The Musculoskeletal Syndrome of Menopause
Hi Readers! This one’s long and more in-depth than usual; my hope is that it may help you, or someone you care about, identify perimenopause (and the musculoskeletal syndrome that is one of its signals) early, and address its underlying causes before it progresses.
If you’d like to learn more about perimenopause and menopause, including what brain-body systems are implicated, how to track symptoms, what evidence-based interventions are, and how to advocate for menopausal hormone treatment (MHT), I’m holding an All-Day Menopause Lab on October 26th where you can learn more and workshop your symptoms. You can learn more and sign up here.
A few years ago, after ten months on a waiting list, I snagged an appointment with a top rheumatologist in Boston. I’d been plagued by multiple joint and tendon issues that seemed to be getting worse. Merely shrugging out of a shirt would strain my right elbow, inflaming it for days. Several nights a week, I woke up to searing pain in my right knee. The wrist I’d broken in a car accident in 2014 started to feel almost… broken again. And shockingly, a recent DEXA scan revealed early osteoporosis. My concern was not the pain, but the underlying sense that something was degrading the integrity and longevity of my joints, tendons, and connective tissue.
From the outset of the appointment, the rheumatologist pronounced my symptoms “psychological.” He recommended a book on psychogenic pain; when I said that it sounded like Dr. John Sarno’s work, he was surprised to learn I’d heard of it. Sarno’s work, I told him, had topped my teacher training reading list for over a decade.
When some of the autoimmune labs came back positive, he waved the results away. The book, he assured me, would take care of everything. I told him I was thinking of seeing a connective tissue disease specialist for Ehler’s Danlos Syndrome, which ran in the family. He grew visibly annoyed. “I feel like you’re still looking for answers,” he told me sharply. “Well, yeah, I thought to myself. “And you should be, too.” Before the appointment even ended, I knew it would be my last.
Eventually, I figured out the underlying cause of all these symptoms, as well as other, seemingly related ones: perimenopause.
Despite his reputation and expertise, the rheumatologist hadn’t thought to ask where I was in the menopause transition. And I wasn’t the only one; countless women share similar stories of their journeys from one specialist to the next, without answers or direction, every so often finding a way to manage individual symptoms outside their true context.
More than 47 million people globally and 2 million in the U.S. enter menopause each year, typically between the ages of 45 and 55—and by the year 2030, that number is projected to reach 1.2 billion.
The numbers for perimenopause are even higher. Most people enter this in-between stage between the ages of 35 and 45.
As of 2020, research shows, more than half of all women globally were unaware of the symptoms of perimenopause, and felt surprised and unprepared for it when it began.
And the longer it takes to detect these symptoms (and the systems in which they cluster), the harder it is to remedy them.
Black and Latine women, smokers and those who began menses early, whose mothers started menses early or began menopause early, who are underweight or have low BMI, who have not had children, or who undergo removal of their uterus or ovaries, tend to start perimenopause earlier.
Survivors of physical and sexual abuse and assault, and those with active PTSD, also tend to enter perimenopause earlier, and many experience greater sleep disturbance, vasomotor symptoms, and genitourinary symptoms.
If you identify as male and you’re reading this, you might be thinking, “This isn’t for me.” If you’re in your twenties or early thirties, or are over 65, you might feel the same.
Yet chances are that someone you love is navigating this transition—and therefore, contending with the vast gap in care that accompanies it. Your understanding may be a gateway for them to access knowledge, agency, and expert medical care.
The menopause transition includes over 75 cardinal symptoms. Many women seek out multiple specialists, from rheumatologists to neurologists, from gastroenterologists to orthopedists, from allergists to urologists to cardiologists. All too often, women are told that these symptoms are part of the aging process, that they’re the “new normal.” Sometimes, a doctor will prescribe an antidepressant, hoping to “calm” a woman’s somatic complaints or at the very least, improve her mood.
Yet even menopause specialists tend to focus on individual symptoms of menopause, a view that can make those symptoms overwhelming.
From an integrative perspective, however, menopause affects not only distinct elements of the mind, brain, and body, but entire overlapping, interacting, and intelligent systems within us.
Intelligent Systems That Crosstalk in Menopause
The most common symptoms of menopause often cluster in key systems of the mind, brain, and body. These include:
The gastrointestinal or enteric nervous system: acid reflux, bloating, low motility, irritable bowel syndrome (or worsening of previous IBS symptoms), a reduction in the diversity of the gut microbiome, and new or exacerbated food allergies
The neurognitive system: new or worsening indicators of ADHD, brain fog, memory issues, difficulties in executive functioning, low concentration, reduced motivation, and a drop in global desire (think libido, but in multiple areas), procrastination, and cognitive slowness
The immune system: an uptick in allergies, inflammation, autoimmune anomalies (new or worsening), asthma, fibromyalgia, and lowered resistance to bacterial and viral infections
The vasomotor system: hot flashes, night sweats, sleep disturbance, and heart palpitations
The Chronobiological System: disturbances in circadian rhythms, sleep apnea, increased sleep onset latency (the time it takes to fall asleep), increased nighttime awakenings, insomnia, and restless legs syndrome (RLS)
The endocrine system: including thyroid issues, blood-sugar dysregulation, parathyroid anomalies
The genitourinary system: urinary incontinence, bladder pain, bladder atrophy, urinary tract infections, reduction in vaginal lubrication (vaginal dryness), pain with intercourse, vulvovaginal atrophy, atrophic vaginitis (thinning, drying, and inflammation of the vaginal walls), loss of libido, and vulvar pain.
The Limbic System: new or recurring panic attacks, anxiety, depression, PTSD, loss of agency, loss of global desire
Because these brain-body systems interact, many signs of menopause occur in more than one system.
For example, gastrointestinal symptoms signal imbalances in the enteric nervous system, or belly brain. These, in turn, affect the oral microbiome and can lead to dry mouth, gum recession, and dental problems, particularly in menopause. Gut microbes can leak into the bloodstream, causing autoimmune reactions. They can also cross the blood brain barrier, where they impact brain health.
And strikingly, researchers believe that the intestinal microbiome is one medium through which aging affects not only inflammation and intestinal permeability, but bone health, leading them to what they call the new gut-bone axis.
Recently, an exciting new brain-body system has emerged in menopause research: the musculoskeletal syndrome of menopause. What exactly is this syndrome? Why isn’t it common knowledge, and what can we do to address it?
The Musculoskeletal Syndrome of Menopause
The musculoskeletal system is an integral part of the body that includes muscles, bones, joints, tendons, ligaments, cartilage, and other types of connective tissue, including cells. This remarkable system facilitates structure (including posture), mobility, stability, and strength. On an experiential level, it gives us a sense of cohesion and, at the same time, the ability to explore and engage with the world around us.
The musculoskeletal syndrome of menopause unites several symptoms previously thought of in isolation and as unrelated to menopause, including:
musculoskeletal pain
arthralgia (mild to severe joint pain in one or more joints)
adhesive capsulitis, also known as frozen shoulder
cartilage matrix fragility with progression of osteoarthritis, often in multiple joints
loss of lean muscle mass (sarcopenia)
unexplained weight gain which, along with sarcopenia, is known as sarcopenic obesity
decreased bone density, which leads to osteoporosis and a higher risk for frailty, fractures, and an enhanced risk of falling
increased tendon and ligament injury
plantar fasciitis
The musculoskeletal syndrome of menopause affects approximately 70 percent of menopausal women, and 25% experience severe symptoms. The syndrome exerts a markedly negative impact on activity level, quality of life, and even longevity. Yet in 40 percent of women who suffer from it, no structural findings will manifest on x-rays, MRIs, or scans, often leading doctors to overlook the syndrome or to misdiagnose it as psychological.
This is because estrogen acts as a regulating factor in nearly all types of musculoskeletal tissue, including bone, tendons, muscle, cartilage, ligaments, fascia, and even adipose tissue (often considered a type of fascia). The midlife drop in estrogen that begins in perimenopause serves as the catalyst for the musculoskeletal syndrome of menopause.
The precipitous drop in estrogen throughout menopause drives five recognized primary changes in health:
an increase in systemic inflammation
a decrease in bone density, leading to osteoporosis
arthritis
sarcopenia
a decrease in the growth of muscle stem cells, also known as satellite cells
As we’ll see, the musculoskeletal syndrome of menopause also leads to another primary change still unrecognized by menopause specialists: a loss of proprioception, our sixth sensory system and a medium for how we know ourselves and engage with the world around us.
Inflammatory Cascades in the Musculoskeletal Syndrome of Menopause
More than half of all perimenopausal women (in other words, beginning in the decade leading up to menopause) report arthralgia, pain in one or more joints. Why might this happen, and what does it have to do with skeletal muscle?
Estrogen regulates inflammation, a process is thought to occur via estradiol, or E2, the most potent estrogen in mammals and the primary form of estrogen during the reproductive years. It does this in part by increasing levels of anti-inflammatory molecules such as interleukin 10 (IL-10).
Estrogen also happens to target IL-10 in the dorsal root ganglion, a cache of sensory neurons that transmit proprioception and pain-related sensations to the central nervous system.
Several research groups have demonstrated that estradiol (E2) can shift macrophages to repair cells after injury and diseases. (Macrophages are white blood cells that surround and attack microorganisms, remove dead cells, and potentiate the action of other immune system cells.) Estrogen also supports T helper cells, which have a
Estrogen also inhibits the release of many pro-inflammatory molecules, so much so that menopause is often referred to as an inflammatory phase that begins in perimenopause and disrupts estrogen-modulating neurological systems.
Researchers believe that the relationship between estrogen and inflammation is reciprocal. The perimenopausal decline in estrogen that continues beyond menopause elevates inflammation—and, in turn, the associated rise in chronic, low-grade inflammation can accelerate ovarian insufficiency.
FOR A DEEP DIVE:
Multiple research studies show that menopause correlates strongly with an increase in pro-inflammatory cytokines, or molecules. Foremost among these are interleukin-6 (IL-6), interleukin 4 (IL-4), interleukin 1 (IL-1), and tumor necrosis factor-α (TNF-α).
Tumor necrosis factor- α can degrade muscle proteins and compromise the capacity for repair in adult muscle tissue. The loss of estradiol in menopause increases the amount of circulating TNF-α and exacerbates the degradation of muscle proteins. During the menopause transition, fat cells also release TNF-α, which can further promote the accumulation of fat cells and impair muscle function.
The inflammatory cascade in menopause, the degradation of muscle proteins, and the slow, incomplete process of muscle tissue and repair all contribute to arthralgia, or joint pain.
This process isn’t confined to the musculoskeletal system or immune system. Neuroinflammation in menopause also affects the brain—and therefore, cognitive and neurological health. This is another of the multiple mechanisms through which the systems of menopause intersect and affect one another.
Estrogens inhibit neuroinflammation, specifically on microglia cells, which drive the neurodegenerative process of diseases such as M.S., Parkinson’s, and Alzheimer’s Disease. As women go through menopause, multiple brain imaging findings indicative of Alzheimer’s Disease emerge, including reduced brain glucose metabolism in the frontal cortex, increased amyloid-β plaque accumulation, and the loss of both gray matter and white matter (communication pathways) in the brain.
And in other cross-system interactions, scientific studies support a link between the rise in pro-inflammatory cytokine activity (the kind that creates inflammation) and postmenopausal bone loss.
Inflammation also plays a role in cardiovascular disease. It increases the amount of pro-inflammatory molecules in the blood. It contributes to the chronic buildup of plaque in arterial walls in several organs, particularly in the heart and brain.
Systemic inflammation also occurs in our enteric nervous system. When intestinal permeability (think leaky gut) occurs, inflammatory cytokines can pass from the gut to the bloodstream and even cross the blood-brain barrier, setting the stage for neurodegenerative disease years and even decades in the future. (You can read more about this link in this column about the gut-brain connection.)
What’s more, multiple studies show strong correlations, and you could even say a causal relationship, between inflammatory markers and depression. People with major depressive disorder (MDD) exhibit chronically heightened inflammatory responses.
They have a pronounced expression of pro-inflammatory molecules known as cytokines in both their blood and cerebrospinal fluid. Inflammatory molecules common in depression include IL-6 and IL-8, TNF-α, and c-reactive protein (CRP). (See this piece for more on depression as an inflammatory disease.)
INFLAMMATION IN MENOPAUSE FOR SURVIVORS
Given the prominent role of inflammation in the mind-brain-body systems of menopause, it’s important to note that survivors of sexual assault may not only enter perimenopause earlier. They may also have a different constellation of symptoms. Take inflammation, for instance: Survivors of childhood sexual abuse carry a higher risk for systemic inflammation—and, as we’ll see, for symptoms related to the musculoskeletal syndrome of menopause. In a systematic review of studies, most reported an increase of inflammatory activity in survivors compared to controls; this included pro-inflammatory cytokines such as IL-6, TNF- α, and C-reactive protein.
According to several new studies, sexual assault and the posttraumatic stress it causes increase the odds that women will develop lupus. One study found that women with posttraumatic stress disorder (PTSD) had nearly triple the risk of developing lupus; women exposed to trauma but without clinically significant PTSD had more than double the risk than those without a trauma history.
As a survivor, I wish I’d had access to this information sooner, along with so much of the additional emerging research in menopause (and perimenopause). It would have helped me anticipate and intervene in the intrusion that these symptoms can confer, especially when we know their full context.
My hope is that if you or someone you know is a survivor, too, this information can give you a greater sense of agency during a time when changes can feel unexpected, unwanted, and engender significant nervous system hypervigilance.
Bone Health and Osteoporosis
Bone is living tissue that is constantly being broken down and replaced.
Estrogen regulates bone metabolism. It does this by facilitating the process of bone homeostasis, a dynamic process that involves regulatory activity among three types of bone cells: osteoclasts, osteoblasts, and osteocytes. This regulatory process maintains appropriate bone mass and achieves a balance between bone formation and bone resorption.
FOR A DEEP DIVE:
In the process of bone homeostasis, osteoblasts and osteoclasts collaborate (along with osteocytes) to form new bone cells and break down old or damaged bone tissue.
Osteoblasts are the cells that make new bone cells, reshape or remodel bones as we age, and help heal damaged or broken bones
Osteoclasts break down old bone tissue so new, healthier bone tissue can replace it
Osteocytes are the most common type of bone cell and “master regulators” of bone homeostasis; they monitor changes in pressure and stress that affect our bones, signal osteoblasts and osteoclasts to repair damaged bone tissue, and maintain the mineralization of bone (they also serve as mechanoreceptors, which respond to mechanical strain, and therefore play a role in proprioception)
Estrogen stimulates the activity of osteoblasts (the cells that make new bone) by increasing their lifespan and inhibiting their breakdown.
Estrogen directly targets osteoclasts, (the cells that break down old bone tissue), and decreases their numbers by promoting the programmed death of their early “cell ancestors” (rather than their mature cell population)
Many researchers have theorized that osteocytes (the major signalers in bone homeostasis) are the main targets of estrogen. In premenopausal women, estrogen deficiency leads to a fourfold increase in osteocyte death in bone biopsy samples.
Estrogen deficiency, therefore, correlates with increased bone turnover and enhanced bone resorption. This disruption in bone metabolism and homeostasis results in osteoporosis, a condition in which the body loses too much bone or makes too little new bone. This means a significant loss of bone, increasing fragility and risk of fracture.
When the creation of new bone doesn't keep up with the loss of old bone, osteoporosis occurs. Bones become weak and brittle: a fall or even mild stressor such as bending over or coughing can cause a break, most frequently in the hip, wrist or spine.
During menopause women have, on average, a 10 percent reduction in bone mineral density. For each year following menopause, they have an average additional reduction of .6 percent in lean muscle mass.
Osteoporosis is a serious medical condition that affects 200 million postmenopausal women globally.
Osteoporosis is usually a “silent” disease. It has no easily identifiable symptoms, and is largely underdiagnosed. Most people are unaware that they have it until they receive the results of a DEXA scan or incur a fracture.
While osteoporosis affects men and women of all races and ethnicities, white and Asian women, especially those who are postmenopausal, are at highest risk.
Fractures secondary to osteoporosis can lead to deformed bone (and slower bone regeneration and healing), disability, and even premature death.
While osteoporosis on its own does not cause death, it increases the risk of fractures, which are highly correlated with mortality. According to a 2022 article, only 33 percent of older adults assigned female at birth who experience a hip fracture regain their independence. The risk of death is substantially higher during the twelve months post-fracture, and the risk remains high for five years.
Osteoporosis is both preventable and treatable. In women at risk of fracture, menopausal hormone therapy is effective in preventing osteoporotic fractures. Furthermore, menopausal hormone therapy preserves or increases bone density at all skeletal locations.
Proliferation of Satellite Cells
Satellite cells are stem cells located on muscle fibers, which bolster plasticity and regeneration. Although “dormant” in a state of equilibrium, these special cells mobilize after injury to repair muscle tissue amid inflammatory states.
Estrogen stimulates the activity of satellite cells. Animal model studies suggest that female mice without ovaries (and therefore, without estrogen) have between 30 and 60 percent fewer satellite cells than their counterparts with intact ovaries. These reduction are associated with estrogen deficiency.
Skeletal muscle houses specific estradiol receptors at the level of muscle fibers. This suggests that estradiol can promote muscle regeneration and foster muscle health by stimulating the proliferative activity of muscle satellite cells.
Without menopausal hormone therapy, the decrease in satellite cells can exacerbate osteopenia and osteoporosis, and may also increase frailty due to faulty cell regeneration.
Sarcopenia in Perimenopause and Beyond
Sarcopenia refers to the age-related loss of lean muscle mass that accelerates starting
Strikingly, experiments in animal models show that just 24 weeks of estrogen deficiency led to a 10 percent decrease in muscle strength. What’s more, the decrease corresponded to a reduction in the skeletal muscle fiber cross-sectional area, a measurement of muscle plasticity. (Think here of the capacity of the muscle fiber to learn and adapt to stimulation or stress.)
Signs of sarcopenia include the atrophy of fast muscle fibers, loss of type II fibers that allow muscles to generate short-term force, and increased intra-muscular adipose tissue.
Often, the first symptom of decline in muscle mass is weight gain despite few, if any, changes in dietary intake or activity level. Yet socially, particularly in body positivity circles, we have come to view weight gain (or discussions of weight gain) as a superficial body-image issue. This can cause women, particularly in yoga and body positivity spaces, to be reluctant to address weight gain with others, including their gynecologists. And when they do address it in medical appointments, they often hear that it’s simply a “side effect” of menopause.
But weight gain in menopause is often both a predictor and cardinal symptom of musculoskeletal issues. It warrants deeper attention and inquiry, particularly in the context of other musculoskeletal symptoms.
The combination of excess adipose tissue and low muscle mass and muscle function is called sarcopenic obesity, a condition which is also a risk factor for frailty, comorbid disease states, and mortality, particularly in the aging population. People with sarcopenia incur a higher risk for metabolic disease and functional impairment compared with the risks incurred by either obesity or sarcopenia alone.
My dad kept a handgrip strength training tool in his living room; much to his children’s amusement, he’d squeeze it daily, gritting his teeth with the effort. I think of this often, now that grip strength has emerged as an indication not just of physical but cognitive health.
Surprising as it may sound, grip strength is widely considered to be a biomarker of overall strength, upper limb function, bone mineral density, risk of fractures and falls, cognitive impairment, mental health, quality of life, and all-cause mortality in older adults. Importantly, a study of postmenopausal women found that this muscle fiber cross-sectional area and grip strength were greater in women using menopausal hormone therapy than in non-users.
And here’s another remarkable example of the way one system intersects with another, seemingly disparate one: in this case, the musculoskeletal and genitourinary system. It turns out that low muscle mass and muscle strength correlate with an increased incidence of urinary incontinence in women of menopausal age.
A recent study found that waking up frequently during the night to urinate (nocturia), urinary urgency, incontinence, and hyperactive bladder were more common in women who had decreased grip strength. And a novel study of women 60 years and older revealed that those who had a greater amount of muscle in the thigh area had a 54 percent lower incidence of urinary incontinence.
Loss of Proprioception in Menopause
You won’t yet find menopause experts talking about this, but a key part of the musculoskeletal syndrome of menopause is also a loss of proprioception, sometimes referred to as our sixth sense and a key part of embodiment. From the Latin roots proprius, meaning “of one’s own,” and capere, “to take or grasp,” proprioception is one of the central ways through which we grasp, or know, ourselves.
Proprioception is more of a system than it is a sense. It encompasses our awareness of movement, the position of our body and its parts in space, and how we occupy space. It also involves our sense of balance, of effort and force and heaviness, and our posture or shape. Proprioception also includes the way we monitor and regulate the space around our bodies—and sometimes others’ bodies too.
At more complex levels, proprioception involves a multilayered dialogue between the body and brain that helps us explore and relate to the world around us. Proprioception doesn’t constitute a separate bodily sense of self; it is our sense of self.
Key participants in this body-to-brain dialogue include sensory neurons embedded in our muscles, tendons, skin, joints, and connective tissue. Called proprioceptors, they continually sense and communicate fine-grained details like the position of your limbs and body parts in space. Important among these are muscle spindles, stretch detectors that listen for and respond to how much and how fast your muscles lengthen or contract.
Estrogen and progesterone alter the stiffness of collagen fibers—and this stiffness, in turn, modulates muscle spindle sensitivity.
Muscle spindle impairment is part of the musculoskeletal syndrome of menopause. It leads to unstable gait, difficulty balancing, and frequent falls. Other elements of proprioception also weaken, such as awareness of limb position, movement, touch, and vibration; these changes exacerbate the risk of falling.
Sarcopenia is not confined to our muscle system. It also precipitates a “forgetting” of movements that we once did automatically, like walking on an uneven surface without thinking about it or racing down the stairs without looking at them. Sarcopenia indicates a disruption in the fluency with which the body and brain communicate. This disfluency occurs with age, and pervades our other inner senses like interoception and body agency.
When the sensory receptors in muscle (and with them, our sense of proprioception) are compromised, we “lose” movements that were formerly automatic. This burdens the executive regions of the brain, such as the prefrontal cortex, with greater responsibility for routine functions. As this loss progresses, it places growing demands on the brain’s energy, attention, and resources. (This may contribute to the acquisition of new symptoms—or worsening of previous systems—in women with ADHD during the menopause transition, and to cognitive decline.)
Losing proprioception isn’t just the loss of movements we used to be able to do with ease. It’s also a loss of our bodily self—and with it, our sense of self—and the capacity to explore the world through our body. Although most of us aren’t taught to value embodiment, we feel its loss all the same.
And in the research for my book in progress, I’ve reviewed many novel studies that connect proprioceptive deficits with depression. This connection makes sense because as this piece explored, the third type of dopamine neuron, D3, is intimately linked with movement. In fact, my sense is that the decline in movement that occurs in the menopause transition is linked to a drop in dopamine (which is deeply influenced by estrogen, as I’ve talked about here, and also related to ADHD).
Fascia, Osteoarthritis, and Pain
Recently, my friend Sara confided that she felt her body was disintegrating. “Everything hurts,” she told me. “What the heck is happening?” She had seen an orthopedic doctor; neither x-rays nor MRI scans had revealed anything other than a touch of arthritis in her spine. Although Sara had just turned fifty, none of the many specialists she saw made an association between the pain she had in multiple joints and the process of menopause. Sara was also a survivor of childhood sexual assault. And emerging research indicates that survivors of childhood physical abuse and sexual abuse have a 1.3 times greater and 1.6 times greater likelihood, respectively, of developing osteoarthritis, chronic back and neck pain, and frequent or severe headache.
Cartilage is comprised of a dense cellular matrix which includes cells that estrogen regulates. It is considered part of the system of fascia, or connective tissue, that links every cell in our bodies and maintains our structural integrity. (Fascia also contributes to vascular support, joint stability, and circulation. It is also intertwined with two of our inner senses of embodiment: interoception and proprioception.)
Estrogen cells play a role in regulating cartilage, as well as inflammation. Osteoarthritis in women increases precipitously around the time of menopause.
A comprehensive review of the relationship between estrogen and arthritis pointed to a correlation between menopausal loss of estrogen and the incidence of osteoarthritis in the knee, hip, and fingers, as well as the severity of hip arthritis.
Evidence suggests that the drop in estrogen during menopause leads to alterations in the connective tissue matrix. Estrogen deficiency correlates strongly with an increase in type I collagen (relative to type II collagen,) which makes fascia stiffer and firmer. At the same time, the hormone relaxin, which inhibits fibrosis and inflammation (and plays a role in bone healing and remodeling), also decreases. (On the opposite end of the continuum between stiffness and softness, the elevation of estrogen at ovulation in menstruating women is associated with increases ligament laxity, which is why sports injuries in women happen more often during ovulation.)
Estrogen supports hyalauronan (hyalauronic acid), a mucoid substance that is a key component in the extracellular matrix. Hyalauronan is found not only in the joints but in the skin and eyes. It is a joint lubricant, aids in wound healing and tissue repair, and is also found in the eyes. By age 50, hyalauronin production is merely 50% of what it was in our youth. The loss of estrogen and subsequent decrease in hyalauronin leads to joint stiffness, slow wound repair, and dry eye syndrome, all of which occur in menopause. And, studies suggest, hyalauronan also plays a role in the health of our nervous system and brain.
Interested in learning more about the other systems of menopause and how to address them? Consider this month’s MENOPAUSE LAB, an all-day practicum on October 26th.
Recommendations for Musculoskeletal Syndrome of Menopause
Prevention and Detection:
A focus on prevention and early detection is critical, before this syndrome progresses
In addition to labwork and testing that addresses the other systems involved in menopause, consider getting the following measures related to the musculoskeletal system, both as a baseline and at regular intervals:
DEXA bone scans starting early in perimenopause, to track changes in muscle mass, adipose tissue composition, and bone density
Vitamin D3 laboratory tests (Vitamin D3 is a hormone that supports bone health and the regulation of inflammation, key nodes of the musculoskeletal syndrome of menopause)
Parathyroid hormone panels (which can include calcium tests)
Regular female hormone panels, particularly for women at risk for early perimenopause
I will add here that the current guidelines for osteoporosis stipulate screening for women 65 and older, as well as those between the ages of 50 and 65 who have risk factors such as a family history of osteoporosis. Given my personal experience (no family history of osteoporosis or other risk factors, yet I still developed the disease, which I am now in the process of reversing), I highly recommend that all women obtain these tests beginning much earlier than the guidelines recommend, particularly if you are in a high risk racial or ethnic category.
Treatment:
Menopausal hormone therapy (MHT) can offset these changes to connective tissue. It slows the rate of estrogen loss, which can minimize the devastating effects of the musculoskeletal syndrome of menopause. According to the North American Menopause Society, “For women aged younger than 60 years or who are within 10 years of menopause onset and have no contraindications, the benefit-risk ration is favorable for treatment of bothersome VMS (vasomotor symptoms) and prevention of bone loss.”
For women aged younger than 60 years or who are within 10 years of menopause onset and have no contraindications, the medical profession now recognizes the benefit-risk ratio of menopausal hormone therapy as favorable for the treatment of bothersome VMS and prevention of bone loss.
For reasons I’ll cover in an upcoming column, many gynecologists—even ones who identify as menopause specialists—do not consider the musculoskeletal syndrome of menopause to be a clinical reason for MHT, and instead prescribe solely to target vasomotor symptoms such as hot flushes, heart palpitations, and night sweats. You may have to do some sleuthing to find a specialist with more in-depth training and expertise, which usually means that they’re more open to MHT than others.)
Research indicates that Vitamin D3 supplementation improves hip bone mineral density in women, and prevents the risk of frailty-related falls. In postmenopausal women aged 50-65 years with an existing Vitamin D deficiency, supplementation with 1000IU (a modest amount) Vitamin D3 for 9 months was associated with reduced bone turnover suggestive of decreased bone loss.
Menopause and women’s health specialists now recommend strength/resistance training with weights beginning in perimenopause, and if one’s joints allow, doing so with higher weights and fewer repetitions. (I already check the boxes for several features of the musculoskeletal syndrome of menopause; lower weights combined with higher repetitions help prevent injuries to my muscles, tendons, and fascia.)
You might also consider walking (as well as gardening, and other forms of exercise) while wearing a weighted vest. While most weighted vests are designed with Navy Seals and extreme athletes in mind (and therefore, these models can be boob-crushing), it’s only a matter of time before someone makes one for women.
A future menopause article or Masterclass will explore this in greater depth, but increasing protein intake is now at the center of the discussion of treatment for women in perimenopause and beyond. The European Society for Clinical Nutrition and Metabolism proposes a daily recommended amount of 1 to 1.2 g of protein for every kg (or 2.2 pounds) of body weight. This recommendation, however, is more than ten years old. In studies, higher protein intake (1.2g per kg or 2.2 lbs. body weight) is associated with greater lean body mass, better physical function, and a lower risk of frailty.
Early in menopause, I’d long taken Vitamin D3 regularly, and had for most of my adult life engaged in regular strength training with weights—except during the first 18 months of Covid, which is when my osteoporosis began to develop. Two two interventions that have made the most difference for me in terms of symptoms as well as a reversal of my bone density issues have been menopausal hormone therapy and increasing my protein intake.
That brings us to proprioception.
We can stimulate our muscle spindles and the connective tissue that surrounds them: One study of older adults with mild mobility and body-sensing deficits showed that wearing textured insoles reduced executive control over walking, prompting a return of automaticity. And large-scale reviews found that compared to conventional therapies like walking, traditional mind–body exercises like Tai Chi and Qigong improved working memory, cognitive flexibility, and inhibitory self-control in older adults with cognitive impairment.
And then there’s novel movement, movements, which I wrote about in this column. You can do this by embracing the strangeness of trial-and-error movements that you are unused to, which is also known as motor learning. You can also try new movements, accessing “sleeping” areas of the body, new actions or sensations within “old” movements, or new types of movement altogether, such as Tai Chi or windsurfing or balance boards.
Note: I highly recommend Mary Clare Haver’s book The New Menopause, available where books are sold.
Sources:
By the year 2030, that number is projected to reach 1.2 billion: Hill K. (1996). The demography of menopause. Maturitas, 23(2), 113–127. https://doi.org/10.1016/0378-5122(95)00968-x
And as of 2020, research shows, more than half of all women globally were unaware of the symptoms: Women’s knowledge of (peri)menopause worldwide 2020. (n.d.). Statista. Retrieved October 10, 2024, from https://www.statista.com/statistics/1242168/womens-knowledge-awareness-perimenopause-menopause-worldwide/
Survivors of physical and sexual abuse and assault, and those with active: Cleland, L., McLeod, G. F. H., Dhakal, B., Fenton, A., Welch, J. L., Horwood, L. J., & Boden, J. M. (2022). Childhood maltreatment and the menopause transition in a cohort of midlife New Zealand women. Menopause (New York, N.Y.), 29(7), 816–822. https://doi.org/10.1097/GME.0000000000001976 See also: Gibson, C. J., Huang, A. J., McCaw, B., Subak, L. L., Thom, D. H., & Van Den Eeden, S. K. (2019). Associations of Intimate Partner Violence, Sexual Assault, and Posttraumatic Stress Disorder With Menopause Symptoms Among Midlife and Older Women. JAMA Internal Medicine, 179(1), 80–87. https://doi.org/10.1001/jamainternmed.2018.5233
One study found that women with posttraumatic stress disorder (PTSD) had nearly triple the risk of developing lupus: Roberts, A. L., Malspeis, S., Kubzansky, L. D., Feldman, C. H., Chang, S.-C., Koenen, K. C., & Costenbader, K. H. (2017). Association of Trauma and Posttraumatic Stress Disorder With Incident Systemic Lupus Erythematosus in a Longitudinal Cohort of Women. Arthritis & Rheumatology, 69(11), 2162–2169. https://doi.org/10.1002/art.40222 Maihofer, A. X., Ratanatharathorn, A., Hemmings, S. M. J., Costenbader, K. H., Michopoulos, V., Polimanti, R., Rothbaum, A. O., Seedat, S., Mikita, E. A., CHARGE Inflammation Working Group, Psychiatric Genomics Consortium PTSD Working Group, Smith, A. K., Salem, R. M., Shaffer, R. A., Wu, T., Sebat, J., Ressler, K. J., Stein, M. B., Koenen, K. C., Wolf, E. J., … Nievergelt, C. M. (2024). Effects of genetically predicted posttraumatic stress disorder on autoimmune phenotypes. Translational psychiatry, 14(1), 172. https://doi.org/10.1038/s41398-024-02869-0
And strikingly, researchers believe that the intestinal microbiome is one medium through which aging affects not only inflammation and intestinal permeability, but bone health: Hu, H., Huang, Y., Liu, F., Wang, Q., & Yao, Y. (2024). How aging affects bone health via the intestinal micro-environment. BIOCELL, 48(3), 353–362. https://doi.org/10.32604/biocell.2024.048311 Fu, L., Zhang, P., Wang, Y., & Liu, X. (2024). Microbiota-bone axis in ageing-related bone diseases. Frontiers in Endocrinology, 15, 1414350. https://doi.org/10.3389/fendo.2024.1414350 See also: Sharma, M. (2024, February 12). The Impact of Menopause on Gut Health: Functional Medicine Strategies for Middle-Aged Women. Rupa Health. https://www.rupahealth.com/post/the-impact-of-menopause-on-gut-health-functional-medicine-strategies-for-middle-aged-women
This remarkable system facilitates structure: Musculoskeletal System—An overview | ScienceDirect Topics. (n.d.). Retrieved October 12, 2024, from https://www.sciencedirect.com/topics/medicine-and-dentistry/musculoskeletal-system
It affects approximately 70 percent of menopausal women: Lu CB, Liu PF, Zhou YS, Meng FC, Qiao TY, Yang XJ, Li XY, Xue Q, Xu H, Liu Y, Han Y, Zhang Y. Musculoskeletal Pain during the Menopausal Transition: A Systematic Review and Meta-Analysis. Neural Plast. 2020 Nov 25;2020:8842110. doi: 10.1155/2020/8842110. PMID: 33299396; PMCID: PMC7710408.
And strikingly, 40 percent of women who suffer will have no structural: Lu CB, Liu PF, Zhou YS, Meng FC, Qiao TY, Yang XJ, Li XY, Xue Q, Xu H, Liu Y, Han Y, Zhang Y. Musculoskeletal Pain during the Menopausal Transition: A Systematic Review and Meta-Analysis. Neural Plast. 2020 Nov 25;2020:8842110. doi: 10.1155/2020/8842110. PMID: 33299396; PMCID: PMC7710408.
The precipitating factor: estrogen, which acts as a regulating factor: Chidi-Ogbolu N, Baar K. Effect of Estrogen on Musculoskeletal Performance and Injury Risk. Front Physiol. 2019 Jan 15;9:1834. doi: 10.3389/fphys.2018.01834. PMID: 30697162; PMCID: PMC6341375.
More than half of all perimenopausal women report arthralgia in the years Wright, V. J., Schwartzman, J. D., Itinoche, R., & Wittstein, J. (2024). The musculoskeletal syndrome of menopause. Climacteric: The Journal of the International Menopause Society, 1–7. https://doi.org/10.1080/13697137.2024.2380363
Menopause is often referred to as an inflammatory phase that begins in perimenopause: McCarthy, M., & Raval, A. P. (2020). The peri-menopause in a woman's life: a systemic inflammatory phase that enables later neurodegenerative disease. Journal of neuroinflammation, 17(1), 317. https://doi.org/10.1186/s12974-020-01998-9
The perimenopausal decline in estrogen that continues beyond menopause: Ağaçayak, E., Yaman Görük, N., Küsen, H., Yaman Tunç, S., Başaranoğlu, S., İçen, M. S., Yıldızbakan, A., Yüksel, H., Kalkanlı, S., & Gül, T. (2016). Role of inflammation and oxidative stress in the etiology of primary ovarian insufficiency. Turkish journal of obstetrics and gynecology, 13(3), 109–115. https://doi.org/10.4274/tjod.00334
Estrogen increases levels of anti-inflammatory molecules such as interleukin 10: Shivers, K. Y., Amador, N., Abrams, L., Hunter, D., Jenab, S., & Quiñones-Jenab, V. (2015). Estrogen alters baseline and inflammatory-induced cytokine levels independent from hypothalamic-pituitary-adrenal axis activity. Cytokine, 72(2), 121–129. https://doi.org/10.1016/j.cyto.2015.01.007
This process is thought to occur via 17β-estradiol: Li YP, Reid MB. NF-kappaB mediates the protein loss induced by TNF-alpha in differentiated skeletal muscle myotubes. Am J Physiol Regul Integr Comp Physiol. 2000 Oct;279(4):R1165-70. doi: 10.1152/ajpregu.2000.279.4.R1165. PMID: 11003979.
Several research groups have demonstrated that estradiol (E2) can shift macrophages: Harding, A. T., & Heaton, N. S. (2022). The Impact of Estrogens and Their Receptors on Immunity and Inflammation during Infection. Cancers, 14(4), 909. https://doi.org/10.3390/cancers14040909
Research studies show that menopause correlates closely with an increase in pro-inflammatory: Cioffi, M., Esposito, K., Vietri, M. T., Gazzerro, P., D'Auria, A., Ardovino, I., Puca, G. A., & Molinari, A. M. (2002). Cytokine pattern in postmenopause. Maturitas, 41(3), 187–192. https://doi.org/10.1016/s0378-5122(01)00286-9
During the menopause transition, fat cells also release TNF-α, which can further: Roth SM, Metter EJ, Ling S, Ferrucci L. Inflammatory factors in age-related muscle wasting. Curr Opin Rheumatol. 2006 Nov;18(6):625-30. doi: 10.1097/01.bor.0000245722.10136.6d. PMID: 17053510.
Estrogens inhibit neuroinflammation, specifically on microglia cells: Vegeto, E., Benedusi, V., & Maggi, A. (2008). Estrogen anti-inflammatory activity in brain: a therapeutic opportunity for menopause and neurodegenerative diseases. Frontiers in neuroendocrinology, 29(4), 507–519. https://doi.org/10.1016/j.yfrne.2008.04.001
Scientific studies support a link between the rise in pro-inflammatory cytokine activity: Experimental and clinical studies strongly support a link between the increased state of proinflammatory cytokine activity and postmenopausal bone loss. Pfeilschifter, J., Köditz, R., Pfohl, M., & Schatz, H. (2002). Changes in Proinflammatory Cytokine Activity after Menopause. Endocrine Reviews, 23(1), 90–119. https://doi.org/10.1210/edrv.23.1.0456
It increases the amount of pro-inflammatory molecules in the blood: Henein, M. Y., Vancheri, S., Longo, G., & Vancheri, F. (2022). The Role of Inflammation in Cardiovascular Disease. International journal of molecular sciences, 23(21), 12906. https://doi.org/10.3390/ijms232112906
In a systematic review of studies, most studies reported an increase of inflammatory activity in survivors: D'Elia, A. T. D., Matsuzaka, C. T., Neto, J. B. B., Mello, M. F., Juruena, M. F., & Mello, A. F. (2018). Childhood Sexual Abuse and Indicators of Immune Activity: A Systematic Review. Frontiers in psychiatry, 9, 354. https://doi.org/10.3389/fpsyt.2018.00354
Estrogen stimulates the activity of osteoblasts, the cells that make: Kousteni, S., Han, L., Chen, J. R., Almeida, M., Plotkin, L. I., Bellido, T., & Manolagas, S. C. (2003). Kinase-mediated regulation of common transcription factors accounts for the bone-protective effects of sex steroids. The Journal of clinical investigation, 111(11), 1651–1664. https://doi.org/10.1172/JCI17261 See also: Khosla S, Oursler MJ, Monroe DG. Estrogen and the skeleton. Trends Endocrinol Metab. 2012 Nov;23(11):576-81. doi: 10.1016/j.tem.2012.03.008. Epub 2012 May 16. PMID: 22595550; PMCID: PMC3424385.
Estrogen decreases the number of osteoclasts: Kim, H.-N., Ponte, F., Nookaew, I., Ucer Ozgurel, S., Marques-Carvalho, A., Iyer, S., Warren, A., Aykin-Burns, N., Krager, K., Sardao, V. A., Han, L., de Cabo, R., Zhao, H., Jilka, R. L., Manolagas, S. C., & Almeida, M. (2020). Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors. Scientific Reports, 10(1), 11933. https://doi.org/10.1038/s41598-020-68890-7 See also: Khosla S, Oursler MJ, Monroe DG. Estrogen and the skeleton. Trends Endocrinol Metab. 2012 Nov;23(11):576-81. doi: 10.1016/j.tem.2012.03.008. Epub 2012 May 16. PMID: 22595550; PMCID: PMC3424385.
Osteocytes, which derive from osteoblasts, are master regulators: Al-Bari, A. A., & Al Mamun, A. (2020). Current advances in regulation of bone homeostasis. FASEB bioAdvances, 2(11), 668–679. https://doi.org/10.1096/fba.2020-00058
In premenopausal women, estrogen deficiency leads to a fourfold increase: Tomkinson A, Reeve J, Shaw RW, Noble BS. The death of osteocytes via apoptosis accompanies estrogen withdrawal in human bone. J Clin Endocrinol Metab. 1997 Sep;82(9):3128-35. doi: 10.1210/jcem.82.9.4200. PMID: 9284757
Osteoporosis is a serious medical condition that affects 200 million: Johnell O, Kanis JA. An estimate of the worldwide prevalence and disability associated with osteoporotic fractures. Osteoporos Int. 2006 Dec;17(12):1726-33. doi: 10.1007/s00198-006-0172-4. Epub 2006 Sep 16. PMID: 16983459.
During menopause, women have, on average, a 10 percent reduction in bone mineral density: Ji MX, Yu Q. Primary osteoporosis in postmenopausal women. Chronic Dis Transl Med. 2015 Mar 21;1(1):9-13. doi: 10.1016/j.cdtm.2015.02.006. PMID: 29062981; PMCID: PMC5643776.
And for each year after menopause, they have an average reduction of .6 percent: Rolland YM, Perry HM 3rd, Patrick P, Banks WA, Morley JE. Loss of appendicular muscle mass and loss of muscle strength in young postmenopausal women. J Gerontol A Biol Sci Med Sci. 2007 Mar;62(3):330-5. doi: 10.1093/gerona/62.3.330. PMID: 17389732.
Fractures secondary to osteoporosis can lead to deformed bone: W. D., & Morin, S. N. (2014). Osteoporosis epidemiology 2013: implications for diagnosis, risk assessment, and treatment. Current opinion in rheumatology, 26(4), 440–446. https://doi.org/10.1097/BOR.0000000000000064
According to a 2022 article, only 33 percent of older adults assigned female at birth who experience a hip fracture: Downey, C., Kelly, M., & Quinlan, J. F. (2019). Changing trends in the mortality rate at 1-year post hip fracture - a systematic review. World journal of orthopedics, 10(3), 166–175. https://doi.org/10.5312/wjo.v10.i3.166 See also: Porter, J. L., & Varacallo, M. (2023). Osteoporosis. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK441901/
In women at risk of fracture, menopausal hormone therapy is effective in preventing osteoporotic: Wells, G., Tugwell, P., Shea, B., Guyatt, G., Peterson, J., Zytaruk, N., Robinson, V., Henry, D., O'Connell, D., Cranney, A., & Osteoporosis Methodology Group and The Osteoporosis Research Advisory Group (2002). Meta-analyses of therapies for postmenopausal osteoporosis. V. Meta-analysis of the efficacy of hormone replacement therapy in treating and preventing osteoporosis in postmenopausal women. Endocrine reviews, 23(4), 529–539. https://doi.org/10.1210/er.2001-5002
Estrogen may also regulate bone homeostasis, a dynamic process: Al-Bari, A. A., & Al Mamun, A. (2020). Current advances in regulation of bone homeostasis. FASEB bioAdvances, 2(11), 668–679. https://doi.org/10.1096/fba.2020-00058
Furthermore, MHT preserves or increases bone density at all skeletal: Wells, G., Tugwell, P., Shea, B., Guyatt, G., Peterson, J., Zytaruk, N., Robinson, V., Henry, D., O'Connell, D., Cranney, A., & Osteoporosis Methodology Group and The Osteoporosis Research Advisory Group (2002). Meta-analyses of therapies for postmenopausal osteoporosis. V. Meta-analysis of the efficacy of hormone replacement therapy in treating and preventing osteoporosis in postmenopausal women. Endocrine reviews, 23(4), 529–539. https://doi.org/10.1210/er.2001-5002
Satellite cells are stem cells located on muscle fibers; these special cells: Hawke, T. J., & Garry, D. J. (2001). Myogenic satellite cells: physiology to molecular biology. Journal of applied physiology (Bethesda, Md. : 1985), 91(2), 534–551. https://doi.org/10.1152/jappl.2001.91.2.534
Although they are “dormant” in a state of equilibrium, these cells mobilize after injury: Dumont, N. A., Bentzinger, C. F., Sincennes, M. C., & Rudnicki, M. A. (2015). Satellite Cells and Skeletal Muscle Regeneration. Comprehensive Physiology, 5(3), 1027–1059. https://doi.org/10.1002/cphy.c140068 See also: Hindi, S. M., & Kumar, A. (2016). TRAF6 regulates satellite stem cell self-renewal and function during regenerative myogenesis. The Journal of clinical investigation, 126(1), 151–168. https://doi.org/10.1172/JCI81655
Without menopausal hormone therapy, the decrease in satellite cells can exacerbate: Wright, V. J., Schwartzman, J. D., Itinoche, R., & Wittstein, J. (2024). The musculoskeletal syndrome of menopause. Climacteric: The Journal of the International Menopause Society, 1–7. https://doi.org/10.1080/13697137.2024.2380363
Animal model studies suggest that female mice without ovaries (and therefore, without estrogen: Velders M, Schleipen B, Fritzemeier KH, Zierau O, Diel P. Selective estrogen receptor-β activation stimulates skeletal muscle growth and regeneration. FASEB J. 2012 May;26(5):1909-20. doi: 10.1096/fj.11-194779. Epub 2012 Jan 25. PMID: 22278942.
Skeletal muscle houses specific estradiol receptors at the level of muscle fibers: Geraci, A., Calvani, R., Ferri, E., Marzetti, E., Arosio, B., & Cesari, M. (2021). Sarcopenia and Menopause: The Role of Estradiol. Frontiers in endocrinology, 12, 682012. https://doi.org/10.3389/fendo.2021.682012
This suggests that estradiol can promote muscle regeneration by stimulating: Cruz-Jentoft, A. J., Baeyens, J. P., Bauer, J. M., Boirie, Y., Cederholm, T., Landi, F., Martin, F. C., Michel, J. P., Rolland, Y., Schneider, S. M., Topinková, E., Vandewoude, M., Zamboni, M., & European Working Group on Sarcopenia in Older People (2010). Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age and ageing, 39(4), 412–423. https://doi.org/10.1093/ageing/afq034 See also: La Colla, A., Pronsato, L., Milanesi, L., & Vasconsuelo, A. (2015). 17β-Estradiol and testosterone in sarcopenia: Role of satellite cells. Ageing research reviews, 24(Pt B), 166–177. https://doi.org/10.1016/j.arr.2015.07.011
People with sarcopenic obesity incur a higher risk for metabolic disease and functional impairment compared to: Donini, L. M., Busetto, L., Bischoff, S. C., Cederholm, T., Ballesteros-Pomar, M. D., Batsis, J. A., Bauer, J. M., Boirie, Y., Cruz-Jentoft, A. J., Dicker, D., Frara, S., Frühbeck, G., Genton, L., Gepner, Y., Giustina, A., Gonzalez, M. C., Han, H. S., Heymsfield, S. B., Higashiguchi, T.,
The combination of excess adipose tissue and low muscle mass and muscle function is called sarcopenic: Laviano, A., … Barazzoni, R. (2022). Definition and Diagnostic Criteria for Sarcopenic Obesity: ESPEN and EASO Consensus Statement. Obesity facts, 15(3), 321–335. https://doi.org/10.1159/000521241
It is characterized by the atrophy of fast muscle fibers: Khadilkar SS. Musculoskeletal Disorders and Menopause. J Obstet Gynaecol India. 2019 Apr;69(2):99-103. doi: 10.1007/s13224-019-01213-7. Epub 2019 Mar 7. PMID: 30956461; PMCID: PMC6430266.
Strikingly, experiments in animal models show that just 24 weeks (six months) of estrogen: Kitajima Y, Ono Y. Estrogens maintain skeletal muscle and satellite cell functions. J Endocrinol. 2016 Jun;229(3):267-75. doi: 10.1530/JOE-15-0476. Epub 2016 Apr 5. PMID: 27048232.
Importantly, a study of postmenopausal women found that this muscle fiber cross-sectional area and grip strength: Taaffe DR, Newman AB, Haggerty CL, Colbert LH, de Rekeneire N, Visser M, Goodpaster BH, Nevitt MC, Tylavsky FA, Harris TB. Estrogen replacement, muscle composition, and physical function: The Health ABC Study. Med Sci Sports Exerc. 2005 Oct;37(10):1741-7. doi: 10.1249/01.mss.0000181678.28092.31. PMID: 16260975.
Grip strength is widely considered to be a biomarker of overall strength: Bohannon RW. Grip Strength: An Indispensable Biomarker For Older Adults. Clin Interv Aging. 2019 Oct 1;14:1681-1691. doi: 10.2147/CIA.S194543. PMID: 31631989; PMCID: PMC6778477.
A recent study found that waking up frequently during the night to urinate: Yang, S.-J., Park, J. H., Oh, Y., Kim, H., Kong, M., & Moon, J. (2021). Association of decreased grip strength with lower urinary tract symptoms in women: A cross‐sectional study from Korea. BMC Women’s Health, 21(1), 96. https://doi.org/10.1186/s12905-021-01241-4
And a novel study of women 60 years and older revealed that: Urinary Incontinence Risk Linked to Thigh Muscle Area in Older Women. (2022, September 12). Renal and Urology News. https://www.renalandurologynews.com/reports/urinary-incontinence-risk-linked-to-thigh-muscle-area-in-older-women/
You won’t yet find menopause experts talking about this, but a key part: Forbes, B. (2023, March 28). Proprioception: We Are Explorers [Substack newsletter]. Bodies of Knowledge. https://boforbes.substack.com/p/07-proprioception-we-are-explorers
From the Latin roots proprius, meaning “of one’s own,” and: Forbes, B. (2023, March 28). Proprioception: We Are Explorers [Substack newsletter]. Bodies of Knowledge. https://boforbes.substack.com/p/07-proprioception-we-are-explorers
Estrogen and progesterone appear to alter the stiffness of: Casey, E., Hameed, F., & Dhaher, Y. Y. (2014). The muscle stretch reflex throughout the menstrual cycle. Medicine and science in sports and exercise, 46(3), 600–609. https://doi.org/10.1249/MSS.0000000000000134
Important among these are muscle spindles: Proske, U., & Gandevia, S. C. (2012). The proprioceptive senses: their roles in signaling body shape, body position and movement, and muscle force. Physiological reviews, 92(4), 1651–1697. https://doi.org/10.1152/physrev.00048.2011
It leads to unstable gait, difficulty balancing, and frequent falls: Kröger, S., & Watkins, B. (2021). Muscle spindle function in healthy and diseased muscle. Skeletal Muscle, 11(1), 3. https://doi.org/10.1186/s13395-020-00258-x
Proprioceptive senses, particularly related to limb position and movement, deteriorate with age: Proske, U., & Gandevia, S. C. (2012). The proprioceptive senses: their roles in signaling body shape, body position and movement, and muscle force. Physiological reviews, 92(4), 1651–1697. https://doi.org/10.1152/physrev.00048.2011 See also: Ferlinc, A., Fabiani, E., Velnar, T., & Gradisnik, L. (2019). The Importance and Role of Proprioception in the Elderly: a Short Review. Materia socio-medica, 31(3), 219–221. https://doi.org/10.5455/msm.2019.31.219-221 See also: Clark, D. J. (2015). Automaticity of walking: Functional significance, mechanisms, measurement and rehabilitation strategies. Frontiers in Human Neuroscience, 9, 246. https://doi.org/10.3389/fnhum.2015.00246
This burdens the executive regions of the brain such as the prefrontal cortex: Clark, D. J. (2015). Automaticity of walking: Functional significance, mechanisms, measurement and rehabilitation strategies. Frontiers in Human Neuroscience, 9, 246. https://doi.org/10.3389/fnhum.2015.00246 See also: Michely, J., Volz, L. J., Hoffstaedter, F., Tittgemeyer, M., Eickhoff, S. B., Fink, G. R., & Grefkes, C. (2018). Network connectivity of motor control in the ageing brain. NeuroImage. Clinical, 18, 443–455. https://doi.org/10.1016/j.nicl.2018.02.001
As this loss progresses, it places growing demands: Michely, J., Volz, L. J., Hoffstaedter, F., Tittgemeyer, M., Eickhoff, S. B., Fink, G. R., & Grefkes, C. (2018). Network connectivity of motor control in the ageing brain. NeuroImage. Clinical, 18, 443–455. https://doi.org/10.1016/j.nicl.2018.02.001
And emerging research indicates that survivors of childhood physical abuse and sexual abuse: Baiden, P., Panisch, L. S., Onyeaka, H. K., LaBrenz, C. A., & Kim, Y. (2021). Association of childhood physical and sexual abuse with arthritis in adulthood: Findings from a population-based study. Preventive medicine reports, 23, 101463. https://doi.org/10.1016/j.pmedr.2021.101463
Osteoarthritis in women increases precipitously around the time of menopause: Stevens-Lapsley JE, Kohrt WM. Osteoarthritis in women: effects of estrogen, obesity and physical activity. Womens Health (Lond). 2010 Jul;6(4):601-15. doi: 10.2217/whe.10.38. PMID: 20597623.
A comprehensive review of the relationship between estrogen and arthritis: Richette, P., Corvol, M., & Bardin, T. (2003). Estrogens, cartilage, and osteoarthritis. Joint Bone Spine, 70(4), 257–262. https://doi.org/10.1016/s1297-319x(03)00067-8
Evidence suggests that the drop in estrogen during menopause leads to alterations in the connective tissue: Muscat Baron, Y., Brincat, M. P., Galea, R., & Calleja, N. (2007). Low intervertebral disc height in postmenopausal women with osteoporotic vertebral fractures compared to hormone-treated and untreated postmenopausal women and premenopausal women without fractures. Climacteric: The Journal of the International Menopause Society, 10(4), 314–319. https://doi.org/10.1080/13697130701460640
Estrogen deficiency correlates strongly with an increase in type I collagen: Fede, C., Pirri, C., Fan, C., Albertin, G., Porzionato, A., Macchi, V., De Caro, R., & Stecco, C. (2019). Sensitivity of the fasciae to sex hormone levels: Modulation of collagen-I, collagen-III and fibrillin production. PloS One, 14(9), e0223195. https://doi.org/10.1371/journal.pone.0223195
At the same time, relaxin, which inhibits fibrosis and inflammation: Fede, C., Pirri, C., De Caro, R., & Stecco, C. (2022). Myofascial pain in females and personalized care: The key role played by sex hormones. European Journal of Pain (London, England), 26(4), 939–940. https://doi.org/10.1002/ejp.1920
Hyalauronan is found not only in the joints but: Garantziotis, S., & Savani, R. C. (2019). Hyaluronan biology: A complex balancing act of structure, function, location and context. Matrix Biology : Journal of the International Society for Matrix Biology, 78–79, 1. https://doi.org/10.1016/j.matbio.2019.02.002
And, studies suggest, hyalauronan also plays a role in the health of our nervous system: Perkins, K. L., Arranz, A. M., Yamaguchi, Y., & Hrabetova, S. (2017). Brain extracellular space, hyaluronan, and the prevention of epileptic seizures. Reviews in the Neurosciences, 28(8), 869. https://doi.org/10.1515/revneuro-2017-0017 See also: Zakusilo, F. T., Kerry O’Banion, M., Gelbard, H. A., Seluanov, A., & Gorbunova, V. (2021). Matters of size: Roles of hyaluronan in CNS aging and disease. Ageing Research Reviews, 72, 101485. https://doi.org/10.1016/j.arr.2021.101485
According to the North American Menopause Society, “For women aged younger than: The 2022 hormone therapy position statement of The North American Menopause Society. (2022). Menopause, 29(7), 767. https://doi.org/10.1097/GME.0000000000002028
Research indicates that Vitamin D3 supplementation improves hip bone mineral density: Mei, Z., Hu, H., Zou, Y., & Li, D. (2023). The role of vitamin D in menopausal women's health. Frontiers in physiology, 14, 1211896. https://doi.org/10.3389/fphys.2023.1211896 See also: Jackson, R. D., LaCroix, A. Z., Gass, M., Wallace, R. B., Robbins, J., Lewis, C. E., Bassford, T., Beresford, S. A., Black, H. R., Blanchette, P., Bonds, D. E., Brunner, R. L., Brzyski, R. G., Caan, B., Cauley, J. A., Chlebowski, R. T., Cummings, S. R., Granek, I., Hays, J., Heiss, G., … Women's Health Initiative Investigators (2006). Calcium plus vitamin D supplementation and the risk of fractures. The New England journal of medicine, 354(7), 669–683. https://doi.org/10.1056/NEJMoa055218
In postmenopausal women aged 50-65 years with an existing Vitamin D deficiency: Nahas-Neto, J., Cangussu, L. M., Orsatti, C. L., Bueloni-Dias, F. N., Poloni, P. F., Schmitt, E. B., & Nahas, E. A. P. (2018). Effect of isolated vitamin D supplementation on bone turnover markers in younger postmenopausal women: a randomized, double-blind, placebo-controlled trial. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 29(5), 1125–1133. https://doi.org/10.1007/s00198-018-4395-y
Many menopause specialists now recommend resistance training with weights: Wright, V. J., Schwartzman, J. D., Itinoche, R., & Wittstein, J. (2024). The musculoskeletal syndrome of menopause. Climacteric: The Journal of the International Menopause Society, 1–7. https://doi.org/10.1080/13697137.2024.2380363 See also: Agostini, D., Donati Zeppa, S., Lucertini, F., Annibalini, G., Gervasi, M., Ferri Marini, C., Piccoli, G., Stocchi, V., Barbieri, E., & Sestili, P. (2018). Muscle and Bone Health in Postmenopausal Women: Role of Protein and Vitamin D Supplementation Combined with Exercise Training. Nutrients, 10(8), 1103. https://doi.org/10.3390/nu10081103
The European Society for Clinical Nutrition and Metabolism proposes a daily: Volpi, E., Campbell, W. W., Dwyer, J. T., Johnson, M. A., Jensen, G. L., Morley, J. E., & Wolfe, R. R. (2013). Is the optimal level of protein intake for older adults greater than the recommended dietary allowance?. The journals of gerontology. Series A, Biological sciences and medical sciences, 68(6), 677–681. https://doi.org/10.1093/gerona/gls229
In several studies, higher protein intake (1.2g per kg or 2.2 lbs. body weight) is associated: Antonio, J., Ellerbroek, A., Silver, T., Orris, S., Scheiner, M., Gonzalez, A., & Peacock, C. A. (2015). A high protein diet (3.4 g/kg/d) combined with a heavy resistance training program improves body composition in healthy trained men and women--a follow-up investigation. Journal of the International Society of Sports Nutrition, 12, 39. https://doi.org/10.1186/s12970-015-0100-0 See also: Silva, T. R., & Spritzer, P. M. (2017). Skeletal muscle mass is associated with higher dietary protein intake and lower body fat in postmenopausal women: a cross-sectional study. Menopause (New York, N.Y.), 24(5), 502–509. https://doi.org/10.1097/GME.0000000000000793 See also: Beasley, J. M., LaCroix, A. Z., Neuhouser, M. L., Huang, Y., Tinker, L., Woods, N., Michael, Y., Curb, J. D., & Prentice, R. L. (2010). Protein intake and incident frailty in the Women's Health Initiative observational study. Journal of the American Geriatrics Society, 58(6), 1063–1071. https://doi.org/10.1111/j.1532-5415.2010.02866.x
It slows the rate of estrogen loss, which can minimize the devastating effects: Wright, V. J., Schwartzman, J. D., Itinoche, R., & Wittstein, J. (2024). The musculoskeletal syndrome of menopause. Climacteric: The Journal of the International Menopause Society, 1–7. https://doi.org/10.1080/13697137.2024.2380363
One study of older adults with mild mobility and body-sensing deficits: Clark, D. J., Christou, E. A., Ring, S. A., Williamson, J. B., & Doty, L. (2014). Enhanced somatosensory feedback reduces prefrontal cortical activity during walking in older adults. The journals of gerontology. Series A, Biological sciences and medical sciences, 69(11), 1422–1428. https://doi.org/10.1093/gerona/glu125
And several large-scale reviews found that compared to conventional therapies: Yao, K. R., Luo, Q., Tang, X., Wang, Z. H., Li, L., Zhao, L., Zhou, L., Li, L., Huang, L., & Yin, X. H. (2023). Effects of traditional Chinese mind-body exercises on older adults with cognitive impairment: A systematic review and meta-analysis. Frontiers in neurology, 14, 1086417. https://doi.org/10.3389/fneur.2023.1086417 See also: Wang, X., Si, K., Gu, W., & Wang, X. (2023). Mitigating effects and mechanisms of Tai Chi on mild cognitive impairment in the elderly. Frontiers in aging neuroscience, 14, 1028822. https://doi.org/10.3389/fnagi.2022.1028822 See also: Zou, L., Han, J., Li, C., Yeung, A. S., Hui, S. S., Tsang, W. W. N., Ren, Z., & Wang, L. (2019). Effects of Tai Chi on Lower Limb Proprioception in Adults Aged Over 55: A Systematic Review and Meta-Analysis. Archives of physical medicine and rehabilitation, 100(6), 1102–1113. https://doi.org/10.1016/j.apmr.2018.07.425