I don’t know that sun sensitivity and lack of tanning ability is directly related to Iodine. But I wanted to include this as a topic, because lack of tanning could be related to Tyrosine metabolism as one potential cause. Tyrosine is a basic precursor to melanogenesis, so anything that affects tyrosine metabolism could potentially affect tanning – and TH, of course, is nothing more than tyrosine residues plus iodine attached. But I started suspecting a tyrosine metabolism abnormality was occurring independent of TH for a number of reasons, including this symptom. Hypothyroid people often have a “pasty white” type of skin, and both hyper and hypothyroidism is associated with vitiligo, a skin de-pigmentation condition.
For the first few years after my floxing, I didn’t feel like I had an extreme sun sensitivity. On the other hand, I wasn’t spending my time outside all day in the sun anymore, or even sunning myself much. So in that way, I’m not really sure this didn’t exist. However, one thing I can say, is that I simply no longer tanned, even while I was ON TH meds. On the few occasions I did try to get some sun, my skin remained that “pasty white”, and no amount of sun brought on a tan anymore. In 2013 and 2014 I was bedridden for much of the time, and again didn’t spend much time in the sun at all. I also was NOT on TH during this time, and was flaring for much of these years as my thyroid axis attempted to normalize and reach steady state status. I noticed the few times I tried to tan, I felt like I had developed a “sun sensitivity” – my legs wouldn’t tan, but they would “burn” with increased neuropathy after just 15-20 minutes in the sun, and it felt like my systemic symptoms worsened a bit too afterwards.
I believe that altered or damaged Tyrosine metabolism is a consideration in me post floxing, in addition to Iodine metabolism – or possibly instead of it. When I did my “Iodine trial”, separating out iodine from the protein component of TH (ie, tyrosine), some of my symptoms cleared up remarkably, supporting this hypothesis. There are any number of reasons this may have occurred, with altered or damaged tyrosine metabolism being only one of them. Cell or antibody mediated attacks against specific tyrosyl residues, whether those residues were located in receptors, transporters, enzymes, signal transduction, or phosphorylation targets within DNA itself was another possible mechanism I considered.
The higher my TH (iodinated tyrosine) serum levels were, the worse some of my symptoms were, in particular the dry, gritty eyes which bothered me so. Interestingly enough, taking tyrosine supplements also felt very “drying” to me, drying out my eyes, chest, and everything else more, also supporting the suggestion that tyrosine is playing a role in this. This could be due to cellular or antibody mediated destruction targeting tyrosine or tyrosine related moieties, such as TH, or even tyrosine protein kinases involved in signal transduction processes. Taking NSAID’s helped the autoimmune inflammatory component of my symptoms greatly, which supports this particular hypothesis. The tyrosine supplements also gave me a bit of what I called an “adrenaline” feeling as well. Tyrosine is a precursor of thyroid hormones, the neurotransmitter dopamine, the catecholamines epinephrine and norepinephrine, the tanning pigment melanin, and is needed to synthesize the benzoquinone structure which forms part of coenzyme Q10. The tyrosine metabolism disorder Alkaptonuria is one of the few conditions known to cause spontaneous tendon ruptures later on in life.
There are actually quite a few phototoxicity studies on the effects of FQ’s with melanocytes (the cells that produce melanin and are responsible for tanning and skin color) and tyrosinase (an enzyme required to produce melanin from tyrosine), as well as various other photoxic mechanisms. Melanosomes are organelles found inside cells and are the site for synthesis, storage and transport of melanin. Note that melanosomes are synthesized not only in the melanocytes of the skin, but in both the retinal pigment epithelial cells and choroidal melanocytes of the eyes as well. This might be another mechanism to consider in the potential increased risks of retinal detachments with FQ’s (as of 2016, there appears to be debate on this issue; check “fluoroquinolone retinal detachment” in PubMed). For those interested in published FQ Phototoxicity studies, see my References lists, search in PubMed, or here are a few to get you started: 1, 2, 3, 4.
Of additional interest to me, is that many of my symptoms in general correlated very well with Neural Crest Cell Derivatives, which includes melanocytes (See Wiki Neural Crest Cells, scroll down to “Cell Lineages” and “Neural Crest Derivatives”). I found myself wondering what underlying factors these derivative cells might still have in common in terms of hormones, neurotransmitters, receptors, transporters, enzymes, signal transduction, growth factors, etc., despite their differentiation. Since both TH and Iodine appeared to affect most, if not all of my symptoms, and TH is known to affect differentiation in embryogenesis, perhaps this is a common link.