Cultivating a Healthy Skin Microbiome

A company is marketing a probiotic spray designed to help cultivate a healthy skin microbiome.  The spray contains Ammonium Oxidizing Bacteria (AOB; specifically the genus Nitrosomonas) that derive their energy solely from consuming the ammonia and urea found in sweat.  Supposedly, if you have enough AOB, you don't smell bad because they consume all your sweat, releasing beneficial nitric oxide gas!



I wanted to learn more about the skin microbiome, and found this comprehensive article with diagrams to show skin follicles, etc the complex topography and ecology of the skin environment.

These new data are based on DNA assays, and with improvements to these techniques, viruses, mites, and fungi are also being inventoried. This is certainly an improvement from the old days when only culturable bacteria were studied.  Here is a classic paper about the microbial correlates of dandruff.  Apparently there is no cause of dandruff, but simply a feedback between bacteria and fungi and the scalp. A fungus called Malassezia spp can release compounds that stimulate epidermis to proliferate.    Fungicides cure dandruff by killing the Malassezia spp, but many people harbor Malassezia spp without dandruff.   Perhaps an "ecological" cure could involve cultivating probiotic bacteria?

The same article also has the classic diagram showing different microbial communities on different body parts, based on their temperature, moisture and oilyness (sebum versus apocrine ).

Interestingly, soap and shampoo may be destabalizing our skin microbiome, in the same way that antibiotics can impact the gut microbiome.  For example, many ingredients in personal care products have been found in laboratory tests to inhibit "good-guy" AOBs, including sodium lauryl sulfate (SLS is one of the harshest detergents), sodium coco-sulfate, and even castile-type soaps. (Source)

To maximize ammonia utilization, AOBsproduce unique enzymes on elaborately folded cell membranes. These membranes are intricately folded so that they can increase the surface area for ammonia-oxidation. This means that they are able to boost both their ammonia-oxidizing capacity and their energy output.  However, this elaborate membrane architecture also renders AOBs particularly sensitive to membrane-disrupting chemicals, such as anionic surfactants found in modern soaps and detergents.

Detergents replaced simple soap in our hygiene routine soon after WWII and form a major part of most bath products. Anionic detergents such as lauryl sulphates, sarcosines and sulfosuccinates can be harsh to the skin and especially the microbiome.

When reading the ingredients list on your cleaning products, you can identify anionic surfactants as those that have the following in their names:

Sodium
Ammonium
Magnesium
Sulfate
Sulfonate
Gluconate

(For example, sodium laurel sarcosinate, magnesium laurel sulfate, and sodium gluconate.)

Nonionic surfactants are gentler to the skin microbiome, although not entirely harmless. (Source) They include:

Ethoxylates
Alkoxylates
Cocamide

All of my soaps and shampoos contain these ingredients, except for Black African soap "made from shea butter and palm kernel oil mixed with ashes".  The detergent in this soap is laurel glucoside, (AKA dodecyl glucoside) a non-ionic surfactant molecule.  Because it is non-ionic, it is a milder detergent, often used in cosmetics, shampoos, etc. Glycosides are produced from lauryl alcohol and glucose.

It may be possible to specially order detergents from companies like this one.  

What is the Microbiome Good for?

How Inhibit Ammonia Production in Large Intestines?
"In general, the treatment of [excess ammonia] has as common elements the reduction of protein in the diet, removal of excess ammonia and replacement of intermediates missing from the urea cycle."

Eating large amounts of protein feeds harmful bacteria: "Protein fermentation by human faecal bacteria in the absence of sugars not only leads to the formation of hazardous metabolic products, but also to the possible proliferation of harmful bacteria [such as Clostridium, Enterococcus, Shigella and Escherichia coli]."

--
text below from:

Increasing the amounts of alimentary proteins results in a spectacular increase of the luminal and faecal ammonia [92]. In humans, the ammonia luminal concentration progressively increases from the ascending to the descending colon [93] in accordance with a higher rate of protein fermentation in
the distal than in the proximal colon. The two environmental characteristics of the proximal colon (low pH and high carbohydrate) explain the reduced net production of ammonia. [13]

Large amounts of ammonia can be absorbed through the large intestine mucosa [96]. Ammonia has been considered as a metabolic troublemaker since this compound is able to inhibit in a dose-dependent manner the mitochondrial oxygen consumption [104]. In addition, high millimolar concentrations of ammonia inhibit short-chain fatty acid oxidation [105,106] in colonic epithelial
cells.

Also of concern is H2S:  H2S is a bacterial metabolite produced through fermentation of sulfur containing amino acids (methionine and cysteine). Interestingly, there is a correlation between the level of meat intake and the level of faecal excretion of sulfide. [110]  H2S at excessive concentrations inhibits colonic epithelial cell respiration [120] and provokes genomic DNA damage [121], [122].

What to do?
inhibit large intestine production of ammonia!
Lactulose (comalose) would help acidify colon, feed good bacteria: http://www.lactulose.eu/97.htm

Pathogenic Bacteria Mediate Inflammatory Effects of Meat

A recent study from Harvard university concluded that, in genetically susceptible mice, dietary saturated fatty acids (SFAs) led to increased pathogens in the gut. (See Rob Wolf's critique of the study.)  The implication appears to be that dietary SFAs feed harmful microbes.  A similar conclusion was also reported for choline...

Researchers have theorized that the evolutionary pressure from pathogenic gut bacteria has led to the link between SFAs and a prophylactic inflammation: our bodies ramp up a defense response to SFAs because these fats feed harmful bacteria.  In contrast, monounsaturated fats (MUFAs) and polyunsaturated fats (PUFAs) are actually antimicrobial.  

However, it appears that pathogenic species are not being stimulated directly by dietary fats, but rather by cholesterol in our own bile.  This makes sense, because most fats should be absorbed before they reach the large colon, but bile is one of the largest inputs to our large intestines.  If this is true, than dietary fats are not the culprit so much as our own bodies' reaction to SFAs.

Even so, the association between saturated fat intake and inflammation has been repeated numerous times.  For example, one study of obese women on a high-fat low-carb diet noted 25% increase in C-reactive protein (CRP, a marker of inflammation) compared to a 43 decrease on a low-fat high-carb diet.  But when I searched for studies confirming this, I found a 2008 study from the University of Aukland, New Zealand, found that in healthy men, a single high-fat (71% of calories) meal did not lead to changes in tumor necrosis factor-α (TNF-α), and CRP.  Also, a 2004 study looking at the acute effect of a high-fat (50% of calories) meal in young healthy men noted no significant changes in CRP.

Jeff Leach at the Human Food Project lays out an interesting theory to explain these divergent results:

"Multiple studies have shown that a high fat diet produces low-grade inflammation, which in turn promotes metabolic disease such as diabetes. Interestingly, the low-grade inflammation correlates with circulating levels of a plasma endotoxin known as lipopolysaccharide (LPS). LPS is the primary structural component of the outer membrane of Gram-negative bacteria. Importantly, LPS only originate in the gut."

He concludes that intestinal permeability and the translocation of inflammatory toxins occurs only in the absence of Bifidobacteria, a type of beneficial bacteria found in mother's milk and fermented dairy products.  Importantly, stimulation of these species with fiber prebiotics like FOS and inulin has been shown to block inflammation from saturated fats.  Indeed, higher dietary intake of fiber has been repeatedly associated with lower markers of inflammation.

Take home message: always eat enough fiber with higher-fat meals.

Another Ecosystem Analogy

"....The idea [is] that fewer excess carbs in the gut leads to more competition which favors indigenous gut microbes over bad or pathogenic bacteria. A good example in this paper likens friendly gut microbes to your lawn. “It is thought that our commensal, or friendly, bacteria serve as a kind of lawn that, in commandeering the rich fertilizer (carbs) that courses through our gut, out-competes the less-well-behaved pathogenic “weeds.” The more healthy grass you have, the fewer weeds will be able to become established.” But if you were to spray your lawn with roundup (like antibiotics) and continue to add fertilizer, soon you will have a weed-filled yard. According to the authors: “Resident microbes hold pathogens at bay by competing for nutrients.”

Source.

Three Weird Examples of Nutrition Science: Obsolete, "Alternative", and Futuristic!

Time is acting strangely.  In our post-modern world, I'm never sure if the newest craze is going to come from the paleolithic or from Star Trek.  Especially when it comes to health and diet, the amount of confusion is almost 100%.

I've collected three examples below....an outdated idea promulgated by the state health department, weird nonsensical claims from an alternate reality, and new cutting-edge research from a man who steals aboriginal poop.


20-years out of date:     2% milk is making you fat!  ...according to NM Department of Health and their new foodstamp guidelines.  (Seems they missed the last 15-20 years of research showing that its actually a high-carbohydrate diet of processed foods that has led to the obesity epidemic, not the extra 1% milk fat in 2% milk!)


Alternate reality: Try pH 8.8 water!  Straight from the Himalayas, with minerals added!  (what minerals? Baking Soda?  I can make water any pH I want by adding baking soda or vinegar....)


20-years in the future:  Jeff Leach, co-founder of the American Gut Project, is definitely a good 10-20 years ahead of his time.   In the tradition of those brave scientists who self-infected themselves with the cutworm parasite in try to cure allergies and autoimmune dieseases, Mr. Leach has given himself a fecal transplant from an aboriginal in Africa.  What happens?  Stay tuned!

American Gut Project

An Ecologist Ponders the Microbiome

Fluctuating nutrient concentrations and the timing of peristalsis may affect microbiome growth and composition, which is hypothesized to affect health. Certainly digestive upset is no fun for anyone, and it makes sense to look at inputs (diet) as the primary drivers.

Ecosystem arguments are used to claim that some forms of digestive upset are due to over- or under-growth of bacteria in the intestines.  For example, Small Intestine Bacterial Overgrowth (SIBO) is treated with what is called the GAPS diet, an effort to restrict all foods that bacteria can digest.

In response, Jeff Leach, of the American Gut Project, made this comparison between diets disturbing the microbiome and ecological disturbances:

"If you think about it from an ecosystem perspective or from an ecosystem restoration perspective, if you take any ecosystem like the gut, the microbiome, and if you starve it... If you starve your backyard and all the diversity of plants, if you just starve it of nutrients, all ships go down with lowering water. And that perturbation, if you will, it wouldn’t be on the same level as an antibiotic, but it is a perturbation; it is an insult. And when you insult an ecosystem, insults like fire, drought, nutrient overload or nutrient deprivation, any of these perturbations typically result in a flourishing of weedy species, in this case, opportunistic pathogens. I know the GAPS diet...from an ecosystem restoration standpoint, it makes absolutely no sense whatsoever to starve your gut microbiome at any level. "

This idea that "a healthy garden needs a healthy soil" is an ecological idea.  Jeff Leach goes on to claim that specific nutrients, like "resistant starch, non-starch polysaccharides like inulin and fructooligosaccharides and galactooligosaccharides, can provide food for the beneficial bacteria in your gut and can increase their levels by orders of magnitude."

Turns out it may be a false analogy, or if the analogy is valid, the hoped-for predictive power of diet on microbiome function may not hold up. While broad temperature-precipitation drivers do determine biome (e.g. tundra versus desert) it is almost impossible to predict the exact species in an ecosystem based on the nutrient inputs to that ecosystem.  And if microbiome bacteria exert their effects in a species-dependent fashion, it may not be possible to predict that eating x will cause bacteria xyz to grow.

Ecologists look (with envy, and skepticism) at nutrition research and commentary because we know how complicated ecosystems can mess with simplistic notions of cause-and-effect.

The Microbiome

This is probably the best article about the microbiome. (Economist.com)

Microbiome and Disease: Experimentation, Gulf War Syndrome, and Mycoplasma

Humans are host to a large number of bacteria which may influence health and disease. Whether or not any given microorganism, such as E coli, becomes pathogenic is not understood. What is becoming increasingly clear is that, in addition to exogenous influences such as diet and exercise, endogenous factors such as bacteria (and genetics!) are crucial determinants of human health. Carl Zimmer, science writer, has proclaimed: "I, for one, welcome our microbial overlords!" after reviewing recent research establishing that certain bacteria can lead to obesity. His famous New York Times fecal transplant article is here.

In the absence of scientific certainty, groups of concerned citizens have begun moving forward, experimenting with antibiotics and probiotics to try to nudge the population dynamics of their microbiome toward healthier states. This emerging field, combined with the failure of the medical community to communicate and collaborate with patients who are sick and aren't being helped by currently available diagnosis or treatment has created fertile ground for web-based DIY experimentation. The community of Chronic Fatigue Syndrome sufferers in particular have latched onto research examining possible links between a tiny gram-negative bacterium called Mycoplasma fermentans and Gulf War Syndrome. The bacteria, which can apparently be a member of normal human microbial flora, is implicated in the vague symptoms of GWS, and by extension, CFS. A definitive book on GWS found little evidence to suggest such a link, but the initiator the research, Dr. Nicholson, has forged ahead nonetheless, starting a nonprofit research lab to investigate and link between Mycoplasma fermentans and health problems.

It is unfortunate that so much of the information available online is anecdotal. If these types of alternative medical practices could keep better data it may be possible to scientifically evaluate them. However, in the absence of peer-reviewed double blind trials, it appears many people are simply grasping for any treatment that offers hope, no matter how unsupported. Indeed, the scientific jury is still out, and this developing field may see fringe transformed into mainstream.

Research into M. fermentans is certainly controversial, but continuing: see, for example:

Kawahito et al. Mycoplasma fermentans glycolipid-antigen as a pathogen of rheumatoid arthritis. Biochemical and Biophysical Research Communications. 2008;369(2):561-566.