If you have migraines, put down your coffee and read this

During medical school, a neurologist taught me that the number one cause of headaches in the US was coffee.

That was news to me! But it made more sense when he clarified that he meant lack of coffee. His point was that for people who regularly drink coffee, missing an early morning cup, or even just having your first cup later than usual, can trigger a caffeine withdrawal headache. And considering how many daily coffee drinkers there are (an estimated 158 million in the US alone), it’s likely that coffee withdrawal is among the most common causes of headaches.

Later in my neurology rotation, I learned that caffeine is a major ingredient in many headache remedies, from over-the-counter medicines such as Excedrin and Anacin, to powerful prescription treatments such as Fioricet. The caffeine is supposed to make the other drugs in these combination remedies (such as acetaminophen or ibuprofen) work better; and, of course, it might be quite effective for caffeine-withdrawal headaches.

But then I learned that for people with migraine headaches, certain drugs, foods, and drinks should be avoided, as they can trigger migraines. At the top of this list? Coffee.

So, to review: the caffeine in coffee, tea, and other foods or drinks can help prevent a headache, treat a headache, and also trigger a headache. How can this be?

Migraine headaches: Still mysterious after all these years

Migraine headaches are quite common: more than a billion people reportedly suffer from migraines worldwide. Yet, the cause has long been a mystery — and it still is.

Until recently, the going theory was that blood vessels around the brain go into spasm, temporarily constricting and limiting blood flow. Then, when the blood vessels open up, the rush of incoming blood flow leads to the actual headache.

That theory has fallen out of favor. Now, the thinking is that migraines are due to waves of electrical activity spreading across the outer portions of the brain, leading to inflammation and overreactive nerve cells that send inappropriate pain signals. Why this begins in the first place is unknown.

Migraines tend to run in families, so genetic factors are likely important. In addition, chemical messengers within the brain, such as serotonin, may also play a central role in the development of migraines, though the mechanisms remain uncertain.

People prone to migraines may experience more headaches after coffee consumption (perhaps by effects on serotonin or brain electrical activity), but coffee itself, or the caffeine it contains, is not considered the actual cause of migraines. Certain foods or drinks like coffee are thought to trigger episodes of migraine, but the true cause is not known.

A new study about coffee and migraines: how much is too much?

In a new study published in the American Journal of Medicine, researchers (including several from the hospital where I work) asked 98 people with migraines to keep a diet diary that included how often they consumed caffeinated beverages (including coffee, tea, carbonated beverages, and energy drinks). This information was compared with how often they had migraines. Here’s what they found:

• The odds of having a migraine increased for those drinking three or more caffeinated beverages per day, but not for those consuming one to two servings per day; the effect lasted through the day after caffeine consumption.
• It seemed to take less caffeine to trigger a headache in those who didn’t usually have much of it. Just one or two servings increased the risk of migraine in those who usually had less than one serving per day.
• The link between caffeine consumption and migraine held up even after accounting for other relevant factors such as alcohol consumption, sleep, and physical activity.

Interestingly, the link was observed regardless of whether the study subject believed that caffeine triggered their headaches.

One weakness of this study is that the researchers did not actually measure caffeine consumption. Instead, they defined one serving of a caffeinated beverage as 8 ounces of regular coffee, 6 ounces of tea, a 12-ounce can of caffeinated soda, or 2 ounces of an energy drink. But caffeine content in different caffeinated beverages can vary widely. For example, an 8-ounce serving of coffee from Starbucks can have twice the caffeine as a similar-sized serving from a Keurig K-Cup. They also did not include caffeine-containing foods in the study, although such amounts tend to be quite small compared with the beverages studied.

The bottom line

There is a lot about the connection between caffeine consumption and migraine headaches that remains uncertain. Until we know more, it seems wise to listen to your body: if you notice more headaches when you drink more coffee (or other caffeinated beverages), cut back. Fortunately, this latest research did not conclude that people with migraines should swear off coffee entirely.

If you like coffee as much as I do, it may seem unfair that you need to keep drinking it to prevent a headache. And if you’re prone to migraines, it might seem unfair that you have to limit your coffee intake to avoid headaches. Either way, you’d be right.

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Popular heartburn drug ranitidine recalled: What you need to know and do

If you or a family member take ranitidine (Zantac) to relieve heartburn, you may have heard that the FDA has found a probable human carcinogen (a substance that could cause cancer) in it. The story is unfolding quickly and many details remain murky. Here is what we know so far and what you should do.

What do we know so far?

On September 13, 2019, the FDA announced that preliminary tests found low levels of N-nitrosodimethylamine (NDMA) in ranitidine, a heartburn medication used by millions of Americans. This week, the drug companies Novartis (through its generic division, Sandoz) and Apotex announced that they were recalling all of their generic ranitidine products sold in the US.

These announcements came after a Connecticut-based online pharmacy informed the FDA that it had detected NDMA in multiple ranitidine products under certain test conditions.

What is ranitidine and which products are affected?

Ranitidine (also known by its brand name, Zantac, which is sold by the drug company Sanofi) is available both over the counter (OTC) and by prescription. It belongs to the class of drugs known as H2 (or histamine-2) blockers. OTC ranitidine is commonly used to relieve and prevent heartburn. Prescription strengths are also used to treat and prevent more serious ulcers in the stomach and intestines. Multiple companies sell generic versions of both the OTC and prescription products.

So far, only Novartis/Sandoz and Apotex have recalled products. Ranitidine distributed by other companies remains on store shelves.

Health Canada, a federal department within the Canadian government, has asked all companies to stop distributing ranitidine drugs there, indicating that “current evidence suggests that NDMA may be present in ranitidine, regardless of the manufacturer.” France has taken the step of recalling all ranitidine products.

What is NDMA and what harm can it cause?

NDMA is an environmental contaminant that is found in water and foods, including dairy products, vegetables, and grilled meats. Its classification as a probable carcinogen is based on studies in animals; studies in humans are very limited.

It is important to know that the NDMA in ranitidine products does not pose any immediate health risks. Neither the FDA nor Novartis/Sandoz or Apotex have received any reports of adverse events related to NDMA found in ranitidine. Although classified as a probable carcinogen, NDMA may cause cancer only after exposure to high doses over a long period of time. NDMA is one of the same impurities that was found in certain heart medications beginning last year and that resulted in the recall of many products.

What should you do if you take ranitidine?

As the FDA and other agencies around the world continue to investigate ranitidine, more details will become available. In the meantime, the FDA is not calling for individuals to stop taking the medication.

However, for many conditions, ranitidine is only recommended for short-term use. If you have been using ranitidine for a while, now would be a good time to discuss with your physician whether you still need it, and whether you might benefit from alternative treatment options, including other drug classes or a different H2 blocker. Based on what is known so far, there is no evidence that other H2 blockers or other heartburn medications are affected by NDMA impurities.

Some people might find antacids useful for relieving heartburn. Lifestyle changes, including avoiding certain foods and beverages, such as spicy foods, large or fatty meals, and alcohol, can also help prevent episodes of heartburn.

Follow me on Twitter @JoshuaJGagne

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Is there a test for Alzheimer’s disease?

After spending 30 minutes hunting for your car in a parking lot, or getting lost on a familiar route, have you ever considered asking your doctor for a blood test or brain scan to find out if you have Alzheimer’s disease?

A number of factors contribute to Alzheimer’s disease. By definition, this form of dementia involves the buildup of a protein in brain called beta-amyloid. Beta-amyloid forms plaques that disrupt communication between brain cells, and ultimately destroys them. For this reason, tests for Alzheimer’s disease focus on beta-amyloid.

Blood tests for Alzheimer’s disease are being developed

Recently, researchers at Washington University in St. Louis measured the levels of beta-amyloid in the blood of 158 mostly normal people (10 had cognitive impairment).

When they compared their findings with those of amyloid brain PET (positron emission tomography) scans performed within 18 months of the blood draw, they found very similar results. Moreover, the few people in their study who had a positive blood test and negative brain scan were actually 21 times more likely to have a positive brain scan in the future. This means that the new blood test may be extremely sensitive at detecting Alzheimer’s disease — that is, it results in few false negatives.

If you’re worried about your memory, should you ask your doctor for this test? Not yet — the blood test is still being evaluated and is not currently available for clinical use.

What about amyloid brain PET scans?

Maybe you’re thinking about having an FDA-approved amyloid brain PET scan. These tests involve the injection of a radioactive dye attached to a molecule that sticks to amyloid plaques in the brain. The radioactivity is then measured by special imaging technology, similar to a CT scan.

Should you get one? You could, but there are two issues to consider. First, they are not paid for by insurance — and they cost about $5,000 — so you either have to pay out of pocket or join a research study at a National Institute on Aging Alzheimer’s Disease Research Center, where you might get one for free. Second, how would the information help you?

No special amyloid brain scans are needed for the straightforward diagnosis and treatment of memory loss. If you are having significant symptoms of memory loss, such as those mentioned above, talk with your doctor about them. Your doctor will likely evaluate your overall health and the medications you take, then do some standard blood tests and brain scans as well as pencil and paper testing. Based on the results of those tests, your doctor may start you on a medication intended to boost your memory function.

Perhaps you don’t have any symptoms of Alzheimer’s disease today, but one of your parents had it. Should you get an amyloid brain scan to find out if you are likely to develop Alzheimer’s in the future?

Unfortunately, there are no medications that can prevent or slow down the development of Alzheimer’s disease. So if you get the scan and it is positive, again, what will you do with the information?

Spinal fluid tests are available now — and paid for by insurance

Perhaps I’ve convinced you that you don’t need to rush out and have an expensive amyloid brain scan. But there are situations when it is important to find out if you or a loved one has Alzheimer’s, versus another brain disease that would be treated differently. In these situations, we often use a spinal fluid test that is quite good at being able to distinguish Alzheimer’s from other brain diseases affecting thinking and memory.

To obtain the spinal fluid, you need to undergo a lumbar puncture, more commonly known as a spinal tap. Although it may sound frightening, it is actually a perfectly safe test. You simply sit or lie down on your side with your back to the doctor and curl into a little ball by bringing your shoulders down and your knees up. The doctor finds the right spot, cleans the area well, gives you some numbing medicine, inserts a thin needle, and takes out a small amount of spinal fluid, which is sent to a lab for analysis.

Exercise daily, eat right, stay social, keep active

Lastly, don’t forget that you can work to prevent Alzheimer’s disease every day by performing aerobic exercise, eating a Mediterranean-style diet, staying socially engaged, and keeping your mind active. These activities are the only things that have been proven to reduce your chances of developing Alzheimer’s disease — regardless of the results of any special tests.

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Vitiligo: More than skin deep

Vitiligo (pronounced vit-uh-LIE-go) is a medical condition in which patches of skin lose their color. This occurs when melanocytes, the cells responsible for making skin pigment, are destroyed. Vitiligo can affect any part of the body, and it can occur in people of any age, ethnicity, or sex.

Affecting approximately 1% of the population, vitiligo can be an emotionally and socially devastating disease. Particularly frustrating to many is its unpredictable progression, which can be slow or rapid.

Thus far, there is no cure for vitiligo. But new hope is on the horizon, thanks to recent research that is improving our understanding of the pathways involved in this condition and potential new ways to treat it.

Body attacks cells responsible for producing skin’s pigment

Vitiligo is generally thought to be an autoimmune disease, in which a person’s immune system mistakenly attacks its own body (in this case, it attacks melanocytes). In addition, the melanocytes of people with vitiligo appear unable to deal with the imbalance of antioxidants and harmful free radicals in the body, which results in cell damage and death.

While most people with vitiligo are otherwise healthy, there is an association between vitiligo and thyroid disease (either over- or underactivity of the thyroid). Less frequently, it occurs together with other autoimmune conditions, such as lupus or type 1 diabetes.

Phototherapy and topical treatments can help

There are a number of treatments aimed at restoring color to depigmented skin. One of the oldest and most effective treatments is phototherapy (light therapy) with ultraviolet B (UVB) light. For this treatment, depigmented skin is exposed to UVB light several times a week, either in a clinic or at home.

Light therapy is often used in combination with topical medications that are applied to the skin. Topical treatments include topical steroids, topical calcineurin inhibitors (such as tacrolimus or pimecrolimus), or topical vitamin D analogues (such as calcipotriol and tacalcitol). Psoralen, a type of medication previously used in conjunction with phototherapy, has largely fallen out of favor. Topical medications may also be used on their own, without light therapy, although when the two treatments are used together, patients typically see better results.

If the depigmented areas are extensive, there is also the option of using topical medications to bleach unaffected skin, bringing it closer in color to the depigmented areas.

If medical treatments are ineffective, surgical treatment may be an option for certain people. Skin grafts can be taken from normally pigmented skin, usually from the buttocks or hips, and transferred to depigmented areas in more visible parts of the body.

New treatments for vitiligo may be on the horizon

Recently, several exciting studies have looked at a class of medications called JAK inhibitors as a possible new treatment option. JAK inhibitors target a type of immune communication pathway that has not been targeted before in vitiligo. These medications are thought to work by reducing levels of inflammatory chemicals that drive disease progression, and by stimulating melanocytes to regrow.

One study, published in JAMA, looked at the JAK inhibitor tofacitinib; another study, published in the Journal of the American Academy of Dermatology, looked at the JAK inhibitor ruxolitinib. Both reported promising results for repigmentation in people with vitiligo when the JAK inhibitor was used together with UVB phototherapy.

Though these initial studies analyzed small groups of patients, several larger-scale studies are underway to assess how both oral and topical JAK inhibitors may improve vitiligo. Preliminary data from these larger trials are showing promising results for repigmentation, especially on the face. The hope is that these results will eventually lead to FDA approval of JAK inhibitors for the treatment of vitiligo. For now, because they are still considered off-label by the FDA for use in vitiligo, these drugs are rarely covered by insurance for the treatment of vitiligo, and therefore can be quite expensive.

Psychosocial support is a key part of vitiligo treatment

A diagnosis of vitiligo can be life-altering. Patients may struggle with self-esteem or depression, and they often have to deal with social stigma, due to misunderstanding about the contagiousness of the condition. As a result, people with vitiligo typically benefit from psychosocial support in addition to medical treatment.

If you have vitiligo (or know someone who does) and would like to learn more about support groups and other available resources, please visit the Global Vitiligo Foundation or Vitiligo Support International.

Follow me on Twitter @KristinaLiuMD

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What donor offspring seek when they do DNA testing

I wrote previously about parents who fear that their donor-conceived children might uncover long-held secrets through DNA testing. Many were unsettled by Dani Shapiro’s memoir Inheritance, which told of how a DNA test done for no particular reason dismantled a family story. Now let’s consider reasons why some people who know they were donor-conceived might pursue DNA testing.

Why might people who were donor-conceived seek DNA testing?

Donor-conceived adults who embark upon DNA testing may, like Shapiro, stumble upon information accidentally. Their experience with DNA testing is not explored in this post, which focuses on those whose choice to do testing followed one of these three paths:

• They were told their conception story at a young age, but had limited information about their donor and his or her family.
• They were only recently told of their donor conception, but grew up knowing something was different or left unspoken (the “unknown known”).
• As adults, they were completely startled to learn that they were donor-conceived.

What might people hope to learn through DNA testing?

So what might these people seek — and hope to find — in DNA testing? Everyone is different and DNA testers have a wide range of reasons for swabbing their cheeks. Yet most have the desire to better understand their personal story. We all have origin stories that circle around our ancestry, ethnicity, and the circumstances of our conception and birth. Whether they grow up always knowing, or learn of donor conception as young adults, personal stories for the donor-conceived are complicated. Questions people hope to have answered include:

• Why did he or she become a donor? Am I simply the product of a transaction, or were there other reasons that motivated someone to donate?
• Who else am I related to? This question is especially compelling for sperm donor offspring, who may have large numbers of genetic half-siblings. This is less often true for those conceived from donated eggs, yet there are the donor’s children, her nieces and nephews, all those she donated to, and in some instances, children born through embryos donated to other families after the original recipient family was complete.
• What is my ethnicity? What does it mean if the ethnicity in my DNA does not match the ethnic identity I was raised with? One woman I spoke with had grown up believing she was Irish on her mother’s side and Jewish (Ashkenazi) on her dad’s side. When the DNA test results came back indicating she is 100% Irish, she felt a sense of loss. She always felt proud to be half Jewish. Did this mean that she is not?
• What abilities and vulnerabilities might I have inherited from the donor? For many, the high beam of this question directs itself to medical issues. This can go both ways: learning one’s actual medical history may relieve worries regarding illnesses in the family, or it may bring new medical concerns. Either way, those who are just learning they were donor-conceived as adults have relied on a family medical history that they now know to be only half complete.
• Most people feel they came from two people. I came from three. What does this mean for my identity? People conceived with donated eggs are often, though not always, told of the donation from a young age. They grow up always knowing that they are gestationally, but not genetically, connected to their mothers. Part of their task as they mature is sorting out as best they can what it means to literally come from three people. (Sperm donor offspring, by contrast, must reconcile with the fact that they have no physical connection to their fathers.)

What does the future hold?

The world of commercially available DNA testing is still in its infancy. These days it is being heavily marketed in the media as a nifty gift, an interesting tool, a key that will unlock doors. Undoubtedly its uses, and its meaning for all of us, will unfold and evolve over time. The questions it raises and the “answers” it provides are surely more complex and multidimensional for the donor-conceived.

For more information

If you’d like further information and support, you may find these organizations helpful.

Donor Conception Network

Donor Sibling Registry

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Jessica Simpson Shows Off 100 Pound Weight Loss Since Birth Of Daughter

"So proud to feel like myself again," wrote the actress and singer, who welcomed her third child on March 19.

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Weekend catch-up sleep won’t fix the effects of sleep deprivation on your waistline

Sleeping in late on a Saturday sounds delicious, right? However, as with many delicious things, there may be a cost to your health and waistline.

Catching up on sleep on the weekend can almost feel like the norm these days. With increasingly full schedules and competing demands, sleep is often sacrificed during the busy workweek. As the week comes to an end, many people look to the less structured weekend to cram in what couldn’t be done during the week, including sleep. In sleep clinic, I now ask “When do you get up on work (or school) days?” and “What about bedtime and wakeup time on days off?” The catch-up time — perhaps a 6 am wake-up for a work day, but 11 am on a weekend — can be close to an entire weeknight’s sleep. But does it matter? We’re paying back our sleep debt, right?

Our average hours of sleep may hide a weekly sleep debt

Despite the fact that number of hours of sleep, when averaged, may approach the seven to nine hours per night recommended by most professional societies, the “average” can hide some truths. The daily amount, quality, and regularity of bed/wake time all seem to matter too. A recent paper in Current Biology shows that our sleep is not very forgiving of being moved around to more convenient times. Researchers found that subjects who cut their sleep down by five hours during the week, but made up for it on the weekend with extra sleep, still paid a cost. That cost included measurable differences: excess calorie intake after dinner, reduced energy expenditure, increased weight, and detrimental changes in how the body uses insulin. Although sleep debt was resolved on paper, the weekend catch-up subjects had similar results (though there were some differences) to those who remained sleep-deprived across a weekend without catch-up sleep.

New research is a reminder that you can’t cheat on sleep and get away with it

First, sleep deprivation, even if only during the workweek, likely has real health consequences. Sleep is often an overlooked factor when considering chronic disease risk, including hypertension, diabetes, heart disease, and even death. There’s ample data, including a recent review in Sleep Medicine, suggesting that too little sleep is a risk factor for these conditions, as well as obesity. Unfortunately, this new study suggests that extending sleep on the weekend doesn’t seem to undo the impact of short sleep.

Second, whether the health impact is due to the decreased sleep alone, or additionally due to changes in timing of sleep on the weekend — an at-home “jet lag” — is unknown. The impact of essentially jumping time zones by staying up later and sleeping later on weekends, may add to the problem. Other behaviors, such as eating or drinking later on weekends, also confuse the body’s rhythm.

What can you do to improve nightly sleep?

As with a lot of medicine, prevention seems to be the best strategy. Although we can’t undo the impact of short sleep by trying to oversleep on the weekends, we can try to carve out a bit more time for sleep at night during the week and improve behaviors that lead to better sleep.

It’s very important to keep bedtime and waketime fairly stable across the weekend, which may also help reduce the jet-lag effect. Short naps of 15 to 20 minutes may help relieve sleepiness, but shouldn’t interfere with the regularity of bedtime and waketime. For some people, keeping a sleep log to track sleep patterns can be eye-opening and provide accountability, in the same way that tracking food choices and behaviors around eating can help with weight loss. Finally, consider reframing your relationship with sleep and prioritize it. Sleep is preventive medicine — we know it helps reduce illness and optimizes your daily well-being.

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Intensive blood sugar control doesn’t have lasting cardiovascular benefits for those with diabetes

In 2009, the New England Journal of Medicine published results from the Veterans Affairs Diabetes Trial (VADT). The study found that intensive glucose (blood sugar) control in older men with longstanding type 2 diabetes did not significantly reduce their risk of major cardiovascular (CV) events, including heart attack, stroke, and death from CV causes, compared with standard blood sugar control.

Researchers recently reported 15-year follow up results from VADT. They found that intensive blood sugar control did not exert any “legacy effect”: the intensive blood sugar control group did not enjoy CV benefits 15 years after the start of the study.

The Veterans Affairs Diabetes Trial

The VADT study originally enrolled over 1,700 veterans with longstanding type 2 diabetes, who were at high risk of cardiovascular disease, and had poorly controlled blood sugar when they enrolled in the study. At the time of enrollment, study participants had been diagnosed with diabetes for an average of 12 years. Their average A1c level, a measure of average blood sugar levels over the previous two to three months, was 9.4%.

The participants were randomly assigned to either intensive glucose-lowering therapy or usual care for about 5.6 years. At the completion of the study, there was a significant difference in blood sugar control: the average A1c in the intensive treatment group was 6.9%, while the average A1c in the usual care group was 8.4%.

Despite the lower A1c levels, there were no benefits shown from intensive treatment on CV outcomes, which included nonfatal heart attack, nonfatal stroke, new or worsening congestive heart failure, amputation for diabetes-related tissue damage, or death from CV causes.

No long-term cardiovascular benefit of intensive blood sugar control

A follow-up observational study was then undertaken to assess whether intensive treatment during the 5.6-year study period had any long-lasting effects, after the interventions were completed. The 10-year VADT follow up showed some benefits to intensive treatment with regard to CV events. At that time, participants in the intensive treatment group still had lower A1c levels compared to the usual care group, despite the gap of several years since the completion of the study.

However, at the newly published 15-year follow-up, the benefits of intensive control on any of the CV outcomes were lost. By this time, both groups had similar A1c levels of about 8%.

This phenomenon may suggest that to achieve the CV benefits, blood sugar control needs to be maintained and that the short-term tight control, without lasting blood sugar control, may not have long-lasting effects.

New evidence supports existing evidence

The new VADT results add to existing evidence from previous large studies that have failed to show any long-lasting benefits of intensive blood sugar control during observational follow-up. One study, however, did show some beneficial legacy effect. The United Kingdom Prospective Diabetes Study (UKPDS) evaluated intensive treatment versus usual care in adults with newly diagnosed type 2 diabetes. When the UKPDS cohort was evaluated 10 years after the completion of the study, the participants from the intensive treatment arm showed benefits with regard to cardiovascular disease, compared to standard care.

Taken together, the evidence suggests that older adults with longer duration of diabetes and/or multiple coexisting conditions may not benefit from intensive blood sugar control. On the other hand, intensive treatment might be beneficial in younger patients, with shorter duration of diabetes and fewer coexisting medical conditions.

Individualize treatment and control other cardiovascular risk factors

Personalization of goals and treatment regimens that can be maintained safely over the long term by the patient might be the best strategy to lower the risk of cardiovascular disease. As I discussed in a previous blog post, treatment of older adults should consider possible dangers of intensive treatment. For example, intensive blood sugar control can overshoot and lead to hypoglycemia, a potentially dangerous condition in which blood sugar falls too low. Hypoglycemic episodes in older adults are particularly harmful and may negate the possible benefits or tighter diabetes control. In older adults, rather than aiming for tight control, we aim for the best control that can be achieved without increasing the risk of hypoglycemia.

For reducing CV risk, the authors of an editorial that accompanied the NEJM study recommend prioritizing interventions that address other CV risk factors. That includes quitting smoking, and managing blood pressure and cholesterol levels with medication, if needed. Newer classes of diabetes medications, such as sodium glucose cotransporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists appear to have CV benefits and low risk of hypoglycemia, and may be considered as well.

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Adult acne: Understanding underlying causes and banishing breakouts

“I’m not a teenager anymore, why do I still have acne?!” This is a question we hear from patients on a daily basis. The truth is, it is quite common to see acne persist into adulthood. Although acne is commonly thought of as a problem of adolescence, it can occur in people of all ages.

Adult acne has many similarities to adolescent acne with regard to both causes and treatments. But there are some unique qualities to adult acne as well.

What causes adult acne?

Adult acne, or post-adolescent acne, is acne that occurs after age 25. For the most part, the same factors that cause acne in adolescents are at play in adult acne. The four factors that directly contribute to acne are: excess oil production, pores becoming clogged by “sticky” skin cells, bacteria, and inflammation.

There are also some indirect factors that influence the aforementioned direct factors, including

• hormones, stress, and the menstrual cycle in women, all of which can influence oil production
• hair products, skin care products, and makeup, which can clog pores
• diet, which can influence inflammation throughout the body.

Some medications, including corticosteroids, anabolic steroids, and lithium, can also cause acne.

Many skin disorders, including acne, can be a window into a systemic condition. For example, hair loss, excess hair growth, irregular menstrual cycles, or rapid weight gain or loss in addition to acne, or rapid onset of acne with no prior history of acne, can all be red flags of an underlying disease, such as polycystic ovarian syndrome, or other endocrine disorders. Tell your doctor if you are experiencing additional symptoms; he or she may recommend further evaluation.

How can I prevent breakouts?

Like most things in life, acne is not always completely in one’s control. There are, however, some key tips we offer to help prevent breakouts:

• Never go to bed with makeup on.
• Check labels: when purchasing cosmetic and skincare products, always look for the terms “non-comedogenic,” “oil-free,” or “won’t clog pores.”
• Avoid facial oils and hair products that contain oil.
• Some acne spots are not actually acne but are post-inflammatory pigment changes from previous acne lesions or from picking at acne or pimples. Wear sunscreen with SPF 30+ daily, rain or shine, to prevent darkening of these spots.

There is some evidence that specific dietary changes may help reduce the risk of acne. For example, one meta-analysis of 14 observational studies that included nearly 80,000 children, adolescents, and young adults showed a link between dairy products and increased risk of acne. And some studies have linked high-glycemic-index foods (those that cause blood sugar levels to rise more quickly) and acne.

With that said, it’s important to be wary of misinformation about nutrition and skin. As physicians, we seek scientifically sound and data-driven information; the evidence on the relationship between diet and acne is just starting to bloom. In the future, the effect of diet on acne may be better understood.

What are the most effective treatment options?

The arsenal of treatment options for acne treatment is robust and depends on the type and severity of acne. Topical tretinoin, which works by turning over skin cells faster to prevent clogged pores, is a mainstay in any acne treatment regimen, and has the added bonus of treating fine wrinkles and evening and brightening skin tone. Isotretinoin (Accutane, other brands), taken by mouth, is the closest thing to a “cure” for acne that exists and is used to treat severe acne. Women who can become pregnant need to take special precautions when taking isotretinoin, as it can cause significant harm to the fetus.

For women with hormonally driven acne that flares with the menstrual cycle, a medication called spironolactone, which keeps testosterone in check, can be prescribed. Oral birth control pills can also help regulate hormones that contribute to acne.

In-office light-based treatments, such as photodynamic therapy, can sometimes help. Chemical peels, also done in-office, may help to treat acne and fade post-inflammatory pigment changes.

Simple, non-irritating skin care products are important for anyone with acne. Choose products that are gentle and safe for skin with acne, and eliminate products that are harsh and can make matters worse. It’s also important not to squeeze or pick at acne lesions, as that can worsen discoloration and scarring.

With proper evaluation by a board-certified dermatologist and commitment to a treatment regimen, almost all cases of acne can be successfully treated. After all, adulthood is stressful enough without breakouts!

Follow me on Twitter @KristinaLiuMD and @JanelleNassim

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Common hormonal treatments linked to abnormal heart rhythms and sudden death in men being treated for prostate cancer

Treatments for advanced prostate cancer that suppress testosterone, a hormone (also called an androgen) that drives the malignant cells to grow and spread, are collectively referred to as androgen deprivation therapies, or ADT. These therapies can significantly extend lifespans in men who have the disease, but they also have a range of challenging side effects.

In 2004, Dr. Marc Garnick, Gorman Brothers Professor of Medicine at Harvard Medical School and Beth Israel Deaconess Medical Center, and editor in chief of HarvardProstateKnowledge.org, reported that in some men, an ADT drug called aberelix lengthens the time it takes for cardiac cells to recharge electrically between beats. Known as the QT interval, this measure is determined with the use of an electrocardiogram. Prolonged QT intervals are worrying because in rare instances they induce potentially fatal heart rhythms. In fact, the FDA has withdrawn several approved medications from the market after they were associated with drug-induced lengthening of the QT interval, leading to documented cases of either fatal or nonfatal cardiac arrhythmias. The decision to withdraw a drug in these cases is based on the strength of the evidence linking to these sorts of cardiac outcomes.

Now a French research team is reporting that many widely used forms of ADT are linked to these sorts of cardiac side effects and their potential consequences. The study was led by Dr. Joe-Elie Salem, a cardio-oncologist at Sorbonne University in Paris.

One of testosterone’s normal effects in the body is to shorten QT intervals. Salem was aware from prior research that the intervals are longer — and the risk of potentially fatal heart attacks greater — in women than in men, possibly because women have lower testosterone levels than men do.

Would ADT — because it suppresses testosterone — elevate risks for men in a similar way that naturally low levels of the hormone do in women? That’s what Dr. Salem and his team wanted to know.

To find out, they combed through a global database of more than 17 million adverse drug reactions reported by doctors, patients, and pharmaceutical companies between 1967 and 2018.

Their investigation showed that seven out of the 10 hormone therapies evaluated were disproportionately associated with prolonged QT intervals, abnormal heart rhythms, or sudden death. The link with sudden death was strongest with enzalutamide, a second-generation ADT drug used after weaker front-line testosterone-suppressing drugs fail.

The frequency of prolonged QT, abnormal heart rhythms, or sudden death among men taking hormonal therapy in the general population is unknown. But in an email, Dr. Salem wrote that the combined incidence is “probably low — less than 1%.”

Importantly, the tendency towards prolonged QT intervals has a range of causes, and some men are born with it — this is called congenital long QT. Dr. Salem and his colleagues are now planning a study that they hope will allow clinicians to predict in advance which men face the greatest risks of these heart problems when taking hormone-suppressing therapy.

In the meantime, Dr. Salem recommends that men have a baseline electrocardiogram before starting testosterone-suppressing treatments. If abnormalities are noted before or after the treatments begin, he says, patients should be monitored further, and taken off any other drugs they might be taking that also have QT prolonging effects. The list of these drugs is quite extensive, and includes various antihistamines, antidepressants, antipsychotics, and antibiotics, among others.

“This new research reflects ongoing efforts to assess cardiac risk factors among men taking ADT, and underscores the need to better understand how prolonged QT intervals cause irregular heart rhythms,” Dr. Garnick said. “This is important because men are not routinely screened with a baseline electrocardiogram before beginning ADT. Future research is needed to determine if a longer baseline QT interval when starting on ADT should be monitored during the course of treatment.”

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Harvard Health Ad Watch: What you should know about direct-to-consumer ads

If you’re like most people, you’ve seen a ton of direct-to-consumer (DTC) drug ads in recent years. They’re all over television, in magazines, online, on billboards, and slapped on the sides of buses, promoting treatments for arthritis, cancer, heartburn, psoriasis, flagging memory — and more. The deluge of drug ads can be overwhelming. Worse, the information is often incomplete, biased, or confusing. That’s why we’re launching the Harvard Health Ad Watch series to highlight some benefits and problems with health product advertisements. We’ll focus on the evidence behind the ads and show you how — and why — to view them with a skeptical eye.

This post briefly explains direct-to-consumer advertising and FDA regulation, as well as rationales and potential drawbacks for these ads. It also alerts you to words to consider very carefully when advertisers clamor for your attention. In later blogs, we’ll analyze some of the most popular health product ads.

How common are DTC ads for health products?

Almost every country in the world bans DTC ads for health products like medications and procedures. Years ago in the US, drug ads were directed primarily at doctors. But in 1997 the FDA eased restrictions to allow pharmaceutical companies to advertise directly to consumers. With restraints lifted, spending on prescription drug ads soared to more than $6 billion a year (and rising).

Do the ads work? Yes, indeed! Estimates suggest drug sales rise by $4 for every dollar spenton advertising. At health care visits, up to a third of patients ask about a drug adthey’ve seen. The ads have been shown to increase the number of prescriptions written for those products. Does this actually improve patient health? That’s far less clear.

The limited role of the FDA in DTC advertising

FDA regulations require that advertising be accurate and promote only approved drugs for approved conditions (called indications). Additionally, ads must state medication risks and ways to get more information. The FDA’s goal is to assure prescription drug information is “truthful, balanced, and accurately communicated” — a lofty aim that receives mixed reviews.

The rationale for DTC ads

Advocates often present the ads as a chance to

• educate people about conditions and treatments they were unaware of
• improve health by encouraging people to take medications they should be taking
• raise awareness of possible side effects, because regulations require consumers to be referred to a website, magazine, or other site for more information
• lessen stigma surrounding certain conditions, such as erectile dysfunction or constipation
• increase detection of unrelated diseases if patients are inspired by DTC ads to see their doctors.

Potential drawbacks to DTC ads

Unfortunately, experience shows that some DTC ads may

• present incomplete or biased information
• spur people to ask for medications they don’t need
• promote medications before long-term safety is known. In one case, a new pain relief drug was pulled from the market due to an unexpected rise in heart attacks and strokes — but not before millions of people saw the ad and began taking it.
• create conflicts between patients asking for a drug and doctors who don’t recommend it
• drive up healthcare costs without adding health benefits (new drugs are much more expensive than generic drugs that may do the same job, yet cost is rarely mentioned in the ads).

Advertising words to consider very carefully

Keep this in mind: the main purpose of DTC drug advertising is to sell a product, not educate consumers. The language of drug ads makes that clear. Consider these common examples.

• “A leading treatment for this condition” Perhaps, but what if there are only two or three drugs available for that condition? When considering any treatment, it’s important to know what the other options are and how they compare — yet it’s unlikely this additional information will be mentioned.
• “No other treatment has been proven better.” This suggests that the advertised drug is great. Yet it might be only as good as — and no better than — older, less expensive, or even over-the-counter competitors. Plus, drug ads are unlikely to mention the option of taking nothing for the condition in question, even though many minor ailments get better on their own.
• “In clinical studies, this medication proved more effective than standard treatment.” So, how good is standard treatment? If a drug helps only 20% of people with a disease and “standard treatment” helps 15%, the added cost and risk of side effects of the new therapy may not prove worthwhile.
• “I don’t care about studies… it works for me” or “This drug gave me my life back.”The power of the anecdote — one person’s story of near-miraculous improvement with a particular treatment — is undeniable. The problem is that studies do Otherwise, we’d all be taking the advice of a proverbial “snake oil salesman” recommending unproven and potentially dangerous drugs because someone said it worked for them. And, of course, in ads promoting drugs or procedures, that “someone” is a paid actor or spokesperson.
• “For some, one pill is all you need for 24-hour relief.” This sounds good, but how many is “some”? If one in 100 get 24-hour relief, the drug may be less effective than the ad suggests. Also, what does “relief” mean? If a drug reduces pain by 10% for 24 hours, that’s a rather modest benefit; a competitor’s drug might reduce it by 80% or even 100%. These details are often left out of drug ads.

The bottom line

As an arthritis specialist, I’ve found patients who ask me about drug ads are often surprised to learn that important information is missing. For example, most of the newest and most effective drugs for rheumatoid arthritis are given by injection under the skin or into a vein, yet many ads for these drugs never mention this!

Also, I think DTC drug advertising has had unexpected costs: these ads tend to “medicalize” everyday aches, pains, and other symptoms while calling for prompt treatment with their medication. For some people, this constant barrage may be terrifying or anxiety-inducing, as if just around the corner there lurks a new deadly or debilitating condition you should hurry to investigate with your doctor.

So, be wary. Even if information in a drug ad can be considered accurate, it may not be thorough, balanced, or unbiased. In the end, it’s another instance of buyer beware. Stay tuned.

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New medication advances treatment for chronic rhinosinusitis with nasal polyps

Chronic rhinosinusitis is a long-lasting medical condition, usually caused by infection or exposure to irritants, such as allergies, that affects one in seven American adults. Symptoms include nasal obstruction, nasal congestion, nasal drainage, loss of smell and taste, and facial pain and pressure. Some people with chronic rhinosinusitis also develop additional symptoms, such as asthma and nasal polyps, that are exacerbated by underlying allergies. A nasal polyp is a noncancerous tumor that grows from the lining of the nose or sinuses and affects the drainage system of the sinuses.

While chronic rhinosinusitis is not a life-threatening condition, the chronic nature and progression of the disease can have a significant impact on quality of life, affecting work, productivity, and sleep, and leading to social and emotional consequences, such as depression and anxiety.

Recently, a new medication has been approved in the treatment of chronic rhinosinusitis with nasal polyps.

What is the new medication and how would it be used?

Current treatment includes a combination of therapies that target symptoms. These include medical and surgical treatments, such as antibiotics, short-term oral corticosteroids, steroid nasal sprays, sinus irrigation, and endoscopic sinus surgery. However, many people continue to experience symptoms despite treatment.

Earlier this year, the FDA approved dupilumab (Dupixent) to treat chronic rhinosinusitis with nasal polyps that is not adequately controlled with standard treatment. It is intended to be used together with the other established treatments.

Dupilumab is a human-derived monoclonal antibody, a type of drug that enlists the body’s immune system to help it do its job. It specifically inhibits IL-4 and IL-13 cytokines, chemicals involved in the inflammatory allergic response that leads to symptoms. It is given by injection, under the skin, every other week. It can be administered in a doctor’s office or self-administered at home.

Several clinical trials, including this study published in JAMA (and funded by the drug’s manufacturer), have looked into the effects of dupilumab on chronic rhinosinusitis with nasal polyps. In the JAMA study, participants received either dupilumab plus a steroid nasal spray or a placebo plus a steroid nasal spray, for 16 weeks. Those treated with dupilumab had significant improvements in nasal congestion and obstruction, sense of smell, and overall decreased need for oral corticosteroids and surgery. In those study participants who also had asthma, lung function improved. There were also reductions in nasal polyp size and improved appearance of the sinuses on imaging studies. Patients experienced improvement of symptoms as early as four weeks into treatment, and continued to experience greater improvement than the placebo group for up to one year.

 Dupilumab is not a cure for chronic rhinosinusitis with nasal polyps. However, it is an exciting advancement in the treatment of a chronic condition that significantly impacts physical and emotional health.

How do I know if I have chronic rhinosinusitis with nasal polyps and if I am a candidate for dupilumab?

Chronic rhinosinusitis is commonly diagnosed by a primary care physician who can then refer you to an otolaryngologist, or ear, nose, and throat (ENT) physician, for specialty care. The ENT may perform a nasal endoscopy exam and recommend additional testing, such as imaging studies, to make the diagnosis of chronic rhinosinusitis with nasal polyps. Depending on the treatments you have tried, the ENT will assess whether you are an appropriate candidate for dupilumab.

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Hallelujah, Instagram Is Banning The Most Toxic Weight Loss Ads

Keeping up with how many Kardashian posts get deleted ― or at least blocked from teen viewers ― as a result.

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This Is What It's Like To Be Overweight And Have Anorexia

Eating disorders as a whole are relatively misunderstood, and the misunderstandings become even worse if you don’t “look” the part.

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Does Botox reduce the frequency of chronic migraine?

Doesn’t it seem like Botox is showing up everywhere as a medical treatment? Botox is a brand of botulinum neurotoxin (BoNT), a protein substance originally derived from the bacterium Clostridium botulinum. In its original form it was the toxin responsible for botulism, the paralyzing illness often caused by eating contaminated food.

BoNT is now used to treat a number of medical conditions including muscle spasms, excessive sweating, overactive bladder, and some eye muscle conditions. However, one of its most common uses is in the preventive treatment of chronic migraine. Chronic migraine, defined as headache occurring more than 15 days a month for more than three months, is rare, affecting only about 3% of the migraine population. Nonetheless, since migraine itself is so common, this condition ends up affecting a large number of people and can be extremely debilitating.

A recent meta-analysis pooled the results of multiple prior studies to investigate the usefulness of Botox, a brand of BoNT, in reducing the frequency of chronic migraine. The results suggested that there was benefit from this treatment; it not only improved quality of life and significantly reduced the frequency of chronic migraine headaches, but did so with few and mild side effects.

How might BoNT work to prevent chronic migraine?

Botox was introduced for treatment of chronic migraine in 2000, after some people receiving injections for cosmetic treatment of facial lines reported improvement of headaches. Initial studies after that observation produced conflicting results. Then in 2010, two large studies showed enough benefit (reduction in headache days and improved quality of life) that the FDA approved this treatment for chronic migraine.

Botulinum neurotoxin is taken up into nerves, where it may modify the release of neurotransmitters, chemicals that carry signals between brain cells. This is the original mechanism responsible for the paralysis in BoNT poisoning.

However, this same process in other nerves may interrupt pain production by blocking the release of pain-producing chemicals such as substance P and calcitonin gene-related peptide (CGRP). Although not yet proven, this process could lead to a turning-down of pain processes inside the brain that may be responsible for chronic migraine. Although this mechanism can reduce headache frequency and severity, it does not seem to change the underlying migraine condition.

What are the risks of this treatment?

Theoretically, the spread of BoNT from the site of injection to other areas could result in muscle weakness or paralysis, and doctors usually avoid using BoNT in people with muscle weakness conditions. In practice, however, body-wide reactions or side effects are rare.

Mild injection-related irritation is sometimes reported. At times, temporary eyelid drooping or a change in facial expression resulting from the loss of forehead lines can be seen. These complications can be avoided by moving subsequent injections to a different location. People typically have no restrictions after their injections, and they may return to work or normal activities.

Who would be a candidate for Botox and who wouldn’t?

Since its introduction Botox has become an accepted treatment for chronic migraine when other standard treatments have failed. Botox can help people feel and function better with fewer missed days of work, and the treatments are often covered by health insurance plans.

Botox is not typically used in people who have 14 or fewer migraine headaches per month. However, it is sometimes used “off label” (outside FDA approval) for other forms of chronic headache, such as chronic tension headache.

Where does Botox fit relative to other treatments to prevent migraine?

A comprehensive migraine management plan consists of maintaining a healthy lifestyle, avoiding migraine triggers as much as possible, and using over-the-counter and prescription abortive medications (to stop a migraine already in progress), as needed.

In chronic migraine, standard treatments, including daily prescription preventive medications alone or in combination, are usually tried before Botox. A disadvantage of Botox is that it must be administered through injection by a medical provider every three months in order to maintain the effect. In addition, those on Botox may need to continue taking their previous prescription migraine medications for optimal results.

Nonetheless, Botox has become a common treatment in headache centers in the US. Botox injections are well-tolerated, beneficial, and appear to be safe for long-term management of chronic migraine.

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Want to travel back in time? Use episodic memory

You can picture the long-ago scene perfectly: The waiter opens your bottle of champagne with the familiar — yet always startling — pop. The bubbles tickle your nose as you sniff the effervescent liquid. You raise your glass as you look into the eyes of your spouse. You see pupils dilate as those eyes look at you in return. “Happy Anniversary,” you say, “to the love of my life.” This is episodic memory in action.

Episodic memory allows you to mentally time-travel back to an episode of your life and relive it in vivid detail. You also use episodic memory to remember the name of someone you recently met at a party. It enables you to remember to take a detour because there is construction along your usual route. In fact, most of the time when you speak about “memory,” you are referring to episodic memory, which involves several parts of the brain.

The hippocampus is crucial for episodic memory

If you drew a line between your ears you would pass through the most critical structure for episodic memory. The hippocampus looks somewhat like a seahorse with a head, body, and tail. It is always turned on, recording thoughts, feelings, perceptions, and sensations that arise from other regions of the brain. One part of the hippocampus binds these disparate aspects of experience into a coherent whole. Another part tags it with an index that will allow the memory to be retrieved minutes, hours, days, or years later.

Learning and retrieving information: the frontal lobes

What you pay attention to determines what you will remember. If you are watching your favorite television show and your spouse walks in and gives you a verbal to-do list, you will have difficulty remembering the list if your attention was focused on the television. You can, however, use your frontal lobes to focus your attention. Located behind your forehead, the frontal lobes also enable us to voluntarily retrieve memories. In fact, when you are searching for a specific memory, it is your frontal lobes that are doing the searching.

Trying to remember whether you learned that medical information from a Harvard Health Blog post or a supermarket tabloid? The frontal lobes also help you remember the source and context of information that you learn.

Providing context: the parietal lobes

Have you had the “aha!” experience where you suddenly recall the information you’re looking for — such as the name of a friend who is walking toward you? The conscious recollection of episodic memory comes from the parietal lobes, located in the top, back part of the brain.

Episodic memory: left brain versus right brain

You have two hippocampi, frontal lobes, and parietal lobes, one on each side. The left-brain system is specialized for words and language. The right-brain system is particularly good at remembering non-linguistic information including images, body language, and tone of voice. So, when you recall a conversation with your friend, your left hippocampus remembers the words that were spoken, and your right hippocampus remembers how they were spoken, your friend’s face, and the emotion conveyed.

Aspects of episodic memory decline in normal aging

One reason it is useful to know about the different parts of the episodic memory system is that frontal lobe functions — such as learning, searching, and ability to recall source — tend to decline in normal aging. For this reason, it’s normal for people to notice three changes in episodic memory as they age:

• Because learning diminishes, information may need to be repeated a couple of times in order to get it into the hippocampus so it can be remembered.
• Because the search process slows, it may take more time or a hint or a cue to retrieve a memory.
• Because the ability to judge source declines, it may be more common to experience trouble recalling where we learned information.

In normal aging, however, once information is learned, a person should be able to retrieve it — even if it takes a bit of time, or a hint or cue. By contrast, if a person cannot retrieve learned information, this suggests some problem in addition to normal aging is present. In future blogs I will discuss what happens to episodic memory in disorders of aging, such as Alzheimer’s disease.

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Sleep driving and other unusual practices during sleep

Most people have talked or walked during sleep at some time in our lives. However, some people exhibit more unusual complex behaviors while asleep, including eating and driving. These types of behaviors, called parasomnias, come about when parts of our brain are asleep and other parts awake at the same time. Parasomnias, while generally considered normal in a healthy child, can be a cause for concern when they develop in adults. Earlier this year the FDA issued a “black box” warning for the sleep medications eszopiclone, zaleplon, and zolpidem, given reports of sleep behaviors that resulted in injuries from falls, car accidents, and accidental overdoses related to their use. The FDA also notes that all medications used to promote sleep reduce alertness and may cause drowsiness the following day, which may impair your ability to drive.

Common parasomnias and why they happen

Traditionally, parasomnias are categorized by whether or not they occur during rapid eye movement (REM, or dreaming) sleep.

REM sleep behavior disorder: During REM sleep the body is paralyzed; however, with REM behavior disorder, our bodies are no longer paralyzed, and thus people with this disorder act out their vivid dreams during sleep. Comedian Mike Birbiglia publicly made his dramatic and dangerous story of his experience with REM-behavior disorder part of his comedy routine.

Non-REM parasomnias: Parasomnias occurring in other stages of sleep are categorized as disorders of arousal. Night terrors, sleepwalking, and confusional arousals (also called “sleep drunkenness”) fall under disorders of arousal, which occur when a person has minimal cognition, though they may appear awake with their eyes open. Abnormal sexual activity while asleep, and without intention or thought, is one type of confusional arousal. Typically patients have no or minimal recall of the event. Non-REM parasomnias usually occur during the first third of the sleep period, in deep (slow wave) sleep. They are often triggered after sleep deprivation (which increases the length of time in deep sleep), stress, or sleep disorders such as sleep apnea.

Sleep-related eating disorder: This condition involves episodes of eating while asleep, when people generally have no recollection of the foods they eat. During a sleep-eating episode people often eat peculiar items, such as unprepared or pet foods, or nonfoods such as cigarettes, cleaning products, or books. Sleep-related eating is associated with certain sleep medications, and it may also be associated with other sleep disorders, particularly restless legs syndrome.

Who is at risk for developing a parasomnia?

• Genetic factors play a role in sleepwalking. If your parents are sleepwalkers, you have a higher risk of this behavior.
• REM behavior disorder is extremely common in patients with certain neurogenerative diseases, such as Parkinson’s disease.
• Common sleep medications, such as those in the FDA black box warning, as well as some antidepressants, antianxiety, and antipsychotic medications, have also been linked to parasomnias, including sleep-related eating disorder.

Black box warnings are significant, so what do if you’re taking a sleep medication and are concerned?

If you are using a medication that now has a warning, and you have experienced an unusual sleep behavior, you should contact your physician and they can work with you on how and when to adjust your medication. You should continue to review your doses with your physician, and use the lowest effect dose. The FDA recently changed the recommended doses of zolpidem and eszopiclone, since they may reduce alertness the next morning. Studies have shown that people may have difficulty with coordination and memory, which correlate with the ability to stay in a driving lane after taking the medications, but people may not be aware that they were impaired.

If you are concerned about medication side effects, you should discuss other options for treatment for your insomnia. I’ve written previously about effective non-medication behavioral options to help you get a good night’s sleep.

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How racism harms children

Racism hurts children, in real and fundamental ways. It hurts not just their health, but their chances for a good, successful life.

That’s the bottom line message of a new policy statement from the American Academy of Pediatrics (AAP). It is a call to action for all of us. If we care about the health and future of all of our children, it says, we need to take real steps to end racism — and to help and support those who are affected by it.

Racism informs our actions when we structure opportunities for and assign value to people based on our interpretation of how they look. Biologically we are truly just one race, sharing 99.9% of our genes no matter what the color of our skin or what part of the world we come from. But historically we have found ways to not just identify differences, but to oppress people because of them. Racism grew out of and helped rationalize colonization and slavery. Despite our biological sameness, people continue to look for differences — and claim superiority. While we have made historical progress, the beliefs and oppression that underpin racism persist; it is, as the AAP statement calls it, a “socially transmitted disease.”

How does racism affect health and well-being in children?

And it truly is a disease. Racism and its effects can lead to chronic stress for children. And chronic stress leads to actual changes in hormones that cause inflammation in the body, a marker of chronic disease. Stress that a mother experiences during pregnancy can affect children even before they are born. Despite improvements in health care, racial disparities exist in infant mortality as well as low birthweight.

These days, it’s important to think about chronic stress for the children of immigrant families. Many live in constant fear of being separated from their parents if they haven’t been already.

Children raised in African-American, Hispanic, and American Indian populations are more likely to live in homes with higher unemployment and lower incomes than white children. This means that they are less likely to have good housing, good nutrition, good access to health care, and access to good education. Such disparities increase their risk of health problems and of receiving less, and lower-quality, education.

Even when minority children live in wealthier areas, research shows that they are often treated differently by teachers. They are more likely to be harshly punished for minor infractions, less likely to be identified as needing special education, and teachers may underestimate their abilities. And when a teacher doesn’t believe in you, you are less likely to believe in yourself.

Referencing the National Center for Education Statistics, the AAP statement notes that in the 2015–2016 school year, 88% of white students graduated from high school. In comparison, only 76% of African Americans, 72% of American Indians and 79% of Hispanics did the same. This is important not just in terms of economic opportunity but also in terms of health: adults with a college degree live longer and have lower rates of chronic disease than those who did not graduate from college.

The juvenile justice system is another place where racism plays out. Minority youth are more likely to be incarcerated, with all the health and emotional consequences this brings, both during incarceration and after. Being incarcerated forever changes a person — and changes how others see them.

Discrimination extends beyond racism

The statement points out that it is important to remember that it’s not just the color of one’s skin that can lead to discrimination and all the problems that brings. Differences in sex, religion, sexual orientation, and immigration status can lead to discrimination, as can having a disability.

The policy statement reminds us that children are being hurt every day by racism and discrimination, and the effects can be not only permanent but continue through generations. There is real urgency to this.

How can we help change course on racism and discrimination?

Fixing racism and discrimination is obviously not easy and cannot be quick. But there are things we can all do immediately.

• We can take a hard look at ourselves, take stock of our beliefs and our biases, and work to change them.
• As part of this, we need to think about and change how we talk about each other, as individuals and as a society.
• We need to speak up when we hear or see racism or discrimination in any form. Empowering ourselves and each other is an important way to begin.
• We need to talk to our children about racism, and teach them healthier ways to think about themselves and each other.
• We need to work to stop institutional racism.
• We need to work with our schools to be sure that all children, no matter what, have access to a good and supportive education. This is no small endeavor, but it needs to be our goal.
• We need to be sure that there are programs in place to not just help people who are poor or struggling, but lift them out of poverty.
• We need to be sure our laws truly protect all people, not just some people.

This is about the future of our children — and our children are our future.

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Your risk of dementia: Do lifestyle and genetics matter?

Globally, Alzheimer’s disease and other forms of dementia are a major burden on individuals and communities. To make matters worse, there are few treatments to combat these complex illnesses. Even the causes of dementia are widely debated. Sadly, clinical trials for drugs to stop or even slow its progress have come up short. Taking a different tack, some experts hope to intervene before people are diagnosed with dementia by encouraging lifestyle changes.

What is dementia and what makes it so complex?

Dementia describes groups of specific diseases characterized by symptoms such as memory loss. The most common type of dementia is Alzheimer’s disease (AD). People with AD have plaques in their brains made of up of tangled proteins, and many researchers have hypothesized that these plaques are the cause of the disease.

Another common type of dementia is vascular dementia. This is thought to be induced by damaged blood vessels in the brain, such as from a stroke.

Experts believe both genetic factors (variants of genes passed down from mom and dad) and modifiable lifestyle factors (diet, pollution, infection, smoking, physical activity) all play a role in the development of dementia, perhaps in concert.

What factors might affect dementia risk?

Genes – which are not considered modifiable —and lifestyle factors like physical activity and diet – which are considered modifiable – play potential roles in different forms of dementia.

A recent study in JAMA attempts to estimate how much genetic and lifestyle factors influence risk for dementia by querying individuals who pledged to be part of a UK-based “biobank.” Biobanks link large collections of biological information, such as genetics, with health and disease status gleaned from medical records. Using data in large biobanks, scientists can look at how the environment—which includes lifestyle choices —and genetics work together to increase (or decrease) risk for disease.

In the JAMA study, researchers tapped hospital records and death registries to collect diagnoses in 200,000 white British individuals age 60 or older.

But how can you measure “lifestyle” and genetic risk?

The investigators hand-picked a list of common lifestyle factors, including smoking, alcohol consumption, physical activity, and diet, and created a score. A low score denoted a “bad” lifestyle. A high score denoted a “good” lifestyle.

However, taking this approach to measure lifestyle risk has several pitfalls:

• First, a vast number of factors comprise lifestyle and environment beyond smoking and physical activity. So any list may be arbitrary. In fact, our research team has argued that choosing a candidate list doesn’t capture our complex lifestyles and may lead to false findings. For example, what exactly constitutes a “healthy” diet?
• Second, using a score makes the individual roles of the factors unclear.
• Third, if connections between factors (for example, weight or history of other diseases) influence both the score and dementia, then the score might be a weak proxy for other variables that weren’t considered. In other words, if weight is associated with diet and dementia, then it is hard to untangle the association of diet.

To create the genetic risk score, the investigators used all genetic variants previously identified by a genome-wide association study (GWAS) of Alzheimer’s disease. These gene variants are strongly associated with patients who have Alzheimer’s compared with healthy controls). Using this information, the researchers constructed a polygenic risk score.

Lifestyle and genetics both play a small role in dementia

The lifestyle score was associated with dementia risk. Second, the genetic score was also associated with dementia. In other words, individuals with worse scores were at higher risk for dementia.  The researchers further found that genetic risk and lifestyle appeared to act independently of each other. For example, individuals with both an unhealthy lifestyle and a high genetic risk score had almost two and a half times more risk than individuals with a low genetic score and healthy lifestyle.

However, this research was not designed to prove whether lifestyle and environment or genes cause dementia. A lot more could explain the differences between people who develop dementia. If populations at high genetic risk changed their lifestyle, and if the lifestyle was known to be the cause of AD (a big if), one out of 121 dementia cases would be prevented in 10 years. This is significant, but what number of lifestyle modifications would it take for the prevention of AD in 10, 50, or even 120 people? Do genetics even matter?

Second, the genes and lifestyle did not appear to work together — or they weren’t synergistic — in dementia risk. Specifically, this means that individuals with both bad genetic and lifestyle scores were not at risk for developing dementia any more than the sum of the parts or the individual scores alone.

New frontiers for AD prevention and treatment

New horizons for prevention and treatment might include how risk might be different for individuals of varied genetic ancestries and ethnicities (most genetic studies have predominantly focused on white individuals) both here in the US and abroad. The risk may also be different between males and females. Finally, biobanks can only describe association, not causation, between changes in lifestyle and dementia risk. To determine causation, randomized trials are required, and a new US-based randomized clinical trial called POINTER is now underway.

Trying to live a healthy lifestyle, despite its elusive definition, seems to be an obvious way to prevent dementia. What remains to be seen is how studies using biobanks can be informative about the millions of people who already may be suffering from the disease.

References

Why Most Published Research Findings Are False. PloS Medicine, August 30, 2005.

Repurposing large health insurance claims data to estimate genetic and environmental contributions in 560 phenotypes. Nature Genetics, January 14, 2019.

Studying the Elusive Environment in Large Scale. JAMA, June 4, 2014.

A Nutrient-Wide Association Study on Blood Pressure. Circulation, November 20, 2012.

Association of Lifestyle and Genetic Risk with Incidence of Dementia. JAMA, July 14, 2019.

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Psychotherapy leads in treating post-traumatic stress disorder

Post-traumatic stress disorder (PTSD) is a common, often debilitating mental health condition that occurs in some people who have experienced trauma. It can have a negative impact on mood, mimicking depression, and is characterized by petrifying episodes in which affected people re-experience trauma. New research suggests psychotherapy may provide a long-lasting reduction of distressing symptoms.

Over the course of a lifetime, many people directly experience or witness trauma, such as sexual assault, violence, or natural disasters. Experts estimate that 10% to 20% of these people will experience acute (short-term) PTSD. Some will go on to develop chronic (long-term) symptoms. Overall, about 8% of all people will develop PTSD during their lifetime, highlighting the need for effective treatments.

What happens when people have PTSD?

Because PTSD spans several categories of symptoms, it can be incapacitating. People are diagnosed with PTSD if they have certain symptoms following a traumatic experience that last for at least a month:

• one or more symptom of re-experiencing the trauma (sometimes called a flashback)
• one or more avoidance symptoms, such as avoiding places or objects that remind you of the original event
• two or more symptoms of arousal and reactivity, such as jumpiness, heart pounding, or sweating
• two or more symptoms of an effect on mood or cognition, such as negative thoughts or problems recalling key portions of the event.

When a person has PTSD, the brain can become sensitized in a state of constant hyperarousal. Nightmares are exceptionally common. People struggling with PTSD often begin to avoid a range of triggering environments. This can further fuel social isolation, making it difficult to hold a job and nurture relationships. Altogether, PTSD can lead to substantial disability and emotional burden on people who have it and society at large.

How is PTSD treated?

Experts have long disagreed on optimal treatment approaches. Current standards of care for treatment may include

• medications, such as antidepressants known as selective serotonin reuptake inhibitors (SSRIs), and alpha-1 blockers such as prazosin (Minipress)
• certain forms of psychotherapy, such as prolonged exposure therapy and eye movement desensitization and reprocessing (EMDR).

However, recommendations made by different expert panels vary substantially on the order in which to try these treatments. For example, the American Psychological Association and the International Society for Traumatic Stress Studies recommend antidepressants known as SSRIs as possible first-line treatment. Most other guidelines, including those from the National Institute of Health and Care Excellence and National Health and Medical Research Council, recommend using SSRIs only if initial attempts at psychotherapy are unsuccessful.

What does the new research tell us?

Rigorous new research supports using psychotherapy first, followed by medication if it fails to offer sufficient relief, or psychotherapy combined with medication from the start. This large meta-analysis, published online in JAMA Psychiatry,combined data from 12 randomized clinical trials and 922 participants. Researchers found that no particular treatment approach was superior to any other at the time of treatment. However, the benefits of psychotherapeutic approaches lasted longer. At their last documented follow up, patients with PTSD who received psychotherapy had significantly greater improvement in symptoms compared with those who received only medications. Additionally, combining both therapy and medications was significantly better in the long term than medications alone.

This meta-analysis presents the strongest argument yet that evidence-based psychotherapies are superior to medications alone in helping to relieve symptoms of PTSD. Combining both approaches also holds merit and is superior to medications alone, though not statistically better than psychotherapy alone.

Which type of psychotherapy is most helpful for PTSD?

Questions remain about which kind of psychotherapy is most effective. Evidence suggests that cognitive behavioral therapy, prolonged exposure therapy, Seeking Safety therapy, and EMDR help many people with PTSD. Yet there are not many head-to-head trials and there is no convincing evidence from those that were done.

The bottom line: Advocate and seek help early

Until more robust comparison research is completed, people who experience trauma must be their own best advocates. As a psychiatrist with experience in this field, I recommend the following:

• Monitor yourself closely after a trauma.
• Be on the lookout for early symptoms, such as mood and sleep disturbances.
• Be aware of whether symptoms seem to be improving or worsening over time.
• Be willing to listen to family members, loved ones, and your healthcare team, who may identify problem areas as they arise.
• Seek treatment early, with a mental health professional who has extensive experience in treating PTSD using one of the above therapeutic approaches.

Taking these steps offers the best opportunity to mitigate symptoms and optimize quality of life following a traumatic event.

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Why are diabetes-related complications on the rise?

Diabetes has grown to become one of the most important public health concerns of our time. A review by the Harvard T.H. Chan School of Public Health has shown that the number of affected people has quadrupled in the last three decades. Type 2 diabetes (T2D), a type of diabetes traditionally occurring in adults and associated with obesity and a sedentary lifestyle, is now the ninth leading cause of death worldwide. It therefore comes as no surprise that this rapidly emerging epidemic is giving rise to a profusion of diabetes-related complications.

What are the usual diabetes-related complications?

As diabetes is a systemic disease, its effects are felt in virtually all parts of the body. Most diabetes-related complications are related to problems in the blood vessels, usually involving changes in blood flow or in the ability of blood to clot.

These complications are generally classified into two broad categories: microvascular (involving small blood vessels) and macrovascular (involving large blood vessels). Microvascular damage is responsible for causing eye, kidney, and nerve complications, while macrovascular complications encompass stroke and heart disease and are currently the leading cause of diabetes-related death and disability. In some areas of the body, such as the lower extremities (legs and feet), as well as in wound healing, both small and large blood vessels may be involved.

What are the trends in diabetes-related complication rates?

A recent viewpoint article in JAMA tackled the changing trends in diabetes-related complication rates. During the early 1990s, patients with T2D had reductions in life expectancy of up to 10 years, coupled with substantial risks for diabetes-related complications. However, through better education and medical care, these risk differences were slashed by as much as 60% between 1990 and 2010. The reduced risks chiefly represented reductions in heart disease, thus improving the long-term outlook for adults with T2D.

Yet between 2010 and 2015 the tides turned again, with an uptick in diabetes-related lower extremity amputations and hospitalizations, and a plateauing of the previously-reported improvements in heart disease and kidney failure. What’s interesting is the fact that this phenomenon figured prominently in young adults (ages 18 to 44).

What may have led to the changing trends in diabetes-related complication rates?

Why, then, do we have this paradoxical rise in complication rates, despite having more cutting-edge diabetes drugs and devices in the market, and learning more than ever about how the disease works? The JAMA article suggested that explaining these trends is especially challenging because of the numerous factors, ranging from individual patient characteristics to institutional issues and governmental policies, that may play a role. The article authors propose several theories:

First is the gradually changing profile of people newly diagnosed with diabetes. These young adults possess high rates of obesity, smoking, and sedentary lifestyles, as well as high blood pressure and cholesterol (lipid) levels, all contributing to an earlier onset of complications. The demographic of T2D is also veering toward a nonwhite population, with Asia being the epicenter of its global rise. Hence, the increase in complication rates may have been due to changes in the types of people who are developing T2D.

Second, there may have been an inadvertent relaxation of blood sugar targets (HbA1C) in these young adults. Intensive blood sugar control can cause low blood sugar (hypoglycemia), which can be particularly dangerous for older adults. When clinical organizations shifted toward less stringent blood sugar management guidelines in the late 2000s, with an eye on preventing hypoglycemia in older patients, this may have had unintended consequences for blood sugar management in young adults.

Third, broader socioeconomic factors may have been at play. The article observed that the complication rate reversal transpired after the noteworthy economic recession of 2008–2009, and at a time when high-deductible health plans started to pose added financial barriers to preventive care. Variations in insurance coverage of healthcare services, plus the skyrocketing costs of insulin and newer medications, may have likewise contributed to the rising complication rates.

On the other hand, it is also entirely possible that things may have simply boiled down to the increasing prevalence of T2D, or to earlier and better detection strategies.

Whatever the case, the exact reasons may be difficult to truly ascertain using observational and epidemiological approaches, which cannot definitively establish cause and effect.

What can someone with diabetes do to lower their risk of complications?

There is no single overarching strategy to lower one’s risk for diabetes-related complications. Prevention of complications and delay of their progression is always a two-way street between physician and patient. It comprises a multifaceted approach of reasonably sufficient blood sugar control that balances the benefits of diabetes medications with the risks of overly aggressive blood sugar control; lifestyle modifications; and regular screenings for eye, kidney, nerve, and heart-related conditions.

Nevertheless, the unexpected reversal of improvements in complication rates is worrisome, given its predominance in the young population. We need more focused studies to determine whether these negative trends are also occurring in other countries and are affecting particular ethnic groups. In addition, we need to know whether present treatments are effective in this younger, ethnically diverse subset of people developing diabetes-related complications.

Follow me on Twitter @marcgreggy

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