Around It
6. Your Gut Bacteria as a Backup Enzyme
7. How Isothiocyanates Work Inside a Cell
8. The Cancer Evidence, Honestly
9. Why the Same Meal Does Different Things in Different People
10. Beyond Cancer
11. Getting the Most From a Head of Cabbage
12. Key Research Papers
13. Connections
14. Featured Videos

What Glucosinolates Actually Are

A glucosinolate is a storage molecule. It has a sugar on one end, a sulfur-containing core in the middle, and a variable side chain that differs from one glucosinolate to the next. That side chain is what makes each one distinct, and it is what eventually becomes the biologically active compound. Fahey, Zalcmann and Talalay's 2001 survey catalogued around 120 different glucosinolates across the plant kingdom, concentrated overwhelmingly in the order Brassicales — cabbage and its relatives, mustard, horseradish, wasabi, radish, watercress, rocket, capers and papaya.

On their own, glucosinolates do essentially nothing in your body. They are water-soluble, chemically stable, and biologically quiet. The plant makes them as a defence system in the same way you might keep a fire extinguisher on a wall — useless until something triggers it. The trigger is tissue damage.

This matters more than it sounds. A great deal of confused writing about cruciferous vegetables treats "glucosinolate content" as if it were the health-relevant number. It is not. The health-relevant number is how much of that glucosinolate gets converted into an isothiocyanate and absorbed — and that conversion can vary by a factor of ten depending on nothing more than how you cooked dinner.

Myrosinase: The Enzyme in the Other Compartment

The trigger is an enzyme called myrosinase. In an intact leaf it lives in specialised cells — often called myrosin cells — kept physically apart from the glucosinolates stored in the surrounding tissue. Nothing happens while the leaf is whole. Break the cells open and the enzyme reaches its substrate, snips off the sugar, and the remainder rearranges itself within seconds.

What it rearranges into depends on the conditions:

• At roughly neutral pH, the product is an isothiocyanate — the biologically interesting compound, and also the pungent, peppery, faintly mustard-like taste you get from raw cabbage, radish and rocket. Allyl isothiocyanate is the compound responsible for the burn in mustard and horseradish.
• In acidic conditions, or in the presence of a plant protein called epithiospecifier protein together with iron, the reaction diverts and produces nitriles and epithionitriles instead. These are far less biologically active. The plant is not making a mistake — different products deter different pests — but from a human health standpoint the nitrile route is largely a dead end.

That branch point has a useful practical consequence. Epithiospecifier protein is destroyed by heat at a lower temperature than myrosinase is. Brief, gentle heating — a short steam rather than a hard boil — can knock out the protein that diverts the reaction while leaving enough myrosinase intact to run it. This is why lightly steamed brassicas can, in laboratory conditions, yield more isothiocyanate than raw ones, even though heavy cooking yields almost none.

Which Ones Cabbage Actually Contains

Here is a distinction that most articles blur, and it is worth getting right, because it prevents you from expecting cabbage to do something it is not especially good at.

Sulforaphane comes from a glucosinolate called glucoraphanin. Glucoraphanin is abundant in broccoli and spectacularly abundant in young broccoli sprouts — which is precisely why the Johns Hopkins group that isolated sulforaphane in 1992 worked with broccoli rather than cabbage. Cabbage contains glucoraphanin, but far less of it. If your goal is sulforaphane specifically, broccoli and broccoli sprouts are the food to reach for.

What cabbage carries in quantity is a different set:

• Sinigrin, which hydrolyses to allyl isothiocyanate. This is the dominant glucosinolate in most green and savoy cabbage and in Brussels sprouts, and it is the compound behind the characteristic smell and bite. Allyl isothiocyanate is a well-studied isothiocyanate in its own right, with the same general phase II enzyme-inducing behaviour as sulforaphane.
• Glucobrassicin, an indole glucosinolate, which breaks down to indole-3-carbinol and from there, in stomach acid, to a condensation product called DIM (3,3'-diindolylmethane). These indoles behave quite differently from isothiocyanates — they interact with oestrogen metabolism and with a receptor system called the aryl hydrocarbon receptor — and they are the reason cruciferous vegetables keep appearing in the hormone-and-cancer literature.
• Glucoiberin, which yields iberin, another sulfur-containing isothiocyanate.
• Progoitrin, which yields goitrin — the compound behind the thyroid concern discussed on the tolerance and safety page. Cabbage is comparatively low in progoitrin; some kale varieties and Brussels sprouts carry considerably more.

Total glucosinolate content in cabbage varies enormously — by variety, by growing season, by soil sulfur, by how long the head has been in storage and how it was handled after harvest. Published figures for brassica vegetables span a range wide enough that quoting a single number for "cabbage" would be misleading. Verkerk and colleagues' review of the whole supply chain makes the point bluntly: what leaves the field and what arrives on the plate can differ several-fold, and most of that loss happens after harvest.

Why Chopping and Resting Matters

The advice to chop cruciferous vegetables and let them sit for a few minutes before cooking is one of the rare kitchen tips that has a real mechanism behind it rather than folklore.

Shredding cabbage ruptures cells and starts the myrosinase reaction. The reaction is fast but not instantaneous. If you throw the shreds straight into a hot pan, you denature the enzyme before it has converted much of anything, and you are left with intact glucosinolates that will pass into your colon largely unchanged. If you shred the cabbage and leave it on the board for a few minutes first, the enzyme gets to work at room temperature and converts a substantial share of the glucosinolates into isothiocyanates before the heat arrives. Isothiocyanates are themselves reasonably heat-stable once formed — it is the enzyme that is fragile, not the product.

How long? The reaction is largely done within minutes rather than hours. Somewhere in the region of five to ten minutes captures most of the available benefit without turning meal preparation into a project. The same logic is why crushed garlic is often rested before cooking, for an unrelated but structurally identical enzyme reaction.

And a related trick worth knowing: if you have already cooked your cabbage to death, you can supply the missing enzyme from outside. Ghawi, Methven and Niranjan showed that stirring a small amount of raw mustard seed powder into cooked broccoli substantially increased sulforaphane formation, because mustard seed is loaded with active myrosinase. A pinch of mustard powder, a spoonful of horseradish, some raw radish or rocket on top — any of these adds enzyme back to an enzyme-free dish. A crunchy raw garnish on a cooked brassica is not just texture.

What Cooking Does — and How to Cook Around It

Cooking hits cruciferous chemistry in three separate ways, and it helps to keep them apart.

1. Heat destroys myrosinase. This is the big one. Once the enzyme is gone, the conversion that produces isothiocyanates cannot happen in your kitchen at all — it can only happen later, and much less efficiently, in your colon.
2. Water leaches glucosinolates out of the tissue. Glucosinolates are highly water-soluble. Boiling cabbage in a large volume of water and pouring the water away removes a substantial fraction of them before they ever reach your plate. Steaming, stir-frying and microwaving with little or no added water avoid most of this loss simply because there is nowhere for the compounds to go.
3. Prolonged heat degrades some glucosinolates outright, independent of leaching.

The human bioavailability data are striking. Vermeulen and colleagues fed volunteers raw or cooked broccoli and tracked sulforaphane metabolites in urine; mean bioavailability was roughly ten times higher from the raw vegetable than from the cooked one. Conaway and colleagues had found the same direction earlier with fresh versus steamed broccoli, with roughly three times more isothiocyanate absorbed from the fresh vegetable. Oliviero and colleagues then mapped how the effect depends on processing conditions, and Rungapamestry and colleagues reviewed the whole cooking question for the Nutrition Society. The findings differ in magnitude — different vegetables, different cooking times, different measurement methods — but they all point the same way.

What that means at the stove:

• Raw is the reliable maximum. Coleslaw, shredded cabbage in a salad, cabbage as a taco base or wrap. This is the form in which the enzyme is fully intact.
• Brief steaming or a fast stir-fry is a good compromise — a few minutes, not twenty. Enough heat to soften and sweeten, not enough to wipe out the enzyme entirely.
• Long boiling is the worst case, and it is also what produces the sulfurous smell that gives boiled cabbage its bad reputation — that smell is literally the sound of the chemistry escaping. If you are making a cabbage soup or a braise, that is fine: the compounds are in the liquid, and you are going to eat the liquid.
• Fermentation is its own category. Sauerkraut and kimchi are made from raw cabbage, and the lactic acid bacteria carry out their own glucosinolate breakdown, producing isothiocyanates and related compounds along the way. See Sauerkraut and Kimchi.

Your Gut Bacteria as a Backup Enzyme

If you eat thoroughly cooked cabbage, the glucosinolates survive the small intestine and arrive in the colon intact. There, a subset of your gut bacteria produce myrosinase-like activity and hydrolyse them, releasing isothiocyanates into the large bowel.

Two things about this backup route are worth knowing. First, it is real — you are not getting nothing from cooked cabbage. Second, it is much less efficient than the plant's own enzyme, and it is enormously variable between individuals, because it depends on which bacteria you happen to be carrying. Studies that measure isothiocyanate excretion after cooked brassica meals find a wide spread across participants, and some people convert very little.

This is one of those places where an honest answer is more useful than a clean one: the colonic route means cooked cabbage still counts, and the variability means nobody can tell you exactly how much it counts for you. The practical response is simply to eat some of your cruciferous vegetables raw or lightly cooked, so you are not depending entirely on a route you cannot measure.

How Isothiocyanates Work Inside a Cell

The mechanism is genuinely elegant and, unusually for nutrition, well characterised.

Your cells carry a protein called Keap1 whose job is to hold down a transcription factor called Nrf2 and send it for destruction. Nrf2 is the master switch for a large battery of protective genes: glutathione S-transferases, NAD(P)H quinone oxidoreductase 1, haem oxygenase 1, and the enzymes that make glutathione, the cell's principal internal antioxidant. Under ordinary conditions Keap1 keeps Nrf2 switched off.

Keap1 is studded with reactive cysteine residues, and isothiocyanates react with them. When they do, Keap1 changes shape and lets go. Nrf2 escapes destruction, moves into the nucleus, binds a DNA sequence called the antioxidant response element, and turns the whole protective battery on. The effect lasts for a day or two — considerably longer than the isothiocyanate itself remains in the body.

Note carefully what this is not. Isothiocyanates are not antioxidants in the way vitamin C is; they do not mop up free radicals directly in any quantity that matters. They are signalling molecules that provoke your own cells into raising their defences. This is sometimes called a hormetic effect: a mild chemical stress that triggers a disproportionate protective response. It is a different and, on the evidence, more durable mechanism than swallowing an antioxidant.

Zhang and Talalay's 1992 isolation of sulforaphane from broccoli, and Fahey and Talalay's 1999 review, are the foundational papers here. The pathway itself is not in doubt.

The Cancer Evidence, Honestly

Now the part that requires discipline, because the mechanism above is so attractive that it is easy to let it stand in for evidence it does not provide.

What the population studies show. Large observational studies that record what people eat and follow them for years have repeatedly found that higher cruciferous vegetable intake is associated with somewhat lower rates of several cancers. Wu and colleagues' 2013 meta-analysis found roughly 18% lower colorectal cancer risk in the highest-intake groups compared with the lowest. Their companion meta-analysis on stomach cancer found a similar-sized association. Higdon and colleagues' review covers the wider literature, including lung and prostate.

What that does and does not mean. These are associations, not causes, and the limitations are not technicalities:

• People who eat a lot of cabbage and broccoli differ from people who do not in dozens of other ways — smoking, exercise, weight, income, overall diet quality, how often they see a doctor. Statistical adjustment reduces this problem but cannot eliminate it.
• Dietary intake in these studies is usually measured by questionnaire, sometimes asking people to recall a year of eating. That measurement is noisy, and noise in the exposure tends to blur real effects and can also manufacture apparent ones.
• The results are not uniform. Some cohorts find nothing. Publication and reporting patterns in nutritional epidemiology mean the pooled figure is probably an upper bound rather than a best estimate.
• The effect sizes, where present, are modest — the kind of difference that matters at population scale and is almost invisible in an individual life.

What is missing. The evidence that would actually settle it — large, long-term randomised trials in which people are assigned to eat more cruciferous vegetables and cancer incidence is counted — does not exist, and realistically will not. Such a trial would need thousands of people, decades, and a way to keep them eating to protocol. What we have instead are short human trials measuring biomarkers.

Those biomarker trials are worth knowing about, because they are the strongest direct human evidence there is. Kensler and colleagues gave a broccoli sprout beverage to adults in Qidong, China, and measured urinary markers of aflatoxin and air-pollutant exposure; the group-level result for aflatoxin adducts was not statistically significant, but among participants whose urine showed the most isothiocyanate, adduct levels were lower — consistent with the mechanism, short of proof of it. Egner and colleagues' later randomised trial in the same region found that the sprout beverage increased urinary excretion of detoxification products of benzene and acrolein, two airborne carcinogens, rapidly and durably over twelve weeks.

That is a real, measured, human, randomised finding — and it is a finding about excreting carcinogens faster, not about getting fewer cancers. The honest summary is therefore: the mechanism is established, the human biomarker effect is demonstrated, the population association is consistent but modest, and the link from those to actual cancer prevention in a person is inferred rather than shown. That is a good reason to eat cabbage regularly. It is not a reason to eat cabbage instead of anything, and it is certainly not a treatment for a diagnosed cancer.

Why the Same Meal Does Different Things in Different People

Isothiocyanates are cleared from the body by conjugation with glutathione, a reaction carried out by glutathione S-transferase enzymes. Two of these, GSTM1 and GSTT1, are commonly deleted entirely — a large minority of people carry no functioning copy of one or the other. People who lack the enzyme clear isothiocyanates more slowly, so the compounds linger longer at the tissues.

Several epidemiological studies have found that the apparent protective association between cruciferous intake and cancer is stronger in people with the null genotype — that is, in people who hold on to isothiocyanates for longer. That is exactly the pattern you would predict if the isothiocyanates were the active agent, which is one of the better arguments that the association is not purely confounding. It also means the average effect in a population conceals real differences between individuals, and nobody is genotyping you before recommending vegetables.

Beyond Cancer

Cancer dominates the cruciferous literature, but it is not the only place these compounds show up.

• Inflammation. Isothiocyanates suppress NF-κB signalling in laboratory models, and the Nrf2 pathway they activate is itself anti-inflammatory. Human data are limited to short trials with biomarker endpoints.
• Detoxification capacity generally. The phase II enzymes Nrf2 switches on are the same ones that handle a wide range of everyday xenobiotics, not just carcinogens. The Qidong trials are the clearest human demonstration.
• Helicobacter pylori. Sulforaphane has activity against H. pylori in the laboratory, including strains resistant to antibiotics, and a small number of human studies have looked at broccoli sprouts for this. Results are suggestive rather than conclusive, and this is not a substitute for eradication therapy. See Bacteria.
• Oestrogen metabolism. Indole-3-carbinol and DIM shift the balance of oestrogen metabolites, which is the basis for a good deal of supplement marketing. The food-level evidence is thin and the supplement doses used in studies are far above anything achievable from cabbage.

A note on supplements, since it comes up constantly: concentrated sulforaphane and glucoraphanin capsules exist, and they are not the same thing as eating a vegetable. Some are standardised for glucoraphanin but contain no active myrosinase, in which case they depend entirely on the colonic route. If you are choosing between a capsule and a plate of shredded cabbage, the plate has better evidence behind it and considerably more fibre.

Getting the Most From a Head of Cabbage

1. Eat some of it raw. Shredded cabbage in a slaw, folded into a salad, or as a crunchy base under something hot. This is the single highest-yield change.
2. Shred first, cook a few minutes later. Let the enzyme work at room temperature before the heat arrives.
3. Cook fast and dry. Steam briefly, stir-fry hot, or roast. Avoid long boils unless you are keeping the liquid.
4. Add a raw brassica garnish to cooked dishes. Mustard powder, horseradish, wasabi, sliced radish or a handful of rocket restores the missing enzyme.
5. Buy fresh and use it reasonably promptly. Glucosinolate content declines during storage, though cabbage holds up far better than most vegetables — a whole head keeps for weeks refrigerated. Cut surfaces degrade much faster, so store it whole and cut what you need.
6. Vary the brassicas. Different species and varieties carry different glucosinolate profiles, so rotating cabbage, broccoli, kale, rocket, radish and watercress gives you a broader mix than eating one of them every day.
7. Do not chase a single compound. If sulforaphane specifically is what you want, broccoli sprouts are the food for it. Cabbage's contribution is a different and perfectly respectable set of compounds, plus fibre, vitamin C and vitamin K, at a fraction of the price.

Key Research Papers

1. Fahey JW, Zalcmann AT, Talalay P. The chemical diversity and distribution of glucosinolates and isothiocyanates among plants. Phytochemistry. 2001;56(1):5–51. — doi:10.1016/S0031-9422(00)00316-2
2. Zhang Y, Talalay P, Cho CG, Posner GH. A major inducer of anticarcinogenic protective enzymes from broccoli: isolation and elucidation of structure. Proceedings of the National Academy of Sciences. 1992;89(6):2399–2403. — doi:10.1073/pnas.89.6.2399
3. Fahey JW, Talalay P. Antioxidant functions of sulforaphane: a potent inducer of Phase II detoxication enzymes. Food and Chemical Toxicology. 1999;37(9–10):973–979. — doi:10.1016/S0278-6915(99)00082-4
4. Traka M, Mithen R. Glucosinolates, isothiocyanates and human health. Phytochemistry Reviews. 2008;8(1):269–282. — doi:10.1007/s11101-008-9103-7
5. Verkerk R, Schreiner M, Krumbein A, et al. Glucosinolates in Brassica vegetables: the influence of the food supply chain on intake, bioavailability and human health. Molecular Nutrition & Food Research. 2009;53(S2). — doi:10.1002/mnfr.200800065
6. Vermeulen M, Klöpping-Ketelaars IWAA, van den Berg R, Vaes WHJ. Bioavailability and kinetics of sulforaphane in humans after consumption of cooked versus raw broccoli. Journal of Agricultural and Food Chemistry. 2008;56(22):10505–10509. — doi:10.1021/jf801989e
7. Conaway CC, Getahun SM, Liebes LL, et al. Disposition of glucosinolates and sulforaphane in humans after ingestion of steamed and fresh broccoli. Nutrition and Cancer. 2000;38(2):168–178. — doi:10.1207/S15327914NC382_5
8. Oliviero T, Verkerk R, Vermeulen M, Dekker M. In vivo formation and bioavailability of isothiocyanates from glucosinolates in broccoli as affected by processing conditions. Molecular Nutrition & Food Research. 2014;58(7):1447–1456. — doi:10.1002/mnfr.201300894
9. Ghawi SK, Methven L, Niranjan K. The potential to intensify sulforaphane formation in cooked broccoli using mustard seeds. Food Chemistry. 2013;138(2–3):1734–1741. — doi:10.1016/j.foodchem.2012.10.119
10. Rungapamestry V, Duncan AJ, Fuller Z, Ratcliffe B. Effect of cooking brassica vegetables on the subsequent hydrolysis and metabolic fate of glucosinolates. Proceedings of the Nutrition Society. 2007;66(1):69–81. — doi:10.1017/S0029665107005319
11. Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacological Research. 2007;55(3):224–236. — doi:10.1016/j.phrs.2007.01.009
12. Wu QJ, Yang Y, Vogtmann E, et al. Cruciferous vegetables intake and the risk of colorectal cancer: a meta-analysis of observational studies. Annals of Oncology. 2013;24(4):1079–1087. — doi:10.1093/annonc/mds601
13. Wu QJ, Yang Y, Wang J, Han LH, Xiang YB. Cruciferous vegetable consumption and gastric cancer risk: a meta-analysis of epidemiological studies. Cancer Science. 2013;104(8):1067–1073. — doi:10.1111/cas.12195
14. Kensler TW, Chen JG, Egner PA, et al. Effects of glucosinolate-rich broccoli sprouts on urinary levels of aflatoxin-DNA adducts and phenanthrene tetraols in a randomized clinical trial. Cancer Epidemiology, Biomarkers & Prevention. 2005;14(11):2605–2613. — doi:10.1158/1055-9965.EPI-05-0368
15. Egner PA, Chen JG, Zarth AT, et al. Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. Cancer Prevention Research. 2014;7(8):813–823. — doi:10.1158/1940-6207.CAPR-14-0103

Further reading: PubMed: glucosinolate, myrosinase and isothiocyanate bioavailability.

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Connections

• All Food
• Cabbage
• Cabbage Benefits
• Cabbage History
• Sulforaphane — the isothiocyanate broccoli is famous for.
• Broccoli — the richest common source of glucoraphanin.
• Brussels Sprouts
• Kale
• Cauliflower
• Watercress
• Arugula
• Radish
• Sauerkraut
• Kimchi
• Glutathione — the antioxidant whose synthesis Nrf2 switches on.
• Colorectal Cancer
• Stomach Cancer
• Goitrogens and Safe Intake — the other side of the same chemistry.

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