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From the Townsend Letter
February / March 2019

Lichen Sclerosus – A Roadmap to Treatment Beyond Steroids
by Sara Wood, ND
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Since her husband passed away six years ago and she wasn't dating, Sheila hadn't given much thought to her vulva until her gynecologist mentioned, during a routine exam, that her lichen sclerosus had progressed and her clitoral hood was starting to fuse. She didn't even remember being told that she had lichen sclerosus, but apparently it was in her chart, observed and "diagnosed" years prior. Sheila was alarmed, though her clitoris had been admittedly underused over the past few years, she certainly didn't want it sealed away! Her doctor told her that the diagnosis may not have been emphasized to her at the time it was originally observed because she wasn't experiencing any symptoms. Bewildered and confused, Sheila returned home to process this new information and to do some research, and she found that she wasn't alone. Online forums were filled with stories like hers, or worse. Many women who were symptomatic, experiencing severe itching or pain, who were still undertreated or told that there wasn't much that could be done. Those that were treated were primarily given steroid creams of varying strengths that sometimes helped, but often they weren't advised on a long-term management strategy. Reasons for this shortcoming in treatment are multifaceted but include the sensitive nature of the subject and the counseling required to fully address it. Unfortunately, many physicians don't have the luxury of time required to discuss the emotional impact of labial fusion, let alone the time needed to discuss underlying causes and possible lifestyle changes.

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It's not a household word, but lichen sclerosus isn't exactly rare; one study found a prevalence of 1.7% in a general gynecology practice,1 although many women have never heard of it until they read it on a pathology report or their doctor prescribes them a steroid cream. For some, like Sheila, the symptoms are mild or even absent and the condition is discovered upon routine exam; for others, itching or pain with sex are what lead them to investigate the problem. Since tissue changes can lead to labial fusion, narrowing of the vaginal opening and even carcinoma (in approximately 3% of cases), even the mildest of cases should be treated and monitored.
Lichen sclerosus (LS) is a chronic inflammatory disease that may initially manifest as white patches on the skin. The tissue becomes fragile and itchy; and because LS is most commonly found on genital tissues, pain with sex is a frequent presenting complaint. LS occurs in women approximately 10 times more often than men and is most common during phases of life with relatively low reproductive hormones (pre-pubertal and post-menopausal).2 Since men make up such a small percentage of LS patients, they are often overlooked in the conversation, although the same general therapies are used for both sexes with the exception of circumcision, which is often an effective treatment in uncircumcised men.3
A diagnosis of lichen sclerosus typically requires a biopsy of the tissue, and the steroid creams that are the standard of care are effective at slowing tissue damage. Unfortunately, many treatment plans stop there, using a combination of different strength steroids to halt the progression of the disease. An important part in truly treating any condition is trying to understand what causes it; and while the definitive etiology of lichen sclerosus isn't known, there is increasing evidence of an autoimmune component. Restoration of hormones, repletion of important nutrients, elimination of inflammatory foods as well as mechanical or chemical irritation and employment of immune modulating agents can have a significant impact. Beyond that, there are new studies on injection treatments that are proving to be very effective for some patients.

BDNF EssentialsWhat Is Autoimmunity?
The immune system is an invaluable component to health, as it identifies and targets infectious organisms including bacteria, viruses, and fungi as well as eradicates random mutations in our own tissues that may lead to malignancy. This is happening behind the scenes, all the time, in every tissue in the body. But occasionally something goes wrong and the immune system targets tissue that is not foreign and is otherwise perfectly healthy. Like friendly fire, the body incorrectly attacks itself for reasons that are largely unknown, although evidence is mounting that one of the initial triggers may be gut dysfunction.4 There are approximately 80 identified autoimmune diseases, some of which are diagnosed with a specific test for an antibody to a target tissue. Others are thought to be autoimmune but do not have an identified "marker." Lichen sclerosus generally falls into this latter category, and there is a high rate of comorbidity with LS and autoimmunity; between 20 and 30% of women with LS have also been diagnosed with another autoimmune disease,5,6 autoimmune thyroiditis is the most common.7 When it comes to long-term treatment of lichen sclerosus, there are many effective ways of addressing underlying immune dysfunction that are often overlooked and can have a profound effect on symptoms as well as the overall progression of the disease.

There is a clear pattern to the demographic of lichen sclerosus patients: women who have low circulating levels of reproductive hormones are more likely to be affected.8 When discussing changing hormone levels in peri and postmenopausal women, estrogen is invariably the first name to come to mind, and a low estrogen state does exacerbate almost all vulvovaginal disorders. Additionally, we know that estrogen helps to modulate the inflammatory response and cytokine expression,9 as well as work to counteract the tissue thinning caused by the primary treatment with topical steroids.10 For these reasons, topical estrogen creams are often prescribed to LS patients, although the literature actually better supports the use of testosterone. It has been observed that lichen sclerosus patients have decreased serum testosterone levels,11 and treatment with topical testosterone is nearly as effective as clobetasol (a high potency steroid) in both establishing remission, and to prevent reoccurrence.12
Sex hormones are only part of the picture. As stated above, there is a close connection between hypothyroidism and LS, and stress hormones have a significant impact as well. Thyroid hormone levels should be evaluated in all patients who have received a diagnosis of lichen sclerosus, or any other autoimmune disease for that matter, as thyroid hormones have a bidirectional relationship with the immune system and can serve as a modulator of immune function and inflammatory processes.13 Repletion of thyroid hormones, if deficient, may play a key role in improving general immune function.
Stress hormones, including cortisol, also have a very direct impact on inflammation and immune processes. Chronic stress has been implicated in increasing the risk of autoimmune disease.14 While cortisol is ordinarily a potent anti-inflammatory agent in the body, chronic overproduction of the hormone can lead to resistance in the immune system and result in an increase in inflammatory markers.15 Furthermore, continued chronic stress can lead to a general state of hypocortisolism through a number of mechanisms, further disrupting control over immune function.16 As with many conditions, the symptoms and treatment of lichen sclerosus itself greatly contribute to chronic stress on top of any additional stressors the patient may be experiencing. Modulating and managing stress is a very complex and difficult task for many people, although it is important to note that the perception of stress is key in its power. Recurring negative thoughts, perseveration, and feelings of helplessness are maladaptive responses that may exaggerate the stress hormones effects on immune tissues.17 In additionally to the emotional or psychological input, physical stressors including genital piercings, sexual trauma, chronic mechanical irritation from tight clothing or ongoing chemical irritation from compounds found in soaps or detergents can lead to inflammation and tissue changes.18 The development of inflammatory tissue changes following trauma or irritation is often referred to as the Koebner phenomenon.19

Diet and Nutrients
While tissue biopsy for diagnosis, laboratory testing to identify hormone deficiency, and prescriptions for steroids, thyroid medication or testosterone require a physician, there are many things that any patient with a diagnosis of lichen sclerosus can do on their own that can greatly improve symptoms. Just the act of taking control can be empowering and reduce some of the negative impact of stress hormones,20 adding additional benefit.
There are few published studies on the influence of diet on lichen sclerosus specifically; however there is an abundance of empirical evidence that supports this approach in autoimmunity in general and we can extrapolate data from studies done on other autoimmune diseases that illustrate the anti-inflammatory benefits of certain foods21 and the role that foods play in triggering a leaky gut and subsequent immune dysfunction.22 When it comes to diet changes, there are several approaches that may be worthwhile for LS patients including the avoidance of individual food sensitivities that are identified through testing and the broader elimination/challenge of foods that have been implicated in compromising intestinal barrier function and stimulating inflammation. The autoimmune paleo diet (AIP) is a modified version of a pre-agricultural diet that promotes gut healing and eliminates inflammatory foods including grains (both gluten and non-gluten containing), dairy, sugar, alcohol, legumes, nuts and seeds, nightshade vegetables, eggs and processed oils.23 While some patients need to be extremely restrictive, others may see significant benefit by eliminating just one or two of the greatest offenders. When inflammatory foods are removed, chronic immune stimulation is reduced which leads to an improvement in symptoms. The gold standard for identification of which foods may be of individual concern is an elimination period followed by provocation. The elimination period should be done for at least 30 days, although in many cases will be done for up to a year. Foods are then re-introduced in a systematic fashion, which enables the patient to identify what the biggest culprits are.

Compromised intestinal function doesn't just lead to immune stimulation directly but can also affect absorption of essential nutrients, which in turn can further disturb immune function. Even in people without autoimmune disease, insufficient levels of vitamin D are remarkably common due to inadequate sun exposure, lack of vitamin D-rich foods and malabsorption. Low serum vitamin D levels have been linked to several autoimmune diseases24-27 as vitamin D plays an important role in establishing and maintaining self-tolerance by stimulating T-regulatory cells. These important immune cells (as their name suggests) work to regulate the immune system, neither stimulating or suppressing it. Recommended dosing of vitamin D varies tremendously. The recommended daily allowance (RDA) is relatively low and was generally established to prevent osteomalacia, a bone density disease that results from frank vitamin D deficiency.28 Supplemental dosages are frequently 3-10 times the RDA and many patients are prescribed large bolus weekly doses. Regardless of how it is supplemented, target serum levels should be 75 nmol/l (30 ng/ml)29 at a minimum and potentially twice that for autoimmune patients.

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