Your face and neck turn red and hot, and suddenly your clothes are sweaty. Your heart rate increases, and maybe you even feel anxious. Then you switch from hot to chilled just as rapidly. One of the most troubling symptoms of menopause is the dreaded hot flash—and related night sweats.
Nearly 80% of women report having experienced hot flashes (also called vasomotor symptoms) by the time they are postmenopausal. Menopause is officially reached when menstruation has ceased for 12 months. After that, one is in postmenopause. Before menopause and postmenopause is perimenopause, which is the years-long transition. During that time, one’s cycle can be erratic, hormone levels change, and symptoms begin.
A 2005 review of several menopause studies encompassing more than 18,000 participants looked at hot flash prevalence at various life stages to assess how common these symptoms are. Based on the various datasets they used, the researchers estimated that among those who haven’t yet entered the menopause transition, 6% to 13% experience hot flashes. For those in the late menopause transition, 33% to 63% have hot flashes. And the prevalence estimate increases to 79% for those who’ve reached menopause.
Although much is still unknown about the cause of hot flashes, research suggests they may have a connection to metabolic health. Therefore, focusing on stabilizing blood sugar and increasing insulin sensitivity could help ease this symptom. More research is needed to determine the mechanisms at play and what people can do to mitigate symptoms. Read on to learn about what is known thus far.
What happens during a hot flash (and what causes it)?
Generally, the human body can tolerate roughly half a degree Fahrenheit change in ambient temperature without the brain stepping in to counteract the change. And that remains true for women in their reproductive years. But when a woman enters perimenopause and hormone levels change, that tolerance for heat also drops.
During a hot flash, the hypothalamus, the part of the brain that helps control body temperature, overreacts to those minor changes in ambient temperature and triggers an excessive vasodilatory response to cool the body. Blood vessels expand, causing skin redness and sometimes sweating. Then the body releases heat rapidly, resulting in a subsequent chill. The experience can be maddening.
Why does the hypothalamus play a role? During the usual trajectory of a menstrual cycle, the hypothalamic-pituitary-gonadal (HPG) axis maintains a tightly controlled feedback loop. As one hormone level rises, it kicks off a set of chain reactions on other hormone levels. These hormone fluctuations occur across the two main phases of the menstrual cycle: the follicular and luteal phases, with ovulation happening between. Changes during perimenopause and at menopause can alter these processes.
Researchers partially attribute the hypothalamus’s excessive response to minor temperature changes to the increase in follicle-stimulating hormone (FSH) in perimenopause and, potentially, to initial fluctuations of estrogen levels also during early perimenopause and their rapid decline in the later stages of the menopause transition.
Here’s how the physiology potentially plays out. Changes in reproductive hormones impact a grouping of neurons in the hypothalamus called the KNDy neurons. Researchers theorize that balanced hormones regulate these neurons and neuropeptides during one’s reproductive years. During perimenopause, however, hormone disruption may cause a neuropeptide called neurokinin B to overstimulate the neuropeptide kisspeptin. The kisspeptin neurons are connected to our thermoregulatory center. So during a hot flash, the brain overreacts to even minuscule temperature changes.
A decline in serotonin may also be to blame. Estrogen stimulates serotonin. When estrogen levels decline during and after menopause, it causes a 50 percent decrease in serotonin, which then causes an increase in the neurotransmitter norepinephrine. Norepinephrine also disrupts the hypothalamus’s ability to regulate temperature.
The connection between metabolic health and hot flashes
Hot flashes have some links with insulin resistance and high blood sugar. A study from 2012 looked at more than 3,000 women, ages 42 to 52, who were in the menopause transition and were part of the Study of Women’s Health Across the Nation. The researchers analyzed annual blood samples from the women, taken over eight years, looking at fasting glucose, insulin, and estrogen levels. Hot flashes and night sweats were associated with higher levels of insulin resistance. The researchers looked at hot flash and night sweat frequency of the women over the past two weeks and compared frequency to the participants’ levels of insulin resistance as defined by the homeostatic model assessment for insulin resistance (HOMA-IR). Compared to women who had no hot flashes, those who had hot flashes one to five days over the past two weeks had 2.37% higher HOMA-IR. And those who had hot flashes on six or more days over two weeks had 5.91% higher HOMA-IR.
The researchers also found a link between higher glucose levels and hot flashes but to a lesser extent. These associations remained independent of body mass index (BMI) or estrogen level.
As part of a smaller 2017 study, researchers looked at hot-flash severity in 151 women ages 45 to 60. They found that the women who reported the most severe hot flashes had the highest fasting glucose and insulin levels compared to those who had either no hot flashes or mild-to-moderate episodes. Finally, a 2018 study of about 150,000 postmenopausal women linked hot flashes and night sweats with an 18 percent increase in Type 2 diabetes risk. Complicating matters is that lower estrogen concentration in perimenopause is associated with a 47% increase in Type 2 diabetes risk.
Researchers don’t know the exact mechanisms for how hot flashes are associated with insulin resistance and high blood sugar, but they have some theories. One is the stress-response theory, and another involves the hormones leptin and adiponectin. These have some overlap and, therefore, may be connected.
Some research points to autonomic nervous system involvement. During a hot flash, the sympathetic nervous system (the fight-or-flight response) is activated while the parasympathetic nervous system (the rest-and-digest system) withdraws. Overactivation or predominance of the sympathetic nervous system (and withdrawal of the parasympathetic nervous system) appears to play a role in the onset of Type 2 diabetes. But researchers point out that the relationship may also work in reverse. Metabolic syndrome may cause sympathetic nervous system overactivation. The hypothalamic-pituitary-adrenal (HPA) axis is essentially the body’s stress response system, so overactivation of the HPA from metabolic syndrome could be triggering the hypothalamus to have an outsized response to minor temperature changes, resulting in hot flashes. But again, we need more research.
The HPA axis overlaps with the HPG axis, which, as noted above, controls the menstrual cycle. These two axes—HPA and HPG—have a reciprocal relationship, with each affecting the other. For example, when overactivated—as occurs with insulin resistance and hyperinsulinemia—the HPA axis can inhibit hormonal secretion on the HPG axis. Animal studies show that the release of cortisol (a stress hormone) can inhibit the natural cycle of the ovaries. Could this inhibition intensify perimenopause-related hormonal changes and, therefore hot flashes? Likewise, changes in sex steroid hormones can impact the HPA axis and, therefore, the stress response. We need more research to determine exactly how and to what extent these two axes impact each other and how those impacts could be a driver of hot flashes.
The stress-response theory is also an underlying theme in older research. Preliminary research from 2007 shows that hot flashes may be more common when blood sugar drops rather than right after eating. Researchers looked at 10 postmenopausal women with an average age of 49 who went off hormone therapy for the study. They underwent blood glucose sampling and monitoring for hot flashes—via skin conduction testing—during eating and fasting periods. The researchers found that eating provided a 90-minute window that was hot-flash-free. Whereas, in the 30 minutes before a meal, when participants hadn’t eaten for a while, hot flashes were more common.
The researchers theorize that declining estrogen levels cause a decrease in glucose transporter 1 (GLUT1), a carrier protein produced in the blood-brain barrier. The hypothesis is that these changes slow the rate of glucose transported into the brain. The lack of energy triggers the hot flash and sympathetic nervous system response, with the aim of getting glucose and oxygen to the brain quickly. More research is needed to confirm, but the study authors point out that stabilizing blood glucose may reduce hot flashes.
How can both low and high blood sugar be related to hot flashes? Researchers are still trying to figure out these mechanisms. However, some research shows that low blood sugar initiates a stress response and, thus, activation of the HPA axis. Theoretically, this activation could trigger the hypothalamus to overreact to a minor increase in heat.
Levels Member story:
Adiponectin and leptin
Changes in the hormones adiponectin and leptin may also play a role in hot flashes. Adiponectin is a protein hormone secreted by fat tissue that helps increase insulin sensitivity and reduce inflammation. Leptin, another hormone secreted by fat tissue, helps regulate appetite, energy balance, and weight.
During menopause, adiponectin appears to decline, and lower levels are associated with hot flashes. One study of more than 300 participants of varying menstrual status found that adiponectin declined to its lowest level during perimenopause before increasing again after menopause, while additional research supports this general trajectory, more research is needed. Low adiponectin levels are associated with metabolic syndrome (a cluster of conditions including insulin resistance and central obesity), especially after menopause. And in a different study of 151 women ages 45 to 60, researchers found that hot flash severity was significantly associated with lower adiponectin levels.
That same study found that hot flash severity was also significantly associated with higher leptin levels. Higher leptin levels are also sometimes associated with insulin resistance. Researchers are still trying to figure out if lower adiponectin and higher leptin levels are a cause of hot flashes, however. Right now, they just note these associations.
The bottom line
Hot flashes appear to have connections to several hormones and processes in the body, including those associated with metabolic health. The specifics of these associations are still unclear because we don’t yet have high-quality studies that provide more insight. As research on this topic progresses, we hope to learn more about the exact mechanisms. For now, we do know that boosting metabolic health has profound effects on overall health. So if you’re entering the menopause trajectory, focusing on metabolic health is likely beneficial and doing so may even help lessen some vexing symptoms, including hot flashes.
Interested in using CGM to manage menopause?
Levels, the health tech company behind this blog, helps people improve their metabolic health by showing how food and lifestyle impact your blood sugar, using continuous glucose monitoring (CGM), along with an app that offers personalized guidance and helps you build healthy habits. Click here to learn more about Levels.