Category Archives: Hormone Replacement Therapy

Menopause starts for most people in their late 40s or early 50s. But in early or premature menopause, the drop in estrogen production and the end of menstrual periods comes much earlier. Premature menopause begins before the age of 40, and can sometimes happen in your 20s.

If youre in your 20s and in premature menopause, you may have questions and concerns about its effects on your health. In this article, you can read about the symptoms of early or premature menopause, what can cause it, and what can be done to treat its symptoms. Youll also learn about the effects premature menopause can have on your health.

Menopause is premature when it occurs before age 40. Premature menopause is sometimes called primary ovarian insufficiency because the ovaries stop producing estrogen the way they should. If youre in your 20s and going through menopause, youre going through premature menopause.

Premature menopause is different from early menopause, which refers to menopause that happens before youre 45 years old. The average age for menopause in the United States is 51 years old. A 2019 research review showed that around 3.7 percent of women experience either primary ovarian insufficiency or early menopause.

The symptoms of premature menopause are the same as those youd experience if you started menopause later. But its important to note that menopause symptoms can vary from one person to another. Some of those symptoms include:

It isnt always possible to determine exactly what has caused premature menopause. Here are some of the known causes and risk factors.

Premature menopause can run in families. If it feels appropriate, you may want to speak with your biological relatives about the age at which they stopped having periods. Knowing about their symptoms could help you get a sense of what to expect.

Smoking is associated with an earlier menopause. 2018 research shows that the more someone smokes, the higher their risk of premature menopause. A research review from 2020 including some mouse studies shows that e-cigarette vapors also affect reproduction. But scientists dont yet know how smoking e-cigarettes affects menopause.

Pelvic or ovarian surgery is sometimes the cause of premature menopause. You may have had a surgery called an oophorectomy to remove your ovaries because of cancer, endometriosis, or another condition. If surgery has caused you to go into menopause, your symptoms may be more severe than if you started menopause more gradually, according to 2019 research.

People who have had chemotherapy or radiation therapy to treat cancer have a higher risk of premature menopause.

A 2015 study also looked at exposure to certain estrogen-disrupting chemicals. It found that exposure to substances found in some pesticides and phthalates also gives you a higher risk of earlier menopause.

Some viruses have been linked in a 2015 research review to premature menopause, though their role isnt clear. HIV, mumps, cytomegalovirus, tuberculosis, malaria, and other viruses may potentially cause ovarian changes and premature menopause.

Autoimmune disorders can sometimes damage the ovaries, bringing about premature menopause. Some conditions associated with premature menopause include:

2019 research found that more than 75 different genes can contribute to primary ovarian insufficiency and premature menopause. Most are genes that influence how ovaries develop and function, how cells divide, or how DNA is repaired in the body. Turner syndrome and fragile X syndrome are genetic conditions that can cause premature menopause.

Premature menopause poses some health risks. Its a good idea to talk with a healthcare professional about these risks so that you can take steps to protect your physical and emotional health going forward. Here are some potential health issues that can arise:

Primary ovarian insufficiency is often diagnosed when someone talks to a healthcare professional about missing several periods. If you have missed three or more periods in a row, its a good idea to talk to a doctor. Heres what to expect during the diagnosis:

If your doctor thinks you may have primary ovarian insufficiency, you may have a pelvic ultrasound to see if a cause can be determined.

Premature menopause cannot yet be reversed, but researchers are trying to improve the outlook. Treatments have different goals, such as:

Your treatments options could include:

It can be a shock to experience menopause in your 20s. In fact, for many, premature menopause comes with mixed emotions, including sadness, anxiety, and frustration. This change can be especially hard if your plans include pregnancy and childbirth, since premature menopause can make it harder to have children.

Whether youre experiencing physical, psychological, or emotional symptoms, its important to take good care of yourself during this transition. Think about whether a therapist, a nutritionist, a support group, or other specialists could benefit you.

Here are some places where you may be able to find support:

Premature menopause, sometimes called primary ovarian insufficiency, happens when your ovaries stop producing as much estrogen, your periods stop, and it becomes more difficult to become pregnant naturally.

Premature menopause brings on all the symptoms usually associated with menopause hot flashes, night sweats, mood changes, concentration difficulties, lower libido, and more. And because premature menopause can alter your life plans and your sense of self, its not uncommon to experience depression and anxiety along with the other symptoms.

Treatment may help with your symptoms. Hormone replacement therapy, while not right for everyone, may also prevent bone loss and heart problems down the road. A healthcare professional can help you decide what treatments are right for you.

Menopause in your 20s can be unexpected. Though you may feel isolated by the diagnosis, you are not alone in dealing with it. As soon as you are ready to reach out, you can find the professional guidance and personal support you need.

Read more from the original source:
Early Menopause in 20s: Symptoms, Causes, Concerns, & More - Healthline

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Menopause can be unbearable for women, bringing hot flashes, brain fog, insomnia and other life-invading symptoms. Local doctors say there is hope, and better ways to cope, for women today thanwhat was available to their mothers.

"People ask me when they will be done with menopause," said Dr. Sarah Hanson, an OB/GYN at York Hospital. "I answer, 'When you're dead.' Menopause encompasses the last half of a woman's life, the part where they are not reproductive anymore."

Hanson points out that what women think of when they say "menopause"are those symptoms ofhot flashes, night sweats, difficulty sleeping. For most women, thosesymptoms have a shelf life. They usually do not last more than a few years.

"What women think of as menopause is usually pre-menopause, or peri-menopause," Hanson said. "That's where the symptoms are happening. That can last three to seven years. The ovaries are no longer preparing to reproduce and hormones get thrown out of whack. But, it is a normal part of a woman's life cycle."

Some women pass through this phase easily, and menopause is like a lamb, often requiring zero medical intervention. Hanson said for others, it is a lion, fraught with symptoms and women seek any relief available to them.

"I spend a lot of my day talking about menopause," said Dr. Caroline Scoones of Harbor Women's Health, who also practices at Portsmouth Regional Hospital. "Here on the Seacoast, we have a wonderful population of women, teens, moms, menopausal women and much older women. At any time, a good 20% of them are chatting with me about menopause."

Scoones said menopause occurs when a woman has not had a period in 12 months.

"It is a transition and women go through transitions their entire lives," she said. "From the time they begin adolescence, when their reproductive systems are ramping up, to the time we enter menopause and our reproductive systems are ramping down, we are experiencing hormonal changes. It's not the same for men. We get the short end of the stick, but it's the wonderful system we are stuck with."

The average age of a woman entering menopause is 51, but Dr. Kristin Yates of Garrison Women's Heath and Wentworth-Douglass Hospital said it can range several years on either side of that age. It's rare but some women begin entering this phase of life as early as their 40s.

"When you are born, you have a certain amount of eggs in your ovaries," Yates said. "That number goes down every month when you ovulate and have a period. Eventually they run out and you no longer ovulate. You stop having periods and the amount of estrogen your body secretes gets lower."

"My first advice is to do nothing," said Hanson. "If you can handle the symptoms, this is normal and there is nothing you have to do. For other women, of course, that's not the option they choose because the symptoms are interfering with their daily life. Our grandmothers just endured it. You can, but you don't have to."

Scoones said the question of what to do relates to how many of the symptoms a woman gets, how they are interrupting every day living, and herpersonal views.

"Are you a super natural type and you do not want to take anything?" said Scoones. "Are you the oppositeand want to go full hog?Or are you somewhere in between? We can help you, or you can choose to tough it out."

Hanson said women who maintain a more healthy lifestyle, with a lot of physical activity, a healthy diet, and who maintain a good body weight generally handle menopause more easily. And, she said, it's good for our overall health anyway, so why not do it?

"People who are overweight or who smoke may have a more difficult time," Hanson said.

Hanson said women in pre-menopausecan experience hot flashes, difficulty sleeping, mood changes and shifts, and a feeling of cloudiness or fogginess, and still perform equally well every day. But, they are uncomfortable.

"These are neurological symptoms, all of them," said Hanson. "We know moods affect hormones,and hormones affect moods. For some women, low-dose birth control pills will be enough to handle the hormonal change."

Scoones said over-the-counter products, like black cohosh or evening primrose work for some women, but not all. Some natural products like Estrovera canhelp some women mitigate symptoms.

"They can be taken daily, with little side effects," said Scoones. "I think about 50% respond to these non-pharmaceutical methods."

Scoones said those with severe symptoms, like thosewho cannot sleep, who drip sweat and who are miserable in general, might consider prescription relief.

Yates said hormone replacement therapies have gone through several schools of thought.

"Women were worried about the risk of blood clotsor strokes," said Yates. "We now know that relatively small doses have low risk, and can be safe and effective. There are some women who are not good candidates, women who have a history of clots, strokes or who have had breast cancer."

"We all did it, then no one did it," she said. "Now we are better able to use low-dose hormone therapymore successfully."

Scoones agreed, saying hormonal therapies are more nuanced now.

"We can tailor hormonal treatments to deal with your particular symptoms," said Scoones. "There are transdermal estrogen treatments. There is an IUD that can be used to treat the heavy flow that usually precedes peri-menopause. We have choices that can help with sleep, anxiety, hot flashes and weight gain."

Hanson said in cases where blood flow is extreme, a procedure called endometrial ablation, an outpatient surgery, can alleviate the situation.

"Some women opt for hysterectomy," she said. "We can do that usinglaparoscopy in many cases, or with the more traditional vaginal application."

If the choice is hormone therapy, Scoones said the North American Menopause Society recommends the lowest effective dose, for the shortest duration of time, usually two to threeyears.

"You are not broken," said Scoones. "This is a natural course of a woman's life and you will not need hormone replacement therapy forever, just until you feel good again."

See the article here:
Menopause is dreadful. But there's hope for how to cope with it better - Foster's Daily Democrat

Introduction

Type 2 diabetes mellitus (T2DM) and osteoporosis are common chronic diseases, and the relationship between the two is becoming a hot research topic.1,2 Previous studies have shown that although bone mineral density (BMD) is normal or elevated,3 T2DM patients increase the risk of fractures compared with non-diabetic patients.46 T2DM can influence bone metabolism by affecting osteoblasts and osteoclasts, and the imbalance between the two may lead to osteoporosis.7 It has been confirmed that there are insulin receptors on the surface of both cells,8 and insulin signaling can regulate the bone formation of osteoblasts and bone resorption of osteoclasts.9 In vitro, it has been shown that the physiological concentration of insulin can increase the proliferation rate of osteoblasts, collagen synthesis, alkaline phosphatase production, and glucose uptake and inhibit osteoclast activity.10 Thus, insulin is an anabolic agent for bone formation, and elevated insulin levels may increase bone density.11,12 It has been widely accepted that insulin resistance is the main problem of T2DM metabolic disorders. It is caused by the defect in the insulin signaling pathway that reduces the cellular insulin response; pancreatic cells overcome the reduced sensitivity by enhancing insulin secretion, thereby developing hyperinsulinemia.9,13 Hyperinsulinemia can also negatively affect sex hormone-binding globulin to increase free sex hormone levels, preventing bone loss.11,14

However, more and more studies have shown a negative association between insulin resistance and bone mineral density,11,15,16 indicating that insulin resistance in T2DM patients may weaken the physiological effects of insulin on bones.1 Therefore, the relationship between insulin resistance and osteoporosis is still controversial. To address this question, in this study, we used a C peptide to evaluate insulin resistance based on the modified insulin resistance homeostasis model (HOMA-IR) and explored the relationship between HOMA-IR (CP) and the risk of osteoporosis in different gender groups of T2DM patients.

This was a cross-sectional study. We selected 575 T2DM patients from the outpatient department of Endocrinology and Metabolism at our hospital from February 2016 to August 2018. This study was conducted in accordance with the Declaration of Helsinki and was approved by the Institutional Ethics Committee of the Third Affiliated Hospital of Soochow University for retrospective analysis (ethics number: 2014-KD-79). The sample size calculation used the method of computer simulation inspection efficiency (see Supplementary Material-Computer simulation inspection efficiency). Since the patients were anonymous, informed consent was not required. Inclusion criteria: T2DM was defined as: fasting blood glucose level 7.0 mmol/l, 2 hours postprandial or random blood glucose level 11.1 mmol/l, glycosylated hemoglobin (HbA1c) 6.5%. Record the patients use of T2DM treatment drugs. The following patient populations were excluded: (1) patients using hormone replacement therapy, bisphosphonates, glucocorticoids, proton pump inhibitors, etc. (14 cases); (2) patients with missing bone density results (311 cases); (3) patients under 18 years old (1 case); (4) patients with missing HOMA-IR (CP) (15 cases). The research flow chart is shown in Figure 1. Among the 250 patients with available BMD data and the 311 patients with missing BMD data, almost all clinical factors were similar (all P > 0.05) (see Supplementary Table S1).

Figure 1 Flowchart of the study.

The general data of the patient was recorded, including menopause information. The height, weight, waist circumference, and hip circumference of patients were measured, and the body mass index (BMI) and waist-to-hip ratio were calculated. The fasting venous blood was collected, and the fasting blood glucose, uric acid, and blood lipid levels were measured using an automatic biochemical analyzer (Beckman Coulter AU5800, Brea, CA, USA). Fasting C peptide was determined by electrochemiluminescence immunoassay (Roche Cobas8000, Indianapolis, IN, USA). HbA1c was measured by high-performance liquid chromatography (D-10 system, Bio-Rad, USA).

Instead of insulin, fasting C-peptide was used to evaluate insulin resistance and islet function according to a modified formula. The modified HOMA-IR [HOMA-IR (CP)] formula = 1.5 + fasting blood glucose (mmol/L) fasting C-peptide (pmol/L)/2800. The modified HOMA-islet [HOMA-islet (CP-DM)] formula = 0.27 fasting C-peptide (pmol/L)/[fasting blood glucose (mmol/L) 3.5].17

The dual-energy X-ray absorptiometry (DXA, Hologic, Discovery-WI, USA) was used to determine the bone density of the lumbar spine (L1-L4) (unit: g/cm2). Trained and certified technicians performed all DXA scans. The diagnosis of osteopenia and osteoporosis was based on the T score of the World Health Organization (the T value was the standard deviation between the patient BMD and the BMD of the young adult reference population). 2.5 < T value < 1.0 was defined as osteopenia, T value 2.5 was defined as osteoporosis.18

Data were expressed as mean standard deviation (SD) (Gaussian distribution) or median (Q1-Q3) (Skewed distribution) for continuous variables and as numbers or percentages for categorical variables. To examine the association between HOMA-IR (CP) and osteoporosis risk, we constructed three distinct models using univariate and multivariable binary logistic regression models, including non-adjusted model, minimally-adjusted model (Adjust I), and fully-adjusted model (Adjust II). Covariates were included as potential confounders in the final models if they changed the estimation of HOMA-IR (CP) on osteoporosis by more than 10% or significantly associated with osteoporosis (P < 0.10). The subgroup analyses were performed using a stratified binary logistic regression model. The effect sizes with 95% confidence intervals were recorded. To investigate the nonlinear relationship between HOMA-IR (CP) and osteoporosis risk, we used a generalized additive model and smooth curve fitting (penalized spline method) to address nonlinearity. Moreover, the two-piecewise binary logistic regression model was used to explain the nonlinearity further.

Modeling was performed with the statistical software R (http://www.R-project.org, The R Foundation) and EmpowerStats (http://www. empowerstats.com, X&Y Solutions, Inc, Boston, MA). P < 0.05 (two-sided) was considered statistically significant.

A total of 234 T2DM patients were included in the study, with 139 males and 95 females, aged 57.5 10.8 years old (range: 2383 years old). Among them, 112 cases were first diagnosed (no hypoglycemic drugs were used), 122 cases were controlled by drugs (including 55 metformin, 37 acarbose, 24 sulfonylureas, 12 insulin, and 5 thiazolidinediones, new hypoglycemic drugs [including glucagon-like peptide-1 (GLP-1) receptor agonists, dipeptidyl peptidase-4 (DPP-4) inhibitors, sodium-glucose cotransporter-2 (SGLT-2) inhibitors] 2 cases, some patients have combined medication). The results of BMD measurement showed that there were 82 cases (35.0%) with normal bone mass, 118 cases (50.4%) with osteopenia, and 34 cases (14.5%) with osteoporosis. The general information and blood indicators of different gender groups are shown in Table 1.

Table 1 Comparison of General Information and Blood Indicators of Different Gender Groups

Compared with male T2DM patients, female patients were older (P = 0.047) and had longer disease course (P = 0.013), and have a higher proportion of drug control (P = 0.012); but their BMI, waist-to-hip ratio, fasting blood glucose, fasting C-peptide, HOMA-IR (CP), HOMA-islet (CP-DM), and HbA1c were not significantly different (all P > 0.05). The osteoporosis percentage in female patients was slightly higher than that in male patients (15.8% vs 13.7%), but the difference was insignificant (P = 0.651).

The univariate logistic regression analysis was performed by taking osteoporosis as the dependent variable (Y = 1) and using the clinical data and blood indicators from different gender groups as independent variables (see Table 2). The results showed that age, uric acid, and HOMA-IR (CP) were all possible related factors for osteoporosis in female patients (P < 0.10), while in male patients, the association between the above indicators and osteoporosis was not significant (P > 0.10).

Table 2 Univariate Analysis of Clinical Data, Blood Indicators, and Osteoporosis of Different Gender Groups

Multivariable logistic regression analysis was used to evaluate the association between HOMA-IR (CP) and osteoporosis by adjusting the covariates. The model with non-adjusted covariates equaled to univariate logistic regression analysis. The minimally-adjusted covariates (Adjust I) included age and uric acid, and the fully-adjusted covariates (Adjust II) included age, BMI, waist-to-hip ratio, disease course, HOMA-islet (CP-DM), uric acid, triacylglycerol, and high-density lipoprotein (see Table 3). For female patients, the increase in HOMA-IR (CP) elevated the risk of osteoporosis in all regression models with non-adjusted, minimally-adjusted, and fully-adjusted covariates, and the association was significant in the fully-adjusted model, with OR = 2.63 (95% CI: 1.155.99, P = 0.022). For male patients, the association between HOMA-IR (CP) and osteoporosis was not significant in all three models (all P > 0.05). The interaction effect between different genders was significant (P for interaction all < 0.05), indicating that the relationship between HOMA-IR (CP) and osteoporosis was affected by gender.

Table 3 Multivariable Logistic Regression Analysis of the Effect of HOMA-IR (CP) on Osteoporosis

GAM was used to test the relationship between HOMA-IR (CP) and osteoporosis risk in female patients. The results showed a nonlinear relationship between the two after correcting for age, BMI, waist-to-hip ratio, disease course, HOMA-islet (CP-DM), uric acid, triacylglycerol, and high-density lipoprotein (degree of freedom was 1.862, P = 0.024). Figure 2 showed the changes of osteoporosis risk with HOMA-IR (CP) in female patients: at first, the changes were very little; after a certain HOMA-IR (CP) value, the osteoporosis risk significantly increased, showing a piecewise linear relationship. By observing the fitted curve, we set the inflection point as 4.00.

Figure 2 The relationship between HOMA-IR (CP) and osteoporosis risk. Adjust for: age, BMI, waist-to-hip ratio, disease course, HOMA-islet (CP-DM), uric acid, triacylglycerol, and high-density lipoprotein.

Abbreviations: HOMA-IR (CP), homeostasis model assessment for insulin resistance based on C-peptide; BMI, body mass index; HOMA-islet (CP-DM), homeostasis model assessment islet beta-cell function based on C-peptide.

The two-piecewise logistic regression model method was used further to evaluate the threshold effect of the fitted curve. The log-likelihood ratio test of HOMA-IR (CP) at the inflection point 4.00 was statistically significant (P = 0.005), suggesting that the two-piecewise regression model was appropriate for describing the relationship between HOMA-IR (CP) and osteoporosis (see Table 4). When HOMA-IR (CP) < 4.00, the risk of osteoporosis in female patients did not change much with HOMA-IR (CP), (P = 0.474); when HOMA-IR (CP) > 4.00, the increase in HOMA-IR (CP) significantly elevated the risk of osteoporosis in female patients, with OR = 26.88 (95% CI: 2.75262.69, P = 0.005).

Table 4 Nonlinear Relationship Between HOMA-IR (CP) and Osteoporosis

The relationship between insulin resistance and the risk of osteoporosis in T2DM patients is still controversial. Our study found that this relationship was significantly affected by gender. In female patients, the higher the degree of insulin resistance, the greater the risk of osteoporosis. However, the relationship was not a simple linear relationship, and there was a threshold effect. When HOMA-IR (CP) > 4.00, the risk of osteoporosis increased significantly.

The incidence of osteoporosis is gradually increasing in recent years, which affects the patients life quality and causes serious social health problems.19,20 Many factors are related to osteoporosis, including age, gender, endocrine, and metabolic diseases.21 The age-related reduction of sex hormones is one reason for osteoporosis, as sex hormones play an important role in maintaining bone health.22 Compared with older males, hormone deficiency is more pronounced in older females.23 Diabetes is also an important cause of osteoporosis. Many studies2,24 have shown that people with T2DM have a higher risk of bone fractures than non-diabetic patients. Our study showed that the proportion of osteoporosis in female T2DM patients was higher than that of male patients, consistent with the previous studies.

T2DM is the most common endocrine system disease in the clinic, with insulin resistance as the basic pathological feature, accompanied by internal environmental disorders and abnormal synthesis and secretion of various cytokines. These effects influence bone metabolism and then cause bone loss and destruction of bone ultrastructure.25 In recent years, studies have shown that insulin directly affects bone cells,14 but the relationship between insulin resistance and osteoporosis is still unclear. Bilic-Curcic et al26 proposed that abdominal obesity and hyperinsulinemia played a protective role in postmenopausal women with T2DM, leading to an increase in the total femoral bone density. A cohort study of the elderly27 showed that insulin resistance was associated with increased bone density. The synergistic effect of excess insulin and other anabolic hormones, such as pancreatic amylin, insulin-like growth factors, and parathyroid hormone, can increase bone density.28 However, our results were different, which might be due to the heterogeneity of the study population, such as age, gender, race, and menopause. In addition, we used a modified HOMA-IR model to evaluate insulin resistance, in which C-peptide replaced insulin. C-peptide is more stable and is considered an effective substitute for insulin.29 Moreover, the bone density we measured was based on the lumbar spine, which might also cause inconsistent results. It has been reported30 that significant insulin resistance in T2DM patients is associated with low bone density. T2DM patients are often accompanied by mild inflammation, and chronic inflammation can lead to the development of osteoporosis through oxidative stress.31 Weber et al (31) speculated that the relationship between insulin resistance and osteoporosis might not be linear, and there was a threshold effect. Our results confirmed this perspective. When HOMA-IR (CP) > 4.00, the higher the insulin resistance of female T2DM patients, the greater the risk of osteoporosis. In our study, the proportion of female patients who had menopause accounted for 85.3%. The sharp decline in estrogen after menopause led to the loss of bone mass. This gender difference may affect the relationship between insulin resistance and osteoporosis.32 In addition, with the increase of insulin resistance, other related factors, such as pro-inflammatory cytokines, have also increased, which exerts an adverse effect on bone health, exceeding the anabolic effect of insulin on bone and leading to decreased bone density.11,33

Our study has some limitations. Firstly, this is a single-center retrospective study. There were only 34 patients with osteoporosis, and there was a high proportion of missing BMD results. The sample size needs to be expanded to obtain a more accurate HOMA-IR (CP) threshold. Secondly, there might be unknown confounding factors that affected our results. For example, serum 25-hydroxyvitaminD27,34 and diabetes medications35 are important factors that affect bone health. Finally, this study only found a significant association between HOMA-IR (CP) and osteoporosis in female patients, and more male patients should be collected for further research. The relationship between insulin resistance and osteoporosis is complex and has not been fully understood. Further research is needed to clarify the relationship between the two.

In summary, the relationship between insulin resistance and osteoporosis risk in T2DM patients is significantly affected by gender. The higher the degree of insulin resistance in female T2DM patients, the greater the risk of osteoporosis. Moreover, this relationship is not simply linear, and there is a threshold effect. This study will help clinicians assess the risk of osteoporosis in T2DM female patients and make appropriate early interventions.

All data generated or analyzed during this study are available from the corresponding author upon reasonable request.

The study was approved by the Institutional Ethics Committee of the Third Affiliated Hospital of Soochow University for retrospective analysis (ethics number: 2014-KD-79).

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

There is no funding to report.

The authors report no conflicts of interest in this work.

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2. Xu Y, Wu Q. Trends in osteoporosis and mean bone density among type 2 diabetes patients in the US from 2005 to 2014. Sci Rep. 2021;11(1):3693. doi:10.1038/s41598-021-83263-4

3. Zhu L, Xu Z, Li G, et al. Marrow adiposity as an indicator for insulin resistance in postmenopausal women with newly diagnosed type 2 diabetes - an investigation by chemical shift-encoded water-fat MRI. Eur J Radiol. 2019;113:158164. doi:10.1016/j.ejrad.2019.02.020

4. Looker AC, Eberhardt MS, Saydah SH. Diabetes and fracture risk in older U.S. adults. Bone. 2016;82:915. doi:10.1016/j.bone.2014.12.008

5. Napoli N, Strotmeyer ES, Ensrud KE, et al. Fracture risk in diabetic elderly men: the MrOS study. Diabetologia. 2014;57(10):20572065. doi:10.1007/s00125-014-3289-6

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7. Sassi F, Buondonno I, Luppi C, et al. Type 2 diabetes affects bone cells precursors and bone turnover. BMC Endocr Disord. 2018;18(1):55. doi:10.1186/s12902-018-0283-x

8. Fulzele K, Riddle RC, DiGirolamo DJ, et al. Insulin receptor signaling in osteoblasts regulates postnatal bone acquisition and body composition. Cell. 2010;142(2):309319. doi:10.1016/j.cell.2010.06.002

9. Conte C, Epstein S, Napoli N. Insulin resistance and bone: a biological partnership. Acta Diabetol. 2018;55(4):305314. doi:10.1007/s00592-018-1101-7

10. Thrailkill KM, Lumpkin CK, Bunn RC, Kemp SF, Fowlkes JL. Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues. Am J Physiol Endocrinol Metab. 2005;289(5):E735745. doi:10.1152/ajpendo.00159.2005

11. Shin D, Kim S, Kim KH, Lee K, Park SM. Association between insulin resistance and bone mass in men. J Clin Endocrinol Metab. 2014;99(3):988995. doi:10.1210/jc.2013-3338

12. Nyman JS, Kalaitzoglou E, Clay bunn R, Uppuganti S, Thrailkill KM, Fowlkes JL. Preserving and restoring bone with continuous insulin infusion therapy in a mouse model of type 1 diabetes. Bone Rep. 2017;7:18. doi:10.1016/j.bonr.2017.07.001

13. Shanik MH, Xu Y, Skrha J, Dankner R, Zick Y, Roth J. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care. 2008;31(Suppl 2):S262268. doi:10.2337/dc08-s264

14. Shanbhogue VV, Finkelstein JS, Bouxsein ML, Yu EW. Association between insulin resistance and bone structure in nondiabetic postmenopausal women. J Clin Endocrinol Metab. 2016;101(8):31143122. doi:10.1210/jc.2016-1726

15. Ahn SH, Kim H, Kim BJ, Lee SH, Koh JM. Insulin resistance and composite indices of femoral neck strength in Asians: the fourth Korea National Health and Nutrition Examination Survey (KNHANES IV). Clin Endocrinol (Oxf). 2016;84(2):185193. doi:10.1111/cen.12958

16. Shah VN, Sippl R, Joshee P, et al. Trabecular bone quality is lower in adults with type 1 diabetes and is negatively associated with insulin resistance. Osteoporos Int. 2018;29(3):733739. doi:10.1007/s00198-017-4353-0

17. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412419. doi:10.1007/BF00280883

18. Golob AL, Laya MB. Osteoporosis: screening, prevention, and management. Med Clin North Am. 2015;99(3):587606. doi:10.1016/j.mcna.2015.01.010

19. Ma C, Tonks KT, Center JR, Samocha-Bonet D, Greenfield JR. Complex interplay among adiposity, insulin resistance and bone health. Clin Obes. 2018;8(2):131139. doi:10.1111/cob.12240

20. Cosman F, de Beur SJ, LeBoff MS, et al. Clinicians Guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):23592381. doi:10.1007/s00198-014-2794-2

21. Rubin MR, Schwartz AV, Kanis JA, Leslie WD. Osteoporosis risk in Type 2 diabetes patients. Expert Rev Endocrinol Metab. 2013;8(5):423425. doi:10.1586/17446651.2013.835567

22. Riggs BL, Khosla S, Melton LJ. Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev. 2002;23(3):279302. doi:10.1210/edrv.23.3.0465

23. Sawicki P, Talalaj M, Zycinska K, Zgliczynski WS, Wierzba W. A cross-sectional comparison of selected anthropometric, laboratory and densitometric parameters in postmenopausal osteoporotic women with and without vertebral compression fractures. Endokrynol Pol. 2021;72(3):191197. doi:10.5603/EP.a2021.0011

24. Fan Y, Wei F, Lang Y, Liu Y. Diabetes mellitus and risk of hip fractures: a meta-analysis. Osteoporos Int. 2016;27(1):219228. doi:10.1007/s00198-015-3279-7

25. Heilmeier U, Patsch JM. Diabetes and Bone. Semin Musculoskelet Radiol. 2016;20(3):300304. doi:10.1055/s-0036-1592366

26. Bilic-Curcic I, Makarovic S, Mihaljevic I, Franceschi M, Jukic T. Bone mineral density in relation to metabolic syndrome components in postmenopausal women with diabetes mellitus type 2. Acta Clin Croat. 2017;56(1):5863. doi:10.20471/acc.2017.56.01.09

27. Napoli N, Conte C, Pedone C, et al. Effect of Insulin resistance on BMD and fracture risk in older adults. J Clin Endocrinol Metab. 2019;104(8):33033310. doi:10.1210/jc.2018-02539

28. Fornari R, Marocco C, Francomano D, et al. Insulin growth factor-1 correlates with higher bone mineral density and lower inflammation status in obese adult subjects. Eat Weight Disord. 2018;23(3):375381. doi:10.1007/s40519-017-0362-4

29. Fasipe OJ, Ayoade OG, Enikuomehin AC. Severity grade assessment classifications for both insulin resistance syndrome and status of pancreatic beta cell function in clinical practice using homeostasis model assessment method indices. Can J Diabetes. 2020;44(7):663669. doi:10.1016/j.jcjd.2020.02.003

30. Arikan S, Tuzcu A, Bahceci M, Ozmen S, Gokalp D. Insulin resistance in type 2 diabetes mellitus may be related to bone mineral density. J Clin Densitom. 2012;15(2):186190. doi:10.1016/j.jocd.2011.11.005

31. Tonks KT, White CP, Center JR, Samocha-Bonet D, Greenfield JR. Bone Turnover is suppressed in insulin resistance, independent of adiposity. J Clin Endocrinol Metab. 2017;102(4):11121121. doi:10.1210/jc.2016-3282

32. Mesinovic J, McMillan LB, Shore-Lorenti C, et al. Sex-specific associations between insulin resistance and bone parameters in overweight and obese older adults. Clin Endocrinol (Oxf). 2019;90(5):680689. doi:10.1111/cen.13947

33. Cao JJ. Effects of obesity on bone metabolism. J Orthop Surg Res. 2011;6:30. doi:10.1186/1749-799X-6-30

34. Gagnon C, Lu ZX, Magliano DJ, et al. Low serum 25-hydroxyvitamin D is associated with increased risk of the development of the metabolic syndrome at five years: results from a national, population-based prospective study (The Australian Diabetes, Obesity and Lifestyle Study: ausDiab). J Clin Endocrinol Metab. 2012;97(6):19531961. doi:10.1210/jc.2011-3187

35. Lee HS, Hwang JS. Impact of type 2 diabetes mellitus and antidiabetic medications on bone metabolism. Curr Diab Rep. 2020;20(12):78. doi:10.1007/s11892-020-01361-5

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Association Analysis of Insulin Resistance and Osteoporosis Risk in Ch | TCRM - Dove Medical Press

The novel hormone irisin has the ability to drive the cognitive benefits of exercise, and therefore holds great promise for treating cognitive decline in Alzheimers disease, researchers atMassachusettsGeneralHospital (MGH) have found. In a study published inNatureMetabolism, the team reported that irisin, secreted by the muscles during exercise, could be an effective therapeutic for addressing deficits of the brain that result from Alzheimers disease.

Preserving cognitive function is a major challenge in an increasingly aging population, saysChristiane Wrann, DVM, PhD,leaderof the Program in Neuroprotection in Exercise at MGHand senior author of the study. Exercise is known to have positive effects on brain health, which is why identifying key mediators of those neuroprotective benefits, like irisin, has become such a critical goal of research.

Using mouse models, the team showed that genetic deletion of irisin impairs cognitive function in exercise, aging and Alzheimers disease, which was in part caused by alterations of newborn neurons in the hippocampus. The hippocampus is the compartment of the brain that stores memories and is the first to show signs of Alzheimers disease.At the same time, the MGH study found that elevating irisin levels in the bloodstream improved cognitive function and neuroinflammation in mouse models for Alzheimers disease.

For the first time, we showed that soluble irisin, and not its full-length parent protein FNDC5, is sufficient to confer the benefits of exercise on cognitive function, explains Wrann, who is also an assistant professor of Medicine at Harvard Medical School. These effects can possibly go well beyond what exercise itself can bring. This is particularly important inasmuch as irisin, a small natural peptide, would be much easier to develop into a therapeutic than the much larger membrane-bound protein FNDC5. While previous research used the parent protein FNDC5, she adds, scientists this time delivered only the irisin portion through an adeno-associated viral vector approach to the liver, similar to gene replacement therapy, and discovered irisin was able to cross the blood-brain barrier and directly affect the brain.

What makes this study particularly strong is that we show irisins effect on cognitive function in not one but four different mouse models, states Bruce Spiegelman of Dana-Farber Cancer Institute and Harvard Medical School, who discovered irisin in 2012 and is a co-author of the current paper. Researchers were further encouraged by the fact that irisin treatment was effective in Alzheimers disease mouse models even after the development of significant pathology. This could have implications for intervention in humans with Alzheimers disease where therapy typically starts after patients have become symptomatic, Wrann says.

Another important finding of the study is that irisin protects against neuroinflammation by acting directly on glia cells in the brain. Co-author Rudy Tanzi, co-director of the McCance Center for Brain Health at MGH, explains: Its hard to imagine anything better for brain health than daily exercise, and our findings shed new light on the mechanism involved: protecting against neuroinflammation, perhaps the biggest killer of brain neurons as we age. Adds Wrann: Since irisin does not specifically target amyloid plaques, but rather neuroinflammation directly, were optimistic it could have beneficial effects on neurodegenerative diseases beyond just Alzheimers.

Reference: Islam MR, Valaris S, Young MF, et al. Exercise hormone irisin is a critical regulator of cognitive function. Nat Metab. 2021;3(8):1058-1070. doi:10.1038/s42255-021-00438-z

This article has been republished from materials provided by Massachusetts General Hospital. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Cognitive Benefits of Exercise Are Driven by the Hormone Irisin - Technology Networks

Posted on 31 August, 2021

What follows is an extract from Yves Rees new book, titled All About Yves: Notes from a transition. Its published here with full permission.

I sink onto the red couch, clutching myself tight. I cross my legs, instinctive self-protection, then think better of it. Too feminine. Better to manspread a little. Before me, a coffee table houses a water jug, two glasses and a box of tissues. Typical shrink set-up.

Would you like some water?

Um, yes please.

The gender psychologist bends his lanky frame to pour from the jug. After handing over a glass, he settles into the armchair opposite. He crosses his legs, I note, but in that loose male wayone foot resting on the opposite thigh, crotch wide open. Still taking up space.

I look down at my own legs, spread them a little further apart. It feels insolent, to be so cavalier with my limbs.

The psychologist studies me over the rim of his glasses. He sports a white shirt and dark jeans, business casual, the slim-cut fabric flattering his elegant lines. No matter what happens, Ill never achieve that lissom shape. Ill remain forever stuck at 57, with a pelvis built to accommodate a human skull.

The psychologist watches me and I squirm under his gaze. I dont know what to do with my hands. Without thinking, I re-cross my legs.

So, he begins. What brings you here?

The psychologist was accredited with the World Professional Association for Transgender Health (WPATH), the global body that oversees trans medicine. Since 1979, WPATH has published Standards of Care to guide the treatment of trans and gender-nonconforming people. By using WPATH Standards, the psych would determine whether I was suffering from gender dysphoria, the medical term for the discomfort or distress that is caused by a discrepancy between a persons gender identity and that persons sex assigned at birth (and the associated gender role and/or primary and secondary sex characteristics).

In other words, gender dysphoria was the wrongness associated with my assigned role of woman. Id been born with female genitals, the world pronounced me woman, and now I was convinced thered been a terrible mistake. That was dysphoria.

The psychologists role was to shine the light of science on my distress. If I was found to have sufficient gender dysphoria, I would be officially transgender. With that diagnosis, I could get the green light for hormone replacement therapy and gender-affirmation surgery. I could carry my transness around like certified document, awash with red wax seals and weighty signatures. The world would have to believe me. Id be a legit member of Club Trans. Without the gender dysphoria diagnosis, I could get nothing. No surgery, no legitimacy. No hormones, unless I could find someone who prescribed testosterone via informed consent. Without the diagnosis, Id be just a fucked-up woman, a lady with issuesdisturbed, perhaps, but not trans. Or not, at least, according to the medical profession.

All About Yves is a timely and thought-provoking memoir about the trans experience.

So, what do you remember of early childhood? the psych asks in our second session. What kind of toys did you like to play with?

Hes in a blue shirt today, a lanyard draped around his neck. I feel like an insect under a magnifying glass, a strange specimen ripe for classification.

Um . . . well, I liked playing with my older brother, I begin. I idolised him. I always admired his clothes and wanted to look like him.

Hmmm, okay. The psych scribbles a few notes. And what were your favourite toys? What games did you play with your friends?

I make some quick calculations. The true answer is that I played with Barbies. Dolls houses. Dress-ups. I read fairytales. All the classic girl stuff. But thats not answer the psychs looking for. Im supposed to say that I rolled around in the dirt with trucks and climbed trees with my catapult and always, always refused to wear pink. Thats what female-to-male gender dysphoria is meant to look like. Thats the trans script Im meant to follow.

Only why is this new script as dull and narrow as the one I left behind?

Well, I played with a mix of toys, I guess. I had Barbies but also played heaps of cricket. We had Lego. I loved doing Warhammer with my brother.

Im spinning a story, telling neat tales of a tomboy childhood, once again inhabiting the character Ive been assigned: the trans person, born in the wrong body, a sick person looking for a cure. This is todays role. I must pull off the performance to get the diagnosis I need.

None of its a lie, not exactlyjust a question of emphasis. I mention the skateboard; omit the pink T-shirts and fairy wings. The full truth is so messy, too messy to fit inside this antiseptic office. The full truth is not woman, but not man either. Rather its something else altogether, something outside the stale binary that limits our imagination.

The psych pauses to take notes, re-crosses his legs. I sip water to fill the space.

And how did you feel about your body during childhood?

Well, I had an eating disorder as a teenager.

An eating disorder? Really? Tell me about that. Hes excited now, pen flying, on the trail of some solid dysphoria points. I can see my tally rising.

This is all a game, I realise, not a quest for truth. The rules are obvious: love everything masculine, disdain everything feminine. Hate your body. Share trauma. Be a fuck-up, but not too muchpsychosis is a disqualification. If you tick all the boxes, accumulate enough points, youll win the grand prize: gender dysphoria diagnosis, the golden ticket that opens all the doors.

The whole farce would be amusing if the stakes werent so high.

Simply put, diagnosis wields immense power, writes trans and disability activist Eli Clare. It can provide us access to vital medical technology or shame us, reveal a path toward less pain or get us locked up. It opens doors and slams them shut.

I would play along with the diagnosis game because I needed doors to open.

All About Yves: Notes from a transition is released today by Allen and Unwin (August 31, 2021). Buy it from all good bookshops or find itonline.

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Notes from a transition: The Diagnosis Game - HerCanberra

LE MARS Dr. Paul Parmelee was recently certified as a Bioidentical Hormone Replacement (BHRT) provider. He will offering BHRT (Pellet Therapy) beginning Aug. 18 in the Le Mars location of Floyd Valley Clinics.

BHRT is a personalized and natural approach to hormone replacement.

Appointments can be made by calling 712-546-3670.

Hormonal imbalances occur when there is too much or too little of a hormone in the bloodstream. Because of their importance, even the smallest hormonal imbalance can cause side effects throughout the body.

Signs and symptoms of hormonal imbalance in women include: fatigue, night sweats, hot flashes or flushes, decreased sex drive, weight gain, trouble sleeping, irritability, anxiousness, mood swings, low mood, and discomfort during intercourse.

Signs and symptoms of low testosterone and hormonal imbalance in men include: low sex drive, fatigue, loss of muscle mass, increased body fat (especially in the waist area), decreased bone mass, mood changes, low mood, irritability, brain fog, elevated blood sugar, stress, anxiousness, and high cholesterol.

If you are experiencing any of these symptoms and would like to learn more, your first step is to make an appointment with Dr. Parmelee. A patients hormone replacement eligibility will be determined during an office visit after conducting an extensive lab analysis.

If hormone replacement therapy would benefit the patient, the pellet will be inserted during an in-office visit. Once in the procedure room, an insertion site, usually somewhere around the upper buttocks, is numbed and a small incision is made. The hormone pellet is then inserted. When completed, the site is covered with a small bandage.

The pellet dissolves, and the body absorbs the contents over several months, leaving nothing behind to remove. After pellet insertion, you may continue most of your normal daily activities almost immediately.

Every patients symptoms are unique, so each journey is customized to fit those needs. Some patients report seeing improvement in as little as four weeks, but full optimization can take up to six months.

Everyone deserves to feel better no matter their age. If you are tired of dealing with the symptoms of hormone imbalance and want to take action, call today. Referrals are not necessary, but check with your insurance company to see if this service is covered. You may proceed at your own cost if you wish to receive treatment.

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FV Clinics to begin offering Hormone Replacement Therapy - Le Mars Daily Sentinel

Testosterone plays a vital role in a range of bodily functions, including muscle and bone health, cognition, red blood cell and sperm formation, and sexual and reproductive function in males.

However, testosterone levels can decline for various reasons, including stress, aging, and certain health conditions, such as hypogonadism.

This article discusses TRT in more detail, including who it is for, the types, how it works, how to get it, what to expect from it, and more.

TRT or androgen replacement therapy (ART) is a treatment that doctors give to males who have testosterone deficiency and are showing symptoms of hypogonadism.

Taking prescription testosterone helps restore the levels of this hormone in the blood, reversing the symptoms of low testosterone. People who take it may notice improvements in alertness, sexual function, energy, mood, and overall well-being.

Doctors prescribe TRT to males with hypogonadism. To receive a definitive diagnosis, blood tests must show that a person has low testosterone levels, which the American Urological Association notes as being below 300 nanograms per deciliter (ng/dl). The individual must also have other symptoms, such as fatigue, breast growth, and sexual dysfunction.

However, doctors do not usually recommend TRT as the first course of action for low testosterone levels, even for males who show such symptoms.

If other conditions or medications cause testosterone levels to drop, doctors usually treat the underlying condition before recommending TRT.

TRT is only available with a prescription. If a person presents with symptoms consistent with low testosterone levels, a doctor will only provide a prescription after taking a thorough medical history and performing physical and lab exams.

As hormone levels fluctuate depending on activity levels, diet, and the time of day, doctors usually take a blood test before noon on 2 consecutive days. They may sometimes also ask for imaging studies and additional tests, such as tests for luteinizing hormone and follicle stimulation hormone, to determine the cause of the low testosterone levels.

There are several ways to administer testosterone:

Injectable testosterone is an inexpensive and common form of TRT. A person can receive short-acting treatment, which involves a shot every 1 or 2 weeks, or long-acting treatment, in which the second shot is 4 weeks after the first, and all others are 10 weeks apart. The dosage and frequency of the treatment may vary depending on the person.

Doctors inject short-acting testosterone under the skin or muscle, while long-acting shots go in the gluteal muscles.

TRT can cause fluctuations in testosterone levels, which can affect energy levels, libido, mood, and the presence of symptoms such as breast tenderness.

People usually apply gels and creams on a daily basis. Gradual absorption causes more stable testosterone levels in the blood.

However, people using topical treatments must be careful to avoid skin-on-skin contact with other people for at least 6 hours after application. It is important to prevent the risk of transferring the medication onto other peoples skin because it may be dangerous for pregnant people and children.

Topical patches stick to the skin and stay in place for 24 hours until the next dose. The downsides to patches are that they are not cosmetically appealing and often cause skin irritations.

A person places a buccal patch above the upper teeth, and it releases testosterone over 12 hours. In comparison with oral medications, patches may be less toxic to the liver. However, these patches can cause headaches and gum and mouth irritation.

Testosterone pellets are small plastic pellets that doctors implant under the skin. The implant goes into a persons upper hip or buttock. The pellets dissolve slowly and can deliver TRT for 36 months.

Inserting implants is a minor inpatient surgical procedure. A doctor makes a small cut and then inserts the pellets in the fatty tissue below the skin. They perform the procedure under local anesthesia.

Learn more about testosterone pellets here.

Oral testosterone is a less common type of TRT that is more expensive and less practical. Its long-term use can potentially cause liver damage.

Most tablets also come with warnings about the drug causing hypertension and stroke. As a result, only individuals who cannot use other forms of TRT resort to taking testosterone by mouth.

A person applies nasal testosterone gel to the inside of the nose. They will need to do this three times a day at intervals of 68 hours, preferably at the same times every day. Some common reactions to this treatment include headaches, nosebleeds, a runny nose, and nasal discomfort.

TRT aims to restore a persons testosterone levels to normal. The individual can expect improvements in their blood testosterone levels within a week.

A person may also note other benefits, such as an increase in bone density and lean body mass, an improvement in well-being, and a boost to energy and libido. It may take from 4 weeks to several months to see positive changes.

TRT is typically a lifelong treatment. Once a person starts TRT, their doctor will continually monitor their response to treatment. People need to have routine checkups at least every 612 months to assess their blood testosterone levels.

A doctor will also monitor changes in symptoms and side effects at 3 and 6 months after the initial treatment and then annually.

TRT costs range from $150 to $1,500 per month and vary depending on various factors, including:

In addition to the possible short-term side effects, TRT may also cause health risks. The Endocrine Society recommends that people with the following conditions do not start using TRT:

It also states that the treatment is unsuitable for males who wish to conceive in the near future.

Males aged 40 years older, preadolescent people, and those with migraine or epilepsy may require special considerations.

The Food and Drug Administration (FDA) explains that the benefits and safety of TRT for treating low testosterone levels due to aging are not known. The organization requires that testosterone products carry warnings mentioning the possible risk of stroke and heart disease.

A 2017 review found that men undergoing TRT have a higher risk for cardiovascular events such as stroke.

Other side effects of taking testosterone include:

High cholesterol may also be a side effect. However, a 2021 study suggests that TRT may improve total cholesterol levels.

The current scientific literature suggests that TRT worsens breast and prostate cancer. However, TRT may offer benefits to people with early stage prostate cancer without stimulating the recurrence or progression of cancer.

The following are commonly asked questions:

TRT costs range from $150$1,500 per month depending on the type of TRT, the mode and frequency of administration, and the insurance coverage.

Yes. Most insurance companies cover all forms of TRT. However, there may be out-of-pocket costs.

Although TRT offers benefits to people with low testosterone levels, it can cause many short-term side effects. It may also put people who take TRT in the long term at increased risk of liver and heart problems.

TRT treatment length is indefinite unless the low levels are due to an underlying cause that is treatable.

TRT is a common treatment for low testosterone levels, but it is not suitable for everyone.

People who are considering TRT need a prescription and proper guidance from a doctor.

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TRT for low testosterone: Options, cost, and side effects - Medical News Today

Two out of every three caregivers in the U.S. are women. That means they provide daily or regular support to children, adults, or people with chronic illnesses or disabilities, says the U.S. Centers for Disease Control and Prevention (CDC). But while women tend to care for others, they tend to sacrifice their own physical or mental health, the CDC adds.

Many of the top health threats to women can be prevented, including the top causes of death among adult women in the U.S. heart disease, cancer, chronic lower respiratory disease, stroke, Alzheimers disease and unintentional injuries. Women tend to be underdiagnosed with heart disease, the No. 1 cause of death for both men and women.

During the COVID-19 pandemic, surveys found that women reported skipping preventive health services, such as their yearly check-up or routine tests, more so than men. Usually, that trend is reversed, with women tending to their healthcare needs more. But during the pandemic, more women took on roles as teachers in their homes and caregivers for elderly family members..

Nonetheless, primary care doctors warn that women who put off taking care of their own health to care for others often end up with conditions that could have been treated more easily in their earlier stages.

Women need to take some time to make sure they get their regular checkups and necessary health screenings, depending on their age and overall health, said Kamaljit Kaur, M.D., a family medicine physician with Baptist Health Primary Care. Even if we only see them once a year for their checkups, we can see subtle changes that could indicate a risk for developing or the presence of disease.

A checkups blood work can show the presence of an infection with elevated white blood cells, anemia or internal bleeding with too few red blood cells, high blood sugar that may indicate diabetes, and thyroid, kidney and liver function. A mental health screening can reveal depression, anxiety and sleep disorders, which can lead to other health problems.

We also discuss vital lifestyle factors such as weight management, proper nutrition and regular exercise to keep risk factors under control for heart disease, diabetes and other potentially serious conditions, said Dr. Kaur.

Here are the top threats to womens health:

Unhealthy diet

The foods you eat affect your health. Eating healthier can lower your risk of heart disease and stroke, diabetes and other chronic conditions.

Not enough exercise

Being physically active is good for your heart and overall health, including mental health. People who are not active have double the risk of heart disease and stroke, and higher risk diabetes, dementia, and some cancers. Exercise is one of the most vital steps you can take to better health.

Unhealthy weight

Most people struggle with their weight at some point in their lives. Being overweight can lead to high blood pressure, high cholesterol, diabetes and sleep apnea. Obesity can double your chance of heart disease. Consult with your doctor about lifestyle modification and the ideal weight range for you.

Smoking

Smoking triples the risk of dying from heart disease and stroke in middle-aged women. Quitting is one of the best things you can do to prevent heart disease and stroke.

Stress

If you feel regularly pressured because of workloads at home and the office, your physical well-being, lifestyle habits, and mental health will suffer and so can your immune system and the ability to fight off disease. Take steps to reduce stress.

Too much alcohol

Heavy drinking and binge drinking are risk factors for high blood pressure, heart disease and stroke. Alcohol may also cause problems by interacting with your medications.

Birth control and hormone replacement therapy (HRT)

Medications that contain estrogen the female hormone increase the risk of heart attack, stroke and mini-stroke (TIA). Consult with your doctor about these medications and their side effects.

Tags: Baptist Health Primary Care, women's health

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Ladies, Here's How to Prevent Top 7 Threats to Your Health - Baptist Health South Florida

Puppies Puppies (Jade Kuriki Olivo), Brain on Estrogen, progesterone, spironolactone, Truvada, Advil and Marijuana, 2018, cow brain, marijuana leaf, progesterone, estrogen, spironolactone, prep and pain killers. Photo: Courtesy the artist.

Jade Kuriki Olivos retrospective at the Kunsthaus Glarus in Switzerland brings together the Brooklyn-based artists work from the past decade. On view through August 22, the show maps the evolution of her practice as she transitioned from working under the guise of Puppies Puppies to living as an openly trans woman. Here, Olivo reflects on this transformation and discusses refusing to hide, the turning point represented by this exhibition, and the weekly Stonewall Protests for Black Trans Liberation that have kept her going over the past year.

I WAS HIDING from the world for a long time. In some ways, it was because it was so terrifying to beor even think about beinga trans woman. It felt like jumping off a cliff when I decided that it was what I wanted and needed in life.

Trans women have been consistently erased from historyour voices have been erasedso it is revolutionary for me, and for every trans person, especially BIPOC, gender-nonconforming, and two-spirit people, to be in control of the way our voices go out into the world. I still dont do many interviews, but unlike beforewhen my ex-husband or someone else would speak for me and I would be in a costume or sleeping on a sleeping pillnow I speak for myself. It means something very differentto be hidden as a trans woman. At other points in history, I wouldnt have been able to exist. So when I came out, I exposed myself fully and physically in a nude performance in Paris as a way of saying, Im here and Im not going to hide anymore. I couldnt be out as a trans woman and have hiding be a part of my work. I also wanted to document the changes in my body as my hormone-replacement therapy continued.

This is part of the arc of my exhibition at the Kunsthaus Glarus. It was emotional pulling this show together because I really wanted people to understand the evolution thats happened within me. The show covers eleven years of work. I called it a retrospective because I was thinking about how the amount of time that one is given, that a person is allowed to exist, is different for different people. Trans women often dont live as long as other people. It creates a different way of relating to time. Its definitely more precious for me, also having had a brain tumor.

The show marks a new way of making work for me. Ive always worked with other artists, so collaboration is nothing new, but Im moving into a more curatorial rolebecoming a conduit or a pathwayso that I can give a platform to other artists, especially a growing family of trans/GNC/2S+ artists. Going forward, when an institution asks me to do a solo show, I will invite another artist to do their own solo show, and they can decide how or if they want that to be associated with me. This is the direction I want to go in, and Im doing sex work and figuring out a way to survive so I can keep moving toward it. This new chapter begins with Bri Williams and Elliot Reeds exhibitions opening at Glarus in September.

Next to giving other artists I believe in space to express themselves, Stonewall Protests is the part of my life I am most passionate about. Stonewall is organized by Qween Jean and Joela Rivera, who have been holding weekly demonstrations for the past year in the wake of the murder of George Floyd. They are really the civil-rights leaders of now. Ive been protesting since the age of sixteen, but when I finally found Stonewall Protests at thirty-one, I was like, Oh my God, you found your family and your home. I also found a reason to keep going at a time when my art practice was not fulfilling me. It is a healing space. Stonewall is first and foremost a leading formation within the current Black Trans Lives Matter movement. The protests relate in some ways to the ballroom scene, which was founded by Black and Latinx trans women in New York City, specifically in Harlem, and brings that culture to protesting. An amazing group of bikers called Riders4Rights block intersections so the space can become a dance floor where people are able to express themselves to their fullest and feel safe enough to do so. There are different chants and a drum line and music made by a fantastic group called Musicians United NYC. A huge part of the Stonewall protests are mutual-aid events which emphasize the need to support one another, as well as the communities some Stonewall protesters live or grew up in.

In different Indigenous histories, trans people have been identified as healers or helpers, and Im drawn to this way of existing as a kind of sacred work. This is a practice I became familiar with through my father, who was Indigenous and taught me what he knew, and from my chosen Indigenous queer family members over time. In articulating all this, and thinking about when art and life blend together, Ive been really grateful to reflect on this evolution. As Puppies Puppies, I was making meme videos, really concealed from the world in this little shell. And now this is whats happening. Its my life and Im here.

As told to Camila McHugh

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Puppies Puppies (Jade Kuriki-Olivo) on transition, retrospection, and year of protest - Artforum