Unusual Colors of Urine – Explained

Sure, the color of our urine changes slightly all of the time because of a number of factors, like how much sweating you did versus the water you drank, but what about when pee turns a strange color that isn’t yellow?

Yellow is obviously the normal color, which comes from urochrome. Lots of different drugs or foods can cause the yellow to go different shades or become really bright. Other foods, like eating lots of carrots, and certain medications such as warfarin, a blood thinner, can create orange urine too. Red urine could be caused by blood, and that can indicate a problem. But beets can also make your pee turn red too.

There are a variety of other colors that can come from a weirder section of the color spectrum. A veritable rainbow of urine colors can be caused by the drug propofol, which is typically used for anesthesia, though green is the typical side effect in that case. A few cases of unusual colors like blue and violet urine can symptomatic of a health problem, as can urine that is not clear and may have a white appearance.

What’s that smell?

Did you know that bacteria make us humans and other animals smell the way we do? On top of that, animals use that smell to communicate with each other.

The “fermentation hypothesis of chemical recognition” says that bacteria in the scent glands of mammals generate metabolites with specific odors that animals use to communicate with each other. What’s more, this hypothesis explains how variations in these chemical signals are actually due to variations in those populations of bacteria.

Let’s start with humans, Corynebacterium is responsible for that distinct “body odor” that emanates from our armpits. That odor is caused by 3-methyl-2-hexenoic acid (3M2H) and 3-hydroxy-3-methylhexanoic acid (HMHA). It turns out that the precursors for these chemicals are cleaved by a zinc-dependent bacterial aminoacylase.

In one study, researchers isolated bacteria from the human axilla (a fancy word for armpit). They identified 19 strains of Corynebacterium and 25 strains of Staphylococcus. Curiously, only isolates of Corynebacterium, not Staphylococcus, produced 3M2H or HMHA from the precursors 3M2H-Gln or HMHA-Gln, indicating that these strains produced an Nα-acylglutamine aminoacylase.

So, what’s the use of human body odor? It’s safe to say that most people think body odor smells bad – it’s definitely not attractive to other humans. Some researchers think that may be the point – or at least it was at some point in our evolution. Body odor may have been used by early humans as a way to assert dominance or repel rivals.
Things are a little more clear cut when it comes to mice, however. Mice use odors to attract mates of the same species and to repel rats. One of these odor chemicals is trimethylamine, which is specific for the olfactory receptor TAAR5. Trimethylamine synthesis requires two steps, one of which involves bacteria. We’ve all smelled trimethylamine before, it’s the stinky smell of bad breath and spoiled food!

In humans, trimethylamine is the byproduct of bacteria metabolizing dietary choline, and researchers wanted to know if the same held true for mice. To figure things out, they collected urine from mice that were fed a choline/methionine-free diet or that were treated with an antibiotic. Sure enough, these mice produced less trimethylamine in their urine than control mice.

Likewise, urine from wild type mice contained trimethylamine that activated its receptor TAAR5 (assayed with a reporter gene), but urine from mice on the choline-free diet or treated with antibiotics did not activate TAAR5. These findings suggest that bacteria produce trimethylamine from dietary choline.

While trimethylamine is produced by commensal bacteria, pathogens produce their own array of odors. Mice have receptors in their vomeronasal organ that recognize formylated peptides that are produced by tissue damage or bacterial infection. There are also chemosensory cells in the respiratory epithelium that detect bacterial quorum sensing molecules called acyl-homoserine lactones.

Next are the meerkats. These members of the mongoose family are native to South Africa. They produce a smelly paste from a pouch beneath their tails. They use this paste to mark their territories, applying it to plants, rocks, and their meerkat pals. Researchers found over 1,000 types of bacteria and some 220 odorous chemicals in the stinky paste. The key finding was that specific odors are produced by specific microbial communities – a specific meerkat family smells the way it does because of its own specific microbes.

The group detected five main phyla of bacteria in the meerkats’ anal pouch – Proteobacteria, Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria. Specific genera of bacteria found in the paste were Porphyromonas, Fusobacterium, Anaerococcus, and Campylobacter.

The researchers also found that subordinate and dominant male meerkats had different bacterial communities in their pouches. However, there were no significant differences among dominant and subordinate females.

Finally, like meerkats, hyenas, deposit a scented paste from anal scent pouches to communicate with other hyenas. In one study, researchers used scanning electron microscopy to look for bacteria in the scent pouches of both spotted and striped hyenas (two groups that differ rather significantly in their lifestyles and behavior).

They found that the bacterial communities differed between spotted and striped hyenas, but all communities were largely made up of fermentative anaerobes – specifically, species from the order Clostridiales. For the spotted hyenas, they identified Clostridiales from the genera Anaerococcus, Clostridium, Fastidiosipila, Finegoldia, Murdochiella, Peptoniphilus, and Tissierella. The bacterial communities differed, however, based on sex and female reproductive status.
Next time you reach for your deodorant, remember all those little bacteria living in your armpits!

The gut Microbiome can Influence the Brain

You may have heard of the microbiome, the community of microbes that lives in our gastrointestinal tract, as it is getting a lot of research attention since genetic techniques advanced in recent years. That gave researchers the power to assess what species were living in our guts and how they were influencing our health. It turns out that they are having a huge impact, and while that is not surprising, it has been interesting to find that they may also be affect our moods and behaviors.

The phenomenon even has a name – the gut-brain axis. There are nerves that go directly from your gut, which has an extensive nervous system of its own, to your brain. The brain is protected from the rest of the body by the blood-brain barrier, so it had been simply assumed that microbes in the gut had no effect on the brain. But the microbes actually end up producing an effect that does transmit to the brain, through the molecules they release. The breakthrough researchers made in that area which showed how microbes in the gut did indeed cause a reaction in the brain, although it’s still not known exactly how that happens, and additional research has indicated that the relationship is quite complex.

Scientists have gone on to show that transplanting the microbiome of one mouse into another can induce behavioral changes.

Fungus can Easily Release Toxins Into the air

It’s known that some common molds can be harmful to human health; researchers have confirmed that several kinds of fungi that grow indoors on wallpaper produce toxins that can easily go airborne. When they are present in the air, people just inhale them, at which point they can cause illness. Some of these fungi, which can cause so-called sick building syndrome, are described in the video below, and the new work has been published in Applied and Environmental Microbiology.
“We demonstrated that mycotoxins could be transferred from a moldy material to air, under conditions that may be encountered in buildings,” explained the corresponding author of the work, Jean-Denis Bailly, DVM, PhD, a Professor of Food Hygiene, at the National Veterinary School in Toulouse, France. “Thus, mycotoxins can be inhaled and should be investigated as parameters of indoor air quality, especially in homes with visible fungal contamination.”

The investigators wanted to gather more data on how mycotoxins from indoor fungi present a threat to human health. For this work, the scientists created a model environment in which the flow of air over contaminated wallpaper was modeled, and the speed and direction of the airflow could be controlled by researchers. They then assayed the bioaerosols generated in the experiment.

“Most of the airborne toxins are likely to be located on fungal spores, but we also demonstrated that part of the toxic load was found on very small particles – dust or tiny fragments of wallpaper – that could be easily inhaled,” noted Bailly.
Three species of fungus were used in this study: Aspergillus versicolor, Penicillium brevicompactum, and Stachybotrys chartarum. These species are well-characterized, as they are known to be common food contaminants. In addition, they “are frequent indoor contaminants,” said Bailly. He explained that they synthesize different mycotoxins. Fungi have mycelia, which are projections that function to harvest nutrients from their environment. The mycelia of these various fungi are also different, which could be leading to the variation in mycotoxins.

There are new questions raised by this research, said Bailly. “There is almost no data on toxicity of mycotoxins following inhalation,” he noted, likely because most research has investigated how they contaminate food. These different fungi also appear to contaminate air at different rates, releasing varied levels of mycotoxins.

Bailly suggested that the demand for homes that are very energy efficient could be aggravating this problem. Such homes “are strongly isolated from the outside to save energy,” while appliances that use water, like coffee makers “could lead to favorable conditions for fungal growth,” he explained.

“The presence of mycotoxins in indoors should be taken into consideration as an important parameter of air quality,” concluded Bailly.

My Eczema Chronicle…

I was just like any normal child born to this world and growing looking forward to a bright future. The story of my eczema started unexpectedly as there’re no one to the best of my knowledge within and outside of my immediate and extended families with eczema. So how I got to have it, is a misery. Around 1999/2000 during my high school days, I noticed these rashes-like looking spots on my left arm. It was very hitching. The Hitching was such that scratching it feels good and painful but noticeably was the more I scratched the more it spread. Before long I noticed my right arm was replicating the rash-like pattern. It became a concern for me. I saw a quite number of doctors and consultants, the best they could do is prescribe drugs and skin medication creams. The interesting thing was that none of this medical practitioners never made mention of eczema. Probably they had no idea was the problem was then. Anyway, neither the drugs nor the creams solved the problem. Months passed and my situation wasn’t getting better rather worse as everything I used and applied had no effect. On a faithful morning, I walked into our sitting room and there was a program on the television called the Morning Express. There was a consultant invited on the show who discussed on the skin and he made mention of Atopic eczema, and as I listened to him, everything he said about eczema fitted my experience and that was the very first time I heard of the word eczema. The sad part for me after I watched the programme was when he said that the cause is unknown and it can only be managed. Thereafter I started researching on eczema but then access to information and internet was very limited in Nigeria. The mobile and the internet boom was still at it infancy. But as a desperate young man seeking solutions, I spent money going to the internet cafés, downloaded as much as I could lay my hands. By then more than half of my hands was covered with eczema and I can barely off my clothes in the public, so I had to wear a long shirt to cover my eczema shame. Much of the information I got could only help me to understand eczema and manage it. And so for the next 10 years, I was managing it. There were times it seems it was going and it just returned again. It was a game of hide and seek. During this period I ensured I avoided scratching, importantly was I avoided dryness which is a trigger factor for scratching. As I took these measures, it worked to a certain level but returned with a bigger explosion!!!. In between this 10 years period, I had the worst eczema when it showed up behind my two knees, it showed below my breast, abdomen, my neck regions, my right foot and upper right leg. It was hell broke loose, and psychologically traumatic for me. I just couldn’t fathom was the root cause of the sudden expansion and spread of the eczema. I must mention that I altered, adjusted my diets in effort to narrow down to the root cause, maybe it something internal from what I take was the problem and the closest I came was my protein intake especially beans but it wasn’t my protein intake. I was helpless and without any alternatives, I started to live with my ordeal and I came to accept it as part of me.

My Eczema from 2009 till Date

Eczema took a better part of me emotionally, psychologically and affected my social interaction. Has I worked to manage it, I also hide it under the clothes. It took some courage after a while in 2008 when I started to wear T-shirt. It wasn’t by choice then but by compulsion because I was doing the National Youth Service Corp and we had to wear T-shirts. It like life has a way of forcing me to face the shame I was running from. Thence, many people saw my hands, and those who either by curiosity or sheer courage asked what happened to me and so I used it to educated them on eczema. I was gradually getting to live, move and interact without fear but I still got those stared look occasionally. The eczema was distinctly dry black on my skin and because I am light skinned, made it more obvious. Sometimes it like you can see through the dried layer waiting to shed off and unleash a fresh eczema rash underneath.
The year 2009, October 30th, I arrived in the UK for my masters. I was focused on the main business…study. Within 3 months into the program without anything extraordinary except that it was a cold winter, I saw my skin started taking shape back to it normal form, I didn’t wanted to rejoice early because of previous similar experiences and I waited quietly expecting for another unsurprising return. And 3 months turned 6 months..no eczema and my eczema skin regions got better. It was a miracle unexplainable and unexpected. I tried to look at what changed or habits but nothing. I picked up many of the foods I stopped eating, no eczema. In a year, my eczema infected skin regions was back to normal. 10-year eczema cleared within a year. It got so better that it would be hard to believe I ever had it.

January 2011 – July 2011

In January, I returned back home to Nigeria. It was a great reunion and with a shocking look on everyone’s face who was aware of my skin problem, saw how everything had disappeared without a trace. A miracle?…yea…you are probably wrong!!!.
My eczema was like a wounded lion waiting to strike. Barely a month to my return, the eczema showed up again…and as usual my two arms. This time, I was lost to what to suspect.. The air,the water (both drinking and bathing), the foods, and the whole house. I was devastated and confused. The question ringing in my brain was “What am I reacting or allergic to”. I took every measures against the eczema and maybe probably one of the factors I mentioned above was the root cause but none worked as I also avoid scratching because it itched alot, and helplessly watched as the eczema took over. Six months on, July, I returned back to the UK, less than a month of returning, the eczema stopped. I began to wonder what was peculiar about these two different environments that one seem to favour the eczema and the other stopped it.
By October 2011, I had fully recovered and prepared to returned to Nigeria. This time I had prepared a list of do and don’t when I arrived home.

October 2011 – February 2012

Between this period I was extremely careful of what I eat, drink, bath, clothes, and importantly avoid excessive heat which I could say was the only difference between the UK and the Nigeria environment. My careful measures could only last me 21/2 months before the eczema show up again.

February 2012 – April 2014

This time I was in South Africa, just like my UK experience. The eczema went into hibernation, I cannot say disappeared or gone because I sensed that something external which I cannot explain triggers it. And for good 2 years of my time doing my doctorate research, there was no sign of eczema. April 2014, I visited Nigeria, just like anyone following would guess/suspect, the eczema woke up from hibernation and within 2-week, it appeared fresh on my skin, 2-weeks after, I returned back to South Africa and I was fine. This time I was suspecting the whole country in addition to the previously mentioned…Funny..yea

April 2014 – March 2015

I was ok till I visited Nigeria in March 2015 for 3 weeks, yea..I thought as much, I probably have Nigeria Eczema Syndrome (NES). It became more psychological that anytime I am in Nigeria I must have eczema. The eczema showed up and I can only bid my time to return back.

March 2015 – June 2016

As the trend follows, I returned back to SA completed my doctorate degree with no eczema (hibernating). By mid-year, I moved to the UK, now a family man. I have since travel to and through few countries with no incidence of eczema. Whilst in the UK, I had an experience in April 2016, I used a body spray and few days after the eczema showed up but it wasn’t much after I discontinued using the spray. By then, we have a four months old baby who suddenly developed skin rashes. I examined him and the pattern of his rashes is exactly like mine. I can’t but help suspects he caught the eczema bug. I thought deep within if my problem is rooted at the gene level. Probably I have a faulty gene somewhere. I had long suspected it but there wasn’t any way to test it out. I could only suspect something external. For the next 8-months plus, we watched our child battled his own skin rashes

June 2016 – till date

So I am back in Nigeria, and if you try guessing and you will be probably be right…the eczema is back. The first 6 months of my return was a welcome back eczema (NES). I have only been able to manage it now. I have tried medications and I had to share a skin medication cream prescription for my boy which seems to work fine for both of us.

The motivation for putting up this eczema chronicle was the recent research article by Nick et al which can be found here. My own take on the research is though, they experimented under a controlled experimental condition. Is their controlled variables apply to most or few of us living with eczema? I wish it could answer what is causing my suppose loss of filaggrin if it is actually the implicating factor to my eczema. I wish to know the epigenetic playing out in my body that is affecting the gene causing the eczema. I hope the next decade will provide concrete answers and our knowledge of stopping eczema is established. While I can only hope for a permanent solution, I desired this skin problem doesn’t manifest in the nearest future on my children and if it does manifest, hopefully a solution should be waiting for them.