The Impact of Estrogens on Resting Energy Expenditure
Written by Ben Bunting: BA, PGCert. (Sport & Exercise Nutrition) // British Army Physical Training Instructor // S&C Coach.
--
In the quest for a better understanding of the human body, scientists have long been intrigued by the role of estrogens in various physiological processes.
One area that has captured attention is the impact of estrogens on resting energy expenditure (REE).
As the metabolic rate at rest, REE plays a crucial role in maintaining a healthy weight and overall energy balance.
Studies have revealed a complex relationship between estrogens and REE.
Estrogens seem to have a direct effect on the mitochondria, the powerhouses of our cells, by influencing their efficiency in converting nutrients into energy.
Furthermore, estrogen receptors are found in many tissues, including adipose tissue, skeletal muscle, and the liver, suggesting estrogens' role in regulating metabolism.
Understanding the intricate relationship between estrogens and REE is not only vital for shedding light on the scientific mechanisms but also for potential therapeutic implications.
Insights gained from this research area could pave the way for novel interventions in managing conditions like obesity and metabolic disorders, offering hope for a healthier future.
As scientists continue to unravel the mysteries of estrogens' impact on REE, it becomes increasingly clear that these hormones hold vast potential for improving our understanding of metabolism and how our bodies function.
Estrogen Explained
Estrogen is an essential hormone in female reproductive and breast health. Additionally, it contributes to cognitive functioning and bone strength.
Ovaries, adrenal glands and fat tissues from both males and females produce estrogen; its levels often spike during puberty, pregnancy and menopause.
Women produce three forms of estrogen (estrone, estradiol and estriol) during each reproductive menstrual cycle that peak and decline.
Each type has its own arrangement or number of atoms that causes it to interact with specific receptors throughout their bodies, binding with them as needed to activate specific cells throughout.
Estrogen works alongside progesterone to control the lining of the uterus before menstruation begins and with placenta during gestation while simultaneously creating secondary sexual characteristics in girls while decreasing male pattern hair formation in boys.
Women with higher estrogen levels tend to have lower cholesterol levels and an decreased chance of heart disease compared with women with lower estrogen levels, due largely to how estrogen affects your blood vessels: decreasing "bad" LDL cholesterol while simultaneously raising HDL levels.
Men, trans-women, children and postmenopausal women all produce estrogen through adrenal glands, liver tissue and fat tissue.
Furthermore, estrogen can also come from foods like vegetables containing phytoestrogens like daidzein, genistein and miroestrol as well as fortified foods with extra estrogen (such as soy).
Estrogen is often taken as part of hormone therapy for people assigned male at birth who wish to transition to female as it works alongside anti-androgenic treatments.
Administration can include orally taking tablets; injection; patch or gel application or slow release suppositories inserted under the vagina.
The Role of Estrogen in Metabolism
The hormone estrogen plays an essential role in female reproduction as well as metabolic processes like skeletal muscle and fatty acid metabolism, bone health and cardiovascular system function.
Ovaries, adrenal glands, and fat tissues produce this steroid; more estrogen is produced by women than by men; cognitive functioning may also benefit.
Estrogens are active compounds that must be broken down and excreted from the body to continue having an effectful role.
Estrogen is broken down in the liver and intestine, where its water-soluble form is then sent onward for elimination through feces or urine from your system.
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 poor diet, obesity, high insulin levels, medications (e.g. hormone replacement therapy), and overexposure to estrogen-producing chemicals in the environment.
A healthy lifestyle and diet can support efficient estrogen metabolism to decrease its toxicity levels in the body.
Estrogens play an essential role in maintaining optimal metabolic health and warding off disease.
They support fatty acid b-oxidation in skeletal muscle, decrease glucose utilization, increase expression of genes related to lipid metabolism and stimulate mitochondrial respiration in skeletal muscle.
Additionally they can decrease cholesterol concentrations in blood and increase triglyceride levels, helping protect against atherosclerosis before menopause.
They may even activate exercise endurance within muscles and promote formation of proteins that transport other nutrients like iron, cortisol or thyroxine into muscle fibers - these substances all help promote optimal health in muscle tissue as well.
Research Studies on Estrogen and Resting Energy Expensive
Research studies have demonstrated the effect of estrogen on resting energy expenditure (REE) for both women and men (D'Eon & Braun, 2002).
Estrogen is a major female sex hormone produced by the ovaries that contains 18 carbon steroid hormones including 17_-estradiol (17_E2), estrone and estriol that interact with orexigenic and anorexigenic (fat-burning) hormones to control food intake as well as body weight distribution and fat distribution.
Puberty alters both boys and girls differently: girls tend to develop more fat due to an increase in estrogen while boys gain muscle mass from testosterone.
At premenopausal (perimenopause), which usually begins 8-10 years before menopause, blood estrogen levels in women begin to drastically decline due to estrogen deficiency.
This could potentially impair fat use as fuel leading to weight gain or metabolic health impairment (restoration can be accomplished using hormone replacement therapy).
REE is composed of both metabolically active and inactive energy sources that include proteins, lipids, glucose, lactate, odd-chain fatty acids and glycerol - the latter two being produced through gluconeogenesis to prevent blood glucose levels from dropping too low during endurance exercise.
High estrogen levels enhance glycerol breakdown and synthesis processes to increase carb availability during physical exertion.
Contrarily, research conducted at the University of Jyvaskyla revealed that menopausal state or blood estrogen levels do not impact middle-aged women's ability to use fat as an energy substrate during both rest and exercise - suggesting higher utilization may not indicate improved glucose tolerance.
Factors That Influence Estrogen's Effect on Resting Energy Expenditure
Female sexual hormones serve multiple functions. Their primary use, however, is reproduction; however, these same hormones also exert profound influences over muscle protein turnover and strength performance.
Two major hormones released by ovary secretions include 17-estradiol and progesterone which comprise the estrogens (D'Eon and Braun 2002).
Young women experience their estrogen levels increasing 10-100-fold throughout each menstrual cycle during follicular phase until reaching peak at ovulation, before decreasing rapidly before rebounding towards another peak at start of luteal phase where progesterone also rises with estrogen.
To avoid pregnancy, many women opt for oral contraceptives which provide low doses of both hormones throughout each cycle (e.g. combining them into one daily pill).
Menopause causes chronic reductions of estrogen, leading to irregular periods and vaginal atrophy.
Low estrogen also results in lower metabolism rates which reduce how much energy an individual expends at rest; this reduced amount can result in weight gain - particularly fat accumulation.
Lack of estrogen may also hinder your body's ability to break down carbohydrates during exercise, leading to lower glycogen stores and decreased performance at submaximal intensities.
Furthermore, gonadal estrogen interacts with other hormones to regulate food intake and body 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).
The impact of estrogen on weight management
Estrogen plays a significant role in weight management due to its influence on resting energy expenditure.
A higher resting energy expenditure results in a greater number of calories burned at rest, making it easier to maintain a healthy weight.
Additionally, estrogen affects fat distribution in the body, with lower estrogen levels often associated with increased abdominal fat.
By understanding the impact of estrogen on weight management, individuals can take proactive steps to optimize estrogen levels and support their overall health and well-being.
1. Follicular phase increases resting energy expenditure
Women during the follicular phase of their menstrual cycle, when estrogen is at its peak, require more energy to move their body mass than non-menstruating women do.
Increased estrogen content during this phase causes glucose appearance and utilization by slow oxidative type I muscle fibers for endurance performance improvement (Oosthuyse & Bosch).
Female sex hormones not only directly impact bone and muscle health, but their low levels also have indirect ramifications on energy metabolism through orexigenic and anorexigenic systems in the hypothalamus.
Estrogen interacts with orexigenic neurons via its interactions with estrogen receptors on orexigenic neurons to influence food intake and body weight regulation.
Estrogens increase fat metabolism during exercise by directly increasing lipolysis in adipose tissue and stimulating the release of leptin (an appetite regulator) from brain endocrine secretions.
Leptin then regulates appetite by inducing release of GLP-1 from gut hormones that decrease food intake. Estrogens further promote fat oxidation during aerobic exercise by activating mitochondrial fatty acid oxidase during intense activity.
Estrogens increase skeletal muscle mass and glycogen storage by inhibiting protein degradation.
They also decrease muscle damage, inflammation, and repair during exercise - particularly during high intensity resistance training.
After menopause, estrogen's positive impact on muscle-skeletal function diminishes as plasma estradiol concentrations decline.
Isacco, Duchet and Boisseau reported that obese postmenopausal women training at 50% of maximum aerobic capacity at 50% fat use less fat as an energy substrate than men despite similar basal plasma esterification values.
This decrease in fatty acid oxidation during exercise may be attributable to decreased plasma estrogen concentration.
Estrogen may have even less of an impact on musculoskeletal systems when pre- or postmenopausal women receive hormone replacement therapy, thus lessening fat oxidation rates further.
2. Low estrogens decrease resting energy expenditure
Estrogen levels fluctuate throughout a woman's menstrual cycle, peaking during the follicular phase - roughly in the middle - just prior to ovulation.
Estrogens play an important role in puberty development by stimulating secondary sexual characteristics like pubic and armpit hair growth; also 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 may be caused by estrogen's interactions with orexigenic and anorexigenic hormones that modulate energy balance; additionally, estrogen increases UCP2 production in adipose tissue which aids fat burning.
Additionally, estrogens have the power to directly bind and activate leptin receptors in the hypothalamus, leading to decreased appetite and an increase in resting energy expenditure.
Furthermore, estrogens may bind and activate adiponectin receptors located within white adipose tissue to increase lipid breakdown and fat burning.
Estrogens can be converted to their active forms via various enzymes, such as cytochrome P450 and 17b-hydroxysteroid dehydrogenases.
Furthermore, estrogens may also be glucuronidated by b-glucuronidase or conjugated to pregnanediol by pregnanediol glucuronide conjugation and taken up by gut microbes for digestion - acting directly on their metabolism while protecting against diet-induced obesity both in women and rodents.
3. Estrogens increase fat storage
Estrogens interact with orexigenic and anorexigenic neuropeptides to suppress food intake, one of the primary reasons they increase resting energy expenditure.
Estrogens may also act directly on adipocytes to promote mobilization of fat storage within them and decrease fat cell size - this may reduce fat storage as well as accumulation in liver tissues due to reduced synthesis of cholesterol production.
Finally, estrogens increase leptin production, helping obese mice reduce food intake and weight gain by acting like leptin receptors on them.
Premenopausal women tend to store fat more in their hips and thighs due to estrogen's effect.
After menopause, however, estrogen declines, prompting women to store more in their stomach and belly instead of lower body areas such as hips and thighs.
Cortisol and insulin hormones play a part in shifting fat storage towards middle areas; estrogens may counter this by decreasing cortisol and increasing insulin; in either case the long term result remains decreased hip/thigh fat storage.
Estrogens also exert an immense effect on gut microbiota, modulating it both for humans and rodents alike.
Indeed, studies of ER family estrogens have demonstrated their effects in both environments - in fact ovariectomy increases energy intake and weight gain while 17b-estradiol (E2) treatment can prevent such weight gain in mice on high fat diets, while 17b-estradiol treatment prevents weight gain by protecting from weight gain altogether.
Gut microbiota may influence metabolic rates by impacting nutrient availability and energy use within the body.
Long-term E2 treatment has been found to enhance glucose tolerance, insulin sensitivity and lipid metabolism in mice fed a high fat diet; plus it's associated with greater diversity of bacteria within their large intestine.
4. Estrogens and muscle mass
Estrogens play many different roles throughout a person's lifetime.
Estrogens increase during puberty, pregnancy and menstruation in women; then decrease during menopause when periods stop being taken and the estrogen levels decline, often leading to hot flashes, vaginal dryness and loss of sex drive as symptoms.
Estrogens also help control muscle building rates when performing resistance training sessions; helping your body gain strength more rapidly as a result.
Though androgens' anabolic effects on muscle mass have long been recognized, less is understood about how estrogens contribute to improving muscle quality.
According to some, estrogens may enhance quality by increasing myosin phosphorylation levels - one of two proteins responsible for muscle contraction alongside actin.
Estrogens may increase muscle cells' ability to produce force and thus make muscle fibers larger, necessary for increased power output.
Furthermore, estrogen may decrease muscle cell apoptosis while stimulating proliferation of muscle stem cells.
Recent studies indicate that estrogens and gut microbes play a crucial role in female energy homeostasis.
Ovariectomy dramatically increases weight gain on high-fat diet mice while estrogen treatment prevents obesity.
These results demonstrate how gut microbiota may exert its own unique influences over energy homeostasis through multiple mechanisms - including direct interactions with estrogens.
Recent experiments demonstrate that E2 can inhibit lipopolysaccharides produced by Gram-negative bacteria, thus providing protection from HFD-related metabolic disorders like fatty liver disease, insulin resistance and type 2 diabetes.
E2 may also interact with leptin to significantly influence female energy metabolism.
All these interactions demonstrate estrogens can alter our gut microbiota with serious consequences on health1.
5. Estrogens and bone density
Estrogens increase bone density by inhibiting osteoclasts' ability to break down bone.
Estrogens achieve this by binding with estrogen receptors inside cells and activating them; this causes various genes to be activated while at the same time inhibiting interleukins production that promote bone resorption.
Estrogens also enhance intestinal calcium absorption while protecting the skeleton against parathyroid hormone (PTH).
Estrogen plays an indispensable role in maintaining bone density by both preventing bone loss and stimulating its formation, an effect which becomes especially potent during periods of low estrogen availability, such as menopause.
Furthermore, estrogen increases bone remodeling rate which helps preserve its density.
Women primarily produce two estrogens known as estradiol and estriol; one produced in their ovaries while another by placenta during gestation.
Women with low estrogen levels are at increased risk for bone loss and osteoporosis.
There are various factors that influence bone density, including weight, smoking, and physical activity levels.
Of the major influences on bone density is body weight. Estrogens may play a minor role by increasing fat storage in bones; however they also increase strength by decreasing likelihood of breakage.
The most widely prescribed form of estrogen therapy involves oral conjugated estrogens administered at an approximate daily dosage of approximately 0.6225 mg, without concurrent progestin therapy.
Studies have demonstrated that taking estrogen alone may help to prevent osteoporosis and hip fracture risk among older women; its exact mechanism remains elusive but may involve fat storage reduction and strengthening bones as possible causes.
How to Optimize Estrogen Levels for a Higher Resting Energy Expendiment
Estrogen interacts with orexigenic and anorexigenic hormones to regulate food intake, body weight and fat distribution in humans.
For those living with obesity, elevated circulating levels of estrogen increase resting energy expenditure through increased expression and production of UCP2 in adipose tissue and muscle; this also occurs due to more interactions between estrogen, leptin and T3.
Lab studies on animals indicate that reduced estrogen levels lead to greater weight gain and slower metabolic rates; similarly, in human women losing estrogen may reduce energy expenditure and fat oxidation rates.
Studies conducted recently by researchers revealed that the rate at which middle-aged women use fat as an energy source varies with their menstrual cycle phase and estrogen levels, with rates being highest during mid-luteal phase with elevated estrogen and lowest after six days of estrogen suppression.
It appears that optimizing estrogen levels prior to and during menopausal years may enhance female energy expenditure, particularly during vigorous physical activity like high intensity workouts.
Lifestyle Changes to Support a Healthy Metabolism and Estrogen Balance
Hormones produced by the endocrine system serve as chemical messengers to the body that control major functions like metabolism, reproduction and managing stress.
Even minor fluctuations in their levels can have devastating repercussions for health; conventional medicine typically only offers temporary fixes; there may be natural methods available that can reset metabolism and balance estrogen levels more permanently.
Hormonal imbalance can result from any number of causes, including thyroid (triiodothyronine) or cortisol (dexamethasone) problems, but you can restore your health through adopting a whole foods diet and taking herbal and nutritional supplements that support healthy metabolism and estrogen regulation.
Increase your metabolism through interval training: go hard and 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 protein. Your body burns more calories digesting and absorbing protein than carbohydrates or fats, so when you eat it your metabolism receives an additional boost.
For best results, opt for grass-fed varieties which contain more omega-3 fatty acids to balance hormones more effectively.
Conclusion
Estrogen plays numerous crucial roles in metabolism and is widely studied among endogenous (natural) steroid hormones.
As part of their role, breast hormones play an essential part in puberty.
Furthermore, pregnancy helps create mammary glands and postpartum lactation necessitates secreting milk for breastfeeding purposes.
Increased glycogen appearance and utilization by slow-oxidative type I muscle fibers during prolonged endurance exercise is also beneficial, increasing glucose availability and improving performance.
When performing prolonged physical exercise, estrogen and progesterone both reduce gluconeogenesis output - an essential metabolic pathway that produces glucose from lactate and odd-chain fatty acids to provide energy for exercise performance during ultra-long endurance events.
Without this process functioning optimally, blood glucose levels drop precipitously and performance can decline considerably, hampering any possible successful performance of an ultra-long endurance event.
Estrogen also increases fat oxidation during rest and moderate intensity exercise and protein utilization during rest and high intensity exercise, and leads to an increase in non-estrogen-binding globulin/albumin ratios, providing females a survival advantage during periods of food scarcity by conserving glucose reserves for their foetuses instead of using it all themselves as energy reserves.
Animal and human studies have demonstrated that exogenous estrogen can reverse the decrease in physical activity, RMR and TDEE seen during menopause.
Furthermore, ovariectomized women have higher fat oxidation during endurance training sessions compared to their pre-menopausal counterparts as well as higher liver triglyceride accumulation, potentially due to reduced basal plasma estrogen concentrations or an overall reduction in fat-free mass due to postmenopausal years.
