Chickens, toads, and gluten sensitivity

Keratosis pilarisBy: Laurie Laforest
Keratosis pilaris is one of the many symptoms attributed to non-celiac gluten sensitivity in alternative medicine circles.  Keratosis pilaris – or “chicken skin” – is a benign skin condition reminiscent of permanent goose bumps.  I first heard the term keratosis pilaris on a episode of The Dr. Oz Show about gluten sensitivity [1], the premise being that keratosis pilaris results from fat malabsorption caused by gluten-induced intestinal damage.  Since my family and I have little patches of this on our elbows and knees, I was eager to learn what was really behind it.
It turns out that the link between “chicken skin” and gluten sensitivity is one of mistaken identity.  Keratosis pilaris is a type of follicular hyperkeratosis where excess keratin – a key protein in our outer layer of skin and in our hair and nails – plugs the hair follicule, sometimes trapping a small hair inside. [2]  Enlargement of the follicule and the presence of the hard keratin plug produces the characteristic rough and bumpy appearance; reddening may also occur.  Keratosis pilaris is quite common – it affects around 50% adolescents (80% of females) and 40% of adults – and seems to have a strong hereditary component. [3]
Phrynoderma – or “toad skin” – is another type of follicular hyperkeratosis that is typically related to malnutrition in developing nations.  Phrynoderma is what alternative medicine folks are actually thinking of (or they should be) when they speak about a diet-related bumpy skin problem.  The exact nutrient deficiency behind phrynoderma is not known, but the condition can be reversed by supplementation with essential fatty acids, vitamin A, vitamin E, or B-complex vitamins; different people seem to respond to different nutrients. [4-7]
So “chicken skin” (keratosis pilaris) is common and benign, while “toad skin” (phrynoderma) is uncommon in the developed world and a sign of a serious problem.  But could it still be possible that gluten sensitivity is at the heart of these conditions?  Most likely not.  Keratosis pilaris is not related to diet, although it does seem to occur more often in people with a high body mass index. [8,9]  Hormones could also play a role, since keratosis pilaris is more common during adolescence.  Still, keratosis pilaris can come and go throughout adulthood and may worsen during the drier winter months.
Even for phrynoderma, the gluten connection doesn’t pan out.  Let’s first consider celiac disease, an autoimmune reaction triggered by gluten that damages the small intestine.  Celiac disease is the worst-case scenario when it comes to gluten sensitivity – fat malabsorption is a classic symptom of untreated celiac disease, and there is a risk that celiac sufferers could be deficient in fat-soluble vitamins like A, D, and E.  But even though it might seem like celiac disease could produce the kind of malnutrition that leads to phrynoderma, phrynoderma is not one of the skin conditions seen alongside celiac disease [10], and fat-soluble vitamin deficiencies are also not found in newly-diagnosed celiac patients as often as one is led to believe on TV [11-13].  Now consider that non-celiac gluten sensitivity is not supposed to involve the characteristic intestinal damage (and, hence, the potential vitamin deficiencies) found in celiac disease [14,15], and you have no reason for the average person to suspect that their rough skin is related to gluten.
If you do have “chicken skin” or other roughening or reddening of the skin, it is best to talk to a dermatologist to properly identify your skin condition or to your doctor if you do suspect that you have celiac disease.  Most people with keratosis pilaris don’t even realize that they have it, but others may be plagued by large, unsightly patches of skin.  Mild cases can be improved by over-the-counter moisturizers; more severe cases can be treated by medicated creams that soften keratin and help remove the outer layer of skin.  Even though there is an abundance of advice on treating keratosis pilaris on the Internet, ask a doctor or pharmacist to direct you to the right products to use.
<a rel=”author” href=”https://plus.google.com/108035110292301860932″>Laurie Laforest</a> – <a href=”http://foodconnections.org/”>foodconnections.org</a>
References
1. The 5 Hidden Signs You Have a Gluten Allergy [Internet]. The Dr. Oz Show. 2014 [cited 2014 Nov 14]. Available from: http://www.doctoroz.com/episode/5-hidden-signs-you-have-gluten-allergy
2. Hwang S, Schwartz RA. Keratosis pilaris: A common follicular hyperkeratosis. Cutis. 2008;82(3):177–80.
3. Alai AN, Elston DM. Keratosis Pilaris Treatment & Management [Internet]. Medscape. [cited 2014 Jun 12]. Available from: http://emedicine.medscape.com/article/1070651-overview
4. Ragunatha S, Kumar VJ, Murugesh SB. A Clinical Study of 125 Patients with Phrynoderma. Indian J Dermatol. 2011;56(4):389–92.
5. Bagchi K, Halder K, Chowdhury SR. The etiology of phrynoderma; histologic evidence. Am J Clin Nutr. 1959 Jun;7(3):251–8.
6. Nadiger HA. Role of vitamin E in the aetiology of phrynoderma (follicular hyperkeratosis) and its interrelationship with B-complex vitamins. Br J Nutr. 1980 Nov;44(3):211–4.
7. Therapeutic Response of Vitamin A, Vitamin B Complex, Essential Fatty Acids and Vitamin E in the Treatment of Phrynoderma: A Randomized Controlled Study. Journal of Clinical and Diagnostic Research. 2014;8(1):116–8.
8. Yosipovitch G, Mevorah B, Mashiach J, Chan YH, David M. High body mass index, dry scaly leg skin and atopic conditions are highly associated with keratosis pilaris. Dermatology (Basel). 2000;201(1):34–6.
9. Yosipovitch G, Hodak E, Vardi P, Shraga I, Karp M, Sprecher E, et al. The prevalence of cutaneous manifestations in IDDM patients and their association with diabetes risk factors and microvascular complications. Diabetes care. 1998;21(4):506–9.
10. Caproni M, Bonciolini V, D’Errico A, Antiga E, Fabbri P. Celiac Disease and Dermatologic Manifestations: Many Skin Clue to Unfold Gluten-Sensitive Enteropathy. Gastroenterology Research and Practice. 2012;2012:1–12.
11. Imam MH, Ghazzawi Y, Murray JA, Absah I. Is it Necessary to Assess for Fat Soluble Vitamin Deficiencies in Pediatric Patients With Newly Diagnosed Celiac Disease?: Journal of Pediatric Gastroenterology and Nutrition. 2014 Mar;1.
12. Villanueva J, Maranda L, Nwosu BU. Is vitamin D deficiency a feature of pediatric celiac disease? J Pediatr Endocrinol Metab. 2012;25(5-6):607–10.
13. Wierdsma NJ, van Bokhorst-de van der Schueren MAE, Berkenpas M, Mulder CJJ, van Bodegraven AA. Vitamin and Mineral Deficiencies Are Highly Prevalent in Newly Diagnosed Celiac Disease Patients. Nutrients. 2013 Sep 30;5(10):3975–92.
14. Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH, Hadjivassiliou M, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC medicine. 2012;10(1):13.
15. Sapone A, Lammers KM, Casolaro V, Cammarota M, Giuliano MT, De Rosa M, et al. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011 Mar 9;9:23.

Opioid peptides: the heroin within?

Screen Shot 2014-11-07 at 10.36.51 PMBy: Emily Brown PhD

If you were to hear the words ‘opioid peptides’, they might not trigger much within your brain, other than that the former sounds a bit like opium and together they sound quite scientific. Opium (also known as poppy tears) is a dried substance or latex that originates, as the alternative name suggests, from the opium poppy. Beautifully intricate pipes of bamboo, ivory, silver, jade and porcelain have been carved over the centuries and used to vaporise and inhale the latex traditionally obtained by scratching immature poppy seed pods by hand. Numerous Empires including the Egyptian, Greek, Roman, Persian and Arab made widespread use of the drug, which was then the most potent form of pain relief available. This analgesic property is conferred by morphine, which constitutes approximately twelve per cent of opium and is chemically processed to produce heroin. Commonly known by the street names H, smack, horse and brown, among others, the effects of heroin will be well known by any ‘Trainspotting’ fans. What writer Irvine Welsh did not reveal, however, is that opiates such as heroin mimic the effects of naturally occurring molecules that can be generated inside our own bodies.

Opioid peptides are small molecules that are produced in the central nervous system (the brain and spinal cord) and in various glands throughout the body such as the pituitary and adrenal glands. These peptides can be divided into three categories (enkephalins, endorphins, and dynorphins), depending on the type of larger precursor molecule from which they are derived. Opioid peptides function both as hormones and as neuromodulators; the former are secreted in the blood system by glands and are delivered to a variety of target tissues where they induce a response, while the later are produced and secreted by nerve cells (or neurons) and act in the central nervous system to modulate the actions of other neurotransmitters.

Neurons are electrically excitable cells that process and transmit information through electrical and chemical signals that travel via synapses, specialised connections with other cells. These signals are transmitted across a synapse from one neuron to another by neurotransmitters. By altering the electrical properties of their target neurons and making them difficult to excite, opioid peptides can influence the release of various neurotransmitters.

Through these two different mechanisms, opioid peptides can produce many effects including pain relief, euphoria and altered behaviour such as food and alcohol consumption. The apparent connection between exercise and happiness has been explained at least somewhat by the release of endorphins, for example. Exercise is commonly recommended as a strategy for stress-relief and mood improvement, but less widely accepted forms of therapy might also be connected to opioid peptides. Evidence suggests that pain relief induced by acupuncture results from stimulation of opioid peptides – these peptides act through receptors on their target neurons, and chemicals that inhibit opioid receptor function have been found to reverse acupuncture-induced analgesia. Painful, stressful or traumatic events or stimuli can induce the release of opioid peptides, with the resulting euphoria and pain relief making the sufferer less sensitive to noxious events. Opioid peptides have been reported to affect the release of specific neurotransmitters such as dopamine and serotonin, but the response of the neurons that receive opioid-peptide stimulation depends on their excitatory versus inhibitory nature, making the outcome difficult to predict.

The words ‘opioid peptides’ may not have left a dazzling feeling of recognition within your memory upon first encounter, but these peptides act within the brain and wider body to influence a number of important functions. Although it is not easy to predict the effect of neuromodulators that alter the release of other neurotransmitters, there is little question that opioid systems play a critical role in modulating a large number of sensory, motivational, emotional and cognitive functions. Alterations in opioid peptide systems may contribute to a variety of clinical conditions, including alcoholism, obesity, depression, diabetes and epilepsy. Many questions still remain, particularly those concerning the exact role of opioid peptides produced within the body in relation to addictive and emotional behaviour and psychiatric disorders. Since these disorders are typically of a complex nature, seeking the answers to these questions is not a simple feat. Advances in genetics and genomics research that aim to explain function by studying our DNA are helping to pave the way. But perhaps if there is one thing that can help motivate our talented scientists to reach their challenging goals, a healthy dose of opioid peptide might be just the thing.

Emily Brown PhD

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