New study suggests unexpected link between long sleep and Alzheimer’s

 But do you have cause and effect correct? Early undetected Alzheimers may cause long sleep!

New study suggests unexpected link between long sleep and Alzheimer’s

Researchers found that older adults who routinely sleep 10 hours or more a night had elevated levels of a blood protein considered an early warning sign of dementia.

Sleeping long hours every night may be linked to elevated levels of a blood protein widely regarded as a telltale sign of Alzheimer’s disease, according to a new study by the University of Texas at San Antonio’s academic health center.

UT Health San Antonio reports that, among the 2,410 participants, those who slept 8.5 to nine hours a night had higher levels of phosphorylated tau 181, or p-tau181, a modified form of tau protein associated with cognitive decline. Researchers said p-tau181 levels increased “most sharply” among sleepers who slept more than 10 hours a night. “A lot of people worry about whether their sleep habits are affecting their brain health,” said Vanessa M. Young, PhD, MS, a postdoctoral research fellow at the center’s Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases. “Because this is a snapshot in time rather than a long-term study, we cannot say that long sleep causes Alzheimer’s, but the findings suggest it may be worth monitoring, and that more sleep is not always better for brain health.”

Participants had an average age of 70. Just over 55 percent were female.

Related video: Alzheimer's disease study (KARE-TV Minneapolis St. Paul)The study follows up onby UT Health San Antonio that found sleeping nine or more hours a night was associated with worse cognitive performance, especially among people diagnosed with depression. The latest study, conducted by some of the same researchers, was more extensive. It accounted for multiple health factors and examined blood-based markers that have been tied to Alzheimer’s and neurodegeneration in relation to participants’ self-reported sleep hours. “Sleep is a promising modifiable risk factor linked to the disease,” researchers said, “but existing evidence has remained limited and inconclusive.” people diagnosed with depression. The latest study, conducted by some of the same researchers, was more extensive. It accounted for multiple health factors and examined blood-based markers that have been tied to Alzheimer’s and neurodegeneration in relation to participants’ self-reported sleep hours. “Sleep is a promising modifiable risk factor linked to the disease,” researchers said, “but existing evidence has remained limited and inconclusive.”

Three other proteins associated with brain cell damage were also tested but, unlike p-tau181, they appeared to have no association with sleep duration, researchers said.

While the study found elevated levels of p-tau181 among habitual long sleepers, UT Health San Antonio said more research is needed to determine whether the association can ultimately be tied to Alzheimer’s risk.

The center’s findings coincide with a study published last week in JAMA that said simple blood tests may be able to predict who will develop cognitive impairment up to a decade before the first symptoms surface. The most accurate test measured levels of a mutation of a different tau protein, phosphorylated tau 217 (p-tau217).

The study of nearly 2,700 older adults on three continents found that people with high levels of the p-tau217 biomarker had a 38 percent chance of developing cognitive impairment within five years and a 78 percent chance within 10 years.

Further research and clinical trials could lead to the development of new therapies that may one day slow or even stop Alzheimer’s progression, researchers said.

An estimated 57 million people worldwide are affected by dementia, the San Antonio study noted, with Alzheimer’s diagnosed in 60 to 70 percent of all cases.

“Even with recent advances in disease-modifying therapies, Alzheimer’s remains a profound medical and societal challenge,” researchers said.

Young suggested that long sleepers might want to bring up the new study’s findings during their next doctor visit. “In plain terms, if you regularly find yourself sleeping nine to 10 hours or more a night,” she said, “it may be worth mentioning to your doctor as a useful conversation starter about your sleep quality and overall brain health.”

This post originally appeared at inc.com.

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A workout or a bad night’s sleep can shape your brain for up to 15 days

 Is your competent? doctor ensuring your correct sleep protocol? It better not include sleeping pills or vampires waking you up early morning to get their blood draw in before you eat. 

A workout or a bad night’s sleep can shape your brain for up to 15 days

A single restless night or a brisk workout can leave detectable imprints on brain connectivity for as long as 15 days, according to a five-month longitudinal study that scanned one healthy adult daily with resting-state fMRI while tracking sleep, exercise, and heart-rate data. The finding shifts the conversation about brain health away from extreme lab-based sleep deprivation and toward the ordinary routines that quietly reshape neural networks over two weeks.

How everyday habits rewire brain networks over two weeks

The core evidence comes from a Registered Report in PLOS Biology that used time-lagged cross-correlations spanning from the previous day back to 15 days. Rather than averaging across dozens of participants in a single session, the researchers built a dense timeline from one person’s daily brain scans and physiological logs collected over roughly five months. That design allowed them to detect delayed associations between a given day’s behavior and connectivity shifts that surfaced days or even two weeks later.

Restless sleep stood out as one of the clearest signals. Nights marked by more awakenings and lower sleep efficiency were followed by altered coupling between the default mode network-the brain system active during mind-wandering and self-referential thought-and other large-scale networks involved in attention and control. These changes did not always appear the very next day; some emerged after several days and could still be detected up to two weeks later, suggesting a slowly unfolding adjustment rather than a quick rebound.

Related video: 4 sleep habits for healthy ageing, and 1 that might need medical help (HuffPost)

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Exercise produced its own delayed signature. Days with more physical activity were associated with shifts in connectivity among sensorimotor, visual, and higher-order networks, again with effects that sometimes peaked days after the workout. The published data describe broad associations rather than precise dose-response curves tied to specific workout intensities, so it remains unclear whether short, moderate sessions and long, strenuous workouts have distinct connectivity footprints. Still, the practical message is clear: a single night of tossing and turning, or a day spent unusually active, does not simply vanish from the brain the next morning. Its echo persists in how neural networks coordinate.

Sleep deprivation experiments confirm the connectivity stakes

The longitudinal results gain weight when placed alongside controlled experiments that deliberately strip away sleep. In one study, researchers measured resting-state connectivity across multiple time points during normal sleep and after a night of total sleep deprivation. One sleepless night produced measurable alterations in between-network communication that exceeded normal day-to-day variability. These shifts appeared consistently across repeated scans of the same individuals, underscoring that the effects were robust and not just statistical noise.

A related line of PLOS Biology research has linked acute sleep loss to a disrupted balance between network integration and segregation, two complementary properties that support attention, memory, and executive function. When integration is too high, networks lose their functional specialization; when segregation is too strong, information struggles to flow between regions. After sleep deprivation, this balance tilts, and cognitive deficits follow, including slower reaction times and reduced accuracy on tasks that demand sustained focus and flexible thinking.

A broad review of neuroimaging work on sleep deprivation effects reinforces the idea that these connectivity shifts touch multiple systems at once. The synthesis highlights altered activity and connectivity in the amygdala, prefrontal cortex, and hippocampus-regions central to emotional regulation, decision-making, and memory consolidation. Together, these converging lines of evidence support a clear mechanism: sleep loss does not just make people feel subjectively tired. It physically reorganizes how brain regions communicate, and that reorganization shows up in objective measures of cognition and mood.

What the single-subject longitudinal study adds is duration. Lab deprivation experiments typically capture the acute hit and, at most, a recovery scan a day or two later. By collecting daily data for months, the dense sampling approach reveals that even routine, subclinical sleep disruption-not just total deprivation-leaves traces that linger well beyond a single “catch-up” night. For anyone who has felt mentally “off” for days after a run of poor sleep, these findings offer a plausible biological explanation: the brain’s network architecture is still in the process of reconfiguring.

Single-subject design and the fitness question

The most obvious limitation is scale. All of the 15-day lag results come from a single participant. Dense longitudinal designs trade breadth for depth: they are powerful for uncovering within-person dynamics that group averages might wash out, but they cannot establish that the same patterns generalize to other people. Individual differences in sleep need, stress, and lifestyle could all shape the lag structure between behavior and connectivity. At present, no multi-subject replication of these specific time-lagged associations has been published.

Another open question concerns baseline cardiorespiratory fitness. In theory, higher fitness might buffer the brain against lingering connectivity disruptions after a poor night’s sleep, perhaps by enhancing vascular health, neuroplasticity, or inflammatory responses. If fitter individuals showed quicker normalization of default mode and attention network coupling after sleep disturbance, that would have direct implications for exercise as a protective strategy. However, the available longitudinal data do not test this interaction. The study reports overall associations between exercise and connectivity but does not stratify results by fitness level or parse different workout intensities. As a result, the “fitness as shield” idea remains an appealing but untested hypothesis.

Equally unresolved is whether the 15-day connectivity shifts predict real-world outcomes beyond controlled laboratory tasks. Deprivation experiments clearly link network disruption to slower responses and more errors on cognitive tests, but no current study tracks whether the lingering connectivity changes documented over two weeks translate into worse driving performance, impaired workplace decision-making, or mood instability in everyday life. Establishing those links would require pairing dense neuroimaging with ecological measures such as digital diaries, wearable sensors, or on-road driving assessments-methodologically demanding work that has yet to be completed.

Methodologically, the longest time lags also push against statistical limits. Signals measured 10 to 15 days apart are more vulnerable to confounds such as unmeasured stressors, illness, or life events, and the relevant thresholds and corrections are detailed mainly in supplementary materials. Until independent teams reproduce the analysis with different participants and scanning protocols, the exact shape and strength of those long-lag effects should be treated as provisional.

What this means for everyday brain care

For readers trying to apply these findings, the most concrete takeaway is to treat sleep consistency as a cumulative investment rather than a nightly reset button. Because even mild disruption can leave traces that last many days, patterns-regular late nights, frequent awakenings, or erratic bedtimes-are likely more consequential than any single bad evening. Prioritizing a stable sleep schedule, a dark and quiet bedroom, and wind-down routines that reduce arousal may help keep network-level fluctuations within a healthier range.

Physical activity still looks promising as a brain-supportive habit, but the details matter less than the regularity at this stage of the evidence. Moderate, sustainable movement most days of the week is a reasonable target while researchers work out how different exercise types and intensities shape connectivity over time. Because the same workouts that support brain function also benefit cardiovascular health, mood, and metabolic risk, they remain a low-regret strategy even as the mechanistic story continues to evolve.

Perhaps the most important conceptual shift is to stop viewing the brain as resetting each morning. The emerging picture is of a system that carries a rolling memory of the past two weeks of sleep and activity, with network configurations reflecting that recent history. Each night’s rest and each day’s movement nudge that configuration in subtle ways. Over months and years, those nudges may add up, for better or worse. While scientists work to refine the details, the practical message is already clear enough to act on: consistent sleep and regular exercise are not just lifestyle advice-they are tools for steering how the brain’s networks wire and rewire themselves over time.

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*This article was researched with the help of AI, with human editors creating the final content.

A New Study Finds Melatonin Could Harm Your Heart Health. Try These 7 Sleep Alternatives

 You'll have to ask your competent? doctor if the pros outweigh the cons, Your doctor better know the answer IF COMPETENT AT ALL!

• melatonin (36 posts to February 2012)

A New Study Finds Melatonin Could Harm Your Heart Health. Try These 7 Sleep Alternatives

A preliminary study conducted by the American Heart Association reveals that adults with insomnia who used melatonin for at least 12 months had about a 90% higher chance of first-time heart failure within five years. This was found using five years of health records from 130,828 adults. Participants in the long-term melatonin use group were also almost twice as likely to die from any cause over five years.

It's important to note that this study hasn't yet been peer-reviewed, and that the data may be skewed because melatonin use in the study was based on prescribed medication entries in electronic health records. In the UK, melatonin must be prescribed, whereas it is available over the counter in countries like the US. That means people in the study using over-the-counter melatonin would have been mistakenly included in the non-melatonin group. As a result, more research is required.

However, if you're looking to curb your long-term melatonin use, or, like me, melatonin simply doesn't work for you, there are alternatives that can help you fall asleep. These are my favorites.

1. Use CBD oils, gummies or creams

CBD, also known as cannabidiol, is derived from hemp plants. CBD is a safe and effective treatment for insomnia that contains almost no THC, the substance in marijuana that alters one's mental state. Many studies suggest that CBD is very effective in promoting sleep and decreasing anxiety. It comes in many forms, such as oils and lotions. Use before bed to promote sleepiness and relaxation.

natural remedies for anxiety, stress and insomnia. Drink a cup of one of these herbal teas at least an hour to two before bed -- this gives you time to relax, enjoy the tea and use the bathroom before lights off. Be sure to look at the nutrition label to make sure no caffeine has been added to the ingredients.

3. Put a drop of lavender oil on your pillow

One of the more popular household remedies -- essential oils. If tea is not your favorite way to relax before bedtime, floral and herbal fragrances are good ways to aid sleep. Some popular essential oils for sleep are lavender, chamomile, and bergamot. Essential oils should never be ingested, but you can put a little drop on your pillow at night. You can also diffuse essential oils into the air or use dried lavender to make a tea. 

4. Drink tart cherry juice

Sour cherry juice from tart cherries can increase melatonin production in those who consume it before bedtime. In the same study, the group that drank the cherry juice spent more time in bed and asleep and achieved higher overall sleep efficiency. This suggests that tart cherry juice has the potential to prevent insomnia. 

5. Try dried passionflower or extract oil

Not to be confused with passionfruit -- passionflower is a fast-growing vine that produces vibrant flowers. Not only is the plant beautiful, but it can even help you fall asleep through herbal tea or extract oil. A recent study concluded that passionflower has the potential to treat insomnia. However, it isn't recommended for those who are pregnant. 

6. Make sure you're getting enough magnesium

Magnesium, a powerful nutrient, is responsible for regulating hundreds of processes in the body -- including sleep. Magnesium is found naturally in foods such as nuts and seeds, spinach, soy milk, yogurt and whole grains. Try lightly snacking on foods high in magnesium an hour or two before bed. If you believe that you aren't getting enough magnesium in your diet and suspect it could help your sleep, try adding a supplement. 

7. Practice yoga and meditation before bedtime

Strenuous exercise before bed is not always a good idea, but practicing light yoga or meditation before bed has been linked to decreased insomnia and better sleep. Go through simple yoga poses, such as cat-cow, forward fold or bridge, focusing on your breath and feeling the stretch. There are also many self-guided meditation apps available.

Alzheimer’s risk may be determined by one daily habit combined with genes

 I'm much better now retired but this is still too ambiguous to be of much help.

Alzheimer’s risk may be determined by one daily habit combined with genes

How much sleep you get may matter even more if you carry certain genetic variants linked to Alzheimer’s disease, according to new research that suggests genes and sleep habits work together to influence brain changes years before symptoms appear.

Researchers at Edith Cowan University examined the aquaporin-4 (AQP4) gene, which helps regulate fluid movement through the brain and plays a key role in the brain’s overnight waste-clearance system, often called the glymphatic system.

Scientists believe this system helps remove proteins such as amyloid-beta that accumulate in Alzheimer’s disease. Because the system is most active during sleep, researchers have increasingly focused on whether sleep quality influences long-term dementia risk.

Co-author Dr. Tenielle Porter said that, while poor sleep and Alzheimer’s risk have long been linked, the new results should not be viewed as evidence that genetic testing is ready for clinical use.

Dr. John Showalter, a physician specializing in dementia and cognitive impairment, agreed on the biological link between sleep and Alzheimer’s disease.

“We know that sleep and all-cause cognitive impairment, including Alzheimer’s disease, are linked,” Showalter told Newsweek. “Obstructive sleep apnea is associated with a 34 percent increase in all-cause dementia and insomnia has been reported to increase risk anywhere from 13 percent to 53 percent.”

Showalter added that excessive daytime sleepiness has also been associated with substantially higher amyloid accumulation over time, making the glymphatic system a particularly important area of Alzheimer’s research.

The new findings suggest some genetic risks may be amplified—or potentially mitigated—by sleep habits, raising the possibility that future prevention strategies could be tailored to an individual’s biology.

What the Study Found

Published in the June 2026 issue of Alzheimer’s & Dementia, the study analyzed 351 cognitively unimpaired adults in their mid-70s who already showed evidence of amyloid-beta accumulation and were enrolled in the Australian Imaging, Biomarkers and Lifestyle Study.

Researchers examined 13 common AQP4 variants alongside self-reported sleep measures, brain imaging and cognitive testing. Certain variants were associated with differences in brain volume, brain atrophy and cognitive performance, and those relationships often changed depending on sleep duration, sleep quality and how long participants took to fall asleep.

Participants carrying some AQP4 variants experienced faster gray matter loss when they reported shorter sleep durations. Others who took longer to fall asleep showed structural brain changes linked to reduced brain volume. Cognitive trajectories also differed depending on the combination of sleep disturbances and genetic profile.

The researchers concluded that sleep appears to act as a modifier of genetic risk, potentially influencing how Alzheimer’s-related changes develop over time.

Showalter said the findings resemble patterns already observed in cardiovascular disease, where genes and lifestyle factors interact rather than operating independently.

“It fits what we often see in medicine,” he said. “Genes may influence risk, but behavior and environment frequently determine how that risk is expressed.”

Researchers Urge Caution

Several of the researchers’ public comments originated from an Edith Cowan University press release issued in June 2026. Newsweek did not ask for additional comments from the study authors beyond those included in the university statement.

“Our study shows that individuals carrying certain AQP4 variants showed faster gray matter loss when they reported shorter sleep,” co-author Ayeisha Milligan Armstrong said in the university release. “It’s not just which genes you carry; it’s how those genes interact with the world around you.”

Importantly, the researchers cautioned against overinterpreting the findings.

“We’re not at the point of recommending genetic testing,” Porter said in the university’s June press release. “Our findings need replication in larger and more diverse cohorts.”

Porter said the research instead highlights how Alzheimer’s risk pathways may differ between individuals and suggests future prevention strategies could become more personalized.

That caution was echoed by Jessica McCarthy, a neuropsychologist specializing in dementia assessment and neurodegenerative disorders. She told Newsweek that the study’s immediate significance lies less in genetics and more in what it says about sleep.

“We cannot, and I mean absolutely cannot, ignore the fact that this study screams the importance of understanding and targeting modifiable risk factors such as sleep, aggressively and early,” she said.

McCarthy noted that sleep quality is influenced by factors throughout life, including mental health, hormonal changes, medical conditions and aging. She argued that public-health messaging should place greater emphasis on sleep hygiene long before people reach old age.

“We absolutely need to be moving, and quickly, in the direction of educating everyone about the importance of sleep hygiene and its longer-term impact on our health,” she said.

She also called for additional research into safer treatments for chronic sleep problems, noting concerns that some sleep medications have themselves been associated with increased dementia risk.

While McCarthy said genetic screening could eventually help personalize prevention strategies, she argued that the more actionable takeaway for readers is straightforward: improving sleep is something people can begin addressing now, regardless of their genetic profile.

The Bottom Line

The findings do not prove that improving sleep will prevent Alzheimer’s disease, nor do they establish that AQP4 genetic variants directly cause cognitive decline.

Instead, the study adds to growing evidence that sleep may be one of the most important—and potentially modifiable—factors influencing long-term brain health, while also suggesting that the effects of sleep may differ depending on an individual’s genetic makeup.

The study was first published online in Alzheimer’s & Dementia on May 29, 2026, appeared in the journal’s June 2026 issue, and was highlighted in an Edith Cowan University press release issued on June 22.

Contact Newsweek editors on this story: Kara Dolman and James Debens.

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11 Signs You Might Be Headed For a Heart Attack

 Stroke probably also falls into this.

11 Signs You Might Be Headed For a Heart Attack

1.  You get angry over the littlest things

Tend to morph into the Incredible Hulk when you’re upset? Those fiery emotions may increase your risk for a heart attack, according to research published in 2015 in the European Heart Journal.

Researchers at the University of Australia questioned 313 patients who had  suspected heart attacks about their anger levels before the onset of symptoms. They found that patients were 8.5 times more likely to have a heart attack in the two hours following an intense outburst of anger, defined as “very angry, body tense, clenching fists or teeth” compared with other times when they were less angry.

The findings suggest that if you have an episode of intense anger, it could increase your risk of heart attack in the subsequent hours. Here are the 9 best ways to control your anger and avoid getting to that point.

(I'm incredibly calm all the time, don't get flustered about anything.)

2.  You spend most of your time in front of a screen©Maskot/Getty Images

Yes, that includes working on your computer. A study published in the Journal of the American College of Cardiology in 2011 found that people who watch TV or work on a computer for four or more hours a day have more than double the risk of a cardiovascular disease event, like a heart attack, than those who spend less than two hours looking at a screen.

Long periods of sitting deplete the body’s supply of lipoprotein lipase, an enzyme that breaks down fat and prevents clogged arteries. If you spend most of your day plopped behind a desk, take a brief walk after every 20 minutes or try a standing desk. You can burn 30 percent more calories when you stand than when you sit. (Don't miss these 15 doctor-approved tips to prevent heart disease.)

(Yeah, doing this blog and my brain games is about 4-5 hours per day; not worried, my outdoor walking keeps me moving. And pee and water/coffee breaks mean doing steps in my 4 level condo, so moving quite regularly.)

3.  You log less than six hours of sleep each night©fizkes/Getty Images

Many adults struggle to get the recommended seven to nine hours of sleep each night, but consistently missing that mark could be bad for your heart. A study published in the Scandinavian Journal of Work, Environment & Health found that Japanese men who got less than six hours of sleep were five times more likely to have a heart attack than men who slept seven or eight hours a night. Don't miss what causes heart disease and how you can prevent it.

(Usually about 7 hours a night, starting at 2-3am. It's great being retired, getting up late is not a problem.

Reading in these 11 posts seems to consider napping very beneficial until you get longer than an hour.

• napping (11 posts to August 2014)

4.  You live in a smoggy area©Maik Mitschke / EyeEm/Getty Images

Smog is just as bad for your heart as it is for your lungs. For a 2016 study published in Environment International, researchers used hourly air pollution measurements in South Boston to determine how exposure to particulate matter (small combustion particles that come from fuel burning and vehicle emissions) affected patients in this area who had heart attacks.

They found that exposure to high concentrations of air pollution increased the likelihood of a heart attack by 48 percent in the two hours before patients first experienced heart attack symptoms. The risk went up to 69 percent when people were exposed to high levels of air pollution for 24 hours before the onset of symptoms. (Here are 9 more things you should know about heart attacks before you have one.)

(Nope.)

5.  It’s daylight saving time©SrdjanPav/Getty Images

Several studies have found that the risk of heart attack goes up the first few days after daylight saving time starts, reports the American Heart Association. One study by Swedish researchers found about a 6.7 percent greater risk of a heart attack in the first three days after we spring forward. U.S. researchers tracked hospital records and found a 24 percent increase in heart attacks on the Monday after the spring time change. The risk slowly dropped the rest of the week.

Since the total heart attack counts for those weeks were not drastically different from other weeks, researchers determined that the time changes didn’t necessarily make the heart attacks happen, but rather made them likely to occur sooner than they otherwise would have. This is probably due to disrupted sleep-wake cycles and increased stress at the start of a new week of work.

(Being retired means this really has no effect on me at all.)

6.  You’re divorced©simarik/Getty Images

Divorce can cause literal heartache and be a heart attack risk factor. Researchers at the Duke University School of Medicine conducted an 18-year-study of nearly 16,000 men and women between the ages of 45 and 80 who had been married at least once. Every two years, researchers assessed the participants’ marital status and overall health.

Divorced women were 25 percent more likely to have a heart attack than those who stayed married. Women who had two or more divorces were 77 percent more likely to have a heart attack.

As for the men, the risk of heart attack stayed the same regardless of whether they were married or divorced—at first. But if they divorced at least twice, their heart attack risk increased by 30 percent.

(Very happily divorced! 

 I'm sure my divorce vastly improved my chances of not getting dementia. My social connections have exploded since then. My epigenetic aging was vastly improved by getting divorced. 

My story; I would still be leading a life of quiet desperation.

Why my stroke was the best thing to ever happen to me)

7.  You live in an area with extreme temperatures©Jeff Greenough/Getty Images

Studies show that both extreme cold and extreme heat can put people at risk for heart attacks. Using data from cardiac patients in the Worcester Heart Attack Study, a study in the journal Epidemiology found that exposure to temperatures lower than 17 degrees F in the two days prior to a heart attack increased patients’ risk by 36 percent.

On the other end of the spectrum, British researchers found that once the temperature reaches 68 degrees F, each increase of 1.8 degree F increased the risk of heart attack by 2 percent over the next one to six hours. On the first day of a hot spell, that risk jumps up to 6.5 percent per 1.8 degree F increase.

(Central Michigan; while summers can get in the 90's, winters have definitely wimped out. In the 13 years living here, maybe 1 year the ground actually froze. I barely ever wear my heaviest winter coat. And with a condo, no snow shoveling or lawn work.)

8.  You lived through a natural disaster©Stocktrek Images/Getty Images

Having a hurricane or earthquake devastate your hometown not only affects you mentally and emotionally but physically as well. Researchers at Tulane Medical Center in New Orleans studied the number of patients that were admitted with heart-related problems in the years after Hurricane Katrina hit the area in 2005.

They found that the number of people admitted to the hospital for heart attacks increased three-fold in the 10 years after Katrina, compared to the number of admissions in 2003 and 2004. Patients were also more likely to have heart attack risk factors after the hurricane, including high blood pressure, coronary artery disease, and diabetes.

(Nope, never got close to being in a tornado.)

9.  You didn't go to college©Sengchoy Inthachack / EyeEm/Getty Images

The four or more years you spend in college may be good for more than a diploma. A study published in the International Journal for Equity in Health analyzed data from more than 267,000 Australian men and women.

The results showed that people with no certifications or degrees were more than twice at risk of a heart attack compared to those with a university degree or higher. Bottom line: The more time you spend in school, the lower your risk for a heart attack.

(Bachelor degrees in Data Processing and Accounting. Got within two courses of a master's in finance.)

10.  You got the flu©PixelsEffect/Getty Images

The American College of Cardiology has long recommended that those with heart disease get annual flu shots, but research shows just how important that shot is.

A 2018 study in the New England Journal of Medicine looked at 364 people hospitalized for heart attacks and found that they were six times more likely to have a heart attack in the week after being infected with the flu.

If you're feeling under the weather, look out for these 7 silent signs you're having a heart attack.

(Have regularly gotten flu shots for the last 20 years. The last time I remember getting the flu was probably 35 years ago.)

11.  Your mother had a heart attack©ER Productions Limited/Getty Images

Or maybe it was your father, or grandparent, or siblings. No matter which relative it was, the American Heart Association says that heart disease and risk factors for heart disease are strongly linked to family history.

There are at least 67 sites in the DNA sequence, or variants, that can increase your risk of a heart attack. Each of these variants raises your risk of cardiovascular disease by about 10 percent. But if you have more variants, your risk adds up.

The good news is, having a family history of heart attacks doesn't guarantee you will have one. Actively maintaining a healthy lifestyle can lower your overall risk. (Start with these 30 proven ways to reduce your risk of heart disease.)

(One grandparent died of a heart attack, one died of a stroke. Dad died of Parkinsons and dementia at 91. Mom still living alone at 96. I'm going to easily break 100 if I'm not too wild in my extracurricular activities. I had my stroke at age 50, so got that out of the way early.)