Traci McCormick, MD

If you take estrogen, are considering it, or have been afraid to take it because of what you’ve heard about the risks, this new study is worth reading.

A large new study published this week in The BMJ looked at the risks associated with menopausal estrogen therapy. But importantly, the researchers didn’t just ask whether women were taking estrogen. They looked at which estrogen they were taking, the dose, how they were taking it, and how long they had been taking it.

And that distinction is important, because estrogen is not one medication.

There is estradiol, which is bioidentical to the estrogen your ovaries naturally produce. There are also other forms of estrogen, including conjugated estrogens and synthetic estrogens such as ethinyl estradiol.

And then there is how you take it.

A pill.

A patch.

A gel or spray.

A va**nal cream, tablet, insert, or ring.

Different estrogen. Different dose. Different route.

And those differences can matter when we talk about risk.

Researchers used Denmark’s national health records to look at women ages 50–69 over an 18-year period. They looked at the specific hormones women were prescribed, the dose, how they took them, how long they used them, and whether they developed a DVT or pulmonary embolism, ischemic stroke, or heart attack.

Women taking oral estrogen had about a 60% higher relative risk of DVT or pulmonary embolism.

But if you take oral estrogen, don’t panic when you see that 60%.

The absolute risk was still small.

Among women not using hormone therapy, there were about 16 blood clots per 10,000 women per year.

With oral estrogen, that increased to about 25 per 10,000 women per year.

So a 60% increase in relative risk sounds pretty dramatic. In absolute numbers, it was approximately 9 additional blood clots for every 10,000 women treated for a year.

Both numbers are true. Both are important when we’re deciding what a risk actually means for an individual woman.

Transdermal estradiol was different.

Women using estradiol through the skin, with a patch, gel, or spray, did not have an overall increased risk of blood clots.

For stroke and heart attack, the increased risk associated with oral estradiol was concentrated in women taking doses greater than 1 mg per day for longer than a year.

There is an important limitation to all of this.

This was an observational study, not a randomized clinical trial.

In an observational study, researchers don’t decide which treatment someone receives. They look at what is already happening in the real world. In this case, they looked at which estrogen women had been prescribed and what happened to them afterward.

In a randomized clinical trial, researchers would randomly assign women to different treatments and then follow them to see what happened. Randomization helps make the groups more similar from the beginning, which gives us more confidence that differences in outcomes are actually related to the treatment.

That matters because women prescribed oral estrogen may have been different in other ways from women prescribed patches or women who weren’t taking estrogen at all.

Researchers can adjust statistically for many of those differences, but they can’t account for everything. This study, for example, did not have information about two pretty important risk factors: smoking and BMI.

So we can say that oral estrogen was associated with more blood clots.

We cannot say from this study that oral estrogen caused those blood clots.

That doesn’t make the findings unimportant. Large observational studies give us valuable information about what happens to people in the real world, particularly when we’re looking at relatively uncommon events.

And if you take oral estrogen, this study is not a reason to panic or suddenly stop taking it.

The absolute risk was small.

Oral estrogen is not automatically a bad choice, and a patch is not automatically the right choice for every woman.

But this study is another reason I think we need to stop asking:

“Is estrogen safe?”

The better questions are:

Which estrogen?

What dose?

Taken how?

For how long?

And in whom?

There’s a big story getting national attention this week that I think all women need to know about.

It’s about UTIs and va**nal estrogen, which sounds very boring, I know. But stay with me, because this is actually extremely important.

When we’re younger, we tend to think of a UTI as a pesky annoyance. You call your doctor, get an antibiotic, and go on with your life.

But as women get older, UTIs can become much more serious. They can lead to hospitalization, sepsis, and even death.

In fact, USA Today looked at CDC data and found that between 1999 and 2023, deaths from sepsis related to UTIs nearly tripled among women ages 45–64.

So I was very glad to see USA Today shining a national spotlight on this issue this week.

The media attention is new.

The medicine behind it is not.

We have known for years that va**nal estrogen can reduce recurrent UTIs in postmenopausal women.

But a large study published in Urology this year gives us some pretty remarkable numbers to look at.

Researchers examined the medical records of nearly 1.9 million women with recurrent UTIs.

Yes. 1.9 MILLION women.

Only about 5% had been prescribed va**nal estrogen within two months of their second UTI.

And look at what they found in women ages 55–69.

Among women prescribed va**nal estrogen, 10.1% were hospitalized, 6.8% developed sepsis, and 1.5% died.

Among women who were NOT prescribed va**nal estrogen, 20.5% were hospitalized, 24.7% developed sepsis, and 7.3% died.

Read those numbers again.

This was an observational study, so it shows an association rather than proving that va**nal estrogen itself caused those differences. But those are differences worth paying attention to.

Especially because va**nal estrogen isn’t some new treatment we just discovered.

We have known for years that falling estrogen levels after menopause affect much more than hot flashes.

Estrogen loss changes the tissues of the va**na and urinary tract. It changes the va**nal microbiome. Those tissues become thinner and more vulnerable, and for some women, recurrent UTIs become a significant problem.

Vaginal estrogen can help restore those tissues and reduce the risk of recurrent UTIs.

And yet I still meet women who have had UTI after UTI after UTI and no one has ever mentioned va**nal estrogen to them.

Another UTI.

Another antibiotic.

Another UTI.

We shouldn’t just accept recurrent UTIs as another inevitable part of getting older.

Especially when we have something that can help prevent them.

Because a UTI in an older woman isn’t always a minor inconvenience. It can mean hospitalization. It can become sepsis. And yes, women can die from it.

So if your mother keeps getting UTIs, ask whether va**nal estrogen might be appropriate for her.

If you are in menopause and suddenly getting recurrent UTIs when you never did before, ask about it.

And if you already use systemic estrogen, such as a patch, don’t assume that necessarily takes care of the va**nal and urinary tissues. Some women still need local va**nal estrogen.

I’m glad USA Today is talking about this.

Not because we suddenly discovered that va**nal estrogen can help prevent recurrent UTIs.

We didn’t.

I’m glad because now a lot more women know to ask about it.

And women can’t make informed decisions about treatments they’ve never been told exist.

Source: LaClair J, et al. Vaginal Estrogen Prescription is Associated with Reduced Risk of Serious Adverse Outcomes in Women of All Age Groups with Recurrent Urinary Tract Infection: An Epic Cosmos Database Analysis. Urology. Published online June 10, 2026.

Hair loss after 40 deserves more than “it’s probably your hormones.”

Hair loss is a symptom, and there are several different processes that can cause it. The first step is figuring out what kind of hair loss is happening.

Are you suddenly shedding hair all over? Is your part gradually getting wider? Are there distinct bald patches? Is the hair breaking? Is your scalp itchy, painful, red, or scaly?

Those differences matter.

One common cause of increased shedding is telogen effluvium. The tricky part is that the trigger often happened 2–4 months before you noticed the shedding. Illness, surgery, major psychological or physiologic stress, rapid weight loss, significant calorie or protein restriction, and medication changes can all be clues.

That’s why I ask patients to mentally rewind the calendar.

Iron deficiency is another important consideration. A CBC alone doesn’t tell us everything about iron stores. You can have a normal hemoglobin and still have low ferritin, which is why ferritin can be useful in the evaluation of diffuse hair loss.

Thyroid disease can also contribute to diffuse thinning or shedding, so TSH, sometimes with free T4, may be appropriate.

Other nutritional testing should be more individualized. B12, folate, vitamin D, zinc, and other tests can make sense when someone’s diet, medical history, rapid weight loss, GI disease, bariatric surgery, or other risk factors make a deficiency more likely.

And hormones can matter, but hair loss after 40 does not automatically mean you need an enormous hormone panel.

If hair loss is accompanied by new or worsening acne, increased facial hair, irregular periods, or rapidly progressive scalp thinning, that history may point toward androgen testing such as testosterone, SHBG, or DHEA-S. The testing should follow the clinical question, not the other way around.

Another very important possibility is female-pattern hair loss. This often develops gradually, with a widening part, thinning over the crown or top of the scalp, and an overall decrease in hair density. Genetics and hormonal changes can contribute.

And here’s the part I really want women to understand:

You can have significant female-pattern hair loss and completely normal bloodwork.

Normal labs don’t mean nothing is wrong. They may simply mean the answer isn’t in the blood.

That’s also why I don’t routinely recommend ordering every test marketed for hair loss. Reverse T3, IgG food-sensitivity panels, hair mineral analysis, microbiome/stool testing, and “adrenal fatigue” cortisol panels generally aren’t part of a routine evidence-based hair-loss evaluation.

More testing doesn’t necessarily produce more answers.

Sometimes the most important “test” is actually looking at the scalp.

Patchy hair loss, significant redness or scaling, pain or burning, scarring or shiny areas of scalp, eyebrow or eyelash loss, or rapidly progressive hair loss deserve a closer examination. In some situations, evaluation by dermatology or even a scalp biopsy may be appropriate.

So if you’re experiencing hair loss, don’t start by asking:

“What giant panel of labs should I order?”

Start with:

What pattern of hair loss do I have?
When did it start?
What happened in the months before it started?
Could nutrition, medications, illness, weight loss, thyroid disease, hormones, genetics, or a scalp condition be contributing?

Then use that information to decide what testing actually makes sense.

Because the goal isn’t to order the most labs.

The goal is to figure out WHY you’re losing hair.

Save this carousel if you’re dealing with hair loss, and bring the checklist with you when you talk with your healthcare provider.

Friends ask me about Wegovy all the time.

“How fast will I lose weight?”

“What should I expect?”

Here is the honest answer: probably not as quickly as social media makes it seem—especially at first.

The first three months are often slow. Wegovy starts at 0.25 mg weekly and increases gradually. Many people lose somewhere in the range of 5–15 pounds during that entire stretch, although individual results vary widely.

That slow schedule is intentional. It gives your body time to adjust and helps limit side effects, which often show up after a dose increase.

Around month four, weight loss may begin to pick up as patients reach the higher doses. By six months, average weight loss in clinical trials was approximately 10–12% of starting body weight.

Then, often sometime after month nine, the pace slows again.

That does not necessarily mean the medication has stopped working. It is often a normal part of metabolic adaptation. At that point, adequate protein, strength training, sleep, and the rest of the treatment plan become increasingly important.

The trial results also deserve some context:

• In STEP 1, participants lost an average of 14.9% of their starting body weight over 68 weeks.
• In STEP 5, average weight loss was 15.2% at two years.
• Longer-term data suggest that weight tends to settle into a plateau rather than continuing to fall indefinitely.

Those are averages from clinical trials—not promises. Some people lose considerably more, some lose less, and some do not tolerate the medication well enough to continue it.

Side effects deserve honest numbers, too.

In the Wegovy trials, nausea occurred in 44% of participants, diarrhea in about 30%, vomiting in 25%, and constipation in 24%. These symptoms were usually most noticeable around dose increases and often improved with time. Approximately 4% of participants in STEP 1 stopped treatment because of gastrointestinal side effects.

Gallstones occurred in 2.6% of participants taking Wegovy compared with 1.2% taking placebo. Pancreatitis and kidney injury related to severe dehydration were uncommon—but uncommon does not mean unimportant. These are prescription medications for a reason, and patients need real medical oversight.

There is one more thing people should understand before starting: stopping the medication commonly leads to significant weight regain.

Wegovy was studied as ongoing treatment for a chronic condition—not as a quick, 12-week diet.

I am sharing this because I would rather people begin treatment with realistic expectations than feel discouraged when their experience does not match what they have seen online.

A GLP-1 can be an excellent tool. But the prescription is only one part of the plan—and anyone considering one deserves a thoughtful conversation with a qualified medical professional who knows their history.