Visceral fat and estrogen dominance -
Some of this is a mystery, Keatley says. Still, you can strive to eat well to maintain a healthy weight. Overall, Jessica Cording, R. Foods to avoid when you want to fight hormonal belly fat. She suggests doing your best to avoid or minimize how much you have of red and processed meat, added sugar, and alcohol.
If you have belly fat and it bothers you, experts generally recommend speaking with a registered dietitian or nutritionist who can help you take a look at your eating plan and exercise routine.
Deena Adimoolam, known by many of her patients as "Dr. Deena", received her medical degree and training at the Icahn School of Medicine at Mount Sinai.
After her many years at Yale, she returned back to Mount Sinai as an Assistant Professor of Medicine and Associate Program Director of the endocrinology fellowship program. Adimoolam has published research and written chapters for major textbooks in the areas of diabetes and obesity.
She is passionate for educating the public on disease prevention and hormone health, and uses various media outlets to do so. She serves as a media expert and has worked with most major news organizations in print, online, and television. She works closely as a spokeswoman for the Endocrine Society - the largest medical organization in the field of endocrinology and metabolism and is very active with other local and national health organizations.
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Skip to Content Health Beauty Fitness Nutrition Life. sign in. BEST WALKING SHOES VALENTINE'S GIFTS FOR HER VALENTINE'S GIFTS FOR HIM BEST HAMSTRING STRETCHES HEALTHY SMOOTHIE RECIPES. Gonzales, there are a number of hormones that can affect the way we carry fat in the abdominal area: Estrogen Estrogen is a hormone present in all bodies.
Testosterone When testosterone is deficient in genetic men hypogonadism , it can lead to muscle loss. Advertisement - Continue Reading Below. How to naturally reset your hormones. Why do hormonal changes cause you to gain belly fat?
A deficiency can halt muscle growth and lead to weight gain. Testosterone deficiency can occur due to certain medical conditions, such as Noonan syndrome. It can also occur due to damage to or the removal of the testicles. Other causes can include infection, autoimmune conditions, chemotherapy , and pituitary gland disease.
A doctor may prescribe testosterone supplements or recommend lifestyle changes, such as more exercise and a reduced-calorie diet. Learn more about low testosterone levels here. There are three types of estrogen in the body:. According to a article , in males, estradiol is essential in modulating the libido, the production of sperm, and erectile function.
Low levels of estrogen can cause low sexual desire and excess fat around the belly. However, according to a article , high estrogen levels can cause weight gain in males under A doctor may recommend dietary and lifestyle changes, alongside medications.
Learn more about estrogen and weight gain here. According to the OWH, females with PCOS may have higher levels of androgens, or male hormones, and higher insulin levels, which is a hormone that affects how the body turns food into energy. As a result, people may gain weight, particularly around the abdomen.
Hormonal birth control methods may help treat PCOS in females who do not want to become pregnant. Drugs such as metformin may ease insulin resistance. Dietary changes, especially the elimination of foods that cause blood sugar spikes, can also help.
Learn more about PCOS, endometriosis, and weight gain here. When a person enters menopause , estrogen levels drop. According to one review article , reduced estrogen levels can increase abdominal fat in menopausal women.
A analysis suggests that hormone replacement therapy may help reduce belly fat. Learn how to lose weight during menopause. Some people retain fluid during their period. This can cause bloating, especially in the stomach, and temporary weight gain.
An older study of menstrual cycles in 62 females found that they reported the most fluid retention on the first day of their periods, with fluid retention steadily declining each day after that.
The researchers did not find a correlation between fluid retention and hormone levels, suggesting something else might explain this phenomenon.
A person can try dietary and lifestyle changes to help reduce fluid retention and bloating during menstruation. A person can learn more about ways to reduce period bloating here.
A person can perform exercises that burn fat, such as running, walking, and other aerobic activity. Reducing the calories a person consumes can also help. A person can learn more about how to reduce belly fat here.
A range of hormone imbalances can lead to abdominal bloating, discomfort, and weight gain. They include thyroid problems, Cushing syndrome, and other health conditions. In males, it may result from low testosterone levels and changes in estrogen levels. In females, it can happen with polycystic ovary syndrome PCOS , fluid retention due to menstruation, and during menopause.
The treatment will depend on the cause. A doctor may recommend medication to balance the hormones that are causing the problem. If a hormonal belly is due to thyroid problems, a doctor may recommend using medication, such as levothyroxine.
We showed that in postmenopausal women, E 1 concentration was higher in visceral than in abdominal subcutaneous AT, whereas E 2 concentrations were similar in the two depots.
Furthermore, the high E 1 concentration in visceral AT was associated with a high BMI. Although the conversion of E 1 to E 2 by reductive 17 β -HSD enzymes was more efficient in subcutaneous than in visceral AT, the production of E 2 in visceral AT was enhanced with increasing waist circumference, and E 2 concentration in visceral AT correlated positively with the mRNA expression of HSD17B7.
These data may suggest that although both AT depots are capable of producing active estrogens, an increase in adiposity is related to both increased E 1 concentration and E 2 production in visceral AT. After menopause, the increasing ratio of circulating androgens to estrogens contributes to the accumulation of visceral AT, and increasing adiposity relates to higher circulating levels of estrogens 27 , It is assumed that E 1 and E 2 produced in peripheral tissues in postmenopausal women act in an intracrine manner 29 , but some could leak into the bloodstream along a tissue to serum concentration gradient, thus possibly influencing circulating concentrations of E 1 , E 2 , and E 1 S 2 , 7 , In the current study, although serum E 2 and E 1 remained within normal postmenopausal concentrations, we found strong positive correlations between circulating and AT estrogen concentrations.
In comparing serum and AT estrogen concentrations, we assumed that 1 mL of serum corresponds to 1 g of AT 5 , Visceral AT E 1 and E 2 levels showed a stronger correlation with serum E 1 S than did subcutaneous AT estrogens.
Taking into account the higher concentration in visceral AT of E 1 , this could suggest that the visceral AT depot has an important role in the regulation of overall estrogen exposure in postmenopausal women.
E 1 is produced in peripheral tissues by both STS and aromatization of androstenedione, and local concentrations reflect the balance of several E 1 -producing and metabolizing pathways To the best of our knowledge, no other studies have reported the activity of STS in the conversion of E 1 S to E 1 in human AT.
Serum E 1 S is the predominant circulating estrogen and a marker of overall estrogenic activity in postmenopausal women Hydrophilic E 1 S requires a membrane transporter to reach tissues from the circulation, and organic anion-transporting polypeptide B, a carrier for E 1 S and a gatekeeper for the STS route, is present in AT We showed that E 1 S is hydrolyzed to E 1 in visceral and subcutaneous AT of postmenopausal women.
Although this does not directly prove that STS is a major producer of intracellular E 1 , our finding suggests that STS may contribute to local E 1 concentrations.
The mRNA expression of estrone-sulfating SULT1E1 has been linked to promotion of adipogenesis in subcutaneous AT 34 , although in other studies mRNA expression of this gene in AT has not been detected 15 , It is possible that AT is more of a target than a source of E 1 S, but the local balance of desulfating and sulfating enzymes requires further investigation.
STS activity in the conversion of E 1 S to E 1 was similar in subcutaneous and visceral AT. E 1 S is one of several substrates of STS; the others include DHEAS, cholesterol sulfate, and pregnenolone sulfate The affinity of STS for E 1 S is greater than that for DHEAS 36 , reflected by differences in the enzyme activity in metabolizing these substrates We did not find a correlation between STS activity and STS mRNA expression.
Little is known about local posttranscriptional modification of STS , but tissue conditions relating to inflammatory factors, for example, most likely play a role In line with previous reports 12 , 15 , we found the mRNA expression levels of STS and aromatase CYP19A1 to be higher in subcutaneous than visceral AT.
Of E 1 -producing enzymes, the mRNA expression level of 17 β -HSD type 2 was markedly higher in visceral than in subcutaneous AT. Because HSD17B2 has been shown to localize mainly in the vascular wall 38 , our finding could relate to a greater number of small blood vessels and increased blood flow in visceral than in subcutaneous AT 39 , In addition to the production of free E 1 from E 1 S in AT, we studied the conversion of E 1 into E 2.
The balance between reductive E 1 to E 2 and oxidative E 2 to E 1 pathways catalyzed by 17 β -HSD enzymes regulates the local concentrations of active estrogens, and E 2 formation from E 1 may be the favored direction in fat tissue The activity of reductive 17 β -HSD enzymes has been shown to increase upon preadipocyte to adipocyte differentiation in both subcutaneous and visceral AT In the current study, the conversion of E 1 to E 2 was more efficient in subcutaneous than in visceral AT , and the ratio of E 2 to E 1 was higher in subcutaneous AT.
This may suggest that subcutaneous AT is more efficient than visceral fat at producing E 2. On the other hand, reductive 17 β -HSD activity in visceral AT correlated positively with increasing waist circumference, suggesting that increased visceral adiposity could lead to more efficient production of E 2.
Visceral AT E 2 concentration correlated positively with the mRNA expression of HSD17B7 , which was more highly expressed in visceral than in subcutaneous AT, further supporting active production of E 2 in visceral AT. However, because E 1 concentration in visceral AT increased with BMI, it is possible that increasing obesity also contributes to overall exposure to active estrogens in postmenopausal women.
Our study has some limitations. First, because of the limited quantity of individual AT samples, we were not able to carry out all measurements and analyses for all women. Also, although we analyzed the mRNA expression levels of enzymes involved in estrogen metabolism in AT, we did not have enough tissue material to measure protein levels or aromatase activity.
However, the number of AT samples in the current study is substantial when compared with those in previous studies. Second, human AT is not a homogenous organ 7 , 38 , and in analyzing whole AT samples, we were looking to examine depot differences between subcutaneous and visceral AT.
We acknowledge the limitations of studying whole tissue samples in fully excluding sample-to-sample differences in AT composition.
Finally, we did not have the opportunity to use body imaging techniques for measurement of subcutaneous and visceral adiposity in the current study. A major strength of the present work is the use of mass spectrometric methods for quantification of estrogens, especially for the relatively low serum concentrations in postmenopausal women.
In conclusion, subcutaneous and visceral AT in postmenopausal women differed in their local production of estrogens. E 1 concentration was higher in visceral than in subcutaneous AT, and increasing adiposity was related to a higher E 1 concentration and increased local production of E 2 from E 1 in visceral AT.
Thus, in postmenopausal women, visceral adiposity could contribute to a higher overall estrogen exposure. We thank Anne Ahmanheimo, Päivi Ihamuotila, and Kirsti Räsänen for their expert technical assistance. Funding sources had no role in the design of the study, data collection and analysis, or interpretation of the results or in the decision to submit the article for publication.
has been a speaker for Mylan and has received funding for congress trips from Mylan and MSD. The remaining authors have nothing to disclose. Li J , Papadopoulos V , Vihma V. Steroid biosynthesis in adipose tissue.
Google Scholar. Siiteri PK. Adipose tissue as a source of hormones. Am J Clin Nutr. Grodin JM , Siiteri PK , MacDonald PC. Source of estrogen production in postmenopausal women. J Clin Endocrinol Metab. Vihma V , Wang F , Savolainen-Peltonen H , Turpeinen U , Hämäläinen E , Leidenius M , Mikkola TS , Tikkanen MJ.
Quantitative determination of estrone by liquid chromatography-tandem mass spectrometry in subcutaneous adipose tissue from the breast in postmenopausal women. J Steroid Biochem Mol Biol. Savolainen-Peltonen H , Vihma V , Leidenius M , Wang F , Turpeinen U , Hämäläinen E , Tikkanen MJ , Mikkola TS.
Breast adipose tissue estrogen metabolism in postmenopausal women with or without breast cancer. Kinoshita T , Honma S , Shibata Y , Yamashita K , Watanabe Y , Maekubo H , Okuyama M , Takashima A , Takeshita N.
Kershaw EE , Flier JS. Adipose tissue as an endocrine organ. Rose DP , Vona-Davis L. Interaction between menopausal status and obesity in affecting breast cancer risk. Smith JD , Borel AL , Nazare JA , Haffner SM , Balkau B , Ross R , Massien C , Alméras N , Després JP.
Visceral adipose tissue indicates the severity of cardiometabolic risk in patients with and without type 2 diabetes: results from the INSPIRE ME IAA study.
Lee MJ , Wu Y , Fried SK. Adipose tissue heterogeneity: implication of depot differences in adipose tissue for obesity complications. Mol Aspects Med.
Drolet R , Bélanger C , Fortier M , Huot C , Mailloux J , Légaré D , Tchernof A. Fat depot-specific impact of visceral obesity on adipocyte adiponectin release in women. Obesity Silver Spring. Blouin K , Nadeau M , Mailloux J , Daris M , Lebel S , Luu-The V , Tchernof A.
Pathways of adipose tissue androgen metabolism in women: depot differences and modulation by adipogenesis. Am J Physiol Endocrinol Metab. Yamatani H , Takahashi K , Yoshida T , Takata K , Kurachi H.
Association of estrogen with glucocorticoid levels in visceral fat in postmenopausal women. Bellemare V , Laberge P , Noël S , Tchernof A , Luu-The V.
Differential estrogenic 17beta-hydroxysteroid dehydrogenase activity and type 12 17beta-hydroxysteroid dehydrogenase expression levels in preadipocytes and differentiated adipocytes. Paatela H , Wang F , Vihma V , Savolainen-Peltonen H , Mikkola TS , Turpeinen U , Hämäläinen E , Jauhiainen M , Tikkanen MJ.
Steroid sulfatase activity in subcutaneous and visceral adipose tissue: a comparison between pre- and postmenopausal women. Eur J Endocrinol. Vermeulen A , Verdonck L. Factors affecting sex hormone levels in postmenopausal women.
J Steroid Biochem. Forney JP , Milewich L , Chen GT , Garlock JL , Schwarz BE , Edman CD , MacDonald PC. Aromatization of androstenedione to estrone by human adipose tissue in vitro: correlation with adipose tissue mass, age, and endometrial neoplasia.
Santner SJ , Feil PD , Santen RJ. In situ estrogen production via the estrone sulfatase pathway in breast tumors: relative importance versus the aromatase pathway.
Mueller JW , Gilligan LC , Idkowiak J , Arlt W , Foster PA. The regulation of steroid action by sulfation and desulfation. Endocr Rev. Marchais-Oberwinkler S , Henn C , Möller G , Klein T , Negri M , Oster A , Spadaro A , Werth R , Wetzel M , Xu K , Frotscher M , Hartmann RW , Adamski J.
Labrie F , Bélanger A , Pelletier G , Martel C , Archer DF , Utian WH. Science of intracrinology in postmenopausal women. Wang F , Vihma V , Soronen J , Turpeinen U , Hämäläinen E , Savolainen-Peltonen H , Mikkola TS , Naukkarinen J , Pietiläinen KH , Jauhiainen M , Yki-Järvinen H , Tikkanen MJ.
Wang F , Vihma V , Badeau M , Savolainen-Peltonen H , Leidenius M , Mikkola T , Turpeinen U , Hämäläinen E , Ikonen E , Wähälä K , Fledelius C , Jauhiainen M , Tikkanen MJ. Fatty acyl esterification and deesterification of 17β-estradiol in human breast subcutaneous adipose tissue.
Fotsis T. The multicomponent analysis of estrogens in urine by ion exchange chromatography and GC-MS--II: fractionation and quantitation of the main groups of estrogen conjugates. Moore JW , Clark GM , Bulbrook RD , Hayward JL , Murai JT , Hammond GL , Siiteri PK.
by seooneclick Jun 5, Uncategorized 0 comments. As ft medicine fstrogen with years Brain health supplements experience estrogn in Brea, Gymnastics diet essentials have found that estrogen dominance is a doimnance cause Visceral fat and estrogen dominance weight gain, especially for the elderly. Keep hope alive, though. By taking the right supplements and making some changes to your diet and lifestyle, you can reverse this imbalance and lose weight more quickly. Read on to learn more! Estrogen dominance arises when there is an excess of estrogen in your body or an imbalance between estrogen and progesterone. Concentration and decision making quiz! Which of your hormones are imbalanced? If Regulating insulin levels struggle with doinance gain, Visveral periods, PMS, fatigue, acne, or sugar sominance estrogen dominance could be to blame. Estrogen dominance is one of the most common hormonal imbalances for women, but it often goes undetected for years and sometimes goes undiagnosed for a lifetime. Estrogen is a group of sex hormones most commonly associated with female reproduction.
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