00:00 – Biofilms, they attach to a surface and bacteria
00:06 – live inside these structures and periodically pieces these break off.
00:26 – Melissa: How do you explain why some people have infrequent UTIs while
00:30 – others have frequent symptoms or just continuous symptoms at a certain point?
00:35 – Ruth: This is a hard question I think everyone struggles with. We all have friends, neighbors,
00:41 – family members, they get a UTI, they take a couple days of antibiotics and they’re fine for another
00:48 – three, five, ten years. And they have another one. Whereas we are in the camp of people who tend to
00:56 – get a UTI repeatedly and sometimes the symptoms don’t go away and therefore we’ve moved from
01:05 – the acute urinary tract infection to the chronic to the now IC label.
01:13 – I think there’s several reasons that this happens and there are some commonalities among
01:21 – people who have these conditions that other people don’t have.
01:26 – When I started looking at the genetics based on some testing some of my patients did, I
01:33 – found some interesting commonalities. The first one is a vitamin D receptor mutation.
01:40 – Now we’ve all heard about vitamin D, the sunshine vitamin, and how important it is for bone health.
01:47 – But it has a key role in preventing urinary tract infections, if you have enough vitamin D.
01:55 – I want to qualify that the way they get a normal reference range is you get your thousand people,
02:05 – you check their vitamin D level, you find the mean, you go out two standard deviations and that
02:10 – is declared to be the normal. And in the United States that goes from 30 to 100. However, if you
02:19 – have a vitamin D receptor mutation, even though you can make vitamin D as well as other people,
02:26 – you can’t hold on to it as well. And because that reference range did not throw out of their normal
02:36 – reference range those people, it was falsely skewed to the bottom. So instead of going out two standard
02:45 – deviations, if you only go out one that cutoff is 50. So I like my patients to keep their vitamin D
02:53 – level between 50 and 80. This provides enough vitamin D for the bladder wall to secrete a
03:00 – protein or a peptide called cathelicidin, that actually helps prevent urinary tract infections.
03:08 – If you have enough vitamin D that will help your body prevent urinary tract infections
03:17 – and if you don’t then you’ll be more prone to them.
03:20 – Melissa: Does this mean for those people they’ll need to supplement with vitamin D forever?
03:25 – Ruth: Absolutely because their bodies will never hold on to it as well as other people and d3 is a preferable form than the d2 because it’s more bioavailable.
03:38 – The other commonality that I found was mutation called CBS – cysteine beta
03:46 – synthase, and that enzyme is important in the methylation pathway in breaking one of the
03:54 – chemicals down into cysteine that helps your body detox and taurine which your heart muscle uses.
04:04 – If you have a CBS mutation, which 100 percent of the patients who did the testing have,
04:10 – instead of making cysteine and taurine you make a truck load of ammonia. And what’s the big deal about
04:19 – ammonia? Well it turns out that ammonia then goes over to the urea cycle, it’s in the urine. And in
04:28 – the veterinary literature there are some excellent studies that talk about ammonia destroying the gag
04:34 – layer of the bladder wall. And that’s basically what happens when you get an IC diagnosis and
04:41 – they look through the cystoscope they see the damage to that bladder lining, that gag layer.
04:49 – So if you can keep the ammonia level down, if you can help the body clear it then that
04:58 – will help reduce the damage to the bladder wall itself. And there’s a supplement called ornithine.
05:04 – It’s over the counter, it’s marketed to help you sleep.
05:12 – And so I’ve started asking my patients to take one of those at bedtime. I can’t prove that it will
05:23 – help 5% or 20% or 50% but theoretically if you can help stop the damage to the bladder wall
05:32 – then the bacteria won’t have a happy home.
05:35 – Melissa: You mentioned happy home. So maybe that’s a good place to segue into biofilms because this is a topic that comes up a lot.
05:42 – Ruth: Absolutely. So let’s talk about biofilms. The big B word. Biofilms are kind of like slime.
05:56 – They attach to a surface and bacteria live inside these structures. And periodically pieces these
06:06 – break off. When your body has an infection it causes inflammation and inflammation triggers
06:16 – fibrin. Fibrin is sort of that spider web stuff that things attach to. We see that with making
06:24 – a clot for instance and it’s part of the body’s normal defense to try to wall off an infection
06:30 – so it doesn’t spread wildly or reproduce quickly. And so when you have an infection in the bladder
06:41 – we know that those bacteria like to attach to the bladder wall.
06:47 – They encase themselves in that structure which utilizes fibrin and they slowly continue to
06:55 – reproduce. This also means that they don’t shed off into the urine as readily, so when you do a
07:03 – urine specimen there’s some sort of an assumption that all the infection is free floating in your
07:10 – urine and that isn’t really the reality. It’s walled off on the bladder wall. And so taking a
07:17 – substance that would help that that biofilm to be broken down or disrupted should help that bacteria
07:29 – spill out into the urine so it could be found on a urine test and then more effectively treated,
07:37 – for instance with an antibiotic.
07:42 – There isn’t any specific test to confirm that you have a biofilm. If
07:50 – on a test they report multiple pathogens that’s a pretty good sign you have a biofilm community.
07:59 – They kind of live like in an apartment building with lots of different residents.
08:03 – The problem with urine cultures is that if they find more than two pathogens
08:08 – they report it as contaminated. If there’s a fungal component that is found
08:14 – on a culture plate they throw it away and report it as contaminated, whereas with the DNA testing
08:23 – we know that there are multiple pathogens and some of those can be fungal as well as bacterial.
08:31 – Melissa: So given that the bacteria can live in these protected biofilms, does that mean the best
08:36 – time to collect a urine sample is actually when you’re experiencing symptoms?
08:42 – Ruth: Probably it is. We did an interesting study some years ago in which we had patients collect urine
08:50 – specimens in the morning and the evening and then MicrogenDX tested those two specimens separately.
08:59 – We discovered that the type of bacteria that are shed at one time in a day
09:04 – is different than either the quantity or the kind that is secreted in or able to
09:12 – be found in a different time of day. And for me that explains why some patients will say
09:19 – oh I don’t have that much frequency during the day but I go to bed at night and I’m up four times
09:26 – or another person will say oh I’m just miserable all day long. I’m going every half hour but I
09:32 – sleep through the night. I think that can be explained by the different bacteria that are able
09:38 – to flourish at one time of day versus another time a day and some of that is dependent upon
09:46 – the urinary environment. When we go to bed at night we put out anti-diuretic hormone. If you
09:53 – have the CBS mutation you’re collecting and concentrating a lot of ammonia in the urine
10:00 – and that’s a pH change that favors the growth of some bacteria over other types
10:05 – of bacteria. Currently MicrogenDX will have you collect specimens at both times a day
10:14 – and send them in separate transport tubes they get combined by the lab
10:19 – 50/50 and that way we get a more realistic view of which bacteria is really present no matter which time of day you’re shedding it.
10:27 – Melissa: Is that true for all practitioners or have you got a special set up with MicrogenDX for that?
10:32 – Ruth: Currently we have a special set up and so practitioners are able to
10:39 – contact my sales rep and he is able to supply them and his patients or her and her patients with
10:49 – the kits that are set up to do the two collections. I think this is important for anybody
10:55 – with chronic urinary tract infections or an IC diagnosis because otherwise it’s very possible that the main pathogen will be totally missed.
11:07 – Melissa: You mentioned being able to disrupt biofilms in certain ways are there particular supplements that you use to do that?
11:18 – Ruth: There are. There’s not a one size fits all. It turns out that when you make this extra fibrin,
11:27 – a person’s body tries to break it down, sort of the breaks and the accelerator on a car and those
11:34 – substances are called thrombin anti-thrombin or TAT, T-A-T complexes and some people are better able
11:44 – to make TAT complexes than other people depending upon their genetics. About 20 percent of the
11:51 – population genetically are known as hypercoagulant. This means that they make a lot of fibrin
12:00 – which goes into atherosclerotic plaque causing blood clots, heart attacks and strokes. And
12:09 – then they aren’t able to break that fibrin down in the biofilms as efficiently as other people.
12:16 – Those same set of genetics that apply to that population are the same ones that I’m
12:23 – finding in my chronic urinary tract infection and IC population.
12:30 – Only instead of 20% it’s closer to 55 or 60 percent. And so I think this is a huge huge player
12:40 – in knowing how to break down the biofilms and how to more effectively treat because we can
12:46 – actually get to the infection. And depending upon whether you have one of those genetic
12:52 – issues or not would dictate which biofilm disruptor would work better for you.
12:58 – So there can’t be a one-size-fits-all. Also some of the biofilm disruptors work
13:05 – by actually punching holes in the biofilm. Some of them are enzymes that break down the fibrin,
13:12 – some of them have substances that prevent the bacteria themselves from making their own biofilms.
13:19 – So it it can be fairly complex figuring out which biofilm disruptor your body needs.
13:30 – Melissa: Do you have any concerns about disrupting biofilms in other parts of the body that are meant to be there?
13:36 – Ruth: Not significantly. First of all, I haven’t seen a problem
13:41 – in giving biofilm disruptors to essentially 100% of my patients. Secondly, if you have one of the
13:50 – genetic issues that doesn’t allow you to break down biofilms efficiently by supplementing a
13:57 – biofilm disruptor, all we’re doing is helping your body work as well as everybody else’s.
14:04 – And finally, biofilms are involved in any infection so people with those chronic
14:14 – infections would benefit from a biofilm disruptor. I don’t care if we’re talking
14:21 – about chronic sinus infections, chronic prostatitis in men, chronic urinary tract infections. I believe
14:30 – fibromyalgia is also connected to the buildup of fibrin in the microvasculature, the small blood
14:37 – vessels. So I think the benefits far outweigh any risks. Finally, the enzymes that are used…
14:50 – Some of them are the ones that are used to help digest food. Some of their enzymes do work in
14:58 – that way as well but the majority of them aren’t the same enzymes.
15:04 – Melissa: That’s good to know, that’s a question that comes up quite a lot. You talked about biofilms and the way they can protect
15:09 – organisms from the body’s natural defenses but what does that mean for antibiotic resistance
15:14 – in general and also their ability to avoid antibiotic treatment?
15:20 – Ruth: Biofilms do have the added problem that they can contribute to antibiotic resistance.
15:26 – Bill Costerton, who’s considered the father of biofilms published an article in 2011 that had
15:43 – demonstrated that the presence of biofilms is a major contributor to antibiotic resistance.
15:51 – Not only can pieces of the natural immune system have difficulty getting to where the infection
15:58 – is and attacking it, likewise antibiotics have difficulty getting to where the infection is
16:05 – and dealing with it. So you end up with partial penetration of the antibiotics through the biofilm
16:14 – and the bacteria get just enough of a dose, kind of like a vaccine, that it becomes
16:20 – very smart and has developed drug resistance. And this is an important part, a big point because,
16:28 – when you’re told that you have an antibiotic resistance to a certain antibiotic people are
16:36 – concerned that now they can never take that antibiotic again and if they get an infection
16:44 – they can’t treat it adequately because they’re resistant to an antibiotic.
16:49 – What really is being said is that the bacteria has developed resistance to that antibiotic.
16:56 – If you have let’s say a resistance to penicillin by the organism they find in your urine,
17:07 – that doesn’t mean that you can’t take penicillin for a sinus infection or a strep throat,
17:13 – because the bacteria in your bladder are most certainly different than what you’re finding
17:20 – with your throat infection or your sinus infection. The other good news is that antibiotic
17:26 – resistance is not permanent. Two years ago Scientific American in August, that would have been
17:34 – I guess 2018, had a brilliant article in which they talked about the price that bacteria pay
17:41 – for developing resistant strains. And that price is they do not reproduce as readily. And so if they
17:48 – don’t see that antibiotic or that family, that class of antibiotics for a number of months,
17:55 – they die out. I see that all the time with my patients. They may have a urine specimen
18:01 – and they may have an organism that has multi-drug resistance but if we don’t give them any of those
18:08 – antibiotics for four months six months, sometimes it takes as long as a year, lo and behold
18:17 – when they come back with future tests that resistance is no longer an issue.
18:23 – Melissa: Which means they may then have more treatment options than they did previously.
18:29 – Ruth: Absolutely, and that’s one reason why it’s important to rotate antibiotics, to not keep giving the same one over
18:37 – and over again. Because with repeated exposures the bacteria are more likely to develop resistance
18:46 – to that particular family of antibiotics or the ones that work that particular way.
18:53 – Melissa: You also mentioned that in a biofilm it’s usually a community of different types
18:57 – of bacteria. Do they actually share antibiotic resistance traits so that one can help another become resistant to antibiotics?
19:05 – Ruth: Unfortunately, yes. These critters are much smarter than we
19:08 – ever used to give them credit for. It turns out that there’s something called quorum sensing
19:15 – which is a very fancy term in physics that I don’t fully understand. It means
19:21 – that these bacteria are able to communicate with one another and they are able to transfer
19:28 – some resistance characteristics between species. One of the labs that I use, Pathnostics, has
19:38 – gotten a very clever trick together in which they actually test for pooled antibiotic resistance.
19:47 – They have demonstrated that bacteria behave very differently in their resistance patterns
19:56 – when they have a community than if you’re only separating out each organism and checking each
20:04 – of those individually for drug resistance characteristics. This testing is
20:11 – only PCR – they only check for 48 pathogens but it’s very helpful when you have
20:19 – multi-drug resistance because you can get actual drug sensitivities not just what the literature says should work.
20:28 – Melissa: So they’re looking at what may be effective treatment
20:31 – for the bacterial community as a whole instead of individual which gives you a better picture potentially.
20:37 – Ruth: Absolutely. So there’s pros and cons of the different companies that do the
20:45 – testing. Some check for more organisms, some do actual sensitivity testing, and so it’s pretty
20:54 – much a judgment call as to what’s the more appropriate test for you at that time based on
21:02 – which pathogens have been treated and which ones haven’t and whether you have multi-drug resistance or not.
21:09 – Melissa: That’s good to know. We do get that question a lot: What is the best test? But
21:14 – it can really depend on your situation it sounds like.
21:17 – Ruth: Absolutely. It’s like everything else in life. There isn’t a one size fits all either in the testing nor in in the treatment protocols.