Chapter 10 Managing acne requires teamwork. There are two sides to the story, the patient side and the physician side. Physicians can provide education, instructions, guidance, specialized knowledge, empathy, encouragement, experience, and prescriptions from their side, but much of what needs to be done has to come from the patient side. From the physician’s point of view, it really is pretty simple to write the prescriptions for topicals or oral medications, even isotretinoin (with birth control pills for female patients as appropriate), and stand in a supportive role for four to six months. The patient will get better with no untoward incidents most of the time. The physician is there for emergencies, but the main challenge is explaining the reasons for the therapy being used and how to use it. The problem is that unless the patient looks after his or her side of the story, the acne (no matter which type) will be right back again. The lifestyle choices made by patients dictate the activity of the acnes. In all the acnes, exogenous hormones are the most important thing to reduce or eliminate. This is best achieved by reduction in dairy content and adoption of a low-glycemic-load diet. I consider this approach essentially proven in acne vulgaris. The results are “pending” (the study is partly done but “on hold” due to lack of funds) in acne rosacea. Increasing clinical experience supports the need to respect the zero dairy and low glycemic load diet in acne inversa/hidradenitis suppurativa (AI/HS) as well. The long timeline of AI/HS makes this a difficult disorder to investigate, because doing so in a “blinded trial” is essentially impossible, and one cannot simply discontinue all dairy and wait a year or so for results. Just blowing out the match will not stop the fire. So we need to look at choices. That means an overview of patient lifestyle choices first, then a practical overview and implementation of physicians’ therapeutic choices. Acne is a disorder of the folliculopilosebaceous units (FPSUs), driven by hormones, and those hormones are to a major extent mediated by lifestyle, whether they are produced within our bodies (endogenous) or are provided from the outside (exogenous). Whether from inside or outside, there are two main hormone types, steroids and short proteins called polypeptides. Detailed discussions of each are at Section 4.2.4.1. What follows is a brief reminder. Endogenous hormones include: Exogenous hormones include: Although the arrival of normal puberty is not a lifestyle choice, its premature arrival is increasingly attributed to dietary influences. Although diet is mainly a parental choice in preteens, it is a lifestyle choice nonetheless. In addition, pregnancy is a lifestyle choice, as are stress, the use of oral contraceptives (or not), and the ingestion of the hormones in dairy products. Most require little explanation, but there are some new players on the field. Acne secondary to stress has for decades been considered a response to adrenocorticotropic hormone (ACTH). (See Section 2.10.) Recent studies show that the FPSU sebocytes have a functional CRH receptor system, and this seems likely to be responsive to hypothalamic-sourced CRH [1]. Sugar and other carbohydrate metabolites are intimately involved with insulin, IGF-1, and GH. Acne is associated with the syndrome X complex, which includes insulin resistance, type II diabetes, polycystic ovaries, infertility, obesity, and hyperandrogenemia. Brand-Miller notes, “Increasing obesity and habitual consumption of high-glycemic-load diets worsens insulin resistance and increases the risk of type 2 diabetes in all populations” [2]. Older studies showed that acne improves with insulin-sensitizing drugs such as the biguanide metformin [3], and its use in treating hidradenitis suppurativa shows definite promise [4]. Investigation of the thiazolidinediones to reduce sebum output has been considered [5], but clinical effectiveness has not yet been demonstrated to outweigh the risk of side effects. Meanwhile, low-glycemic-load diets reduce testosterone and fasting glucose levels while increasing sex hormone–binding globulin (SHBG) and improving insulin resistance. Although the relationships are complex, the net effect is a strong dietary influence on acne. Polyunsaturated fatty acids (PUFAs) in Westernized diets tend to include omega-6/omega-3 ratios higher than those in the Paleolithic diet. Dietary manipulation that yields increased omega-3 and lowered omega-6 intake tends to suppress inflammation [6]. Although there is no formal study to show that an increased intake of lean meats will attenuate acne, “consumption of fish was associated with a protective effect” [7]. Oral contraceptives are now available containing progestins that are not only non-androgenic but also androgen blockers. Drospirenone has fewer metabolic side effects than cyproterone acetate, so it is generally favored, but recent concerns about thrombo-embolic events (blood clots) associated with these two progestins have led to a shift toward norgestimate and norelgestromin. These are both less efficient molecules for treating acne but can be supplemented with spironolactone (see Section 10.2). Milk and the many products derived from it are the source of numerous hormones, growth factors, and other chemicals. The list includes over 60 molecules. (See Section 8.3.1.) Why all the growth factors in milk? Milk is designed to make things grow [8]. Milk also contains several important precursors of 5α-dihydrotestosterone (DHT). In addition to progesterone, there are several 5α-reduced compounds including 5α-pregnanedione and 5α-androstanedione [9], each of which is only a few enzymatic steps away from the most powerful acnegen, DHT. Even the simple ingestion of milk invites more acne. There is a fourfold disparity in area under the curve (AUC) comparisons between the rise in serum insulin levels induced by the ingestion of milk when compared to the AUC expected based on milk’s carbohydrate (mainly lactose sugar) content [10]. This reactive hyperinsulinemia opens the androgen receptors and empowers the androgens that drive the increased production of intraductal keratinocytes. These are the cells whose failed terminal differentiation and failed separation from each other lies at the base of the formation of the comedo, and that takes us back to where the story begins. To stop the acnes, it is necessary to start at the beginning. Only by stopping the beginning of the process can we prevent progress to the end of the process. Prevention means no dairy at all during the teen years—and it also usually means limited dairy after the teens. Failure of prevention reflects poor lifestyle choices and means years more acne. This part of the story is up to the patient. Just “going to the doctor” doesn’t do the job. Patients need to follow the rules in this partnership, otherwise, as I occasionally point out, the “my way/your way” rule applies. If you do it my way and it doesn’t work, it may be my fault; I will try something else. If you do it your way and it doesn’t work, it is likely your fault; You get to try another dermatologist.
Putting it all together
10.1 Lifestyle choices and the acnes
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
