Constipation

SIBO, IBS, and Constipation: Unrecognized Thiamine Deficiency?

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In many of my clients, chronic upper constipation and gastroesophageal reflux disease (GERD) are misdiagnosed as bacterial overgrowth. Unfortunately, they are often non-responsive to antimicrobial treatments. Yet, sometimes the issues are fixed within a few days of vitamin B1 repletion. This has shown me that often times, the small intestinal bacterial overgrowth (SIBO) is simply a symptom of an underlying vitamin B1 or thiamine deficiency.

GI Motility and Thiamine

The gastrointestinal (GI) tract is one of the main systems affected by a deficiency of thiamine. Clinically, a severe deficiency in this nutrient can produce a condition called “Gastrointestinal Beriberi”, which in my experience is massively underdiagnosed and often mistaken for SIBO or irritable bowel syndrome with constipation (IBS-C). The symptoms may include GERD, gastroparesis, slow or paralysed GI motility, inability to digest foods, extreme abdominal pain, bloating and gas. People with this condition often experience negligible benefits from gut-focused protocols, probiotics or antimicrobial treatments. They also have a reliance on betaine HCL, digestive enzymes, and prokinetics or laxatives.

To understand how thiamine impacts gut function we have to understand the GI tract. The GI tract possesses its own individual enteric nervous system (ENS), often referred to as the second brain. Although the ENS can perform its job somewhat autonomously, inputs from both the sympathetic and parasympathetic branches of the autonomic nervous system serve to modulate gastrointestinal functions. The upper digestive organs are mainly innervated by the vagus nerve, which exerts a stimulatory effect on digestive secretions, motility, and other functions. Vagal innervation is necessary for dampening inflammatory responses in the gut and maintaining gut barrier integrity.

The lower regions of the brain responsible for coordinating the autonomic nervous system are particularly vulnerable to a deficiency of thiamine. Consequently, the metabolic derangement in these brain regions caused by deficiency produces dysfunctional autonomic outputs and misfiring, which goes on to exert detrimental effects on every bodily system – including the gastrointestinal organs.

However, the severe gut dysfunction in this context is not only caused by faulty central mechanisms in the brain, but also by tissue specific changes which occur when cells lack thiamine. The primary neurotransmitter utilized by the vagus nerve is acetylcholine. Enteric neurons also use acetylcholine to initiate peristaltic contractions necessary for proper gut motility. Thiamine is necessary for the synthesis of acetylcholine and low levels produce an acetylcholine deficit, which leads to reduced vagal tone and impaired motility in the stomach and small intestine.

In the stomach, thiamine deficiency inhibits the release of hydrochloric acid from gastric cells and leads to hypochlorydria (low stomach acid). The rate of gastric motility and emptying also grinds down to a halt, producing delayed emptying, upper GI bloating, GERD/reflux and nausea. This also reduces one’s ability to digest proteins. Due to its low pH, gastric acid is also a potent antimicrobial agent against acid-sensitive microorganisms. Hypochlorydria is considered a key risk factor for the development of bacterial overgrowth.

The pancreas is one of the richest stores of thiamine in the human body, and the metabolic derangement induced by thiamine deficiency causes a major decrease in digestive enzyme secretion. This is one of the reasons why those affected often see undigested food in stools. Another reason likely due to a lack of brush border enzymes located on the intestinal wall, which are responsible for further breaking down food pre-absorption. These enzymes include sucrase, lactase, maltase, leucine aminopeptidase and alkaline phosphatase. Thiamine deficiency was shown to reduce the activity of each of these enzymes by 42-66%.

Understand that intestinal alkaline phosphatase enzymes are responsible for cleaving phosphate from the active forms of vitamins found in foods, which is a necessary step in absorption. Without these enzymes, certain forms of vitamins including B6 (PLP), B2 (R5P), and B1 (TPP) CANNOT be absorbed and will remain in the gut. Another component of the intestinal brush border are microvilli proteins, also necessary for nutrient absorption, were reduced by 20% in the same study. Gallbladder dyskinesia, a motility disorder of the gallbladder which reduces the rate of bile flow, has also been found in thiamine deficiency.

Malnutrition Induced Malnutrition

Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals. In fact, this is indeed something I see frequently. And sadly, as thiamine is notoriously difficult to identify through ordinary testing methods, it is mostly missed by doctors and nutritionists. To summarize, B1 is necessary in the gut for:

  • Stomach acid secretion and gastric emptying
  • Pancreatic digestive enzyme secretion
  • Intestinal brush border enzymes
  • Intestinal contractions and motility
  • Vagal nerve function

Based on the above, is it any wonder why thiamine repletion can radically transform digestion? I have seen many cases where thiamine restores gut motility. Individuals who have been diagnosed with SIBO and/or IBS and are unable to pass a bowel movement for weeks at a time, begin having regular bowel movements and no longer require digestive aids after addressing their thiamine deficiency. In fact, the ability of thiamine to address these issues has been known for a long time in Japan.

TTFD and Gut Motility

While there are many formulations of thiamine for supplementation, the form of thiamine shown to be superior in several studies is called thiamine tetrahydrofurfuryl disulfide or TTFD for short. One study investigated the effect of TTFD on the jejunal loop of non-anesthetized and anesthetized dogs. They showed that intravenous administration induced a slight increase in tone and a “remarkable increase” in the amplitude of rhythmic contractions for twenty minutes. Furthermore, TTFD applied topically inside lumen of the intestine also elicited excitation.

Another study performed on isolated guinea pig intestines provided similar results, where the authors concluded that the action of TTFD was specifically through acting on the enteric neurons rather than smooth muscle cells. Along with TTFD, other derivatives have also been shown to influence gut motility. One study in rats showed an increase in intestinal contractions for all forms of thiamine including thiamine hydrochloride (thiamine HCL), S-Benzoyl thiamine disulphide (BTDS -a formulation that is  somewhat similar to benfotiamine), TTFD, and thiamine diphosphate (TPD). A separate study in white rats also found most thiamine derivatives to be effective within minutes.

Most interestingly, in another study, this time using mice, the effects of thiamine derivatives on artificially induced constipation by atropine and papaverine was analyzed. The researchers tested whether several thiamine derivatives could counteract the constipation including thiamine pyrophosphate (TPP), in addition to the HCL, TTFD and BTDS forms. Of all the forms of thiamine tested, TTFD was the ONLY one which could increase gut motility. Furthermore, they ALSO showed that TTFD did not increase motility in the non-treatment group (non-poisoned with atropine). This indicated that TTFD did not increase motility indiscriminately, but only when motility was dysfunctional. Finally, severe constipation and gastroparesis identified in patients with post-gastrectomy thiamine deficiency, was alleviated within a few weeks after a treatment that included three days of IV TTFD at 100mg followed by a daily dose of 75mg oral TTFD. Other symptoms also improved, including lower limb polyneuropathy.

To learn more about how thiamine affects gut health:

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This article was first published on HM on June 1, 2020. 

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Recovery From Alcohol Induced Gastric Beriberi and Dysautonomia

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Early Alcoholism: A Precursor to Thiamine Deficiency and Dysautonomia

When I was in my 20’s, I was an alcoholic student in a Nordic country. I was a perpetual student enrolling every year, but getting very little done. I mostly read and drank. I stopped drinking in 2015 because it was too tiring to be drunk all the time. Stopping wasn’t difficult. I didn’t get any joy of alcohol anymore anyway. I became fit, resumed studies, and graduated in 2018. I went on a vegetable-based low carb diet and took B vitamins thinking I might need them after years of drinking. I felt fine. I was a little overweight but not too much. I also took a handful of basic vitamins and magnesium, in addition to the B complex. I had four years of a pretty healthy life before everything fell apart and I developed a variety of dysautonomia symptoms related to thiamine deficiency.

The Emergence of Dysautonomia

In February 2020, I became ill with a myriad of symptoms. I had costochondritis. (Defined as “an inflammation of the connective tissue where the ribs attach to the breastbone .Characterized by dull to sharp pain at the front of the chest wall that may radiate to the back or abdomen.”) I had constipation to the point of impaction, I couldn’t regulate my temperature, and kept shivering under several blankets. I wasn’t able to swallow properly because food got stuck in my throat.

In March the Covid-panic was at its worst and I sat tight at home, thinking I’d just need to weather it out rather than make an appointment with my doctor and risk getting Covid. During this time, I had constant vertigo and had to hug the walls of my house as I moved around. Vertigo made me motion sick.

In May things looked up, the panic had changed into hopeful masking. The state I lived in hadn’t gotten its first wave yet and so I made an appointment with my doctor. I left with motion sickness medicines and routine labs done, which showed nothing remarkable. I was able to recover from the costochondritis and constipation. I was using laxatives now regularly. It didn’t bother me after the agony of an impacted colon.

I was now having fulltime dysautonomia, with hypothermia and vertigo being the most prominent symptoms. I still had difficulty swallowing but it was something I decided was psychosomatic because of the stress. I just ate very carefully and avoided things that would make me choke.

Stumbling Onto Thiamine Deficiency

I ran into Hormones Matter blog after joining a reddit group r/dysautonomia. One poster kept repeatedly posting “thiamine deficiency” to people describing their symptoms and quoting parts of Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition by Lonsdale & Marrs. I bought the book and read it.

I went to see my doctor again, telling her that I wasn’t recovering. I asked to get whole blood B1 tested, she refused saying I don’t look like I had beriberi, with a chuckle. That hurt. Pictures of beriberi patients are invariably people who are emaciated to the point of starvation. I am still slightly overweight.

I began high dose thiamine in October 2020 on my own.

I started taking Allithiamine and later Thiamax. I tolerated the TTFD (thiamine tetrahydrofurfuryl disulfide, a thiamine derivative used in the formulations for Allithiamine and Thiamax) fabulously. I titrated the dose per symptoms until I felt fine. I was startled how high I needed to go. At times in December, I was at 400-500 mg TTFD per day + 300 mg of benfotiamine during the night. I would notice the effect wearing off in 4 hours and needed to re-dose because all the symptoms came back.

My Experience with Thiamine Supplementation

My experience with TTFD was head clarity and enormous sense of wellbeing. Benfotiamine made my temperature regulating issues go away and gave me good sleep. I was often having bouts of hypothermia when ill and shivering under blankets. Benfotiamine helped in this more than TTFD.

TTFD solved the constipation and swallowing issues, which would support the vagal lesion theory. Lonsdale describes gastroparesis and dysphagia as a “central lesion” in the GI tract affected by beriberi. I noticed the effect of feeling GI peristalsis kick start and make a sort of “chugging” motion after I took TTFD. If I ate steak, I made sure to take TTFD before because it made my swallowing effortless. Previously, I always had choking hazard because bits of meat would get stuck in my throat and I had to flush them down with water.

I took other B vitamins individually to supplement. The amounts were the same as most B complexes. I took 300 mg of magnesium taurate through the day and 1/2 teaspoon of potassium chloride in water through the day as well. I began taking 150 mcg of molybdenum and 200 mcg of selenium. I took one drop of iodine a day too. I listened to Elliot Overton’s talks about TTFD.

Titrating the Supplements Down After Recovery

Over the spring, I was able to reduce TTFD, going down about 50mg a month, most months. If I felt symptoms coming back – the coldness, vertigo – I decided I wasn’t ready for nipping more off and resumed the previous months’ dose where I felt fine. I have been off of TTFD now since June and completely symptom free from my dysautonomia, constipation, vertigo, swallowing difficulties, continuous nausea – all since April.

I’m still intolerant to many supplements, but I can take Thorne’s Basic B to keep covering the B’s. I still take magnesium and potassium with the B complex, occasionally molybdenum and selenium in small doses. Iodine, if I remember. I don’t know if they contributed any, but they may have.

I must mention that years past when I took Basic B, I felt nothing. Now, I feel a bit energized after taking it and I have a bowel movement. This is similar to my experience with TTFD. I believe that TTFD has enabled me to uptake the regular thiamine HCL, and that for some reason with my history of heavy drinking and bad nutrition, my early beriberi-affected system was not able to transport thiamine HCL that was in the B complex. However, now it feels like it does. I will try to get the other nutrients from food.

What I did not do:

  • megadose any other B vitamin
  • address any oxalate issue
  • make any dietary changes. I kept eating the same low carb I always ate
  • address any histamine issue

I did not do any of those because I was making progress with TTFD and B complex with the usual minerals.

My illness wasn’t long compared to others that I have read about. That may be also why recovery was swift. I also had a pretty good nutritional status to begin with, with magnesium and potassium on board – and probably no other vitamin deficiencies. This is my story. I am forever grateful for Drs. Lonsdale and Marrs for the book and this website.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Understanding Female Digestive Problems

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It is well-documented in research that some digestive problems, such as irritable bowel syndrome (IBS), Crohn’s disease, gastroparesis, and gallstones, are more common in women than men. Others occur equally in both sexes, but affect women more severely.[1] I know far more women than men with digestive issues and wondered why this was so, especially since I suffer from a pancreatic-biliary condition called Sphincter of Oddi Dysfunction (SOD) where 75-95% of sufferers are women.

Female Anatomy: An Opportunity for Digestive Issues

The exact nature of why women experience more digestive problems than men is not always clear.  Though much about these digestive differences is still a mystery, there are two prominent differences: women’s anatomy and hormones.  The ovaries and uterus are located below the intestines in women’s anatomy.  Since the intestines are such close neighbors, conditions affecting the uterus and ovaries may also affect the intestines.

Two examples of this are endometriosis and referred pain. Endometriosis, a collection of built up and shed uterine tissue, can spread outside the female organs. Endometriosis can affect the intestines, where endometrial tissue may cause intestinal blockage. However, it can also spread and attach to other digestive organs as far up as the pancreas and liver though this is rare.  Also, the close proximity of the uterus to the colon may cause a situation of “referred pain” or sensitivity between the two organs. The uterus and colon share central nervous system neuronal activity partly through the hypogastric nerve.[2] Therefore, pain and sensitivity in the uterus can refer to the colon and vice versa.

Cycling Hormones Contribute to Digestive Difficulties

The other prominent difference is in women’s hormones.  In many ways, these hormones work in concert with the digestive system to work properly. The imbalances of estradiol and progesterone can influence the movement of food through the intestines—some by speeding the process up, causing diarrhea, nausea and abdominal pain; and others by slowing things down and causing bloating and constipation.[3]

Estrogens can significantly alter various clinical manifestations of IBS, including changes in motility (intestinal movement) and visceral hypersensitivity (pain).[4] In the case of visceral hypersensitivity, even the slightest pain-inducing alterations in the esophagus, small intestine, colon, rectum, and pancreatic/biliary region can be more painful in women than men.

I and many other women (rarely men) have at one time or another been told by a physician our digestive symptoms were “all in our heads”. This female labeling could not be further from the truth.  Ovarian hormones can alter pain processing by interacting with neuromodulator systems and the emotional system responsible for visceral pain perception.  Estradiol can cause hyper-responsiveness to stress which may promote immune activation and impairments of gut barrier function.[5]  In other words, our hormones may very well be responsible for the onset of these conditions and the exacerbation of symptoms.

Probably the most obvious affect women’s hormones have on the digestive system is estradiol’s effect on the gallbladder.  Women are twice as likely as men to have gallstones because estradiol raises cholesterol levels in the bile and slows gallbladder movement.[6] Female hormones have also been tied to other liver and biliary diseases, along with pancreatic conditions like pancreatitis.

Pregnancy and Progesterone

Women are at higher risk of developing gallstones during pregnancy.  This is because estrogen concentrations (estrone, estradiol and estriol) are high. Pregnant women experience other hormone-related symptoms.  In the first trimester, morning sickness can be debilitating. No one knows the exact cause of morning sickness but hormone fluctuations have long been suspected. Later in the pregnancy, an increase in the hormone progesterone contributes to constipation by slowing the waves of muscle contractions that move food down the digestive tract.[7]  In addition, progesterone causes the stomach’s esophageal valve to relax, causing gastroesophageal reflux disease (GERD), where food and acid move up into the esophagus. Since progesterone relaxes many of our muscles this may be the reason some women with my condition, SOD, find relief from symptoms during pregnancy. SOD is a disorder where the biliary and/or pancreatic sphincters spasm shut causing pain and other symptoms.

What is the Solution?

The long and short of it is there is no one solution. No one size fits all. Everyone is different. I have had surgeries and conventional treatments for my digestive conditions that proved helpful.  However, in many instances when symptoms were not completely disabling, I experienced just as effective, lasting relief through natural remedies and medications. Practicing deep breathing, meditation, yoga, and mindfulness have helped immensely.  Finding the right diet and sticking to it has always been a challenge, but if I eliminate even a few known food triggers, I am much better off. Dieting, stress, anxiety, depression, and exercise can drastically affect hormones—both for the good and bad. Therefore, addressing these factors can help digestion indirectly by “repairing” hormone problems.

Although some supplements and medications may be helpful, be careful. I have experienced horrible secondary conditions and adverse reactions from herbal supplements, medications, and even some vitamins and minerals that purported to aid my digestive problems. Be cautious. Less is more with pills—even the herbal kind.

In conclusion, besides the estrogens and progesterone, there are other female-dominant hormones like human gonadotropic hormone, luteinizing hormone, and prolactin which may affect the digestive system. Studies are sparse regarding the role of progesterone and the estrogens on the digestive system, and almost non-existent for these rarely talked about hormones.  Therefore, research is desperately needed in the field of hormones and digestive health.  I believe once we unlock some of the mysteries surrounding hormones and the digestive system we will uncover a treasure trove of treatments and cures.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

References

  1. U.S. Office on Women’s Health.
  2. Winnard, KP, et al. “Cross-organ interactions between reproductive, gastrointestinal, and urinary
    tracts: modulation by estrous stage and involvement of the hypogastric nerve”. American Journal of Physiology. 2006 Dec;291(6):R1592-601. Epub 2006 Aug 31.
  3. “Digesting It All!” Connections: An Educational Resource for Women’s International Pharmacy.
  4. Mulak, A and Tache, Y. “Sex difference in irritable bowel syndrome: do gonadal hormones play a role?” Gastroenterology Poland. 2010;17(2):89-97.
  5. Meleine, M and Matricon, J. “Review article: Associations between immune activation, intestinal permeability and the irritable bowel syndrome”. World J Gastroenterol. 2014 Jun 14;20(22):6725-43. doi: 10.3748/wjg.v20.i22.6725.
  6. Stinton, L. and Shaffer, E. “Epidemiology of Gallbladder Disease: Cholelithiasis and Cancer”. Gut Liver. 2012 Apr; 6(2): 172–187.
  7. Lingen, J. “The Second Trimester: Constipation, Gas, & Heartburn”. Healthline. March 5, 2012.

This article was published previously on Hormones Matter in September 2015.

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Hysterectomy: Impact on Pelvic Floor and Organ Function

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My life and health were turned upside down after my unwarranted hysterectomy. I touched on the internal and external anatomy changes in a previous article. I am going to go into more detail here on the effects of hysterectomy on the internal anatomy.

Female Anatomy

The uterus sits in the center of the pelvis held in place by four sets of ligaments. The uterus separates the bladder and the bowel and holds those organs in their rightful positions. Once the ligaments are severed and the uterus removed, the bladder and bowel drop down and, without the uterus to separate them, are now adjacent to each other. The nerves and blood vessels that are severed during hysterectomy may also alter the functions of pelvic organs. This female anatomy video explains the anatomical (and other) effects of hysterectomy.

What Every Woman Wants to Know about Hysterectomy

Pelvic Floor Disorders after Hysterectomy

What do medical studies say about the effects of these anatomical changes on the pelvic floor and organ function?

This 2014 U.S. study concluded that hysterectomy is one risk factor for developing pelvic floor disorders. The others are higher Body Mass Index (BMI) and greater parity. There are a number of studies that came to this same conclusion.

This large 31 year Swedish study concluded that hysterectomy, particularly vaginal hysterectomy, even in women with no vaginal births is associated with pelvic organ prolapse surgery. The number of vaginal births further increases this risk.

According to this large Swedish study, vaginal hysterectomy had a higher risk of surgery for pelvic organ prolapse or stress urinary incontinence than other modes of hysterectomy.

Of course, women who undergo pelvic organ prolapse surgery represent only a subset of those who suffer symptoms of bladder and/or bowel dysfunction.

Bladder Function after Hysterectomy

A number of studies have shown no short-term urinary adverse effects of hysterectomy. However, longer-term follow-up shows an increased risk. This large Swedish study over a 31 year period (1973 to 2003) showed a 2.4-fold risk of urinary stress incontinence surgery in women who had hysterectomies for benign conditions. This Danish study of women aged 40 to 60 years also showed a 2.4-fold risk of stress incontinence in women who had a hysterectomy. A small China study showed a 7.6% rate of pelvic organ prolapse and 67.4% rate of urinary incontinence 6 years post total hysterectomy.

A systematic review of 12 MEDLINE articles that used original data published over a 32 year period (January 1966 to December 1997) “was consistent with increased odds for incontinence in women with hysterectomy….Among women who were 60 years or older, summary odds ratio for urinary incontinence was increased by 60% but odds were not increased for women younger than 60 years.” Another review of this same data consistently found an increased risk of incontinence many years after hysterectomy.  However, this study also concluded that “Oral estrogen replacement therapy seems to have little short-term clinical benefit in regard to incontinence and is associated consistently with increased risk of incontinence in women aged 60 years and older in epidemiologic studies.”

The latter statement begs the question “Is the association of oral estrogen and incontinence solely from the oral estrogen or could it be that it’s caused by hysterectomy that prompted the use of estrogen?”

Hysterectomized women of ALL ages were at increased odds for urge (1.9) and bothersome urge (2.6) urinary incontinence (but not stress incontinence) according to this Netherlands study of 1,626 women. This French study of 1,700 women also concluded that hysterectomy increases risk of urge, as well as stress, incontinence regardless of age.

In contrast, this analysis of studies done on urodynamics before and after hysterectomy concluded that “Hysterectomy for benign gynecological conditions does not adversely impact urodynamic outcomes nor does it increase the risk of adverse urinary symptoms and may even improve some urinary function.”

This small study compared incontinence / continence at 1 to 3 years post-hysterectomy and again at 4 to 6 years post-op.  Interestingly, some women went from being continent to incontinent while others went from being incontinent to continent.

Why the conflicting results? There are a few things that come into play, the more obvious ones being study design and size as well as the follow-up period. Mostly, the results depend on the reason for the hysterectomy and whether a bladder suspension was done at the same time. Two common reasons for hysterectomy are fibroids and uterine prolapse. Both conditions can cause urinary symptoms such as frequent urination and incontinence. So symptoms may improve after hysterectomy and if the bladder was suspended at the time of hysterectomy (in the case of prolapse), that would also explain improvement.

Bowel Function after Hysterectomy

Some studies show that hysterectomy negatively affects bowel function. While this small and short-term 2004 study (comparing pre-operative to 6 and 12 months post-operative) concluded that vaginal hysterectomy does not increase incontinence or constipation, abdominal hysterectomy may increase risk “for developing mild to moderate anal incontinence postoperatively and this risk is increased by simultaneous bilateral salpingo-oopherectomy.” In contrast, this small 2007 study found that vaginal hysterectomy significantly increased anal incontinence at the three-year point and at one and three years for abdominal hysterectomy. However, there was “no significant rise in constipation symptoms or rectal emptying difficulties in either cohort through the follow-up.”

This contradicts this small case control study that showed significant short-term decreased bowel frequency and increased urinary frequency after hysterectomy. It also contradicts this larger Netherlands retrospective study in which 31% of women reported severe bowel function deterioration and 11% reported moderate bowel changes after hysterectomy. In the control group which consisted of women who underwent laparoscopic cholecystectomy, 9% reported “disturbed bowel function.”

Constipation, straining, lumpier stools, bloating, and feelings of incomplete evacuation were reported by women who had undergone hysterectomy in this small study.

Abdominal hysterectomy is associated with a significant risk of fecal incontinence and rectoanal intussusception according to this small retrospective study.

Post Hysterectomy Fistula

Hysterectomy increases risk of fistula as documented in the below excerpt from this article:

The uterus precludes fistula formation from the sigmoid colon to the urinary bladder.

As well as this excerpt from this article:

The most common types of fistula are colovesical and colovaginal, against which the uterus can act as an important protective factor.

Diverticulitis is a known risk factor for fistula formation. This large study looked at the risk of fistula formation in hysterectomized women with and without diverticulitis using data from women hysterectomized between 1973 and 2003. Women who had a hysterectomy but no diverticulitis had a 4-fold risk of fistula surgery compared to women who did not have a hysterectomy or diverticulitis. Women who had a hysterectomy and diverticulitis had a 25-fold risk of fistula surgery whereas non-hysterectomized women with diverticulitis had a 7-fold risk.

Vaginal Vault Prolapse

The International Continence Society defines vaginal vault prolapse as “descent of the vaginal cuff below a point that is 2 cm less than the total vaginal length above the plane of the hymen.” This Obstetrics and Gynecology International article states that “it is a common complication of vaginal hysterectomy with negative impact on women’s quality of life due to associated urinary, anorectal and sexual dysfunction.”  The article cited above explains the mechanism for this common complication in section 2 titled “Anatomic Background.”

Table 3 in section 12 compares vaginal and abdominal corrective surgery outcomes using a 5 year follow-up.  Vaginal had significantly higher post-operative incontinence and recurrence rates. The re-operation rate due to recurrence was 33% in the vaginal group versus 16% in the abdominal group.

Surgical mesh is used for many pelvic organ prolapse surgeries. And as shown by the TV ads, surgical mesh has high complication rates. It can cause infection and the mesh can protrude into the vagina leaving sharp edges having obvious negative effects on male partners. And removal of all traces of mesh may be impossible because tissue grows around the mesh.

Women who have not had a hysterectomy and have pelvic organ prolapse may choose to use a pessary instead of undergoing surgery to suspend the uterus (and bladder) or undergo hysterectomy. But a pessary may be difficult to hold in place in women who have had a hysterectomy since the walls of the vagina are no longer supported by the uterus and cervix.

Hysterectomy Consequences

Hysterectomy can have serious consequences on bladder and bowel function and increase risk for future surgeries, but the research is mixed, primarily due to differences in methodology.  Pelvic organ prolapse is also a possibility. Important variables that increase or decrease the risk for future problems include the reason for the hysterectomy and pre-operative bladder and bowel function. If endometriosis, fibroid or other conditions compromise or affect bladder and bowel function pre-surgery, then odds are they will be affected post-surgery and whether there is improvement or further damage depends upon a number of factors, including the surgeon’s skill. In contrast, and I think where most women are interested, is whether these problems can arise post-hysterectomy when no such problems existed pre-surgery. The answer is yes, there is an increased risk for both urinary and bowel incontinence post hysterectomy.

Additional Resources

This RadioGraphics article details the pelvic organ sequelae that can be caused by obstetric and gynecologic surgeries and the imaging techniques for diagnosing them.

This Medscape article details the Long-term Effects of Hysterectomy.

 

 

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