Lower Estrogen Naturally: How the Liver Breaks Estrogen Down
Estrogen is not simply used up. It is reworked in the liver and ushered out through the gut. Once you understand this path, you see more clearly what can truly support estrogen balance and what only sounds good.
When women ask me how they can lower their estrogen, I often hear the hope for a pill that makes the problem disappear. The body does not think like that. Estrogen is not waste that simply vanishes. It is a messenger that the liver carefully reworks and the gut ushers out. Once you understand this path, you stop chasing a miracle cure. Instead you support a system that quietly keeps your hormone balance steady every single day.
Perhaps you have heard the term estrogen dominance, and the internet advised you to lower your estrogen. DIM, calcium-D-glucarate, broccoli extract, liver detox. The list is long and the promises are big. And yet one question stays open: how does estrogen actually leave your body? Until you understand that, you cannot judge what is truly sensible.
That is exactly what this article is about. We look at how the liver breaks estrogen down in two phases. We understand why the gut and a single bacterial enzyme co-decide how much estrogen returns to your circulation. And we honestly place what cruciferous vegetables, DIM and calcium-D-glucarate can do, and where the hype begins. By the end you will know where it is worth starting.
Lowering estrogen really means: supporting its breakdown
The first thinking error is already in the word. We talk about lowering estrogen as if there were a dial you turn down. In reality, estrogen is a vital messenger that is constantly formed, used and broken down again. It is rarely about suppressing it wholesale. It is about breakdown and excretion working well, so that no more active estrogen stays in circulation than necessary.
Picture estrogen as a guest who should be welcomed well, but who eventually has to leave too. The liver is the door it walks through. The gut is the way out. If the door sticks or the way is blocked, the guest stays longer than is good. That is one of the layers behind what is colloquially called estrogen dominance.
In the pillar of this cluster you read that estrogen dominance usually describes a relative ratio, often a shortfall of progesterone. The liver and the gut are the second layer of this picture. They co-decide how much estrogen ultimately stays in circulation. And now you know why the question about breakdown matters more than the search for a lowering agent.
You do not have to fight your estrogen. You may keep the path for its breakdown clear. That is a kinder and more accurate thought. The body has a clever mechanism for packaging and excreting estrogen. Your task is not to battle the hormone, but to support the liver and the gut in their normal work.
Phase 1 and phase 2: how the liver reworks estrogen
The liver breaks estrogen down in two consecutive phases. Both belong together. The first phase makes estrogen reactive, the second makes it ready for excretion. Only both steps together manage to remove the hormone from the body.
In phase 1, enzymes from the cytochrome P450 family attach an oxygen group to estrogen. This forms so-called hydroxyestrogens. Depending on which enzyme is at work, the result tends to be 2-hydroxyestrone, regarded as favourable, or 16-alpha-hydroxyestrone and 4-hydroxyestrone, described as more active or more problematic. Which path predominates depends on genes, diet and lifestyle.
Which liver enzymes rework estrogen, and why direction matters
Review A comprehensive review by Mokhosoev and colleagues in 2024 in Cells describes how the cytochrome P450 enzymes CYP1A1, CYP1A2 and CYP1B1 convert estrogen into 2- and 4-catechols. The authors stress one important point: the 4-hydroxy catechols can form reactive intermediates via quinones that may damage cell components. By contrast, they describe the 2-hydroxy and the subsequently methylated metabolites as rather protective. So it is not breakdown as such, but its direction and completeness, that co-decide whether mostly harmless or mostly burdensome substances remain at the end.
Mokhosoev IM, Astakhov DV, Terentiev AA, Moldogazieva NT. Cells. 2024;13(23):1958. doi:10.3390/cells13231958 · PMID: 39682707
In phase 2, these intermediates are processed further. The body couples them to water-soluble groups, mainly through methylation and through glucuronidation. Only then do they become water-soluble enough to pass through the bile into the gut and finally out. Methylation needs building blocks such as magnesium and certain B vitamins; glucuronidation needs protein and a working liver.
This explains why a sole focus on phase 1 falls short. If phase 1 runs fast but phase 2 lags behind, reactive intermediates can accumulate. A good estrogen detox needs both phases in balance. And now you know why detox promises that turn only one dial distort the picture.
The gut co-decides: the estrobolome and beta-glucuronidase
Here comes the part many overlook. The liver has done its work and passed the packaged estrogen via the bile into the gut. But that does not settle the matter. Because in the gut sit bacteria that can cut this packaging open again.
A group of gut bacteria produces the enzyme beta-glucuronidase. It splits exactly the bond with which the liver marked the estrogen for excretion. This frees the estrogen again, and it can be taken back up across the gut wall into the blood instead of being excreted. This loop is called the enterohepatic circulation. The totality of gut bacterial genes that influence estrogen this way has its own name: the estrobolome.
How the gut flora co-steers estrogen levels via one enzyme
Review Baker and colleagues described the estrogen-gut axis in 2017 in Maturitas. Their core point: the gut flora regulates circulating estrogen through the secretion of beta-glucuronidase, an enzyme that breaks packaged estrogen back into its active form. When the gut flora is out of balance and its diversity reduced, this mechanism can be disrupted and the amount of estrogen in circulation altered. The authors link this to pictures such as obesity, metabolic syndrome, endometriosis and PCOS. So the gut is a real player in estrogen balance, not a mere appendage.
Baker JM, Al-Nakkash L, Herbst-Kralovetz MM. Maturitas. 2017;103:45-53. doi:10.1016/j.maturitas.2017.06.025 · PMID: 28778332
A further review by Kwa and colleagues in 2016 in the Journal of the National Cancer Institute coined the term estrobolome more precisely and described how its activity co-determines estrogen metabolism in the body (doi:10.1093/jnci/djw029, PMID: 27107051). A more recent review by Kumari and colleagues in 2024 in Molecular Nutrition and Food Research confirms this direction and stresses that plant compounds from food also act via the gut bacteria (doi:10.1002/mnfr.202300688, PMID: 38342595). And now you know why a healthy gut is no side stage when it comes to estrogen.
The four levers of estrogen detox at the cellular level
When I look at estrogen breakdown through the lens of clinical psychoneuroimmunology, I see four levels that work together. Each explains one part at the cellular level. Together they explain why some women seem to clear estrogen less well than others.
Liver phase-1 enzymes
The cytochrome P450 enzymes CYP1A1, CYP1A2 and CYP1B1 decide which hydroxyestrogens estrogen is reworked into. Genetic differences and compounds from cruciferous vegetables may influence whether the favourable 2-hydroxyestrone or the more active paths predominate. This first switch co-determines which intermediates arise at all and are passed on to the second phase.
Liver phase-2 coupling
In the second phase, the intermediates are coupled to water-soluble groups through methylation and glucuronidation. Only this makes estrogen ready for excretion. These steps need building blocks such as protein, magnesium and B vitamins. If phase 2 cannot keep up, reactive intermediates can accumulate instead of being cleanly excreted.
Gut and beta-glucuronidase
In the gut, the bacterial enzyme beta-glucuronidase can cut packaged estrogen open again, so it returns to the blood. A gut flora that is out of balance with high enzyme activity could thus contribute to more estrogen circulating. A diverse gut flora and enough fibre may dampen this reflux.
Excretion via bile and stool
In the end, the packaged estrogen has to leave the body via bile and stool. Fibre binds estrogen in the gut and supports transport out. A sluggish digestion or a low-fibre diet can prolong the dwell time. Here the circle closes: what the liver packages, the gut must reliably carry out.
These four levers are not a treatment plan. They are a map. They show that estrogen breakdown can stall in several places, and that there are therefore several sensible starting points rather than just one. And now you know why it rarely takes a single miracle remedy, but rather a coherent whole.
DIM and cruciferous vegetables: what the human studies really show
Broccoli, Brussels sprouts, cauliflower and cabbage contain glucosinolates. When chopping and chewing, indole-3-carbinol is formed, and in the acidic stomach DIM, that is 3,3-diindolylmethane, is formed from it. These compounds may influence the phase-1 liver enzymes via a switch called the aryl hydrocarbon receptor and shift estrogen breakdown towards the more favourable 2-hydroxyestrone.
This is well studied, and there really are controlled human studies on it. That is rather rare in the supplement field and worth a closer look.
DIM shifts the estrogen breakdown ratio
RCT, placebo-controlled Thomson and colleagues studied 130 women taking tamoxifen in 2017 in Breast Cancer Research and Treatment, in a randomised, double-blind, placebo-controlled trial over twelve months. Under DIM, the ratio of 2- to 16-alpha-hydroxyestrone in urine rose markedly, while it stayed practically unchanged under placebo. Sex hormone-binding globulin also rose. Important for an honest reading: at the same time the tamoxifen metabolites in the blood fell. This shows that DIM may shift metabolism, but also interacts with medication.
Thomson CA, Chow HHS, Wertheim BC, et al. Breast Cancer Res Treat. 2017;165(1):97-107. doi:10.1007/s10549-017-4292-7 · PMID: 28560655
An indole-containing formula raises the favourable breakdown ratio
RCT, crossover Green and colleagues tested a dietary supplement with indole-3-carbinol and green tea in 2022 in the Journal of Complementary and Integrative Medicine, in 148 premenopausal women in a randomised, double-blind, placebo-controlled crossover trial. After twelve weeks, the ratio of 2- to 16-alpha-hydroxyestrone in urine was markedly higher than under placebo. This supports the observation that indole compounds may shift estrogen metabolism in a direction discussed as favourable. Whether this eases noticeable symptoms was not the study aim and remains open.
Green T, See J, Schauch M, et al. J Complement Integr Med. 2022;20(1):199-206. doi:10.1515/jcim-2022-0301 · PMID: 36201753
A review by Williams in 2021 in Frontiers in Nutrition places this soberly: to reach the DIM amounts from supplements through vegetables, you would have to eat kilos of Brussels sprouts daily (doi:10.3389/fnut.2021.734334, PMID: 34660663). An older review by Higdon in 2007 in Pharmacological Research stresses that, while indole-3-carbinol and DIM do change estrogen metabolites in urine, the effect on concrete diseases remains unclear (doi:10.1016/j.phrs.2007.01.009, PMID: 17317210).
"DIM lowers my estrogen." That is imprecise. The studies show that DIM mainly shifts the ratio of the breakdown products, not reliably the total level. And a shifted urine ratio is a research marker, not proof that you feel better. DIM may also interact with medication. It can be a thoughtful building block, but it is no hormone off-switch.
Calcium-D-glucarate, alcohol, and an honest line between hype and substance
A second popular supplement is calcium-D-glucarate. The idea is elegant: it may inhibit beta-glucuronidase in the gut, exactly the enzyme that frees packaged estrogen again. If the enzyme is slowed, less estrogen could be reabsorbed and more could leave the body.
Calcium-D-glucarate and beta-glucuronidase
Review, animal-model basis A review in Alternative Medicine Review in 2002 summarises that oral calcium-D-glucarate may inhibit beta-glucuronidase, an enzyme of phase-2 detox and of the gut flora. Raised activity of this enzyme is linked to a higher risk for hormone-dependent pictures. As a possible application, the authors explicitly name the regulation of estrogen metabolism. Important for the framing: the robust data come mostly from animal models. Controlled human studies on hormonal symptoms in women are largely missing.
Calcium-D-glucarate. Altern Med Rev. 2002;7(4):336-339. PMID: 12197785 · doi: not assigned
So calcium-D-glucarate is a good example of the narrow line between mechanistically plausible and clinically proven. The mechanism makes sense. But the bridge to noticeably fewer symptoms in women has not yet been built by good human studies. That does not mean it is useless. It means honesty about the evidence belongs to the picture.
A factor with better plausibility is alcohol. The liver is the central organ of estrogen breakdown, and alcohol taxes the same metabolism. In observational data, alcohol intake is linked to higher estrogen levels. Less alcohol is therefore one of the few measures supported both mechanistically and in observational studies, and it may noticeably relieve the liver.
A plant-compound-rich diet may also act on estrogen balance. In a small controlled dietary study in healthy women, a soy-based, isoflavone- and fibre-rich diet lowered circulating estradiol levels across the cycle, with fibre and energy intake also playing a role (Lu 2000, Cancer Research, PMID: 10945618). That is a hint, not a proof. But it fits the picture that diet as a whole moves more than a single extract.
Three levers that may support estrogen breakdown
Before turning to supplements, it is worth looking at the basics. They are not spectacular, but they support exactly the paths we have described here. These three levers are a start, not a treatment plan. You find your individual path with medical guidance.
Eat plenty of fibre and colourful vegetables
Fibre binds estrogen in the gut and may support excretion via the stool, instead of pulling it back in the enterohepatic circulation. Cruciferous vegetables additionally provide indole compounds that may influence liver metabolism. You do not have to eat kilos of Brussels sprouts. A consistently vegetable- and fibre-rich diet supports the breakdown path on several levels at once.
Care for liver and gut in everyday life
Little alcohol relieves the liver, the central breakdown organ. Enough protein for the phase-2 building blocks, a stable weight and calm blood sugar support the rework. A diverse gut microbiome with fermented foods and a regular digestion may help the packaged estrogen actually leave the body.
Use supplements deliberately and with guidance
DIM and calcium-D-glucarate are mechanistically interesting but clinically thinly supported, and DIM may interact with medication. If you consider them, do so not as a miracle remedy but as a conscious building block after medical consultation. Especially with hormone-dependent conditions, when trying to conceive, in pregnancy, while breastfeeding or alongside other medication, this belongs in professional hands.
These levers share a common denominator: they support the natural path instead of trying to outsmart it. That is less glamorous than a detox promise, but it is what physiology allows. And now you know why the basics come first.
You do not lower estrogen, you keep its exit clear
Your body knows how to break estrogen down. The liver packages it, the gut carries it out. Your task is not the battle against a hormone, but the care of the paths that usher it out. When you support liver and gut, you give your body the chance to find its own balance. That is not denial. It is cooperation with your physiology.
Frequently asked questions about lowering estrogen via the liver
Can you lower estrogen naturally?
Deliberately pushing down your absolute estrogen level with lifestyle is hard, and usually not the real goal. It makes more sense to support estrogen metabolism. Estrogen is reworked in the liver in two phases and passed via the bile into the gut, from where it is excreted. When this path runs well, less active estrogen stays in circulation. Factors such as fibre, a healthy gut, less alcohol and stable blood sugar may favourably influence this breakdown and excretion path. The sober framing matters: much of this shifts the ratio of estrogen metabolites rather than the total level, and the data on clinical symptoms is limited. Persistent symptoms belong in medical hands.
How does the liver break estrogen down?
Breakdown runs in two phases. In phase 1, cytochrome P450 enzymes such as CYP1A1, CYP1A2 and CYP1B1 attach a chemical group to estrogen and form hydroxyestrogens, mainly 2-hydroxyestrone, 4-hydroxyestrone and 16-alpha-hydroxyestrone. These intermediates differ in activity. In phase 2, they are coupled to water-soluble groups, for example through methylation or glucuronidation, so they can be excreted via bile and gut. Only both phases together make estrogen ready for excretion. A review describes that the methylated metabolites and conjugated products tend to be protective, while uncontrolled catechol and quinone intermediates may favour cell damage.
What does the gut have to do with estrogen levels?
A great deal. The gut hosts a group of bacteria whose genes together form the so-called estrobolome. These bacteria produce the enzyme beta-glucuronidase. It can cut open and release estrogen that the liver has already packaged for excretion. The freed estrogen is then taken back up into the blood instead of being excreted, a process called the enterohepatic circulation. An altered gut flora with high beta-glucuronidase activity could therefore lead to more estrogen circulating in the body. Fibre binds estrogen in the gut and may support excretion. So the gut is a real player in estrogen balance, not a side stage.
Does DIM help break estrogen down?
DIM, or 3,3-diindolylmethane, is formed from indole-3-carbinol, a compound from cruciferous vegetables such as broccoli and Brussels sprouts. In controlled human studies, DIM shifts the ratio of estrogen metabolites towards 2-hydroxyestrone, which is regarded as more favourable. In a randomised study of women taking tamoxifen, this ratio rose markedly under DIM. Importantly, DIM mainly changes how estrogen is broken down, not necessarily the total level, and the benefit for concrete symptoms is not yet well established. DIM may also interact with medication; in one study tamoxifen levels fell. Intake should therefore be discussed with a doctor, especially with hormone-dependent conditions, when trying to conceive, in pregnancy, while breastfeeding or alongside other medication.
What is calcium-D-glucarate and can it help?
Calcium-D-glucarate is the calcium salt of D-glucaric acid, which occurs naturally in fruit and vegetables, especially oranges, apples and cruciferous vegetables. It may inhibit beta-glucuronidase in the gut. The idea: if this enzyme is slowed, less already-packaged estrogen can be cut open and reabsorbed, so more is excreted. This effect is mechanistically plausible and described in animal models. Robust human studies on hormonal symptoms in women are largely missing, however. Calcium-D-glucarate is therefore an interesting concept with a thin clinical evidence base in humans, not a proven remedy against estrogen dominance.
Do broccoli and cruciferous vegetables help estrogen metabolism?
Cruciferous vegetables such as broccoli, Brussels sprouts, cauliflower and cabbage contain glucosinolates, from which indole-3-carbinol and then DIM are formed when chopping and chewing. These compounds may influence estrogen metabolism via the aryl hydrocarbon receptor and the liver enzymes and shift the ratio of metabolites. One important caveat: to reach amounts comparable to supplement doses through food, you would have to eat enormous quantities of vegetables. The realistic benefit of a cruciferous-rich diet lies more in the sum of fibre, plant compounds and a healthy gut. Plenty of vegetables is therefore sensible, but not a targeted hormone medication.
What role do alcohol and the liver play in estrogen?
The liver is the central organ for estrogen breakdown. Anything that burdens the liver may, in theory, impair this breakdown. Alcohol is regarded as a relevant factor here, since it taxes liver metabolism and is linked in observational data to higher estrogen levels. A liver-friendly lifestyle with little alcohol, a stable weight, enough protein for the phase-2 building blocks and calm blood sugar may support the liver's work. This is no detox miracle, simply the basis for the normal breakdown path to function well. Working here supports the whole system rather than turning a single hormonal dial.
What does the 2-hydroxy to 16-hydroxy ratio mean?
In liver phase 1, estrogen can be reworked in different ways. Two important paths lead to 2-hydroxyestrone, regarded as rather favourable, and to 16-alpha-hydroxyestrone, described as more estrogen-active. The ratio of these two metabolites in urine has been discussed since the 1990s as a possible marker of estrogen metabolism. Compounds such as indole-3-carbinol and DIM can shift this ratio in favour of 2-hydroxyestrone. The sober framing matters: this ratio is a research marker, not a clear disease value. A shifted ratio does not prove a disease, and an improved ratio does not yet prove a clinical benefit for your symptoms.
What is hype and what can really help with lowering estrogen?
Hype means promises that a single product can lower estrogen quickly and precisely or remove estrogen dominance. The body does not work like that. What has a solid basis: plenty of vegetables and fibre, a healthy gut, little alcohol, a stable weight and calm blood sugar. This supports the natural breakdown and excretion path. What is mechanistically interesting but clinically thinly supported: targeted supplements such as DIM or calcium-D-glucarate. They tend to shift the metabolism of the breakdown products rather than reliably easing symptoms. The honest path is to support the basics first and to use supplements only deliberately and with medical guidance.
When should I see a doctor about an estrogen problem?
Persistent or new symptoms belong in medical hands instead of being attributed too quickly to estrogen dominance. You should seek urgent assessment for suddenly changed or very heavy bleeding, bleeding after menopause, newly appeared lumps in the breast, or an absent period without pregnancy over several months. Behind symptoms that look like an estrogen excess, very different causes can hide, from a progesterone deficiency through the thyroid to stress. Good diagnostics look at the whole system and interpret lab values in the context of your cycle phase and your symptoms. Supplements do not replace medical assessment.
All topics in the "Hormone Guide" cluster
This article is Spoke 15. Back to the pillar and overview. Each topic illuminates one part of the connected system.
- Hormonal Imbalance in Women (overview/pillar)
- Estrogen Dominance: recognising symptoms and addressing them naturally
- Xenoestrogens: hormone disruptors in everyday life
- Coming off the pill: what happens in the body
- Progesterone deficiency: symptoms and testing
- PMS: symptoms and what can ease them
- PMDD: when PMS hits the mind
- Perimenopause: symptoms and when it begins
- Menopause: symptoms and what can ease them
- PCOS: causes and symptoms
- Hormonal acne from within
- Endometriosis: an integrative view
- Hormone-free contraception compared
- Loss of libido in women
- Testing hormones: which test, when
- Lower estrogen naturally (liver)
- Cycle-based nutrition
- Thyroid and female hormones
- Insulin resistance and hormones
- Cortisol, stress and female hormones
- Chasteberry and herbal hormone helpers
Connections to other topics
Because the estrobolome and beta-glucuronidase in the gut co-decide how much estrogen returns to circulation, a healthy gut is central to estrogen breakdown.
Estrogen breakdown is one layer behind the picture of estrogen dominance. Here we place what hides behind the term and why progesterone often plays a role too.
A stable weight and calm blood sugar relieve the liver. Why women respond differently to fasting and what this has to do with hormone balance.
Tiredness and exhaustion are quickly blamed on hormones. Iron deficiency is a common, easily overlooked contributing cause that deserves its own attention.
The thyroid and estrogen are linked via binding proteins in the liver. Why normal values are not always enough and how the two can be connected.
Chronic stress taxes metabolism and the liver. An honest take on cortisol and the HPA axis, closely interwoven with hormone balance.
Sources and further reading
- Mokhosoev IM, Astakhov DV, Terentiev AA, Moldogazieva NT. Human Cytochrome P450 Cancer-Related Metabolic Activities and Gene Polymorphisms: A Review. Cells. 2024;13(23):1958. doi:10.3390/cells13231958 · PMID: 39682707 [Review]
- Williams DE. Indoles Derived From Glucobrassicin: Cancer Chemoprevention by Indole-3-Carbinol and 3,3'-Diindolylmethane. Front Nutr. 2021;8:734334. doi:10.3389/fnut.2021.734334 · PMID: 34660663 [Review]
- Thomson CA, Chow HHS, Wertheim BC, et al. A randomized, placebo-controlled trial of diindolylmethane for breast cancer biomarker modulation in patients taking tamoxifen. Breast Cancer Res Treat. 2017;165(1):97-107. doi:10.1007/s10549-017-4292-7 · PMID: 28560655 [RCT]
- Green T, See J, Schauch M, et al. A randomized, double-blind, placebo-controlled, cross-over trial to evaluate the effect of EstroSense on 2-hydroxyestrone:16α-hydroxyestrone ratio in premenopausal women. J Complement Integr Med. 2022;20(1):199-206. doi:10.1515/jcim-2022-0301 · PMID: 36201753 [RCT]
- Baker JM, Al-Nakkash L, Herbst-Kralovetz MM. Estrogen-gut microbiome axis: Physiological and clinical implications. Maturitas. 2017;103:45-53. doi:10.1016/j.maturitas.2017.06.025 · PMID: 28778332 [Review]
- Kwa M, Plottel CS, Blaser MJ, Adams S. The Intestinal Microbiome and Estrogen Receptor-Positive Female Breast Cancer. J Natl Cancer Inst. 2016;108(8):djw029. doi:10.1093/jnci/djw029 · PMID: 27107051 [Review]
- Kumari N, Kumari R, Dua A, et al. From Gut to Hormones: Unraveling the Role of Gut Microbiota in (Phyto)Estrogen Modulation in Health and Disease. Mol Nutr Food Res. 2024;68(6):e2300688. doi:10.1002/mnfr.202300688 · PMID: 38342595 [Review]
- Calcium-D-glucarate. Altern Med Rev. 2002;7(4):336-339. PMID: 12197785 [Review]
- Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res. 2007;55(3):224-236. doi:10.1016/j.phrs.2007.01.009 · PMID: 17317210 [Review]
- Lord RS, Bongiovanni B, Bralley JA. Estrogen metabolism and the diet-cancer connection: rationale for assessing the ratio of urinary hydroxylated estrogen metabolites. Altern Med Rev. 2002;7(2):112-129. PMID: 11991791 [Review]
- Bradlow HL, Sepkovic DW, Telang NT, Osborne MP. Multifunctional aspects of the action of indole-3-carbinol as an antitumor agent. Ann N Y Acad Sci. 1999;889:204-213. doi:10.1111/j.1749-6632.1999.tb08736.x · PMID: 10668495 [Review]
- Lu LJ, Anderson KE, Grady JJ, Kohen F, Nagamani M. Decreased ovarian hormones during a soya diet: implications for breast cancer prevention. Cancer Res. 2000;60(15):4112-4121. PMID: 10945618 [Human study, controlled, n=10]