There are different forms of Inflammation, ranging from acute to chronic. Inflammation plays an important part in the immune response and is designed to help us survive – it is the immune system’s response to infections and injury.
The inflammatory response has helped us to survive in the evolutionary environment. Throughout evolution, the inflammatory response has stayed the same – our environment however, has changed drastically in the past couple of centuries (not a long time in evolutionary terms!).
The changes in our environment are thought to parallel the rise in chronic disease. Could inflammation be one of the reasons?
When speaking about urinary tract infections, we usually speak about bacterial infections. Fungi (a.k.a yeasts or mold) are different organisms from bacteria and they can cause infections such as thrush in some parts of the body. Fungal infections in the vagina for example are a well-known condition. But can there also be fungal infections in the urinary tract?
Last week I had a look at how hormones affect the urinary tract. Changes in the female hormones oestrogen and progesterone and even the ‘male’ hormone testosterone appear to affect urinary tract symptoms.
Oral contraception affects hormone levels in the body and may therefore also affect urinary tract symptoms.
Other contraception may not affect hormones but may have an impact on the urinary tract in other ways.
Today I would like to take a look at what we know about different forms of contraception and bladder health.
Today I’d like to take a closer look at the role of hormones on bladder health. Hormones have been known for a while to play a role in lower urinary tract symptoms such as UTIs, interstitial cystitis and stress incontinence. Hormones may be the reason why women generally seem to be more prone to bladder problems than men and also why some symptoms may get worse at certain times of the month.
There is new(ish) evidence emerging that recurrent UTIs, also known as chronic cystitis, are not always caused by a reinfection with a new pathogen but rather can be a relapse of the same pathogen.
It turns out that pathogenic bacteria have the ability to invade the cells of the bladder and live there in a dormant sleep-like state.
This is called an ‘intracellular bacterial community’.
In this state, the bacteria remain undetected by standard urine testing and unaffected by antibiotic treatment. They also remain undetected by our own immune system.
Now and again they can leave the cells, causing a relapse of the urinary tract infection.
The current gold-standard testing for UTIs involves culturing the bacteria present in a clean-catch midstream urine sample (MSU) in a lab dish.
On top of that, a dipstick test is often used to indicate the presence of infection markers in urine.
The guidelines for these testing methods have been established in the 1950s. With the discovery of the urinary microbiome, inadequacies of this method have come to light.
It turns out that urine is in fact not sterile and that many microbial species cannot be cultured in a lab.
Therefore, current testing for UTIs fails patients by missing infections.
In last week’s post I talked about the urinary microbiota – the bacterial communities that have recently been discovered to be present in the urinary tract.
We know now that microbes that live in and on our bodies play a crucial role in health and illness. There are friendly and pathogenic microbes (bacteria, fungi etc.) plus opportunistic microbes that can become pathogenic when left unchecked.
When the delicate balance of good vs bad microbes is disturbed we become prone to an array of health conditions and infections. This is called a ‘dysbiosis’.
The human bladder and urine have long been considered to be sterile. Emerging evidence challenges this paradigm.
Recent advances in gene sequencing have made it possible to look at the human microbiome (the collective bacteria that live in and on our bodies) and more and more studies are showing an important link between the microbiome and our health.
Standard urine testing methods are limited in their ability to show the true bacterial composition of the urine and their main use is to show certain strains of bacteria that typically overgrow in urinary tract infections.
In my last post I looked at the GAG layer in the bladder and how damage to it can cause problems for the bladder lining, a.k.a the bladder urothelium.
When the bladder urothelium gets damaged it can lose its integrity and become ‘leaky’ or ‘hyper-permeable’. Molecules that shouldn’t normally leave the bladder can get into the space (‘interstitium’ – hence interstitial cystitis) between the layers of the tissue and into the blood.
Happy 2017, y’all! I hope this year will bring relief from all your bladder issues – keep on learning and searching! In today’s post I would like to address something that I personally have been messing around with in the past month. It is the connection between low metabolism and overactive bladder.