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A landmark presentation at The Menopause Society Annual Meeting found that 94% of women experience digestive health symptoms during perimenopause — making gut disruption one of the most prevalent but least-discussed features of this transition. More than half report severe constipation. Nearly half report acid reflux symptoms they had never experienced before. Almost all describe bloating.

You wake up with a flat stomach. By eleven o’clock you are uncomfortably bloated. By evening, you look — and feel — as though you are several months pregnant. The clothes that fitted you at nine in the morning don’t close by lunchtime.

You have been tested. IBS: negative. Coeliac: negative. SIBO: negative. You have eliminated gluten, then dairy, then FODMAPs, then almost everything. Nothing works consistently. You are not eating differently from how you ate two years ago. You are not under more stress. But your gut has become a different organ — unpredictable, reactive, and swollen in a way that feels new and, frankly, frightening.

Here is what no one has told you: this is not a gut problem. It is a hormone problem that is expressing itself through your gut. And in early perimenopause, it is one of the most common — and most misunderstood — symptoms women experience.

Two Mechanisms Converging at Once

To understand perimenopause bloating and distension, you need to understand what progesterone was quietly doing for you all those years — and what happens when it starts to decline.

In a regular cycle, progesterone rises after ovulation in the second half (the luteal phase). This rise serves two purposes that are directly relevant to gut symptoms.

First, progesterone is mildly diuretic. It competes with aldosterone at the mineralocorticoid receptor in the kidneys, reducing sodium and water retention. This is the counterbalance to oestrogen, which promotes water and sodium retention via aldosterone signalling. In a well-regulated cycle, these two hormones keep fluid balance reasonably stable across the month.

Second, progesterone affects gut motility. Research on progesterone and gastrointestinal function shows a complex picture: at physiological concentrations, progesterone exerts a modulatory influence on gut smooth muscle, and progesterone withdrawal — the sharp drop before menstruation — is widely understood to promote intestinal movement. This is why many women notice looser stools just before their period. That reliable monthly loosening is progesterone withdrawal at work.

In early perimenopause, ovulation becomes irregular. When you do not ovulate, the corpus luteum does not form, and progesterone is not produced in any meaningful quantity. The result is what clinicians call oestrogen dominance — not necessarily an excess of oestrogen in absolute terms, but an unchecked oestrogen effect in the absence of its progesterone counterbalance.

Without progesterone, two things happen simultaneously:

1. Fluid accumulates — oestrogen drives sodium retention via aldosterone signalling, and there is no progesterone competing at the mineralocorticoid receptor to blunt that effect. Research confirms that progesterone (and some progestogens) mitigate oestradiol effects on water and sodium retention through competition with aldosterone for the mineralocorticoid receptor.
2. Gut motility slows — the intestinal stimulation that progesterone withdrawal once reliably triggered no longer occurs with the same regularity.

The result is a gut that is simultaneously waterlogged and sluggish. Both mechanisms drive bloating and distension. Together, they create the pattern you recognise: progressive swelling through the day, worst in the evening, often better (though not gone) after a night’s rest.

The Progesterone Shift is my approach to understanding and addressing this exact imbalance — the dual loss of progesterone’s diuretic and gut-stimulating effects. Learn more here.

The Gut-Oestrogen Axis: The Star Amplifier

If fluid retention and slowed motility were the only mechanisms, we would expect perimenopause bloating to be a manageable, temporary inconvenience. The reason it can become so severe — and so resistant to dietary interventions — is a third mechanism: the gut-oestrogen axis.

Before exploring the estrobolome, it is worth establishing something that most women — and many clinicians — do not know: oestrogen receptors line the entire gastrointestinal tract. Oestrogen receptor alpha (ERα) and oestrogen receptor beta (ERβ) are expressed in the oesophagus, stomach, small intestine, and colon, as well as in the enteric nervous system — the network of neurons embedded in the gut wall that governs motility, secretion, and gut sensation. Chen et al.’s 2019 review in Oncology Letters documented the roles of oestrogen and its receptors throughout GI disease, noting that oestrogen exerts regulatory effects on gut function via these receptor pathways and that their disruption contributes to conditions ranging from gastroesophageal reflux to irritable bowel syndrome. Hill-Yardin et al. (2021) specifically identified ERα-expressing neurons in the myenteric plexus of the colon, demonstrating that colonic motility changes with oestrogen fluctuation across the cycle.

This matters because it means oestrogen withdrawal — and oestrogen volatility — is not a peripheral influence on gut function. It is a direct one, acting on the nervous system that runs the gut itself.

A second consequence of slowed transit deserves specific mention: gas accumulation through fermentation. When gut transit slows, food residue spends longer in the colon where gut bacteria ferment it, producing methane and hydrogen gas as metabolic byproducts. This adds a physical gas volume to the fluid retention already present — which is why perimenopause bloating is often not just a feeling of fullness or heaviness, but actual visible abdominal distension. Johnson et al. (2019) in the American Journal of Physiology documented the role of oestrogen in modulating gut motility and visceral sensitivity through the brain-gut axis, with altered motility patterns directly influencing both gas accumulation and abdominal discomfort.

The Estrobolome

The estrobolome is the collection of gut bacteria whose metabolic activity directly regulates oestrogen levels in the body. Specifically, certain gut bacteria produce an enzyme called beta-glucuronidase (β-glucuronidase). This enzyme is central to what happens to oestrogen after the liver has processed it.

Here is the normal sequence: Oestrogen is metabolised in the liver and conjugated (packaged) with glucuronic acid, rendering it inactive and water-soluble. It is then excreted via bile into the gut, ready to leave the body in the stool. However, if gut bacteria with high beta-glucuronidase activity are present in sufficient numbers, they deconjugate — or unpackage — the oestrogen before it can be excreted. The now-reactivated oestrogen is reabsorbed through the gut wall and returns to general circulation via the hepatic portal vein. This process is known as enterohepatic recirculation of oestrogen.

The landmark 2019 paper by Li et al. provided experimental evidence that gut microbial GUS enzymes actively reactivate oestrogens as components of the estrobolome, demonstrating that bacterial beta-glucuronidase enzymes in the gastrointestinal tract are a contributing factor in the regulation of systemic oestrogen levels. Ma et al.’s 2023 review confirmed that gut microbial beta-glucuronidase is a vital regulator in female oestrogen metabolism throughout a woman’s life, and that when the balance between gut bacteria and beta-glucuronidase activity is disrupted, oestrogen metabolism is disturbed — with consequences for oestrogen-related conditions including menopausal symptoms.

How Gut Dysbiosis Worsens Oestrogen Dominance

In a diverse, healthy gut microbiome, beta-glucuronidase activity is modulated. In a dysbiotic gut — one with reduced microbial diversity, altered species balance, or an overgrowth of beta-glucuronidase-producing bacteria — that activity rises unchecked. The consequences for perimenopausal women are significant:

• Higher beta-glucuronidase → more oestrogen reabsorption → elevated circulating oestrogen → worsened oestrogen dominance
• Elevated oestrogen worsens fluid retention and further suppresses gut motility
• Slower gut transit means oestrogen spends longer in the gut, giving beta-glucuronidase more time to act on it — which means even more reabsorption

This is a self-reinforcing cycle. The disrupted gut worsens oestrogen dominance, and oestrogen dominance further disrupts the gut. Every factor that promotes gut dysbiosis — processed diet, antibiotic use, chronic stress, alcohol, low fibre intake — also amplifies hormonal bloating in early perimenopause.

This bidirectional relationship between the gut microbiome and circulating oestrogen is why dietary interventions that focus purely on elimination (removing foods that “trigger” bloating) so frequently fail. The bloating is not caused by the food. It is caused by the hormonal environment in which the food is being digested.

The Four Amplifiers

Beyond the core progesterone-oestrogen imbalance and the gut-oestrogen axis, four additional factors can significantly amplify bloating and distension in early perimenopause.

1. Liver and Gut Function

As described above, the liver-gut axis is the most clinically important amplifier for bloating. The liver’s capacity to conjugate and excrete oestrogen efficiently depends on:

• Methylation capacity — supported by B vitamins (B2, B6, B12, folate)
• Phase II liver detoxification pathways — supported by compounds such as DIM (diindolylmethane) and I3C (indole-3-carbinol), found in cruciferous vegetables
• Gut microbial diversity — the foundation of healthy beta-glucuronidase regulation
• Bowel transit frequency — stool is the primary exit route for conjugated oestrogen

When any of these factors is compromised, oestrogen recirculation increases, and bloating worsens.

2. The Insulin-Oestrogen Loop

Insulin resistance and oestrogen dominance have a bidirectional relationship. Elevated insulin can contribute to fluid retention independently of oestrogen signalling, and disrupts gut motility signalling. More directly for bloating: refined carbohydrates and high-glycaemic foods that rapidly ferment in the intestine produce gas as a byproduct. This intestinal fermentation adds a separate mechanical bloating mechanism on top of the hormonal fluid retention — and the two compound each other. Blood sugar stability is not only relevant to weight and energy; it directly affects the degree of bloating that perimenopausal women experience.

3. Chronic Stress and the Gut-Brain Axis

Chronic psychological stress activates the hypothalamic-pituitary-adrenal (HPA) axis, elevating cortisol. Cortisol has well-documented effects on gut function: it alters gut motility, increases intestinal permeability, and can produce IBS-like symptoms through direct action on the enteric nervous system. Research confirms that HPA axis overactivation disrupts cortisol balance, exacerbating intestinal permeability and inflammation, and that elevated cortisol and dysregulated stress hormones significantly contribute to altered colonic transit and visceral sensitivity in functional gut disorders. The gut-brain axis is not a metaphor — it is a physiological pathway through which chronic stress directly worsens gut symptoms.

Note: what chronic stress does not do is steal progesterone via the “pregnenolone steal” mechanism. This concept — that cortisol production diverts the precursor pregnenolone away from progesterone synthesis — has been widely circulated but lacks robust scientific support. It is not a mechanism Sandra works from. The cortisol-gut relationship is real; pregnenolone steal is a myth.

4. Xenoestrogens

Environmental oestrogens — synthetic compounds found in plastics (BPA, phthalates), conventional skincare, pesticides, and some household products — bind oestrogen receptors and add to the overall oestrogenic burden on the body. In a woman already experiencing oestrogen dominance through loss of progesterone, xenoestrogen exposure adds additional fuel. Reducing exposure through dietary and household choices is a practical step with cumulative benefit.

For a full explanation of how these amplifiers interact in early perimenopause, see Sandra’s Early Perimenopause page.

The IBS Misdiagnosis Problem

Perimenopausal women are frequently diagnosed with IBS. The diagnosis typically follows a run of negative investigations — colonoscopy, coeliac screen, SIBO test, food intolerance panels — and a pattern of gut symptoms that does not fit any structural or infectious cause. IBS becomes the diagnosis of exclusion.

In many of these women, the underlying driver is hormonal. The gut symptoms are a consequence of oestrogen dominance and the disrupted gut-oestrogen axis, not a primary gut disorder.

The clinical pattern helps distinguish them:

IBS	Perimenopause-driven bloating
Typically chronic and long-standing	Appeared or significantly worsened in the last 1–3 years
Consistent diet triggers across the cycle	Symptoms worsen independent of what was eaten
Relatively stable across the menstrual cycle	Cyclical — worse in the luteal phase (post-ovulation), better after the period
No clear relationship to other hormonal symptoms	Often accompanies other luteal-phase symptoms: low mood, breast tenderness, fatigue
Not typically progressive cycle-to-cycle	Progressively worsening cycle on cycle

Research on gonadal hormones and IBS symptoms in women confirms that an increase in gastrointestinal symptoms including bloating has been reported during the perimenopause period in women with and without IBS, and that declining ovarian hormone levels may underlie the occurrence or exacerbation of these symptoms. Studies on IBS in midlife women further confirm that hormonal changes of the menopausal transition are relevant to gastrointestinal symptoms, and that this population is frequently underserved by standard GI investigation.

The same hormonal data from The Menopause Society also points to two other gut symptoms that commonly accompany bloating but are rarely connected to it clinically. Acid reflux and GERD affect approximately 49% of perimenopausal women — a prevalence far higher than in age-matched premenopausal women. Chen et al.’s review of oestrogen receptors in GI disease confirms that fluctuating oestrogen directly affects the lower oesophageal sphincter, reducing its muscular tone and allowing stomach acid to move upward. Women who develop reflux in their 40s with no prior history are frequently given proton pump inhibitors without any consideration of the hormonal mechanism driving the sphincter dysfunction. Treating the gut in isolation, while the hormonal disruption continues, produces partial and temporary results at best.

This matters clinically because the treatment for IBS (typically dietary restriction, antispasmodics, or fibre supplementation) does not address the hormonal and estrobolome drivers of perimenopausal bloating. Women who have been on low-FODMAP diets for a year with no lasting improvement deserve a hormonal lens applied to their symptoms.

The Constipation-Oestrogen Loop

Data from The Menopause Society found that 54% of perimenopausal women report severe constipation — a figure that, given the mechanism below, should come as no surprise. Constipation deserves its own section because it is widely treated as a minor inconvenience to manage with more water and fibre. In early perimenopause, it is something quite different. It is an active driver of oestrogen recirculation.

Here is the mechanism: Conjugated (inactivated) oestrogen, packaged by the liver and excreted into the gut via bile, is waiting to leave the body. In ideal transit — a bowel movement every day — it leaves within a predictable window. But in constipation, it sits in the colon. For every additional day of constipation, beta-glucuronidase-producing bacteria have more time to deconjugate that oestrogen. More deconjugation means more reabsorption through the gut wall. More reabsorption means higher circulating oestrogen. Higher circulating oestrogen further slows gut motility — which worsens constipation.

This loop can become entrenched quickly. The woman who develops constipation in early perimenopause — because progesterone withdrawal is now irregular and the intestinal stimulation it once provided has become unreliable — finds that the constipation itself is amplifying the oestrogen dominance that caused the constipation in the first place.

Every day that stool is not moving is another day of compounding hormonal imbalance. This is not a digestive inconvenience. It is a central mechanism in perimenopausal oestrogen dominance.

What Helps: My Approach

Sandra’s non-hormonal approach to perimenopause addresses bloating and distension by working on the underlying hormonal and gut mechanisms — not by chasing symptoms with dietary elimination.

Gut Microbiome Restoration

The foundation of addressing estrobolome dysfunction is restoring microbial diversity. Not all probiotics are relevant here — the strains matter. Lactobacillus plantarum has demonstrated capacity to modulate gut barrier integrity and reduce inflammatory signalling in the gut wall. Bifidobacterium longum and Bifidobacterium lactis support healthy transit and contribute to a microbial environment less favourable to excessive beta-glucuronidase activity. Muscogiuri et al.’s 2023 review in Current Nutrition Reports confirmed that specific probiotic strains have demonstrable roles in menopause-related conditions, with Lactobacillus-dominant supplementation associated with improved gut symptom scores in perimenopausal women. Wang et al.’s 2022 paper in Nutrients — specifically examining lactic acid bacteria in menopause — identified Lactobacillus and Bifidobacterium species as having direct relevance to gut microbiome modulation and oestrogen metabolite handling in menopausal women.

Beyond probiotics, Calcium D-Glucarate is a compound that directly inhibits beta-glucuronidase activity in the gut. It works by binding to the enzyme rather than changing the microbial environment itself — it is a chemical inhibitor of the reactivation step. Sulforaphane (from broccoli sprouts or supplement form) supports Phase II liver detoxification and also modulates glucuronidase activity as a secondary effect. These compounds are not general gut supplements — they are specific tools for the estrobolome, used when oestrogen recirculation is the identified driver.

Prebiotic fibre from diverse whole food sources — chicory, Jerusalem artichoke, garlic, leek, cooked and cooled potato — feeds the beneficial microbial species and sustains the diversity that underpins low beta-glucuronidase activity. The goal is not a short-term probiotic course but a genuine, sustained shift in the microbial environment.

Histamine Load and Mast Cell Calming

This is the mechanism that is most often missed entirely. The gut wall contains a substantial population of mast cells — immune cells that release histamine and other inflammatory mediators when activated. Oestrogen directly stimulates mast cell degranulation: mast cells carry oestrogen receptors, and oestrogen volatility in early perimenopause acts as a chronic trigger for mast cell activation in the gut wall. The result is histamine-mediated gut wall inflammation, increased intestinal permeability, and visceral hypersensitivity — all of which worsen bloating, cramping, and distension.

This matters practically because histamine intolerance can develop or worsen in perimenopause even in women who ate freely before. Foods that are high in histamine — aged cheeses, fermented foods, wine, leftover cooked meat, vinegar-containing products — can suddenly trigger gut reactions that were not present previously. This is not a fixed intolerance; it is a hormonally-driven mast cell overactivation state.

Quercetin is a plant flavonoid with well-established mast cell stabilising properties. Weng et al.’s 2012 study published in PLoS ONE found that quercetin was more effective than cromolyn (a pharmaceutical mast cell stabiliser) in blocking human mast cell cytokine release — including histamine, prostaglandins, and interleukins. For perimenopausal women with gut reactivity, quercetin works upstream of the histamine cascade rather than simply limiting exposure.

DAO (diamine oxidase) is the enzyme responsible for breaking down histamine in the gut wall. DAO activity can be reduced by oestrogen fluctuation, alcohol, and certain medications, which allows histamine to accumulate. DAO enzyme supplementation taken before meals can provide direct degradation support while the underlying mast cell reactivity is being addressed.

A temporary histamine reset — typically four to six weeks of significantly reduced dietary histamine load — can lower the overall burden sufficiently that the mast cell activation resolves to a more manageable baseline. This is a transitional intervention, not a permanent dietary restriction.

Ensuring Daily Bowel Movement

Given the constipation-oestrogen loop, daily elimination is a clinical priority, not a lifestyle preference. Practical measures include:

• Adequate dietary fibre from whole food sources (not supplemented bran, which can worsen bloating)
• Consistent fluid intake throughout the day
• Regular movement, particularly walking, which directly stimulates colonic motility
• Morning routine: a warm drink upon waking, time to sit without rushing
• Magnesium glycinate or citrate — well-tolerated forms that support bowel transit without harsh laxative effect

Natural prokinetics — compounds that stimulate the migrating motor complex (MMC), the wave of contractile activity that sweeps the small intestine clean between meals — are an important addition for women with sluggish transit. The MMC only activates in a fasted state; disrupted eating patterns (continuous grazing, late meals) suppress it. Ginger and artichoke leaf extract have direct prokinetic activity through cholinergic stimulation of the gut wall. Giacosa et al.’s 2015 randomised controlled trial in Evidence-Based Complementary and Alternative Medicine demonstrated that combined ginger and artichoke extract supplementation significantly reduced bloating, epigastric fullness, and upper GI discomfort compared to placebo in functional dyspepsia — a condition that shares substantial mechanistic overlap with perimenopause-driven gut sluggishness. Ginger also reduces nausea and accelerates gastric emptying, making it particularly useful when upper GI symptoms (early satiety, reflux, nausea) accompany the bloating.

Digestive Secretions

An underappreciated driver of bloating and sluggish digestion is hypochlorhydria — low stomach acid production. Stomach acid is the first line of digestive processing: it activates pepsin for protein breakdown, sterilises food against pathogenic bacteria, and triggers the cascade of digestive signalling downstream (bile release, pancreatic enzyme secretion, appropriate pyloric emptying). When stomach acid is insufficient, protein is incompletely broken down, the pylorus retains food for longer, and fermentation by gut bacteria increases — all of which worsen bloating and gas.

Acid production declines with age, stress, and certain nutrient deficiencies. The nutrients most directly relevant are zinc (required for carbonic anhydrase, an enzyme involved in acid production) and B vitamins — particularly B1, B3, and B6, which support the gastric parietal cell function that produces hydrochloric acid. Addressing these deficiencies restores a foundation for healthy digestion that no amount of elimination can replace.

Digestive enzyme supplementation — broad-spectrum enzymes including amylase, protease, lipase, and where appropriate lactase or cellulase — provides direct support for macronutrient breakdown at the point of digestion. This reduces the volume of incompletely-digested material reaching the colon for fermentation. Digestive enzymes are not a permanent solution; they are a supportive bridge while the underlying secretory capacity is being restored through zinc and B vitamin repletion.

Blood Sugar Management

Removing refined and rapidly-fermentable carbohydrates reduces two bloating mechanisms at once: intestinal gas production from fermentation, and insulin-driven fluid retention. Whole food carbohydrates, adequate protein at each meal, and avoiding prolonged fasting all contribute to blood sugar stability and, consequently, reduced bloating.

Liver Support

Efficient oestrogen conjugation and excretion requires:

• Cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, kale) — contain DIM and I3C, which support Phase II oestrogen metabolism pathways
• B vitamins — B2, B6, B12, and folate support methylation, the process by which oestrogen is packaged for excretion
• Reduced alcohol — alcohol directly impairs the liver’s ability to conjugate oestrogen, and even moderate intake meaningfully raises circulating oestrogen in perimenopausal women
• Hydration — supports both liver function and bowel transit

The Gut-Brain Axis: Vagal Tone

The gut-brain axis runs in both directions, and the vagus nerve is its primary highway. Under chronic stress, vagal tone falls — the parasympathetic signal that drives digestive secretion, gut motility, and appropriate immune regulation in the gut wall is suppressed. The physiological state of chronic threat does not prioritise digestion. The result is reduced stomach acid production, impaired bile flow, slower transit, and heightened gut wall reactivity — the entire digestive system operating below optimal function.

Vagal tone is not fixed. It responds directly to specific practices:

• Diaphragmatic breathing before meals — three to five slow, deep breaths activating the full diaphragm shifts the nervous system toward parasympathetic dominance and primes digestive readiness before food is introduced. This is not relaxation for its own sake; it is a physiological trigger for digestive secretion.
• Somatic movement — gentle, rhythmic movement (walking, yoga, swimming) that engages the body without activating the sympathetic threat response supports sustained vagal tone throughout the day, not just immediately before meals.
• Consistent meal timing — the migrating motor complex and digestive enzyme release are entrained to circadian rhythms. Irregular eating, skipped meals, and late meals disrupt this entrainment and suppress vagal digestive signals.
• Cold water on the face or neck — triggers the diving reflex via the trigeminal-vagal pathway, producing a rapid shift toward parasympathetic dominance; a practical tool in acute stress states.

For perimenopausal women — who are often in a state of sustained HPA axis activation driven by erratic hormone fluctuations — vagal retraining is a structural intervention, not a complementary add-on. The gut cannot function well in a body that is perpetually signalling emergency.

Xenoestrogen Reduction

Switching to glass or stainless steel food storage, choosing certified organic produce where possible, reviewing skincare for parabens and phthalates, and reducing plastics in cooking all reduce the xenoestrogen load on a body already managing oestrogen dominance.

The Progesterone Shift is Sandra’s structured approach to reversing oestrogen dominance in early perimenopause — addressing the liver, gut, blood sugar, stress response, and environmental exposures together. Explore the programme here.

Case Study: Rachel

Rachel is a composite case. Details are illustrative and do not represent any individual client.

Rachel was 44 when she noticed her bloating had changed. She had experienced mild premenstrual bloating for years, but this was different — persistent, progressive through the day, and no longer clearly tied to her period. By her luteal phase, the distension was significant enough that she avoided social engagements. She described feeling “pregnant by six in the evening.”

She had been fully investigated. Colonoscopy: normal. Coeliac screen: negative. SIBO breath test: negative. She had been trialling a low-FODMAP diet for eight months with no consistent improvement.

Her cycles were still regular on paper — 28-day cycles — but she reported that the quality of the second half had changed. She was more anxious and low in the luteal phase, sleeping badly, and noticing breast tenderness she had not had before. These were signs of anovulatory cycles: regular menstruation without ovulation, and therefore without the progesterone surge that ovulation once provided.

Sandra’s assessment identified estrobolome dysfunction as the primary driver: chronic mild constipation (every second or third day), a dietary pattern low in fermentable fibre and high in refined carbohydrates, regular alcohol intake, and significant work-related stress. The gut-oestrogen recirculation loop was running continuously.

The protocol addressed the estrobolome and oestrogen dominance directly. Targeted probiotics and prebiotic fibre to shift the microbial environment. Daily bowel movement as a clinical goal, supported by magnesium, consistent hydration, and walking. Cruciferous vegetables and B vitamins for liver support. Refined carbohydrates reduced substantially. Alcohol suspended for the initial eight weeks.

Within eight weeks, bloating had reduced significantly. The evening distension that had dominated her social life was markedly less severe. By twelve weeks, her luteal phase symptoms had also improved — less anxiety, better sleep, reduced breast tenderness. The gut and the hormone picture had improved together, because they are the same picture.

References

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