Photo by Coline Haslé
Rosacea is one of the most common skin disorder I see in my clinic and it is yet another condition that affects more women than men… It is a chronic skin condition with periodic ups and downs and considered non-curable by the medical profession. Recent research however highlighted that just like allergies, rosacea is the result of the immune system’s over-reaction to the environment.2
Symptoms and triggers
The main symptoms include red or pink patches, visible tiny broken blood vessels, small red acne-like bumps or red cysts, sometimes even pink or irritated eyes and it may spread to other parts of the body also. Unlike traditional or teenage acne, it usually starts in the mid 30’s. The redness in rosacea, often aggravated by flushing due to hot beverages, alcohol intake, smoking, spicy foods and emotional stress that cause small blood vessels in the face to enlarge (dilate) and become more visible through the skin, appearing like tiny red lines (called telangiectasias).1
Excessive alcohol consumption is especially detrimental, as it damages the gut lining, thus increasing the absorption of vasoactive amines (chemicals that affect blood vessel tone and can trigger dilation), potential allergens, and other toxins from the gut. It impairs liver function and detoxification and known to lead to many nutrient deficiencies necessary for skin health. Lack of Vitamin C and antioxidants weaken blood vessel walls, enabling damage. 1
Local infections promote inflammation and swelling, causing small red bumps that often resemble teenage acne – hence it is sometimes called acne rosacea. And just like in acne, there is an imbalance in sebum production, which may rapture the follicles, making them vulnerable to infection. Studies have shown increased density of mites in patients with rosacea compared with controls, including Demodex folliculorum.3
Hormonal imbalances are also triggering factors. In menstruating women, the brain’s hypothalamus signals the pituitary to tell the ovaries to ovulate. During perimenopause, as levels of estrogen and progesterone fall, the ovaries stop responding, which causes the hypothalamus and pituitary to send stronger signals; this signaling overactivity can trigger the vasomotor center, specifically the arcuate nucleus of the hypothalamus, which controls capillary dilation, resulting in menopausal flushing or hot flashes.1
Blood sugar imbalances are often linked to promoting episodes of flushing. The skin cells of acne patients have been found to be insulin insensitive and to utilize sugar so poorly that one researcher has referred to acne as “skin diabetes”.1
While previous studies and treatment options focused on triggers, recent molecular studies highlighted a possible cause; a common link between the triggers of rosacea and the cellular response, suggesting that an altered innate immune response is involved in the disease pathogenesis. In innate immunity, the pattern recognition system, which includes the Toll-like receptor (TLR) families, respond to environmental stimuli such as UV, microbes, physical, and chemical trauma. Triggering the innate immune system normally leads to a controlled increase in cytokines and antimicrobial molecules in the skin.2
One of these protective antimicrobial molecules is a peptide known as cathelicidin. Individuals with rosacea however, expressed abnormally high levels with different molecular weights of cathelicidin in their epidermis. These forms of cathelicidin peptides (LL-37) promote and regulate inflammatory messages, such as leukocyte chemotaxis, angiogenesis and expression of extracellular matrix components, whereas the types most commonly found on normal skin function mostly as antibiotics and have little to no action in inflammation.2
The reason for this seem to be explained by genetically higher expression of the environment-detection systems called toll-like receptor 2 (TLR2) on the skin surface. This hyper-sensitive reaction to the environment activate the production of local serine protease kallikrein 5 (KLK5, also known as stratum corneum tryptic enzyme), which processes cathelicidin peptides from a precursor protein in the epidermis.2
TLR2 involvement has also been suggested in other dermatoses resembling rosacea. Glucocorticoid (steroid) induced rosacea-like dermatitis, so-called perioral dermatitis, includes erythema, pustules, and papules somewhat similar to that seen in rosacea. Propionibacterium acnes – a common bacteria to cause skin infections, enhanced glucocorticoid-dependent TLR2 induction.2
Vitamin D is a well-known immune regulator and its deficiency has been highlighted in the pathogenesis of many skin disorders including atopic dermatitis where cathelicidin induction is suppressed. However, Vitamin D might be problematic in rosacea patients. A small study found excess levels in rosacea sufferers – possibly due to sun-exposure, which may exacerbate the problem.5 Cathelicidin transcription in epidermal keratinocytes (skin cells) is regulated by the active form of vitamin D 1,25(OH)2D3. TLR2 stimulation by UV light amplifies this by increasing the activation of the vitamin. Thus, human epidermal keratinocytes can produce more 1,25(OH)2D3 locally by TLR2 stimuli, and this in turn enables the epidermis to produce more cathelicidin.2,4 It is not known that supplemental Vitamin D without sun exposure could lead to the same results and, until further is known, Vitamin D levels should be monitored and optimised.
The root of the problem
As with any other skin conditions, the root of the problem often resides in our digestive system where we also house 80% of our immune cells and regulate normal immune function. Insufficient production of stomach acid and lack of adequate pancreatic enzymes, especially lipase necessary for fat absorption is common in patients with rosacea and is considered a causative factor. Many cases associating rosacea with digestive discomforts, ulcerative colitis, Crohn’s disease, celiac disease, Helicobacter pylori gastritis and alteration of intestinal mucosa can be found in the literature.2
It is most often linked to Helicobacter Pylori infection which interfere with the break-down and absorption of the food we eat and allows putrefying bacteria and yeasts to feast on our undigested food particles, producing toxins that overwhelm the liver, interfere with normal immune responses and irritate the skin. A recent study indicated that rosacea patients have significantly higher prevalence of small intestinal bacterial overgrowth and its eradication may completely resolve the problem.6
Zinc deficiency is very common in skin conditions in general and it is the most common deficiency I test for in my clinic. Its benefits are multifaceted; zinc is often called the wonder-mineral with its myriads of purposes in each cell of our bodies. It regulates sebum production, it is a crucial regulator of the immune system and is needed as a co-factor form many other nutrients to work effectively.7,8 The clinical benefits of retinoic acid (Vitamin A) for rosacea is well documented and could be partially explained by its ability to decrease TLR2 expression and function.9,10 We need adequate Zinc levels for vitamin A to get around in our body attached to Retinoid Binding Protein, which is a zinc-dependent molecule. This mineral however tends to be low in people with digestive discomforts, as we need adequate hydrochloric acid to get zinc out of our food, and we need adequate zinc to make hydrochloric acid and digestive enzymes – the typical catch 22 situation.8
Find Your root!
You can try the best topical lotions and ointments; unless the root cause is addressed the symptoms will keep reappearing. Doctors prescribe antibiotic treatments and it is helpful in the short term as it reduces both the bacteria living on the skin that cause infection of the raptured follicle and the putrefying bacteria in the gut. However, it does not address fungal overgrowth, it leads to dysbiosis (imbalanced gut flora), hyper-permeability of the intestinal membranes and stimulate immune reactions – hence the symptoms can return after the course with a vengeance.
Every treatment plan should start with thorough investigations. Your GP can find out if you have Helicobacter Pylori infection in the stomach. Private functional tests can identify small-intestinal bacterial overgrowth or other dysbiotic imbalances and your digestive – eliminative capacity. Food sensitivities should be identified and problematic foods carefully eliminated to allow the immune system to re-boot.
Tailored anti-microbial and probiotic therapy re-balance the bowel flora and the immune system at the same time. Soothing and healing the intestinal membranes and optimizing digestion and elimination are also crucial. These steps lead to enhanced barrier functions and normalize immune reactions. Rosacea is a complex problem; a tailor-made nutrition plan addressing all aspects of the underlying causes is the only solution.
Contact me to find Your ‘root’ to better health!
1, Pizzorno, LU., Pizzorno, Jr JE. & Murray, MT. 2002. Rosacea. Natural Medicine Instructions for Patients. Elsevier Science Ltd. 311-14.
2, Yamasaki, K. & Gallo, R.L. 2011. Rosacea as a Disorder of Innate Immunity. Journal of Investigative Dermatology Symposium Proceedings; 15: 12–15. doi:10.1038/jidsymp.2011.4
3, Kligman AM. & Christensen, MS. 2011. Demodex folliculorum: requirements for understanding its role in human skin disease. J Invest Dermatol 131:8–10. doi:10.1038/jid.2010.335
4, Schauber, J. & Gallo, R. L. 2008. The vitamin D pathway: a new target for control of the skin’s immune response? Experimental Dermatology; 17(8), 633–639. doi: 10.1111/j.1600-0625.2008.00768.x
5, Ekiz, O. et al. 2014. Vitamin D Status in Rosacea Patients. Cutan Ocul Toxicol; 33(1): 60–62. doi:10.3109/15569527.2013.797907
6, Parodi, A. et al. 2008. Small Intestinal Bacterial Overgrowth in Rosacea: Clinical Effectiveness of Its Eradication. Clinical Gastroenterology and Hepatology; 6:759–764. doi:10.1016/j.cgh.2008.02.054
7, Chasapis CT, Loutsidou AC, Spiliopoulou CA & Stefanidou ME. 2012. Zinc and human health: an update. Arch Toxicol.;86(4):521-34. doi: 10.1007/s00204-011-0775-1.
8, Gropper, SC., Smith, JL. & Groff, JL. 2005. Advanced Nutrition and Human Metabolism. Fourth Edition. Wadsworth, Thomson Learning, Inc. 436-46.
9, Zouboulis CC. 2006. Retinoids–which dermatological indications will benefit in the near future? Skin Pharmacol Appl Skin Physiol.;14(5):303-15
10, Scheinfeld N. 2006. Schools of pharmacology: retinoid update. J Drugs Dermatol.;5(9):921-2.