What are metabolism and weight changes?

All humans take in energy (in the form of food) and then burn that energy as the fuel to keep all life functions, like breathing and brain activity, happening. Metabolism can be defined as the conversion of food into chemical energy that is used to power the body’s activities and to build all parts of the body’s structure, including bones, muscle and fat. 

Changes in weight, whether increasing or decreasing, can be simplistically viewed as energy imbalances happening between energy in and energy out. This energy in and out is called total energy expenditure. 

The  term ‘total energy expenditure’ is made up of three interacting components: 

  • the base rate at which your body burns calories to stay alive and functioning properly (your metabolic rate); 
  • the energy used to break down food (dietary thermogenesis); and 
  • physical activity (which determines how much energy is used during physical activities of daily living like moving around, breathing and exercising). 

In sedentary adults (those who are generally inactive), base or resting metabolic rates account for about 60% to 70% of total energy output, the dietary thermogenesis for around 10%, and physical activity for the remaining 20% to 30%. These proportions change if physical activity is increased, depending on the amount and intensity of the activity. As more energy is used due to increased physical activity, the rate at which your base metabolism burns energy increases. So, with movement and physical activity, not only does the amount of energy burned increase directly as a result of the activity, but it also increases the rate at which your body burns energy while resting. 

Energy from food is stored in the form of adipose tissue (fat) beneath the skin (called subcutaneous fat) and around the organs (called visceral fat or central adiposity). This is normal and healthy, and because central adiposity is not the same as subcutaneous belly fat, even those who may be considered normal or underweight may still be impacted by central adiposity. Central adiposity can increase as a result of a sedentary lifestyle, a decrease in healthy recreational movement and exercise,  decreased quality of sleep, shift work, and a poor diet.

However, changes to the proportions of central adipose tissue versus subcutaneous adipose tissue can lead to obesity and to other serious health concerns such as metabolic syndrome. This syndrome is a cluster of conditions such as high blood pressure and abnormal cholesterol levels that increase the risk of heart disease, stroke and type 2 diabetes. [1] [2] [8]

Women in the menopausal transition typically gain weight and experience changes in the composition of their body fat [3]. The increase in body mass index (BMI – one commonly used measure of adiposity), is seen in multiple studies regardless of menopausal status, so menopausal changes are not the only cause. However, the increased storage of central adipose tissue is clearly linked to menopausal stage. [3] 

Subcutaneous body fat is positively associated with vasomotor symptoms (primarily hot flashes), so the more body fat you have, the more likely you are to have vasomotor symptoms. This is consistent with the model of body fat acting as an insulator. The relationship between fat gain and hot flashes is most pronounced among Caucasian and Chinese women, compared to African-American or Japanese women. However, no consistent associations between subcutaneous fat gain and night sweats was observed in the study.[7]

Self-care for metabolic and weight changes

We all need and deserve movement and physical recreation for good health, and the menopausal transition is an excellent time to prioritize what you need for optimal health. 

Recall that we defined metabolism as the conversion of food into chemical energy, which is then used to power the body’s activities and to build the body’s structures. We will refer to the use of energy as energy expenditure, and resting energy expenditure is the same as basal metabolic rate (or resting metabolic rate). Any physical activity directly increases energy expenditure, and it also causes an increase in resting energy expenditure. Given this, some of the most effective and meaningful self care activities surrounding weight gain and metabolism will involve body movement and activity. [8]

In the US, the recommended minimal level of physical activity for health benefits is 500 MET-min/week. One MET, or metabolic equivalent, is defined as the amount of oxygen consumed while at rest and it is used as a proxy for resting metabolic rate. Multiplying the MET can express how much energy is used during physical activity. So, moderate intensity activity, such as walking at 5 km/hr, uses about 3.3 MET. Vigorous activity, such as jogging at 8 km/hr, uses about 6 MET. Meeting the suggested 500 MET-min/week is achievable by walking for about 150 min (2.5 hours) per week or just over 20 mins per day. [8] This may or may not be easy for you to achieve immediately, but starting any movement is a step in the right direction!

In addition to movement, the following can also help you manage your weight and metabolism:

  • Eat a balanced and healthy diet with a variety of fruits and vegetables. If you can, seek help from a qualified nutritionist. 
  • Good sleep hygiene (getting enough rest in a positive sleep environment) is essential because key hunger-regulating hormones (leptin and ghrelin) regulate food intake and they are released at night.
  • Avoid stress eating and night eating if possible.
  • Dehydration can make you feel hungry when all you need is water. 
  • Journal “trigger events” so you can have more awareness of when you eat in an unhealthy way, and then try to find ways to avoid the triggers or make adjustments to your lifestyle (e.g. stop eating while watching tv). 
  • Start a mindfulness practice, such as meditation. This releases stress and also helps to increase body positivity and acceptance of your individual life.
  • Seek food security. Your healthcare provider or nutritionist can help take control of an economical and enjoyable home-made food menus.

Therapy for metabolic and weight changes

At age 40 find a reliable, educated primary care provider familiar with recognizing and treating symptoms of perimenopause and menopause. The North American Menopause Society provides a list of menopause practitioners here.

Get a physical check-up with a healthcare provider before you start an exercise program and to get recommendations for the best program based on your physical health (e.g. taking into account any joint problems you have). Psychological counselling or therapy can help with eating disorders and re-train eating habits.

Estrogen hormone therapy in younger post-menopausal women (aged 50-59 years), reduces fat mass, improves bone-mineral density, and preserves lean body mass, reducing the risk of type-2 diabetes specifically and overall mortality risk generally. However, because of the relationship between fat mass and lean body mass, net weight may not change. Hormone therapy has not been seen to increase weight. [8]

Elevated follicle stimulating hormones (FSH) levels are natural during the menopausal transition, but they act to reduce bone mass and increase central adiposity.  New therapeutic drugs are aimed at reducing the secretion of FSH or blocking FSH action using a specific antibody. These may be more effective and better tolerated by women who can’t or prefer not to use hormone therapy with estrogen [9]

The Science

Metabolism

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Metabolism

Metabolism is essentially all the chemical reactions in the body’s cells that convert food into energy. When your metabolism is stable you are receiving just enough fuel to power all your body’s functions, including breathing, adjusting your hormone levels, and moving around, among many other functions, without needing to store excess fuel as fat.

Your metabolic state, however, does not exist in isolation. It is intricately connected to your immune system and the capacity of your body to defend itself against infections and pathogens. The interrelationship between these two systems is called immunometabolism.

Metabolic dysfunction can be at the root of two key health indicators – inflammation and insulin resistance. Inflammation is the body’s response to insults or injuries. Insulin resistance lowers the sensitivity of your body to insulin, meaning you need larger amounts of insulin to lower your blood glucose levels compared to someone with high insulin sensitivity.

Mitochondria, small organelles inside each cell, are also key players in metabolism. Known as the ‘powerhouses’ of the cell, mitochondria take energy from food and turn it into energy that can be used by the cells in many tissues, including cardiac and skeletal muscle, and adipose tissue – commonly known as fat.

Estrogen and metabolic dysfunction

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Estrogen and metabolic dysfunction

Studies have shown that premenopausal females with sufficient estrogen show less inflammation and lower insulin resistance compared to age-matched males. Another study showed that female mice with no ovaries developed inflammation and insulin resistance when fed a high-fat diet, and that these detrimental metabolic effects were reversed with an estrogen replacement. The conclusion is clear – estrogen helps maintain metabolic function. [6]

In addition, estrogen has been found to stimulate intracellular signaling pathways which can be linked to improved mitochondrial function. All of this suggests that female adipose tissue (which presents with less inflammation compared to that of males) likely also contains more or better functioning mitochondria. [6]

Higher fat burning rates among human females compared to males diminishes after menopause, due to changes in estrogen levels. In the lab, reducing estrogen levels in mice leads to increased obesity and reduced energy use. Replacing those lowered estrogen levels increases energy use and reduces obesity in both humans and animals. [6]

Fat

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Fat

Exploring the research requires understanding some details about adipose tissue, also known as fat.

Fat contributes to metabolic balance, but when that balance is off, fat becomes dysfunctional and obesity results [8]

Fat is stored in five major ‘depots’ in the body, although the majority of research has focused on the first two depots:

(i) subcutaneous fat – under the skin, all over the body in obese individuals
(ii) visceral or intraperitoneal fat – fat is attached to the organs, including the stomach, the small intestine and the large intestine. Also called central adipose tissue or central adiposity, this type of adipose tissue poses greater health risks because it releases proteins and other molecules that contribute to insulin resistance and inflammation more than other adipose tissues do. The inflammation not only affects your organs and tissues, but contributes to narrowing blood vessels, increasing the risk of cardiovascular disease.
(iii) retroperitoneal and pelvic fat – usually classified with visceral fat because they are hard to tell apart using imaging.
(iv) intra- and extra-pericardial fat – found around the heart and large blood vessels.
(v) intramuscular fat – in the muscle tissue

Energy is stored long-term in the body in droplets containing triacylglycerol (which are three fatty acids that make up most dietary fats; also commonly called triglycerides) within cells.

There are two main types of fat, brown adipose tissue (BAT) and white adipose tissue (WAT). There are similarities between these types of fat in that they both produce and secrete hormones (including estrogen), and immune factors (including macrophages* and T lymphocytes** that are both important elements of the immune system).

However, WAT and BAT differ in their cell structure and metabolic function. White adipose cells contain only a few mitochondria in addition to a single large lipid droplet, and their primary function is to store energy. Brown adipose cells, on the other hand, contain many mitochondria, multiple smaller lipid droplets, and their primary function is to release heat for thermoregulation.

Studies indicate that improvements in how fat tissue is burned as energy may be caused by enhanced mitochondrial function in fat cells. The interrelationship is clear: Healthy fat cells (brown fat) have highly functional mitochondria, whereas unhealthy fat cells (white fat) on the other hand, have dysfunctional mitochondria that inefficiently burn fat. [6]

*Macrophage

A type of white blood cell specialized to surround and kill microorganisms, destroy dead cells, and stimulate the action of other immune system cells.

**T lymphocyte

A type of cell in the immune system specialized to kill infected cells, stimulate the action of other immune system cells, and regulate the immune response.

 

Role of hormones

Follicle stimulating hormone (FSH)

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Follicle stimulating hormone (FSH)

FSH regulates follicle development and maturation during the menstrual cycle, but research clearly indicates that FSH has functions that extend beyond reproduction.

Towards the end of the menopausal transition there is a sharp increase in FSH levels, coinciding with a rapid increase in the onset of central adiposity, leading to the conclusion that FSH is a fat-stimulating hormone. [3] Increasing FSH levels and decreasing estradiol (a type of estrogen) were each associated with increases in visceral fat. [5]

Studies have also shown a relationship between high FSH levels and low lean body mass in women. Lean mass is the total weight of your body after subtracting the weight of all of the adipose mass, so it includes the weight of your organs, skin, bones, muscle mass, and any water in your body.

FSH has a strong influence on fat, and FSH inhibition has been shown to help reduce body weight and increase brown adipose tissue (BAT), a process called ‘beiging fat’, or turning it from white to brown fat. [6]

Estrogens

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Estrogens

In pre-menopausal women, estrogens combine with the genes in adipose tissue to increase subcutaneous fat and decrease central adiposity. As estrogens decline in perimenopause, total adiposity increases (by approximately 5% of body weight) and lean body mass decreases by a slightly smaller amount, although often there is no net body weight increase (because these changes can counterbalance each other). Estrogen hormone therapy has been shown to help reverse these trends. [8]

There is scientific support for a significant role of estrogens in the regulation of female adipose tissue. Estrogen has been shown to influence: eating, energy expenditure (metabolism), amount of adipose tissue, distribution of adipose tissue, and the function of adipocytes, which are energy storing cells inside in fat (adipose) tissue. [8]

Changes in Metabolism and Weight

MYTH

Hormone therapy with estrogen, combined with regular movement, good nutrition, and good sleep can help women decrease their weight.

MYTH

Absolutely not – as the science shows, fat is complex and influenced by multiple factors including female hormones, and metabolism. Will power can help you make positive choices, but losing weight occurs over the long term, so behavioural changes around food and movement are very important to stoke your metabolism. 

MYTH

Healthy weights can be achieved and maintained. While hormones affect metabolism and fat deposition, achieving a healthy weight and comfort with your changing body is always possible. 

MYSTERY  

Obesity research is starting to find some of these answers, but frustratingly at the moment it remains a mystery.

Compiled References

  1. Baber, R. J., Panay, N., Fenton, A., & IMS Writing Group (2016). 2016 IMS Recommendations on women’s midlife health and menopause hormone therapy. Climacteric : the journal of the International Menopause Society, 19(2), 109–150. https://doi.org/10.3109/13697137.2015.1129166
  2. Björn, I., Bäckström, T.,Lalos, A. & I. Sundström-Poromaa (2006) Adverse mood effects during postmenopausal hormone treatment in relation to personality traits. Climacteric, 9(4), 290-297. doi: 10.1080/13697130600865766
  3. Brinton, R. D., Yao, J., Yin, F., Mack, W. J., & Cadenas, E. (2015). Perimenopause as a neurological transition state. Nature reviews. Endocrinology, 11(7), 393–405. https://doi.org/10.1038/nrendo.2015.82
  4. Bulan, S. E. (2019). Physiology and Pathology of the Female Reproductive Axis. In Melmed, S., Koenig, R., Rosen, C., Auchus, R. & F. Goldfine (Eds.), Williams Textbook of Endocrinology (14th ed., pp. 574-641). Elsevier.
  5. Minkin, M.J.(2019).  Menopause Hormones, Lifestyle, and Optimizing Aging. Obstetrics Gynecology Clinics of North  America, 46(3), 501–514. https://doi.org/10.1016/j.ogc.2019.04.008
  6. Sabia, S., Fayosse, A., Dumurgeir, J. et al. (2021). Association of sleep duration in middle and old age with incidence of dementia. Nature Communications, 12(2289).  https://doi.org/10.1038/s41467-021-22354-2
  7. Zaidi, M. (2018) FSH, Bone Mass, Body Fat, and Biological Aging. Endocrinology, 159(10), 3503–3514. doi: 10.1210/en.2018-00601
  8. Schmidt, P. J., Nieman, L. K., Danaceau, M. A., et al. (1998). Differential Behavioral Effects of Gonadal Steroids in Women with and in Those without Premenstrual Syndrome. New England Journal of Medicine, 338(4), 209-216. https://doi.org/10.1056/NEJM199801223380401
  9. Drogos, L. L., Rubin, L. H., Geller, S. E., Banuvar, S., Shulman, L. P., & Maki, P. M. (2013). Objective cognitive performance is related to subjective memory complaints in midlife women with moderate to severe vasomotor symptoms. Menopause (New York, N.Y.), 20(12), 1236–1242. https://doi.org/10.1097/GME.0b013e318291f5a6
  10. Greendale, G. A., Huang, M. H., Wight, R. G., Seeman, T., Luetters, C., Avis, N. E., Johnston, J., & Karlamangla, A. S. (2009). Effects of the menopause transition and hormone use on cognitive performance in midlife women. Neurology, 72(21), 1850–1857. https://doi.org/10.1212/WNL.0b013e3181a71193