The Impact of Estrogens on Resting Energy Expenditure
Scientists are fascinated with estrogen’s influence on various physiological processes within human beings.
One area that has garnered much interest recently is estrogens’ effects on resting energy expenditure (REE).
REE is essential in supporting weight maintenance and energy balance. As it measures resting metabolic rate at rest, REE plays a significant role in keeping an ideal energy balance that allows healthy weight management.
Studies have uncovered an intricate relationship between estrogens and REE.
Estrogens appear to exert direct influences over mitochondria – the powerhouses of our cells – by changing how efficiently they convert nutrients to energy and create vitality for life.
Additionally, estrogen receptors have been observed in numerous tissues including fat tissue, skeletal muscle and the liver – suggesting estrogen’s importance in managing metabolism.
Understanding the intricate relationship between estrogens and REE is both scientifically interesting and potentially therapeutically significant, providing crucial insight into their scientific mechanisms as well as offering potential treatment benefits.
Research in this area could open doors for developing innovative interventions to manage conditions such as obesity and metabolic disorders, offering hope of a healthier tomorrow.
Scientists continue to gain more insights into estrogens’ effect on REE, making it evident that these hormones possess vast potential to advance our knowledge about metabolism and body functioning.
What is Estrogen?
Estrogen plays an essential role in women’s reproductive and breast health as well as cognitive functioning and bone strength.
Ovaries, adrenal glands, and fat tissues in both males and females produce estrogen; its levels tend to spike during puberty, pregnancy, and menopause.
Women produce three forms of estrogen (estrone, estradiol, and estriol) during each reproductive menstrual cycle that peak and fall over time.
Each type has its own configuration or number of atoms that enable it to interact with receptors throughout its body and activate specific cells as needed.
Estrogen works together with progesterone to regulate uterine lining before menstruation begins and placental development during gestation while simultaneously creating secondary sexual characteristics in girls and decreasing male pattern hair formation in boys.
Women who have higher estrogen levels often enjoy lower cholesterol levels and have a reduced chance of heart disease compared with women who don’t produce as much estrogen, likely as a result of estrogen’s influence on your blood vessels; it lowers “bad” LDL cholesterol while simultaneously raising “good” HDL levels.
Men, trans-women, children, and postmenopausal women all produce estrogen via adrenal glands, liver tissue, and fat tissue.
Estrogen can also come from food sources like vegetables containing phytoestrogens such as daidzein, genistein, and miroestrol; plus fortified products (like soy) with additional estrogen levels (for instance).
Estrogen can be prescribed as part of hormone therapy to those born male who wish to transition, in combination with anti-androgenic treatments, in order to achieve female gender identity transition.
Administration can include taking tablets orally; being given injections; patch or gel application or inserting slow-release suppositories under the vagina.
Estrogen as an Agent in Metabolism
Estrogen plays an essential part in female reproduction as well as multiple metabolic processes affecting muscle, fatty acid, and bone health, cardiovascular system functioning, and overall cardiovascular wellbeing.
Ovaries, adrenal glands, and fat tissues produce estrogen; more women produce this steroid than men; this may enhance cognitive performance as well.
Estrogens are active compounds that must be broken down and excreted from the body for them to continue having an effective role.
Estrogen is broken down in your liver and intestine, then excreted through urine or stool out of your system as water-soluble forms that will eventually leave through stool or urine.
Unfortunately, these processes are complex, with various factors having an influence over their effectiveness.
Genetic and environmental influences also can have an effect on this process, including diet, obesity, high insulin levels, medications (e.g. hormone replacement therapy), or overexposure to estrogen-producing chemicals in the environment.
An active lifestyle and diet are integral in supporting optimal estrogen metabolism to lower its toxic levels in the body.
Estrogens play an invaluable role in maintaining optimal metabolic health and protecting us against diseases.
These agents promote fatty acid b-oxidation in skeletal muscle, decrease glucose consumption, increase expression of genes related to lipid metabolism, and stimulate mitochondrial respiration within this organ system.
Additionally, they may help reduce cholesterol concentrations in blood and increase triglyceride levels; thus defending against atherosclerosis before menopause.
Muscle strengthening exercises may even stimulate exercise endurance within muscles while increasing protein synthesis that transports other essential nutrients like iron, cortisol, or thyroxine into muscle fibers – all helping promote optimal health in muscular tissue as a result.
Research Studies Showing Estrogen Influencing Resting Energy Expensive
A number of research studies have established the connection between estrogen and resting energy expenditure (REE) for both women and men (D’Eon & Braun, 2002).
Estrogen is a major female sexual hormone produced in the ovaries that contains 18 carbon steroid hormones such as 17_estradiol (17_E2), estrone, and estriol that interact with orexigenic and anorexigenic (fat-burning) hormones to control food consumption as well as weight distribution and fat distribution in the body.
Puberty affects boys and girls differently: girls often develop more fat due to an increase in estrogen while boys gain muscle mass as their testosterone production rises.
At premenopausal (perimenopause), which typically begins 8-10 years before menopause, blood estrogen levels begin to drastically drop due to estrogen deficiency.
Hormone replacement therapy could restore metabolic health impairment or potentially impair fat use as fuel leading to weight gain or metabolic health impairment; a restorer can often help.
REE is composed of both metabolically active and inactive energy sources such as proteins, lipids, glucose, lactate, odd-chain fatty acids, and glycerol; with these latter two produced through gluconeogenesis to maintain steady blood glucose levels during endurance exercise.
Increased estrogen levels enhance glycerol breakdown and synthesis processes to increase carb availability during physical exertion.
Research at the University of Jyvaskyla revealed, however, that neither menopausal status or blood estrogen levels influence middle-aged women’s ability to utilize fat as an energy substrate during rest and exercise – suggesting higher utilization may not indicate improved glucose tolerance.
Factors That Affect Estrogen’s Effect on Resting Energy Expenditure
Female sexual hormones have multiple purposes. Their primary use, of course, is reproduction; but, these same hormones also exert enormous influences over muscle protein turnover and strength performance.
Ovary secretions contain two major hormones released by ovary tissue; 17-estradiol and progesterone make up estrogen (D’Eon and Braun 2002).
Young women experience their estrogen levels increasing 10-100-fold throughout each menstrual cycle during the follicular phase up to peak at ovulation before gradually declining before rebounding to another peak at the start of the luteal phase where both progesterone and estrogen rise together.
Women hoping to avoid pregnancy often opt for oral contraceptives that provide low doses of both hormones in each cycle (i.e. combining them into one daily pill).
Menopause leads to chronic decreases of estrogen, leading to irregular periods and vaginal atrophy.
Low estrogen also results in reduced metabolism rates which reduce how much energy an individual expends at rest; this reduced amount can cause weight gain through fat accumulation.
Reducing estrogen intake could impede your body’s ability to process carbohydrates during exercise, leading to reduced glycogen stores and diminished performance at submaximal intensities.
Gonadal estrogen interacts with other hormones to control food consumption and fat distribution; for instance, lower estrogen in middle-aged and postmenopausal women leads to greater fat accumulation as well as less response to anabolic stimuli such as training (Hansen et al. 2009b).
Estrogen plays an essential part in weight management due to its influence on resting energy expenditure.
An increase in resting energy expenditure means more calories burned when at rest, making it simpler to sustain healthy weight levels.
Estrogen can have an influence on fat distribution in the body; lower estrogen levels tend to correlate with an increase in abdominal fat storage.
By understanding how estrogen impacts weight management, individuals can take proactive measures to optimize estrogen levels and support overall health and well-being.
1. Follicular Phase Raise Resting Energy Output
Women during their menstrual cycles’ follicular phases when estrogen production peaks require significantly more energy to move their bodies than non-menstruating women do.
Increased estrogen content causes glucose to form and be utilized by type I muscle fibers for endurance performance improvement (Oosthuyse & Bosch).
Female sex hormones not only directly influence bone and muscle health, but their low levels have indirect ramifications on energy metabolism through orexigenic and anorexigenic systems in the hypothalamus.
Estrogen interacts with orexigenic neurons via estrogen receptors on these neurons to influence food intake and body weight regulation.
Estrogens help improve fat metabolism during exercise by directly increasing lipolysis in fat tissue and stimulating brain endocrine secretions that produce leptin (an appetite regulator).
Leptin can effectively regulate our appetite by stimulating gut hormones to secrete GLP-1 and decreasing food consumption, while estrogens assist fat oxidation during aerobic exercise by activating mitochondrial fatty acid oxidase activating mitochondrial fatty acid oxidase for maximum efficiency during intense activity.
Estrogens increase skeletal muscle mass and glycogen storage by inhibiting protein degradation.
Furthermore, muscle protective supplements reduce muscle damage, inflammation, and repair during rigorous resistance training activities such as high-intensity resistance training sessions.
After menopause, estrogen’s beneficial impact on muscular-skeletal function diminishes as plasma estradiol concentrations drop.
Isacco, Duchet, and Boisseau reported that obese postmenopausal women training at 50% maximum aerobic capacity at 50% fat used less fat as an energy substrate despite similar baseline plasma esterification values.
Reduced fat oxidation during exercise could be attributable to reduced plasma estrogen concentration.
Estrogen may have less of an effect on premenopausal women receiving hormone replacement therapy, thus decreasing fat oxidation rates further.
2. Lower estrogens decrease resting energy expenditure
Estrogen levels vary throughout a woman’s menstrual cycle, reaching its highest point just prior to ovulation during a woman’s follicular phase – roughly in the middle.
Estrogens play an instrumental part in puberty development by stimulating secondary sexual characteristics like pubic and armpit hair growth; helping control vaginal and uterine development as well as contributing to breast formation during puberty.
Low estrogen levels have been linked with weight gain and body fat increase among women.
This could be caused by estrogen’s interactions with orexigenic and anorexigenic hormones which regulate energy balance; additionally, estrogen increases UCP2 production in fat tissue which promotes fat burning.
Estrogens also possess the power to directly activate leptin receptors within the hypothalamus and reduce appetite while increasing resting energy expenditure.
Estrogens may bind and activate adiponectin receptors found within white adipose tissue to increase lipid breakdown and fat burning.
Estrogens can be converted to their active forms using various enzymes such as cytochrome P450 and 17b-hydroxysteroid dehydrogenases.
Additionally, estrogens may also be broken down through b-glucuronidase enzyme activity or conjugated to pregnanediol via pregnanediol glucuronide conjugation by gut microbes in order to be digested by gut bacteria – both techniques acting directly on their metabolism while protecting against diet-induced obesity in both women and rodents.
3. Estrogens Increase Fat Storage
Estrogens interact with orexigenic and anorexigenic neuropeptides to suppress food intake; one reason they increase resting energy expenditure.
Estrogens may act directly on adipocytes to encourage mobilization of fat storage within them and decrease fat cell size – this may help decrease both fat accumulation as well as accumulation in liver tissues due to reduced cholesterol synthesis production.
Estrogens increase leptin production, helping obese mice reduce food consumption and weight gain through acting like leptin receptors.
Premenopausal women typically store fat more in their hips and thighs due to estrogen’s effect, due to estrogen being the prime player in fat storage.
After menopause, estrogen declines dramatically and women may store fat more readily in their stomach and belly than in lower body areas such as hips or thighs.
Cortisol and insulin hormones play an integral part in shifting fat storage towards middle areas; estrogen may offset this tendency by decreasing cortisol and increasing insulin; the long-term result will still be less hip/thigh fat storage.
Estrogens also exert an immense effect on gut microbiota, altering it both for humans and rodents alike.
Studies of estrogens from the ER family have clearly illustrated their effects in both environments – in fact, ovariectomy increases energy intake and weight gain while 17b-estradiol (E2) treatment can protect from such weight gain in mice on high-fat diets while 17b-estradiol treatment prevents further weight gain by protecting from future weight gains altogether.
Gut microbiota may exert significant influences on metabolic rates by altering nutrient availability and energy use within the body.
Studies on long-term E2 treatment have found it can improve glucose tolerance, insulin sensitivity, and lipid metabolism of mice fed high-fat diets; plus it’s linked with a greater diversity of bacteria within their large intestine.
4. Estrogens and Muscle Mass
Estrogens play multiple roles over one’s lifespan. They contribute significantly to muscle health.
Estrogen levels increase throughout puberty, pregnancy and menstruation in women before gradually declining during menopause when periods stop being taken and estrogen levels decline, often causing symptoms like hot flashes, vaginal dryness and loss of sexual drive as symptoms.
Estrogens help regulate muscle building rates during resistance training sessions; helping your body gain strength more rapidly as a result.
Though androgens’ anabolic effects on muscle growth have long been acknowledged, less is understood about how estrogens contribute to improving muscle quality.
According to some, estrogens could help improve quality by increasing myosin phosphorylation – one of two proteins responsible for muscle contraction along with actin – at higher rates.
Estrogens may increase muscle cells’ ability to generate force and make muscle fibers larger, increasing power output and helping achieve increased power output.
Estrogen may reduce muscle cell apoptosis while simultaneously stimulating the proliferation of muscle stem cells.
Studies indicate that estrogens and gut microbes play an integral part in female energy homeostasis.
Ovariectomy induces dramatic weight gain in mice fed a high-fat diet while estrogen treatment protects them from obesity.
These results demonstrate how gut microbiota can exert their own unique influences over energy homeostasis through multiple mechanisms – including interactions with estrogens directly.
Recent experiments demonstrate how E2 can inhibit lipopolysaccharides produced by Gram-negative bacteria and protect from HFD-related metabolic conditions like fatty liver disease, insulin resistance, and type 2 diabetes.
E2 may interact with leptin to significantly impact female energy metabolism.
All these interactions demonstrate estrogens’ effect on our gut microbiota with potentially severe health impacts.
5. Estrogen and Bone Density
Estrogen can increase bone density by suppressing osteoclasts’ ability to break down bone.
Estrogens accomplish this by binding to estrogen receptors inside cells and activating them; this activates numerous genes while simultaneously suppressing interleukin production which promotes bone resorption.
Estrogens promote intestinal calcium absorption while shielding bones against parathyroid hormone (PTH).
Estrogen plays an essential part in maintaining bone density by both preventing loss and stimulating its formation, with this effect becoming especially powerful during periods of decreased estrogen availability such as menopause.
Furthermore, estrogen increases bone remodeling rate which aids in maintaining its density.
Women usually produce two estrogens known as estradiol and estriol; one is produced in their ovaries during gestation while one is produced during placenta development.
Women who have low estrogen levels are at greater risk for bone loss and osteoporosis.
Bone density can be affected by factors like body weight, smoking habits, and physical activity levels.
Body weight is one of the primary determinants of bone density. While estrogens play a minor role by encouraging fat storage within bones, they also increase strength by decreasing likelyhood of breakage.
Estrogen therapy is one of the most frequently recommended forms, usually administered orally as conjugated estrogens at approximately daily dosage of approximately 0.6225 mg, without concurrent progestin therapy.
Studies have demonstrated that estrogen alone may help older women reduce osteoporosis and hip fracture risk; its exact mechanism remains undetermined but may involve fat storage reduction and strengthening bones as possible causes.
How to Increase Estrogen Levels for Increased Resting Energy Expenditure
Estrogen is one of several hormones that interact to control food intake, body weight distribution, and body fat distribution among humans.
Obese individuals benefit from higher circulating estrogen levels due to an increase in the expression and production of UCP2 in fat tissue and muscle; additionally, this happens through interactions between estrogen, leptin, and T3.
Animal studies demonstrate that lower estrogen levels lead to greater weight gain and slower metabolic rates; similarly, in human women losing estrogen may decrease energy expenditure and fat oxidation rates.
Studies conducted recently by researchers demonstrated that middle-aged women’s use of fat for energy differed with menstrual cycle phase and estrogen levels; with rates being highest during the mid-luteal phase with elevated estrogen and decreasing after six days of estrogen suppression.
Optimizing estrogen levels prior to and during menopausal years could potentially improve energy expenditure for female athletes involved in vigorous physical activities like high-intensity workouts.
Lifestyle Changes for Healthy Metabolism and Estrogen Balance
Hormones produced by the endocrine system act as chemical messengers within our bodies to control functions such as metabolism, reproduction, and stress relief.
Even small fluctuations in estrogen levels can have profound repercussions for health; traditional medical solutions often only offer temporary solutions; natural methods may offer longer-term solutions that reset metabolism and balance estrogen levels more permanently.
Hormonal imbalance may stem from any number of reasons, including thyroid (triiodothyronine) or cortisol (dexamethasone) issues; to restore health through holistic eating practices and taking supplements that support metabolism regulation.
Interval training can boost your metabolism: fast for 30-60 seconds before returning to regular speed for 8-12 cycles – this type of workout provides greater metabolic stimulation than steady-paced exercises, keeping it revved throughout the day!
Eat proteins to give your metabolism a boost! Your body burns more calories digesting protein than it does digesting carbs or fats; by eating protein regularly your metabolism receives an additional boost.
For optimal hormone balance, seek grass-fed varieties that contain more omega-3 fatty acids to balance hormones effectively.
Conclusion
Estrogen plays multiple integral roles in metabolism and is one of the best-studied endogenous (natural) steroid hormones.
Breast hormones play a significant role in puberty development.
Pregnancy helps create mammary glands while postpartum lactation necessitates their development in order to produce enough milk for breastfeeding purposes.
Enhancing glycogen accumulation and utilization by slow-oxidative type I muscle fibers during prolonged endurance exercise is beneficial, increasing glucose availability and optimizing performance.
When engaging in extended physical exercise, estrogen and progesterone both decrease gluconeogenesis output – an essential metabolic pathway that produces glucose from lactate and odd-chain fatty acids for energy during ultra-long endurance events.
Without proper insulin regulation, blood glucose levels may fall rapidly and performance decline significantly, potentially derailing any long-endurance race success.
Estrogen increases fat oxidation during rest and moderate-intensity exercise and protein utilization during rest and high-intensity exercise, increasing non-estrogen binding globulin/albumin ratios which provide females a survival advantage during periods of food scarcity by conserving glucose reserves for their fetuses instead of using all available energy reserves themselves as energy reserves.
Animal and human studies have proven that exogenous estrogen can reverse the declines seen during menopause in physical activity, RMR, and TDEE levels.
Ovarectomy surgery also significantly increased fat oxidation during endurance training sessions compared to premenopausal women as well as liver triglyceride accumulation; possibly because basal plasma estrogen concentrations had declined or due to postmenopausal years reduced fat-free mass mass.
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