Abnormal sensitivity to sunlight and bright lights is known as photosensitivity and sometimes referred to as “sun flare” or photophobia. In the context of the MP, the ultimate cause ofphotosensitivity is the Th1 inflammatory disease process – not the treatment itself. Exposure to natural or bright artificial light in a photosensitive person can lead to flares of internal disease activity, including exacerbation of any inflammatory disease symptoms.
Photosensitivity can occur either when the skin is exposed to bright natural light or the eyes are exposed to either natural or artificial light. Photosensitivity symptoms can occur immediately after exposure or begin 1 to 3 days later, sometimes persisting 5 days or more.
Individuals who are photosensitive prior to the MP will likely become more photosensitive on the MP. Individuals who have no signs of photosensitivity may or may not become photosensitive on the MP. Individuals with limited inflammatory symptoms (suggesting early disease) are the most likely to be able to tolerate more light exposure while on the MP. There is no certain way to tell in advance precisely how photosensitive an individual will be while on the MP. Only after an individual has begun treatment can photosensitivity be assessed.
Even though the exact mechanisms by which Th1 disease leads to photosensitivity remains clouded, photosensitivity is well associated with Th1 disease. Examples of photoaggravated diseases include lupus erythematosus, erythema multiforme, atopic eczema, psoriasis, viral exanthemata, pemphigus, dermatitis herpetiformis, rosacea, and multiple sclerosis.1 2 3 Even so, the variety of MP treatable illnesses for which there is a photosensitivity component and the severity of thephotosensitivity reaction is widely underestimated by the majority of clinicians and researchers. This may be due to the time window for an adverse reaction, which is often hours or days after light exposure.
The photosensitivity observed among the MP patient cohort is not due to the medications. It is part of the healing process.
If you see photos of me from the period 1987-1999, a decade before the MP, when I was taking no medication whatsoever, you will see me with those 98% Zeiss glasses, which I had to wear everywhere.
Once you start cutting the vitamin D so that your immune system can start functioning properly again, the photosensitivity sets in, and it will stay for 6-24 months, gradually decreasing as you progress on the MP.
As you recover you will get to the point where you can’t see anything through those dark glasses any more.
Trevor Marshall, PhD
Note that photosensitivity occurs with sufficient frequency that it is listed as an adverse side effect for patients who take at least one form of Benicar, Benicar HCT, a form which contains thiazide, a diuretic which is contraindicated for MP patients. The reason why it is not more common is that people who take Benicar irregularly (by MP standards) have not taken it consistently enough for a full Benicar blockade to be in place.
Some people feel worse when they begin to avoid sun exposure, causing symptoms such as fatigue, dizziness, headache,photosensitivity, irritability, sleep disturbances, and brain fog. It is also common to become more sensitive to natural light after avoiding sun exposure because the resulting fluctuations in the level of 1,25-D can exacerbate symptoms even if the level of 1,25-D is relatively low. Wearing the required sunglasses may relieve symptoms by calming the neurological effects of light, but it can also make it more difficult to tolerate light without the sunglasses.
In individuals with chronic inflammatory diseases, 1,25-D is rapidly synthesized from 7-dehydrocholesterol when sunlight falls on the keratinocytes of the skin. According to the Marshall Pathogenesis, many of the keratinocytes of Th1 patients are parasitized by bacteria, they produce interferon-gamma (which is part of the bacterial defense mechanism) and TNF-alpha. These cytokines cause the cells of patients to produce much more 1,25-D in their skin than their healthy counterparts. Studies show that all 25-D produced in the skin of individuals with Th1 disease from sunlight is hydroxylated directly into 1,25-D, leaving no 25-D to be stored in fatty tissues. In healthy people, however, there will be remnant 25-D generated. Photosensitivity does not seem to be correlated with a patient’s level of 25-D.
…you cannot judge your level of photosensitivity by your level of 25-D. It is far more likely that exposure of the skin to the sun will directly produce 1,25-D in a Th1 patient than 25-D. This is both because of the metabolism, as described in our paper and because an earlier in-vitro study showed just that.
Trevor Marshall, PhD
In patients who get enough natural light on their skin on a regular basis, 1,25-D can elevate high enough to become immunosuppressive and stop bacterial killing. A study of frequent tanners found that the practice has an addictive quality – an effect which, according to the Marshall Pathogenesis, is due to systematic immunosuppression of high levels of 1,25-D.4
However, most MP patients do not get enough regular continuous light exposure on their skin to offset the olmesartan (Benicar) blockade. They can, however, get a surge of natural light exposure that causes an increase in symptoms due to rapid fluctuation of hormones including 1,25-D.
The majority of sunscreens are ineffective in blocking vitamin D production or blocking sun flare symptoms in Th1 patients.
A recent study in mice cast doubt upon the skin as a major producer of 25-D, even though they it was shown that UV exposure on the skin likely does suppress the immune system through multiple pathways.5 It is possible the effect on the body is to cause the catalysis of 25-D systemically, although nobody seems quite sure of that just yet.
I find it hard to continue to cling to the pragma that the skin produces 25-D solely under the influence of UV light. The actual situation is clearly a lot more complex than this, and lines up with some members’ experience that even indirect sunlight can cause them severe discomfort.
So I would caution members against any outdoors exposure which gives disquieting symptoms. Photosensitivity is eventually lost as the immune system recovers. Additionally, some of our members never really experience noticeable problems out-of-doors. Photosensitivityseems to depend on the individual’s microbiota at any point in time.
Trevor Marshall, PhD
The eyes have a complete, self-contained, renin-angiotensin system (RAS) in them. They are connected directly to the brain via the optic nerve. Any type of bright light (artificial or solar) falling on the eyes causes, via the RAS, the production of a small amount of systemic 1,25-D. Whether exposure of a Th1 patient’s eyes to light generates excess quantities of 1,25-D, which then enters the brain or systemic circulation, is not yet well understood.
There is no data on this, and very little we can use to try and guess at the probabilities involved. Even the circulations are somewhat in question at the moment.
It is important for folk who exhibit photosensitivity while they recover their health (which is nearly everybody) to protect their eyes fastidiously. The exact mechanism(s) remain(s) clouded, however.
Trevor Marshall, PhD
The optic nerve directly connects each eye to the brain, possibly the body’s most sensitive organ. Thus, light is transmitted to the brain via the eyes. Coursing through the portion of the brain known as the amygdala are nerves connecting it to a number of important brain centers, including the neocortex and visual cortex. Many types of angiotensin receptors are known to be active in the brain. This can have the profound effect of stimulating portions of the brain to cause significant neurological symptoms.
This stimulation of the brain causes many of the neurological symptoms that are so bothersome to individuals with Th1 inflammation. Neurological symptoms include fatigue, irritability, aggressiveness, lack of concentration, brain fog, loss of memory, poor judgement, confusion, anger (Lyme rage), mood swings, anxiety, inattentiveness, poor problem-solving, fear, neurosis and even psychosis.
Decreasing the light that falls on the eyes will make the brain comparatively stable and symptom-free, thus, it will be easier to deal with the surges in immunopathology which will inevitably occur.
The first test of a patient’s suitability for the MP is typically the therapeutic probe, which includes Benicar, antibiotics, and the restriction of vitamin D, of which light can catalyze the creation. The therapeutic probe offers early insight into any photosensitivityassociated with the disease process, especially sub-clinical inflammation. In deciding how much light to expose themselves to while on a therapeutic probe, patients are advised to work with their physician and to err on the side of caution. Safety should be the primary concern, especially for patients with cardiac, respiratory, and neurological symptoms.
MP patients who expose themselves to light from all sources will soon know if they can tolerate light, and to what degree, based on their symptoms.
There is no typical length of time between natural light exposure and a symptom flare. Some will feel the effects within an hour or two while others may not experience an increase in symptoms for a day or longer. An MP patient’s reaction to light exposure may be delayed. Before beginning the MP and avoiding light, many people do not associate this delayed reaction with their disease symptoms since daily exposure and a consistent elevated 1,25-D can mask the effect of this inflammatory process. Once one diligently begins avoiding all sources of sun and bright light, it is easier to correlate the sun or light exposure with its effect on symptoms when the exposure to sun and bright lights is sporadic.
While rare, it is important to note that some MP patients may be at high risk for an acute adverse event caused by sunlight exposure or because the innate immune system, once activated by the MP, continues to kill the bacteria. All MP patients should report adverse symptoms to their physician and understand how to manage a significant adverse event should it occur. MP patients are encouraged to report regularly on the website in order to get early help managing symptoms. A range of measures is available to dampen intolerable symptoms.
Most of the original clinical experience of the MP research team had been with individuals who were so ill they were unable to work or to tolerate even moderate outdoor activities. Others were sufficiently sick to be motivated to make accommodations in their workplace and home in order to avoid light. When they began the MP, these very symptomatic early-adopters almost always noticed a high level of photosensitivity (which resulted in an emergence of or an increase in neurological symptoms during and/or after exposure to sunlight).
Later, however, re-evaluation of reports from the enlarged MP patient cohort has led the MP research team to conclude that people who are less ill may not experience significant photosensitivity. Generally speaking, patients who are more ill and/or more photosensitive prior to beginning the MP will be more photosensitive while on the treatment. However, immunopathology is highly variable, and as puzzling as this concept may appear to some, a bad reaction to light exposure can be life-threatening.
As MP patients’ vitamin D metabolism is “reset,” their sensitivity to light diminishes. This will be a gradual process. Later on in the Protocol, MP patients should be able to handle “normal” amounts of sunlight because, in the short period between maintenance doses of antibiotics, they will maintain low bacteria loads.
Photosensitivity is just that, photosensitivity, and it will gradually disappear with time. You need to keep an eye on your general immunopathology and make sure you are progressing on-track to recovery, but otherwise, when you can enjoy the outdoors again, it is a good idea to do so. A little at a time.
As one progresses through Phase 2, the risk of setback from occasional exposures becomes less and less. Eventually the risk disappears (although you will probably never want to sunbathe again). The only way to find out is to try a few “baby-steps” and see. I usually say it takes 18-24 months to get back to any sort of “normal” sensitivities, though.
Trevor Marshall, PhD
In the case of immunopathology – which is generated during the MP and a key part of the recovery process – inflammation from intracellular bacteria affects many areas of the brain, making it difficult to differentiate between neurological symptoms from light stimulation and from immunopathology. Dr. Brian Fallon’s study on Lyme found from SPECT data that the main metabolic changes in the brain were in the region of the parahippocampal gyrus.6 This area is responsible for receiving sensory input from the outside world, integrating it, and projecting it onto the hippocampus, which controls memory, and the amygdala, which is in charge of fear, aggression, and mood. Negative symptoms associated with memory, fear, aggression, and mood can certainly be exacerbated by light.
There are two different and independent phenomena, which occur when one is on the MP, both of which are correlated with a temporary rapid rise in 1,25-D: photosensitivity symptoms and immunopathology. Differentiating between immunopathology andphotosensitivity symptoms is very important as the former is necessary for progress on the treatment and the latter is not.
Exposure of skin (and perhaps the eyes also, as discussed above) to light does not result in immunopathology. It causes 1,25-D to go up. The rise in 1,25-D causes symptoms of hypervitaminosis-D. This may feel like immunopathology but it is a flare in disease symptoms and a hormonal shift due to elevated 1,25-D, not the result of the immune system killing bacteria. A sun flare would be similar to pre-MP inflammation.
The increase in 1,25-D due to sun exposure will increase inflammation everywhere and may not be perceived as photosensitivity but will be evident as any type of symptom, including even worsening lab test results.