Gut health (SIBO) and your skin

The modern evolution of medicine necessitates that training doctors specialise in a specific organ – the brain, the skin, the heart. Indeed if suffering from an ailment in any area of the body a general practitioner will refer their patient to such a specialist. In the context of rosacea, acne, psoriasis, eczema and all other skin conditions this means a dermatologist. However recent scientific research infers the human body cannot be devised apart in this manner. That the skin cannot be treated as an organ in isolation from the body. That in fact all organs are complexly intertwined into feedback loops and in such a situation overall or holistic health is of greater importance.

Scientists call this the dawning of the gut-brain-skin connection.

An interweaving of biology’s causing what happens in the gut to affect the skin and therefore the brain i.e. a person’s mood. The simplest example of this is a high consumption of sugar causing a quick release of insulin (a hormone) which therefore causes the experience of a sugar-high – a feel-good spike of energy. In turn, the very same hormone cascade initiated by sugar is also associated with oily skin and acne1.

What published studies are now beginning to show as most important to general health and wellbeing is a diverse and good population of gut bacteria – what is also known as a healthy microbiome. Skin conditions such as rosacea and acne which show interim resolution by administration of antibiotics may be caused by the opposite – an overgrowth of bad gut bacteria.

Gut health and skin problems

Most people view their guts solely as a food passage. A means of digestion and waste disposal. In actual fact, the gut is home to the major proportion, in cell count of a person’s immune function. Meaning the gut is home to a complex messaging system with the ability to trigger the release of neurotransmitters and immune function messengers. In addition, the gut is also a defender of overall health ensuring the absorption of vital vitamins and nutrients, but the rejection of potential toxins. To perform optimally a person’s gut lining must, therefore, be healthy.

If a person has poor gut health i.e. is suffering from leaky gut syndrome or small intestinal bacterial overgrowth (a condition we explain in detail soon) bad gut bacteria populations grow, the permeability of the gut lining is increased and potential toxins may be absorbed. Activation of the immune function then leads to a body-wide potential for inflammation – the underlying symptom of almost all skin conditions.

Bottom line: What the gut absorbs, enters the bloodstream and can therefore easily and quickly reach and affect all areas of the human body – including the skin.

Gut health and skin problems: SIBO/Leaky gut

The theory of a gut-brain-skin connection was first evolved in 1930 by 2 dermatologists – John H. Stokes and Donald M. Pillsbury2. Now considered ahead of their time, many of the theories these 2 suggested are currently being proven true. An evolution which has led to poor gut health being nicknamed leaky gut and clinically referred to as small intestinal bacterial overgrowth (SIBO).

The original theory was born from the observation that almost 40% of people with acne had a condition called hypochlorhydria i.e. when a person’s production of hydrochloric acid/stomach acid in digestive organs is absent or low. Stokes and Pillsbury believed this reduction in stomach acid could cause migration of bacteria from the colon towards areas of the small intestine therefore ultimately leading to an altered intestinal microflora. They also proposed psychological stress could attenuate this bacterial change3. Subsequent research has confirmed hypochlorhydria is a significant risk factor for SIBO.

It is now known SIBO can not only compromise the absorption of vital vitamin and minerals but can also promote the absorption of toxins. Bacterial strains usually not present in the small intestine may compete for nutrients and when digesting these produce toxic metabolites which can cause direct injury to the small intestine4. It is, therefore, no surprise that SIBO has recently been associated with increased intestinal permeability.

The links between SIBO and skin conditions is recent but building, for example;

  • A recent study showed SIBO is 10 times more prevalent in patients with acne rosacea5
  • 66% of patients with acne show overreaction to the introduction of bad bacteria pointing towards increased absorption and therefore SIBO/leaky gut6
  • Rosacea patients have a significantly higher rate of SIBO compared with controls 46% vs. 5%7
  • Patients with psoriasis are noted to have significantly reduced biodiversity in their microbiome. A 2006 study showed 21% tested positive for SIBO with appropriate treatment successfully improving skin lesions8.
  • Imbalanced gut microflora in infants and children is recognised as a risk factor for atopic dermatitis9.

Bottom line: When a person’s gut microflora is compromised i.e. has an overgrowth of bad bacteria, their growth may lead to excreted metabolites which damage the small intestine. With a damaged intestine, gut found toxins may be absorbed therefore triggering a person’s immune function of which the main consequence is inflammation.

What are the symptoms of SIBO?

The most common gut related symptoms of SIBO are abdominal bloating, flatulence, indigestion and abdominal pain10. These symptoms can range from mild to severe with the inherent symptoms of SIBO also having the potential to cause malabsorption syndrome and chronic tiredness.

Undiagnosed SIBO may also be a cause of inflammatory skin conditions such as acne, rosacea, eczema, and psoriasis.

Can leaky gut cause rosacea?

Of all the skin conditions currently being linked with SIBO, rosacea has the strongest body of evidence. Classically doctors will prescribe antibiotics to mediate the inflammatory symptoms of rosacea. Without the cause of rosacea currently proven, it is known that rosacea symptoms may be temporarily resolved with antibiotics.

Cutaneous lesions of some patients with SIBO before and after treatment with rifaximin (an antibiotic). All patients had complete resolution of cutaneous lesions after normalization of breath tests (diagnosis for SIBO).”

This same study found when SIBO was resolved with antibiotics patients experienced an almost complete regression of rosacea lesions – an outcome which was persistent for at least 9 months in 96% of patients. 78% of patients participating in this trial experience a full clearing of their lesions. Of the patients who showed relapsing of rosacea, SIBO had recurred.

It is therefore proposed antibiotic therapy may send rosacea symptoms into remission because in at least 50% of rosacea patients, SIBO is the cause. In theory, increased intestinal permeability allows bacterial products into the bloodstream heightening levels of inflammatory immune mediators and therefore leading to the inflammation which causes visual symptoms of rosacea.

Note: This study points out that the type of antibiotic used is important. Rifaximin used in this trial is poorly absorbable and therefore has a greater likelihood to impact the gut. Other antibiotic strains do not produce such favourable outcomes. We will be discussing natural ways to treat SIBO soon.

Bottom line: While SIBO or leaky gut is not a 100% validated cause of rosacea in around 50% of rosacea patients, it looks highly likely to be a primary trigger.

Can leaky gut cause acne?

Acne is another skin condition for which an accepted mode of treatment is antibiotics. While the theory of leaky gut and SIBO is relatively young, to date there are no published studies comparing SIBO prevalence in acne sufferers to control groups. However, there is an interesting link which looks likely to point at least to an involvement of SIBO.

Acne is in part a hormonally provoked skin condition which can be caused in adulthood due to high a sugar diet. High sugar foods or high glycaemic index (GI) foods cause the release of hormones known as insulin and insulin-like growth factor (IGF-1). IGF-1, in particular, is positively linked to oily skin and acne.  

Interestingly emerging research has shown specific gut bacteria can influence insulin levels in addition to glucose turnover rates[11]. A bacteria known as bifido-bacteria is thought to be most important. What links these findings together even more tightly is that acne is a common side effect of puberty and that a period of insulin resistance is commonly experienced during puberty12.

Dairy has been positively associated with acne and is a source of IGF-1. Interestingly fermented milk Is not positively associated with acne. During the process of fermentation of probiotic bacteria in particular lactobacilli use IGF-1 as a food source resulting in a 4 fold lower level of IGF-113.

Bottom line: Acne is positively linked with IGF-1, a hormone which is released in partnership with insulin. A healthy gut microbiome may be able to help influence insulin release and therefore IGF-1 levels resulting in a reduced risk/improvement of acne symptoms.

Can leaky gut cause eczema?

Eczema is a skin condition which presents most often in childhood with over 20% of the developed population experiencing eczema during childhood14. While there are currently no published studies linking eczema to SIBO there are many published studies linking eczema symptoms to a changing gut microflora. For instance, it is known that abnormal intestinal microflora is a risk factor for the development of eczema. Other studies show when intestinal microdiversity is improved, eczema severity significantly decreases15.

Bottom line: A diverse gut microflora may help avoid the presentation of allergic-type skin conditions such as eczema.

What causes SIBO?

There are many risk factors for the development of SIBO. Most fit into one of two groups – dietary or lifestyle related. For example the most well-supported include;

  • High sugar diets
  • High glycaemic index diets
  • Low fibre diets
  • Lack of omega-3 dietary fats – omega-3 deficient diets directly increase SIBO16
  • Large consumption of processed foods
  • Stress
  • Temperature extremes
  • Impaired movement of food through the upper GI tract
  • Overuse of antibiotics17
  • High alcohol consumption18

How do you treat SIBO naturally?

While antibiotics can be used to help correct SIBO – at least temporarily – the overuse of antibiotics is also a risk factor for SIBO. Antibiotics work by reducing a person’s microbial count i.e. antibiotics cannot distinguish between good or bad bacteria and therefore cull both species.

Treating SIBO naturally is therefore of particular interest not only for positively resolving SIBO but for creating long-term changes which continue a patients resolution of SIBO. Natural treatments for SIBO include;

  • Probiotic administration – particularly of Lactobacillus and Bifidobacterium19
  • Increased omega-3 consumption
  • Increased levels of dietary fibre
  • Reduced consumption of sugar, high GI foods, and processed foods
  • Effective stress management e.g. with exercise or meditation

Note: Studies show probiotics can increase the absorption of omega-3 fatty acids, therefore, making both changes concurrently has a synergistic effect20.

High sugar diets lead to an increased intestinal permeability21,22 and therefore an effective SIBO diet would not only reduce the consumption of sweet treats such as cakes, pastries, and chocolate bars but would also reduce the consumption of high glycaemic index foods such as white bread, white pasta, white potatoes and white rice. A SIBO diet should contain a higher proportion of natural foods/foods in their raw and most natural condition partnered with a regular serving of omega-3 rich fatty fish such as salmon, mackerel and anchovies.

Lifestyle also imparts a significant effect on a person’s gut microflora. High-stress events such as exams are positively correlated with reduced micro-biodiversity. Experimental studies show psychological stress is associated with an increased small intestinal transit time which provokes an overgrowth of bacteria which therefore compromises the intestinal barrier23.

Bottom line: Natural treatment for SIBO should include an appropriate strain of probiotics, increased consumption of omega-3 in addition to a well-balanced SIBO diet low in sugar and processed foods.

 

Sources and references
  1. Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women. Mark Cappel, David Mauger, Diane Thiboutot

    Arch Dermatol. 2005 Mar; 141(3): 333–338. doi: 10.1001/archderm.141.3.333

  2. Stokes JH, Pillsbury DH: The effect on the skin of emotional and nervous states: theoretical and practical consideration of a gastrointestinal mechanism. Arch Dermatol Syphilol 1930, 22:962-93.

  3. Bowe WP, Logan AC. Acne vulgaris, probiotics and the gut-brain-skin axis – back to the future? Gut Pathogens. 2011;3:1. doi:10.1186/1757-4749-3-1.

  4. Toskes PP: Bacterial overgrowth of the gastrointestinal tract. Adv Intern Med 1993, 38:387-407.

  5. Parodi A, Paolino S, Greco A, Drago F, Mansi C, Rebora A, et al: Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Clin Gastroenterol Hepatol 2008, 6:759-64.

  6. Strickler A, Kolmer JA, Schamberg JF: Complement fixation in acne vulgaris. J Cutaneous Dis 1916, 34:166-78.

  7. Parodi A, Paolino S, Greco A, et al.: Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Clin Gastroenterol Hepatol 2008, 6:759–764.

  8. Ojetti V, De Simone C, Aguilar Sanchez J, et al. Malabsorption in psoriatic patients: cause or consequence? Scand J Gastroenterol. 2006;41(11):1267-1271.

  9. Bisgaard H, Li N, Bonnelykke K, et al. Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school age. J Allergy Clin Immunol. 2011;128(3):646-652.

  10. Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Andrea Parodi, Stefania Paolino, Alfredo Greco, Francesco Drago, Carlo Mansi, Alfredo Rebora, Aurora Parodi, Vincenzo Savarino Clin Gastroenterol Hepatol. 2008 Jul; 6(7): 759–764. Published online 2008 May 5. doi: 10.1016/j.cgh.2008.02.054

  11. Burcelin R: Intestinal microflora, inflammation, and metabolic diseases. Abstract 019, Keystone Symposia – Diabetes Whistler, British Columbia, Canada; 2010.

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  14. Flohr C, Mann J. New insights into the epidemiology of childhood atopic dermatitis. Allergy. 2014;69(1):3-16.

  15. Nylund L, Nermes M, Isolauri E, et al. Severity of atopic disease inversely correlates with intestinal microbiota diversity and butyrate-producing bacteria. Allergy. 2015;70(2):241-244.

  16. Ralph HJ, Volker DH, Chin J: Effects of omega-3 fatty acid deficiency on rat intestinal structure and microbiology. Asia Pac J Clin Nutr 2004, 13(Suppl):S79.

  17. Dukowicz AC, Lacy BE, Levine GM. Small Intestinal Bacterial Overgrowth: A Comprehensive Review. Gastroenterology & Hepatology. 2007;3(2):112-122.

  18. Mucosal bacterial growth in the upper gastrointestinal tract in alcoholics (heavy drinkers). T. Hauge, J. Persson, D. Danielsson Digestion. 1997; 58(6): 591–595.

  19. Bowe WP, Logan AC. Acne vulgaris, probiotics and the gut-brain-skin axis – back to the future? Gut Pathogens. 2011;3:1. doi:10.1186/1757-4749-3-1.

  20. Puch F, Samson-Villeger S, Guyonnet D, Blachon JL, Rawlings AV, Lassel T: Consumption of functional fermented milk containing borage oil, green tea and vitamin E enhances skin barrier function. Exp Dermatol 2008, 17:668-74.

  21. Cani PD, Delzenne NM: Interplay between obesity and associated metabolic disorders: new insights into the gut microbiota. Curr Opinion Pharmacol 2009, 9:737-43.

  22. Cani PD, Possemiers S, Van de Wiele T, Guiot Y, Everard A, Rottier O, et al: Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut 2009, 58:1091-103.

  23. Wang SX, Wu WC: Effects of psychological stress on small intestinal motility and bacteria and mucosa in mice. World J Gastroenerol 2005, 11:2016-21.