Stress Can Cause Spotting — Here's Why It Happens and What to Do
Spotting generally occurs as small droplets of blood in your underwear or as a pink, red, or brown tinge in your discharge.
'The color of your spotting is determined by the amount of time that's passed since the blood was released from the lining of the uterus,' says Jane van Dis, MD, OB-GYN, a medical advisor with menstrual company FLEX.
It typically occurs on either side of your menstrual period (before your period starts in earnest or after you think it has ended), but it can happen at any point in your monthly cycle.
Keep reading to learn more about how stress affects your menstrual cycle and how to manage it.
How stress affects your menstrual cycle
High stress levels can prompt your endocrine system to release stress hormones, including cortisol, a steroid hormone produced by your adrenal glands.
The entire endocrine system is connected, and increased cortisol can have a ripple effect. When cortisol levels rise, both estrogen and testosterone can decrease.
Likewise, fluctuating sex hormones can also affect your stress levels. An unexpected change in your estrogen levels can disrupt your menstrual cycle, resulting in spotting, missed menstruation, or other irregularities.
'Anything that impacts you as a person has the potential to impact the menstrual cycle and therefore cause spotting,' explains reproductive health specialist Felice Gersh, MD, author of 'PCOS SOS: A Gynecologist's Lifeline To Naturally Restore Your Rhythms, Hormones, and Happiness.'
The stress may contribute to spotting if you recently experienced a life change. Causes can include changes like:
a breakup
moving
increasing work responsibilities or losing your job
a recent diagnosis, whether your own or a loved one's
Stress-induced spotting is usually accompanied by other symptoms of stress, including:
difficulty sleeping
difficulty concentrating
changes in appetite
generalized fatigue
muscle aches
digestive upset
sexual dysfunction
Illnesses can also cause physical stress that may have a similar effect.
How to manage stress-related spotting
'Spotting, by its name, implies that an individual is releasing a smaller amount of blood than they would during their period,' says van Dis.
A panty liner should be enough to protect your underwear. If you choose to free-bleed (menstruating without blocking or collecting menstrual blood) and end up staining your underwear, blood-removal tips can help.
However, if you are bleeding so much that you need a sanitary pad or tampon to catch the blood, it is likely too much to be considered spotting. You may have another type of vaginal bleeding.
If the bleeding isn't from stress or your menstrual period, it's best to talk with a healthcare professional about your symptoms. Other causes of abnormal vaginal bleeding can include:
pregnancy or miscarriage
a growth in your uterus or cervix
hormone imbalance
medication changes
an infection
breakthrough bleeding
Cycle-related changes also occur with perimenopause. This is the phase that precedes menopause.
Managing stress to prevent stress-related menstrual changes
Managing your overall stress levels can help reduce stress-related spotting.
'You could incorporate meditation, journaling, grounding, or nature walking into your routine,' says Gersh.
Other stress reduction methods she recommends include:
physical therapy
massage therapy
acupuncture from a licensed practitioner for myofascial release therapy, deep tissue massage, or another form of bodywork
Prioritizing your overall health can also help you manage your stress levels. That means:
drinking enough water
eating nutrient-dense meals
monitoring caffeine intake
getting regular physical activity
limiting alcohol, nicotine, and other substance use
If you continue to feel stressed, less focused, or more irritable than usual, it may be time to talk with a mental health professional. The right therapist can help you deduce the root of your stress and give you tools to manage it.
When to consult with a doctor or other healthcare professional
'If you have a regular period and this is your first time spotting, you'd be wise to rule out pregnancy as the underlying cause if there's a chance that you could be pregnant,' says Gersh.
You can find out if you're pregnant by taking an at-home pregnancy test 10 or more days after you last had vaginal intercourse with a person who produces sperm.
You can also ask a healthcare professional to order a blood test, which can usually detect pregnancy a few days earlier.
If this is the first time you've ever spotted and there's no chance you're pregnant, Gersh says it's probably OK to assume that stress, or some other lifestyle change, is the cause.
But if you're experiencing other unusual symptoms or bodily changes, she recommends consulting a healthcare professional.
Frequently asked questions
What does stress spotting look like?
Spotting usually looks like light bleeding in your underwear. It can be pink, red, or brown and may occur with other discharge. It's typically a small amount (enough that you could use a pantyliner but not need a pad or a tampon).
Spotting usually looks like light bleeding in your underwear. It can be pink, red, or brown and may occur with other discharge. It's typically a small amount (enough that you could use a pantyliner but not need a pad or a tampon).
What can trigger spotting?
Some possible triggers for light bleeding between periods can include stress, changing or skipping hormonal birth control, rough sex, or implantation bleeding due to pregnancy. If you have more than a small amount of blood, there could be another cause.
Some possible triggers for light bleeding between periods can include stress, changing or skipping hormonal birth control, rough sex, or implantation bleeding due to pregnancy. If you have more than a small amount of blood, there could be another cause.
Why am I only spotting when I wipe?
If you only notice blood when you wipe after urinating, you may want to get checked out for other causes of bleeding, such as a urinary tract infection (UTI), which can cause blood in your urine.
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Medscape
17 minutes ago
- Medscape
Calcium Deposition Can Increase Osteoarthritis Risk
Calcium crystal deposition may be a risk factor for knee osteoarthritis (OA), according to a new study. In an analysis including more than 6400 middle-aged to older adults, individuals with knee chondrocalcinosis were 75% more likely to develop knee OA than those without the condition at baseline. Because knee chondrocalcinosis and OA are often observed together, it is commonly considered a feature of the OA disease process, said Jean W. Liew, MD, an assistant professor of rheumatology at Boston University, Boston, and coauthor of the study. 'This study suggests that calcium crystal deposition is a cause of knee OA rather than just a consequence,' she told Medscape Medical News . The analysis included data from two independent cohorts: the Rotterdam Study (RS) and the Multicenter Osteoarthritis Study (MOST). RS enrolled individuals aged 55 years or older residing in Rotterdam, the Netherlands. MOST, which recruited participants from Birmingham, Alabama, and Iowa City, Iowa, enrolled adults aged 50-79 years with preexisting knee OA or at increased risk for OA due to overweight status, knee injury, or knee symptoms. Researchers examined the association between baseline knee chondrocalcinosis, measured via x-ray, and development of radiographic knee OA over time. Radiographic knee OA was defined as a Kellgren and Lawrence grade (KLG) ≥ 2 or if the individual had undergone knee replacement at follow-up. The analysis, published online on August 5, 2025, in Annals of the Rheumatic Diseases , included 3737 individuals from the RS cohort and 2750 individuals from the MOST cohort. At baseline in the RS cohort, 76.1% of participants had no signs of radiographic knee OA (KLG = 0), and 4.3% had knee chondrocalcinosis. For the MOST cohort, 68.5% had no signs of radiographic knee OA, and 5.0% had knee chondrocalcinosis at baseline. The analysis found that knee chondrocalcinosis increased the risk for incident radiographic knee OA after adjustment for age, sex, and BMI. The pooled odds ratio (OR) between both groups was 1.75 (95% CI, 1.25-2.27; P < .001). There were no cases of regression of chondrocalcinosis during follow-up, which suggests that chondrocalcinosis does not resolve over time, Liew and colleagues wrote. In a subgroup analysis including only individuals with KLG of 0 at baseline, the results were similar (OR = 1.77; 95% CI, 1.04-3.01; P = .035). More severe chondrocalcinosis was also associated with increased risk of developing knee OA. Commenting on the study for Medscape Medical News , Sara Tedeschi, MD, MPH, noted that these findings 'strongly suggest that [chondrocalcinosis] is a risk factor for the new development of osteoarthritis in people who don't currently have radiographic osteoarthritis.' Tedeschi is the head of crystal-induced arthritic diseases at Brigham and Women's Hospital in Boston. 'One of the unique features of this paper,' she said, 'is that they were able to look at knees that had chondrocalcinosis at baseline but no osteoarthritis at baseline and were able to follow them forward' with years of follow-up data. Treatment Options Liew now wants to explore whether treatments for inflammation related to calcium crystal deposition could also help prevent or delay progression of OA in this subset of patients. 'It's time to look at designing studies focused on this subgroup of people (with chondrocalcinosis on imaging) and testing whether treatments that work for crystal-associated arthritis like gout or calcium pyrophosphate deposition disease would also work for knee OA,' she said. 'Hints of such benefits have appeared in previous cardiovascular randomized controlled trials of colchicine, where patients receiving the drug had a lower risk of joint replacement as a secondary outcome,' noted Tedeschi. It's 'one interesting therapy to consider' for potential future trials, as are other anti-inflammatory medications like interleukin-1 inhibitors, she added.
Yahoo
an hour ago
- Yahoo
Editorial: Saving lives no more — RFK risks us all in targeting mRNA vaccine research
Showing that his loyalty to his own anti-vax mentality is greater than his loyalty to President Donald Trump, Robert F. Kennedy Jr., the dangerous quack atop the Department of Health and Human Services, has announced that he will be rescinding a half billion dollars in grants and contracts for the development of mRNA technology and vaccines. It was mRNA that was key to both the Pfizer-BioNTech and the Moderna COVID vaccines that were created under Trump in his first term, but RFK does not like life-saving vaccines and so he's pulling the plug. Part of the problem with policymaking at the level of the federal government is that the impacts are often too large, too long-winded, too abstract to really be able to nearly encompass their full breadth, particularly for busy people who have their own immediate concerns to worry about. In this case, though, we can point to very clear, very grim and almost unavoidable repercussions directly caused by this decision: many people worldwide — including in the United States — will die deaths that could have been prevented. Setting aside all of the jargon, at its most basic level a vaccine is about allowing the body to ward off or survive pathogens that would otherwise be extremely dangerous and debilitating or kill a person outright. The model itself is far from new; inoculations in some form of another, including the basic utilization of a dead virus to create antibodies that can attack a live one, date back centuries. What's mainly changed since then is that we have only advanced our understanding and technology to keep infectious diseases from running rampant in our society. One such technological leap was the mRNA process, an innovation so significant that its pioneers won the Nobel prize. The effectiveness and the safety of this process has been well-documented in research settings, but we don't even have to parse the studies to know this because we all collectively lived it. As Trump's Operation Warp Speed produced, the first and most widespread COVID inoculations were mRNA-based vaccines, which enabled us to blunt the rampaging pandemic and much more quickly return our society to a semblance of normalcy. Those COVID vaccines have already been synthesized, but the real issue here are the ones that haven't, or even the inoculations for viruses that we have not even identified or think to be a threat today. Whether we like it or not, our relationship to infectious diseases is something akin to an arms race, in which we are constantly trying to counteract pathogens that, by dint of evolution, are constantly finding ways to elude our defenses and sicken us. We've stayed largely on top of this arms race over the last six decades or so in particular because of constant efforts that have developed sophisticated tools to fight back, including mRNA. A disarmament here for no other reason than ideologically-driven conspiracy that drives Bobby Kennedy is going to mean that we give the diseases an opening, which they will no doubt exploit to sicken and kill us. There are quite simply no two ways about it, and any pause in the research could have dire consequences, even if it is reversed later. Ongoing and sometimes multimonth or even multiyear projects will lose funding and might have to be shut down, with all their efforts wasted. There's no way to really put the genie back in the bottle so we have to stop it in the first place, which means RFK must be fired immediately or impeached and removed by Congress. Many lives hang in the balance. _____
Fast Company
an hour ago
- Fast Company
How tech pinpoints urban heat islands and makes cooling projects easier
It's summer, and it's been hot, even in northern cities such as Boston. But not everyone is hit with the heat in the same way, even within the same neighborhood. Take two streets in Boston at 4:30 p.m. on a recent day, as an example. Standing in the sun on Lewis Place, the temperature was 94 degrees Fahrenheit (34.6 degrees Celsius). On Dudley Common, it was 103 F. Both streets were hot, but the temperature on one was much more dangerous for people's health and well-being. The kicker is that those two streets are only a few blocks apart. The difference epitomizes the urban heat island effect, created as pavement and buildings absorb and trap heat, making some parts of the city hotter. A closer look at the two streets shows some key differences: Dudley Common is public open space sandwiched between two thoroughfares that create a wide expanse of pavement lined with storefronts. There aren't many trees to be found. Lewis Place is a residential cul-de-sac with two-story homes accompanied by lots of trees. This comparison of two places within a few minutes' walk of each other puts the urban heat island effect under a microscope. It also shows the limits of today's strategies for managing and responding to heat and its effects on public health, which are generally attuned to neighborhood or citywide conditions. Even within the same neighborhood, some places are much hotter than others owing to their design and infrastructure. You could think of these as urban heat islets in the broader landscape of a community. Sensing urban heat islets Emerging technologies are making it easier to find urban heat islets, opening the door to new strategies for improving health in our communities. While the idea of reducing heat across an entire city or neighborhood is daunting, targeting specific blocks that need assistance the most can be faster and a much more efficient use of resources. Doing that starts with making urban heat islets visible. In Boston, I'm part of a team that has installed more than three dozen sensors across the Roxbury neighborhood to measure temperature every minute for a better picture of the community's heat risks, and we're in the process of installing 25 more. The Common SENSES project is a collaboration of community-based organizations, including the Dudley Street Neighborhood Initiative and Project Right Inc.; university researchers like me who are affiliated with Northeastern University's Boston Area Research Initiative; and Boston city officials. It was created to pursue data-driven, community-led solutions for improving the local environment. Data from those sensors generate a real-time map of the conditions in the neighborhood, from urban heat islets like Dudley Common to cooler urban oases, such as Lewis Place. These technologies are becoming increasingly affordable and are being deployed in communities around the world to pinpoint heat risks, including Miami, Baltimore, Singapore, and Barcelona. There are also alternatives when long-term installations prove too expensive, such as the U.S.'s National Oceanic and Atmospheric Administration volunteer science campaign, which has used mobile sensors to generate onetime heat maps for more than 50 cities. Making cooler communities, block by block Although detailed knowledge of urban heat islets is becoming more available, we have barely scratched the surface of how they can be used to enhance people's health and well-being. The sources of urban heat islets are rooted in development—more buildings, more pavement, and fewer trees result in hotter spaces. Many projects using community-based sensors aspire to use the data to counteract these effects by identifying places where it would be most helpful to plant trees for shade or install cool roofs or cool pavement that reflect the heat. However, these current efforts do not fully capitalize on the precision of sensors. For example, Los Angeles's massive investment in cool pavement has focused on the city broadly rather than overheated neighborhoods. New York City's tree planting efforts in some areas failed to anticipate where trees could be successfully planted. Most other efforts compare neighborhood to neighborhood, as if every street within a neighborhood experiences the same temperature. London, for example, uses satellite data to locate heat islands, but the resolution isn't precise enough to see differences block by block. In contrast, data pinpointing the highest-risk areas enables urban planners to strategically place small pocket parks, cool roofs, and street trees to help cool the hottest spaces. Cities could incentivize or require developers to incorporate greenery into their plans to mitigate existing urban heat islets or prevent new ones. These targeted interventions are cost-effective and have the greatest potential to help the most people. But this could go further by using the data to create more sophisticated alert systems. For example, the National Weather Service's Boston office released a heat advisory for July 25, 2025, the day I measured the heat in Dudley Common and Lewis Place, but the advisory showed nearly the entirety of the state of Massachusetts at the same warning level. What if warnings were more locally precise? On certain days, some streets cross a crucial threshold—say, 90 F—whereas others do not. Sensor data capturing these hyperlocal variations could be communicated directly to residents or through local organizations. Advisories could share maps of the hottest streets or suggest cool paths through neighborhoods. There is increasing evidence of urban heat islets in many urban communities and even suburban ones. With data showing these hyperlocal risks, policymakers and project coordinators can collaborate with communities to help address areas that many community members know from experience tend to be much hotter than surrounding areas in summer. As one of my colleagues, Nicole Flynt of Project Right Inc., likes to say, 'Data + Stories = Truth.' If communities act upon both the temperature data and the stories their residents share, they can help their residents keep cool—because it's hot out there.
