How To Tell if You Have “Cortisol Face” And What to Do About It

If you have been anywhere near wellness content lately, you have encountered cortisol face or “moon face”.

Posts claim that stress is literally reshaping people’s faces. The coverage tends to split into two camps: content that oversells the trend or content that dismisses it entirely. The more useful truth sits in the middle.

Cortisol face is not a medical term, but the facial feature it describes is real.

Endocrinologists at Ohio State University’s Wexner Medical Center clarify that what it points to has been documented in medicine as moon facies, caused by fat accumulation and soft tissue swelling. Moon facies is the clinical term. Cortisol face is the social media translation. They describe the same phenomenon but carry very different implications for how concerned you should be.

When the body produces too much cortisol it can cause Cushing’s syndrome, a hormonal disorder whose symptoms include weight gain, inflammation and facial rounding, per the Cleveland Clinic. That is what people online are calling cortisol face or moon face. Cushing’s syndrome affects about 40 to 70 people per million according to the NIH, and its symptoms extend well beyond a round face to include skin that bruises easily, a puffy neck and a worsening upper-back hump.

Can Everyday Stress Change Your Face?

UCI Health endocrinologist Dr. Mehboob Hussain says everyday life stressors are unlikely to be the cause of facial puffiness. More common culprits include a high-salt diet, eczema, allergies and sleep position.

That said, chronically elevated cortisol from sustained stress, poor sleep or overexercising does produce real effects. It increases sodium retention, causes the body to hold water in soft tissues including the face, and shifts fat distribution toward the face and midsection. A

board-certified endocrinologist at Trinity Health confirms that inappropriately elevated cortisol over a long period can cause more rounding and weight gain in the face and abdomen. There is a wide gap between that and a hectic week at work.

What to Watch For

University of Colorado endocrinologists recommend looking for multiple symptoms together. Signs worth bringing to a doctor include persistent facial rounding developing over weeks or months alongside weight gain in the abdomen, thin arms and legs, purple stretch marks, increased acne or facial hair in women, easy bruising or muscle weakness.

Texas A&M’s Dr. Maria Olenick offers a practical rule: true moon face does not just appear or disappear from one day to the next. Temporary morning puffiness, swelling after a salty meal or a rounder face with no other symptoms are probably not cause for concern. One additional flag: long-term corticosteroid medications like prednisone are the most common non-tumor cause of clinical moon face, so mention any facial changes to your doctor if you are on these.

What Actually Lowers Cortisol

Sleep is the most evidence-supported starting point. Chronic sleep issues are directly associated with higher cortisol levels per Healthline.

A meta-analysis of 58 randomized controlled trials found mindfulness and relaxation interventions were the most effective approaches for measurably reducing cortisol.

Moderate exercise helps, but high-intensity overtraining can raise cortisol further, worth knowing if punishing workouts are already part of a stressed routine.

OSF HealthCare notes that magnesium-rich foods including leafy greens, avocados and dark chocolate support cortisol balance, while refined sugars can spike blood sugar and trigger further release. Walking in natural settings has measurably reduced salivary cortisol in peer-reviewed research.

Alcohol and caffeine both raise cortisol and are worth pulling back when symptoms are present. When to See a Doctor If facial changes are persistent, cluster with other symptoms or have not responded to lifestyle changes over several weeks, get evaluated.

UCI Health notes that blood, urine and saliva cortisol tests are available, and a primary care provider can handle initial testing before referring to an endocrinologist if needed.

The biology behind cortisol face is real. A rough week probably is not causing it. But if changes persist and stack up alongside other symptoms, it is worth taking seriously.

This article was created by content specialists using various tools, including AI.

Read more at: https://www.miamiherald.com/living/article315266634.html#storylink=cpy

 

Osilodrostat maintained cortisol control in Cushing’s syndrome

Osilodrostat, a drug that normalized cortisol in 89% of patients with Cushing’s syndrome who took it during a phase II study, continued to exert a sustained benefit during a 31-month extension phase.

In an intent-to-treat analysis, all of the 16 patients who entered the LINC-2 extension study responded well to the medication, with no lapse in cortisol control, Rosario Pivonello, MD, said at the annual meeting of the Endocrine Society.

“We also saw significant improvements in systolic and diastolic blood pressure and decreases in fasting plasma glucose,” said Dr. Pivonello of the University of Naples Federico II, Italy. “Surprisingly, after 31 months, we also observed declines in body mass index and weight.”

Osilodrostat, made by Novartis, is an oral inhibitor of 11 beta–hydroxylase. The enzyme catalyzes the last step of cortisol synthesis in the adrenal cortex. The drug was granted orphan status in 2014 by the European Medicines Agency.

In the LINC-2 study, 19 patients took osilodrostat at an initial dose of either 4 mg/day or 10 mg/day, if baseline urinary-free cortisol exceeded three times the upper normal limit. The dose was escalated every 2 weeks to up to 60 mg/day, until cortisol levels were at or below the upper limit of normal. In this study, the main efficacy endpoint was normalization of cortisol, or at least a 50% decrease from baseline at weeks 10 and 22.

Overall response was 89%. Osilodrostat treatment reduced urinary-free cortisol in all patients, and 79% had normal cortisol levels at week 22. The most common adverse events were asthenia, adrenal insufficiency, diarrhea, fatigue, headache, nausea, and acne. New or worsening hirsutism and/or acne were reported among four female patients, all of whom had increased testosterone levels.

The LINC-2 extension study enrolled 16 patients from the phase II cohort, all of whom had responded to the medication. They were allowed to continue on their existing effective dose through the 31-month period.

Dr. Pivonello presented response curves that tracked cortisol levels from treatment initiation in the LINC-2 study. The median baseline cortisol level was about 1,500 nmol per 24 hours. By the fourth week of treatment, this had normalized in all of the patients who entered the extension phase. The response curve showed continued, stable cortisol suppression throughout the entire 31-month period.

Four patients dropped out during the course of the study. Dr. Pivonello didn’t discuss the reasons for these dropouts. He did break down the results by response, imputing the missing data from these four patients. In this analysis, the majority (87.5%) were fully controlled, with urinary-free cortisol in the normal range. The remainder were partially controlled, experiencing at least a 50% decrease in cortisol from their baseline levels. These responses were stable, with no patient experiencing loss of control over the follow-up period.

The 12 remaining patients are still taking the medication, and they experienced other clinical improvements as well. Systolic blood pressure decreased by a mean of 2.2% (from 130 mm Hg to 127 mm Hg). Diastolic blood pressure also improved, by 6% (from 85 mm Hg to 80 mm Hg).

Fasting plasma glucose dropped from a mean of 89 mg/dL to 82 mg/dL. Weight decreased from a mean of 84 kg to 74 kg, with a corresponding decrease in body mass index, from 29.6 kg/m2 to 26.2 kg/m2.

Serum aldosterone decreased along with cortisol, dropping from a mean of 168 pmol/L to just 19 pmol/L. Adrenocorticotropic hormone increased, as did 11-deoxycortisol, 11-deoxycorticosterone, and testosterone.

Pituitary tumor size was measured in six patients. It increased in three and decreased in three. Dr. Pivonello didn’t discuss why this might have occurred.

The most common adverse events were asthenia, adrenal insufficiency, diarrhea, fatigue, headache, nausea, and acne. These moderated over time in both number and severity.

However, there were eight serious adverse events among three patients, including prolonged Q-T interval on electrocardiogram, food poisoning, gastroenteritis, headache, noncardiac chest pain, symptoms related to pituitary tumor (two patients), and uncontrolled Cushing’s syndrome.

Two patients experienced hypokalemia. Six experienced mild events related to hypocortisolism.

Novartis is pursuing the drug with two placebo-controlled phase III studies (LINC-3 and LINC-4), Dr. Pivonello said. An additional phase II study is being conducted in Japan.

Dr. Pivonello has received consulting fees and honoraria from Novartis, which sponsored the study.

Rare Nasal Cancer May Have Caused Cushing’s Syndrome

A very rare case of Cushing’s syndrome developing as a result of a large and also rare cancer of the nasal sinuses gives insights into how to screen and treat such an anomaly, of which fewer than 25 cases have been reported in literature.

Paraneoplastic esthesioneuroblastoma (ENB), a very rare type of nasal tumor, may sometimes produce excess adrenocorticotrophic hormone (ACTH), leading to symptoms of Cushing’s syndrome, according to a recent case report that describes a case of ACTH-secreting ENB. The report aims to demonstrate the importance of recognizing its pathophysiology and treatment.

The case report, “A Case of Cushing’s Syndrome due to Ectopic Adrenocorticotropic Hormone Secretion from Esthesioneuroblastoma with Long Term Follow-Up after Resection,” was published in the journal Case Reports in Endocrinology.

It describes a 52-year-old Caucasian male who had a history of high blood pressure, severe weakness, abnormal production of urine, extreme thirstiness, and confusion.

He was scheduled to undergo surgery for a 7-centimeter skull base mass; the surgery was postponed due to severe high serum potassium concentrations and abnormally high pH levels. His plasma ACTH levels also were elevated and Cushing’s syndrome was suspected. Since imaging of the chest, abdomen, and pelvis did not show any ectopic (abnormal) sources of ACTH, the ENB was suspected to be the source.

Surgery was performed to remove the tumor, which was later found to be secreting ACTH. Consequently, following the procedure, his ACTH levels dropped to normal (below detection limit) and he did not need medication to normalize serum potassium levels. He then underwent subsequent chemoradiation and has shown no sign of recurrence 30 months after the operation, which is considered to be one of the longest follow-up periods for such a case.

Researchers declared it “a case of olfactory neuroblastoma with ectopic ACTH secretion that was treated with resection and adjuvant chemoradiation.”

“Given the paucity of this diagnosis, little is known about how best to treat these patients and how best to screen for complications such as adrenal insufficiency and follow-up,” they wrote. “Our case adds more data for better understanding of this disease.”

From https://cushingsdiseasenews.com/2018/04/03/rare-nasal-cancer-caused-cushings-syndrome-case-report-says/

Metabolomic Biomarkers in Urine of Cushing’s Syndrome Patients

Int. J. Mol. Sci. 2017, 18(2), 294; doi:10.3390/ijms18020294 (registering DOI)
Department of Food Sciences, Faculty of Pharmacy, Medical University of Gdańsk, Al. Gen. J. Hallera 107, 80-416 Gdańsk, Poland
Laboratory of Environmental Chemometrics, Faculty of Chemistry, University of Gdańsk, ul. Wita Stwosza 63, 80-308 Gdańsk, Poland
Department of Endocrinology and Internal Medicine, Medical University of Gdańsk, ul. Dębinki 7, 80-211 Gdańsk, Poland
Department ofEnvironmental Analytics, Institute for Environmental and Human Health Protection, Faculty of Chemistry, University of Gdańsk, ul. Wita Stwosza 63, 80-308 Gdańsk, Poland
Author to whom correspondence should be addressed.
Academic Editor: Ting-Li (Morgan) Han
Received: 5 December 2016 / Revised: 9 January 2017 / Accepted: 19 January 2017 / Published: 29 January 2017
(This article belongs to the Section Molecular Diagnostics)
Download PDF [1853 KB, uploaded 29 January 2017]

Abstract

Cushing’s syndrome (CS) is a disease which results from excessive levels of cortisol in the human body. The disorder is associated with various signs and symptoms which are also common for the general population not suffering from compound hypersecretion. Thus, more sensitive and selective methods are required for the diagnosis of CS.

This follow-up study was conducted to determine which steroid metabolites could serve as potential indicators of CS and possible subclinical hypercortisolism in patients diagnosed with so called non-functioning adrenal incidentalomas (AIs).

Urine samples from negative controls (n = 37), patients with CS characterized by hypercortisolism and excluding iatrogenic CS (n = 16), and patients with non-functioning AIs with possible subclinical Cushing’s syndrome (n = 25) were analyzed using gas chromatography-mass spectrometry (GC/MS) and gas chromatograph equipped with flame ionization detector (GC/FID). Statistical and multivariate methods were applied to investigate the profile differences between examined individuals. The analyses revealed hormonal differences between patients with CS and the rest of examined individuals.

The concentrations of selected metabolites of cortisol, androgens, and pregnenetriol were elevated whereas the levels of tetrahydrocortisone were decreased for CS when opposed to the rest of the study population. Moreover, after analysis of potential confounding factors, it was also possible to distinguish six steroid hormones which discriminated CS patients from other study subjects.

The obtained discriminant functions enabled classification of CS patients and AI group characterized by mild hypersecretion of cortisol metabolites. It can be concluded that steroid hormones selected by applying urinary profiling may serve the role of potential biomarkers of CS and can aid in its early diagnosis.

 

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

From http://www.mdpi.com/1422-0067/18/2/294

Froedtert and MCW researchers investigate Cushing syndrome incidence in bariatric surgery patients

Researchers at the Medical College of Wisconsin determined that Cushing syndrome, an endocrine disorder, may be the potential cause for weight gain and metabolic complications for patients who have undergone bariatric surgery for obesity. The study, published in the journal Obesity Surgery, was conducted by Ty B. Carroll, MD, assistant professor of endocrinology; James W. Findling, MD, FACP, professor of endocrinology ; and Bradley R. Javorsky, MD, assistant professor of endocrinology. The physicians practice at Froedtert Hospital in Wauwatosa and Community Memorial Hospital in Menomonee Falls.

Cushing syndrome can occur when the human body is exposed to high levels of cortisol for an extended period of time. Cortisol is a hormone in the body which affects blood pressure regulation and cardiovascular system functions. Cortisol also helps regulate the body’s conversion of proteins, carbohydrates and fats from diet into usable energy. However, when the level of cortisol becomes too high, Cushing syndrome can develop.

Cushing syndrome is associated with a variety of symptoms including weight gain and fatty tissue deposits in the body. According to the American Association of Neurological Surgeons, 10 to 15 million people are affected each year by Cushing syndrome.

Bariatric surgery is a procedure performed to help with extreme cases of obesity. Weight loss is achieved by reducing the size of the stomach with a gastric band, removal of a portion of the stomach or resecting and rerouting the small intestine to a small stomach pouch. Bariatric surgery is often used as an option for individuals unable to lose weight through diet and exercise, or have serious health problems caused by obesity.

According to the American Society for Metabolic and Bariatric Surgery, 179,000 bariatric surgeries were performed in the U.S. in 2013. However, despite successes in normal weight loss cases, bariatric surgery does not provide long term weight loss for individuals diagnosed with Cushing syndrome. Cushing syndrome often goes undiagnosed as a potential cause for weight gain and metabolic complications until after the surgery is performed.

MCW researchers in this study analyzed the incidence of Cushing syndrome in patients who underwent bariatric surgery for weight loss. During the investigation, the researchers performed a retrospective chart review on a series of 16 patients diagnosed with Cushing syndrome from five tertiary care centers in the U.S. who underwent bariatric surgery. The results from the study found 12 of the analyzed patients were not diagnosed with Cushing syndrome prior to their bariatric surgery. The remaining four patients had Cushing syndrome surgery prior to bariatric surgery, without recognition that their Cushing syndrome was persistent until after the weight loss surgery. The findings from the research indicate that Cushing syndrome may be often overlooked in patients undergoing bariatric surgery.

According to the researchers, testing for Cushing syndrome should be performed prior to bariatric surgery in patients with persistent hypertension, diabetes mellitus or excessive weight regain.

From http://www.lakecountrynow.com/usersubmittedstories/366480371.html