Kava Ichthyosis
Today’s fact of the day will be revisiting another topic covered previously, and that topic is the skin effects we see commonly known as “kava dermopathy”. The previous fact comes from data prior to 2013, and there has been further research regarding it since.
Several mechanisms have been proposed for the cause of kava dermopathy.
Niacin deficiency has been tested and ruled OUT as a cause (Ruze 1990). In the paper we’re referencing today, the researchers are connecting kava skin effects to the known properties of kava to inhibit certain human CYP450 enzymes.
It was noticed that the condition Lamellar Ichthyosis (pronounced “ik-thee-ow-suhs”) was quite similar to the condition seen in daily kava drinkers. Normally this condition is found expressed as a rare recessive genetic skin disorder present at birth. It is one of three skin disorders called “Autosomal Recessive Congenital Ichthyoses”. The genes involved with this condition provide the instructions to make enzymes and proteins for the normal development, function, and shedding of skin cells (“Lamellar Ichthyosis - NORD (national Organization for Rare Disorders)” 2015).
Kava is a known inhibitor of CYP450 enzymes including but not limited to CYP4A11, and CYP2C9 (Nelson et al. 2004). The 2C9 enzyme is structurally similar to one that is intimately involved with Ichthyosis Type 3. This CYP pathway is linked to this syndrome due to the observation that multiple medications have been seen to induce this type of acquired ichthyosis and they are, like kava, metabolized by the CYP450 enzymes. These researchers ultimately suggest that “Kava dermopathy” should be renamed to “Kava Ichthyosis” (Hannam et al. 2014).
Summary: Kava skin effects are being researched, and we’re beginning to see that kava’s ability to inhibit certain enzymatic pathways in the body may be one of the causes for what we now know as “kava ichthyosis”. It does this through suppression of CYP4F22, which plays an essential role in skin hydration among other vital skin effects.
Hannam, Sarah, Michael Murray, Lucia Romani, Meciusela Tuicakau, and Margot J Whitfeld. 2014. “Kava Dermopathy in Fiji: An Acquired Ichthyosis?” International Journal of Dermatology 53 (12): 1490–94.
https://doi.org/10.1111/ijd.12546.
“Lamellar Ichthyosis - NORD (national Organization for Rare Disorders).” 2015. February 11, 2015.
https://rarediseases.org/rare-diseases/ichthyosis-lamellar/.
Nelson, David R., Darryl C. Zeldin, Susan M. G. Hoffman, Lois J. Maltais, Hester M. Wain, and Daniel W. Nebert. 2004. “Comparison of Cytochrome P450 (CYP) Genes from the Mouse and Human Genomes, Including Nomenclature Recommendations for Genes, Pseudogenes and Alternative-Splice Variants.” Pharmacogenetics 14 (1): 1–18.
https://doi.org/10.1097/00008571-200401000-00001.
Ruze, P. 1990. “Kava-Induced Dermopathy: A Niacin Deficiency?” The Lancet 335 (8703): 1442–45.
https://doi.org/10.1016/0140-6736(90)91458-m.
Today’s fact of the day will be revisiting another topic covered previously, and that topic is the skin effects we see commonly known as “kava dermopathy”. The previous fact comes from data prior to 2013, and there has been further research regarding it since.
Several mechanisms have been proposed for the cause of kava dermopathy.
- Interference with cholesterol metabolism.
- The presence of an alpha-methylene-butyrolactone group which enables lactones to attach to skin proteins and forming antigens which eventually lead to a state of allergy.
- Reduction in glandular secretions.
- Accumulation of plant flavopigments or kavalactones.
- Chronic allergic dermatitis.
- A pellagra-like dermatitis.
- Dehydration.
- Niacin deficiency.
- Mast Cell Activation
Niacin deficiency has been tested and ruled OUT as a cause (Ruze 1990). In the paper we’re referencing today, the researchers are connecting kava skin effects to the known properties of kava to inhibit certain human CYP450 enzymes.
It was noticed that the condition Lamellar Ichthyosis (pronounced “ik-thee-ow-suhs”) was quite similar to the condition seen in daily kava drinkers. Normally this condition is found expressed as a rare recessive genetic skin disorder present at birth. It is one of three skin disorders called “Autosomal Recessive Congenital Ichthyoses”. The genes involved with this condition provide the instructions to make enzymes and proteins for the normal development, function, and shedding of skin cells (“Lamellar Ichthyosis - NORD (national Organization for Rare Disorders)” 2015).
Kava is a known inhibitor of CYP450 enzymes including but not limited to CYP4A11, and CYP2C9 (Nelson et al. 2004). The 2C9 enzyme is structurally similar to one that is intimately involved with Ichthyosis Type 3. This CYP pathway is linked to this syndrome due to the observation that multiple medications have been seen to induce this type of acquired ichthyosis and they are, like kava, metabolized by the CYP450 enzymes. These researchers ultimately suggest that “Kava dermopathy” should be renamed to “Kava Ichthyosis” (Hannam et al. 2014).
Summary: Kava skin effects are being researched, and we’re beginning to see that kava’s ability to inhibit certain enzymatic pathways in the body may be one of the causes for what we now know as “kava ichthyosis”. It does this through suppression of CYP4F22, which plays an essential role in skin hydration among other vital skin effects.
Hannam, Sarah, Michael Murray, Lucia Romani, Meciusela Tuicakau, and Margot J Whitfeld. 2014. “Kava Dermopathy in Fiji: An Acquired Ichthyosis?” International Journal of Dermatology 53 (12): 1490–94.
https://doi.org/10.1111/ijd.12546.
“Lamellar Ichthyosis - NORD (national Organization for Rare Disorders).” 2015. February 11, 2015.
https://rarediseases.org/rare-diseases/ichthyosis-lamellar/.
Nelson, David R., Darryl C. Zeldin, Susan M. G. Hoffman, Lois J. Maltais, Hester M. Wain, and Daniel W. Nebert. 2004. “Comparison of Cytochrome P450 (CYP) Genes from the Mouse and Human Genomes, Including Nomenclature Recommendations for Genes, Pseudogenes and Alternative-Splice Variants.” Pharmacogenetics 14 (1): 1–18.
https://doi.org/10.1097/00008571-200401000-00001.
Ruze, P. 1990. “Kava-Induced Dermopathy: A Niacin Deficiency?” The Lancet 335 (8703): 1442–45.
https://doi.org/10.1016/0140-6736(90)91458-m.
