Science explains why some people smell worse than others despite keeping themselves squeaky clean.
The body is crawling with microbes that have evolved with the person, depending on the innate metabolism, history of infections, microbiome swaps, diet and lifestyle.
The body's ecosystem of microorganisms can increase the risk for dangerous diseases for which we have unreserved levels of sympathy. It can also lead to unlikable conditions such as unpredictable and embarrassing outbursts of odor emitting through the pores - odor so bad it ruins social lives and careers.
Analysis of our metabolism is crucial to comprehending the responses of our genes and microbes to the stresses of daily life, and to elucidating the causes and consequences of health and disease.
We applied metabolomic approach to an elusive condition that has always evaded diagnosis: socially and psychologically distressing odors that occur without a known or apparent cause. Learn about our preliminary results and participate in our anonymous survey to help us better understand and help with this condition.
In a Skype call held on May 7, 2017, by MEBO Research, moderated by María de la Torre, the main objective was to discuss strategies for managing body odor (associated with conditions such as TMAU or other metabolic disorders) through lifestyle and dietary changes.
Key points discussed:
Hormonal influence: The discussion covered how hormonal changes in adolescents (up to around age 21), women (during the menstrual cycle), and stressful situations (through adrenaline release) can influence or trigger odor symptoms (1:08–2:07; 14:31–15:24).
Diet and nutrition:
Natural, whole foods are preferable to processed foods in order to avoid unnecessary chemicals (3:33–4:05).
Foods high in sulfur (such as garlic and onions) should be limited or thoroughly cooked (for example, sautéed) so that odor-causing compounds evaporate before consumption (4:05–5:23).
It was emphasized that choline is an essential nutrient and should not be completely eliminated from the diet, as a deficiency can cause serious damage to the nervous system and increase anxiety (9:58–11:30).
Body detoxification process: It was explained that the body needs time to eliminate odor-causing chemicals that have accumulated in fatty tissues over the years. Drinking plenty of water and engaging in cardiovascular exercise can help speed up this process by mobilizing these compounds so they can be eliminated through sweat, urine, and breathing (5:26–7:43; 12:51–13:47).
Emotional well-being: The discussion addressed how social fear and anxiety about possibly smelling bad can create a vicious cycle that negatively affects psychological well-being (10:38–11:30).
One of our community members found this TMAU short film and shared it with me. For the first time ever, it was actually optimistic and full of hope.
I do believe we have come a long way, as we continue steadfastly on the path looking for answers that we hope will arrive sooner than later. There is currently more hope now because there are many "fronts" from which we are expecting new discoveries, and that is most promising, uplifting and inspiring.
Thank you TheoMeta for doing this film and for allowing me to post it in the MEBO Blog! Sharing the hope saves lives. We must keep sharing.
Danny Kunz has donated a very interesting PowerPoint presentation for the MEBO Conference 2017 consisting of metabolic pathway simulations on Apocrine Bromhidrosis compared to Trimethylaminuria. This presentation also discusses the role of the eccrine glands in bromhidrosis.
We are most grateful to Danny, who is a part of this, "loosely coupled group of patients (and non-patients) with academic degree and without academic degree integrating our separate research capabilities and representing an addressable unit."
This theory is supported by high throughput simulations backed by large enzyme databases, which makes it a very persuasive presentation. In other words, this group has done a computer simulation of bromhidrosis backed up by large enzyme databases, as Danny explains in the presentation. Their theory is that bromhidrosis is an apocrine and eccrine sweat glands metabolic disease.Danny also says in his presentation that thyroid function with and without elevated hormone, TSH, may plays a role in bromhidrosis, and the group recommends supplementation and diet for this.
Even though the simulations discussed in this PowerPoint presentation do not have the aspect of medical proof yet, it provides a very compelling theory that calls for further research.
TOPIC OF THE PRESENTATION:
1.Fecal (indole) breath and body odorand it's recommended supplementation and diet,
2.Apocrine and eccrine sweat glands metabolicdisease in bromhidrosis,
a.Discussions on isovaleric acidand amino acid leucinein eccrine bromhidrosis,
b.Recommends aThyroid functions blood test, with and without elevated Thyroid Stimulating Hormone (TSH),and recommended supplementation and diet.
This very interesting presentation raises question on whether TMAU2 to TMAU1 relation pattern could be transferred to the Bromhidrosis pattern as well.
Nobody likes strong smells coming from other human beings. It's just that social convention: you are nice, if you smell nice, and you are a monster - like Shakespeare's Caliban - if you smell bad.
But it could be the brunt of the genetic or environmental misfortune
The term microbiome refers to a collection of bacteria that inhabit a particular niche in our body, and we have a number of these microbiomes.
~90% of an adult human is bacterial.
10x more bacterial cells than human cells.
Microbiome provides essential functions, i.e., Feeds us, forms us and protect us.
Bacteria typically in our gut will digest complex molecules providing us with nutrients.
They form us; the bacteria helping us to develop an immune system, and they protect us because if we are inhabited by non-pathogenic bacteria, they will protect us from being inhabited by pathogenic bacteria that can cause disease.
We have bacteria that inhabit the esophagus, the stomach, the small intestine, the cecum, and the colon.
How do we acquire a microbiome? A baby is born without microbiomes, but it will inherit its mother's microbiome, particular if it's born from the vaginal delivery; and baby born by caesarean section will develop its microbiome slightly delayed from that of a vaginal birth.
Slide #3 PRIMARY TMAU – FMO3, DIET AND MICROBIOME:
Why is the gut microbiome relevant to Primary Trimethylaminuria?
When we eat food, gut microbial action in the gut breaks down the bond of the Trimethylamine group, by liberating nitrogen, methyl group, and other atoms that might be linked to them, and liberate the molecule resulting in trimethylamine (TMA).
This [odorous] trimethylamine (TMA) molecule is very quickly absorbed [into the bloodstream] and is taken to the liver.
In the liver we have this enzyme called FMO3, which is able to catalyze a reaction, which adds an oxygen (the O here in the diagram) onto the nitrogen (N) to form the molecule called trimethylaminuria-N-Oxide (TMAO) [non-odorous], which is then were very rapidly excreted through the kidneys.
And so, the cause of trimethylaminuria [TMAU1] is when the FMO3 gene carries a mutation, such that the enzyme that is encoded by this gene, cannot carry out this reaction very efficiently.
Flavin containing Monooxygenase 3 is the metabolic enzyme in the liver that adds the oxygen atom (O) to trimethylamine (TMA) to make it non-odorous.
Slide #4 MULTIPLE MICROBIOME-MEDIATED PATHWAYS CAN LEAD TO TMA PRODUCTION
A gut free of bacteria does not produce TMA.
Several bacterial phyla produce TMA.
In the gut we have many different pathways that can be carried out by different bacteria to produce trimethylamine (TMA).
Bacteria can actually convert trimethylamine (TMA) [odorous] into trimethylamine-N-Oxide [non odorous], and use it themselves. So this would be by bacterial enzyme.
Slide #5 FISH DIET:
There are a number of different constituents of the diet that have been shown when you culture bacteria to be able to give rise to trimethylamine. These include choline, betaine, carnitine, and also trimethylamine n-oxide (TMAO) [from fish and seafood] itself.
Marine fish that live in the sea or in deep fresh water lakes are the richest dietary source of TMA because to protect their protein from breaking down in salt water and pressure changes, the fish Flavin Containing monooxygenase enzyme (protein) is increased to produce a lot of TMAO, which protects their proteins in the muscles of the fish from breaking down.
In humans eating fish (high in TMAO) our gut bacteria converts it to TMA with our gut bacteria’s TMAO reductase enzyme and the bacteria uses the TMA for itself. The rest of the TMA is passed from the gut to the liver to be metabolized by the FMO3 metabolic enzyme to add an oxygen atom to make it TMAO (non-odorous).
Slide #6 How do we actually measure the content of a particular foodstuff?
The two methods [of measuring the content of TMA in foods], chemical digestion and biological digestion, don't always give the same answer. One is a very harsh chemical condition, and the other one is reliant on the biological digestion of the foodstuffs in the gut by the bacteria that reside in the gut of that Individual.
So just looking at a table doesn't necessarily give you the amount of trimethylamine (TMA) that's might be released when a human eats this particular foodstuff.
Slides #7 and #8 TABLES OF DIETARY SOURCES of TMA:
Lists TMA content of foods, including fruits, vegetables, and chicken, mushroom, pork, egg, beef, soya, lamb, mackerel, and cod, indicating significant differences between chemical digestion and biological digestion.
Slide #9 DIETARY INDOLES INHIBIT FMO3 ACTIVITY:
Researchers identified an inhibitor of FMO3 activity in brussel sprouts.
We are most grateful to Professor Elizabeth Shephard, PhD, for her continual monumental support through the years to the MEBO Mission by educating us through her three PowerPoint presentations, by working with United States and United Kingdom governmental agencies and councils, and by spearheading MRC funded research into a therapeutic for TMAU.