Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, June 27, 2026

Statins may trigger muscle side effects by activating inflammatory danger signals

 Friends have discontinued statins because of side effects and always have never been believed.

Statins may trigger muscle side effects by activating inflammatory danger signals

New experimental findings reveal how statins may push vulnerable muscle cells into a stress state, suggesting future strategies to reduce muscle symptoms without compromising cardiovascular protection.

A recent study published in the journal Science Advances uncovered biological mechanisms that drive muscle-related side effects following statin therapy. The researchers found that statins reduced isoprenoid production, protein prenylation, and yes-associated protein (YAP) signaling.

In experimental models, statins also activated nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasomes, promoted nuclear forkhead box O (FOXO) accumulation, and increased caspase-1 activity. These alterations increased atrogin-1 levels, promoted muscle atrophy, and reduced muscle function in experimental models. By better defining these pathways, the findings could inform future strategies to reduce statin-associated muscle effects while preserving cardiovascular benefit.

Healthcare providers routinely prescribe statin medications to people with lipid imbalances, such as elevated low-density lipoprotein (LDL) levels. These medications help reduce the risk of heart attacks, strokes, and death. However, some statin users experience muscle pain and weakness. Due to these side effects, they may take reduced doses or discontinue the drug altogether. These side effects may occur even when routine blood tests do not show evidence of muscle injury. However, the biological mechanisms underlying them are unclear. Most previous studies examined complications such as severe muscle toxicity and extensive muscle breakdown (rhabdomyolysis), but these are rarely observed among statin users.

About the Study

In the present study, researchers investigated why some people develop statin myopathy, or muscle-related side effects, following statin therapy. They developed a model of mild statin-related muscle problems for analysis. They exposed mouse muscle cells (C2C12 myotubes) to lipopolysaccharide (LPS), a bacterial component that stimulates the immune system. These LPS-primed cells developed an inflammasome-primed state and became much more sensitive to statins.

With LPS priming, a clinically relevant dose (1 μM) of fluvastatin increased atrogin-1 expression, an effect usually observed with 10 μM of the drug in cells without priming. As a result, lower statin doses could trigger molecular changes associated with muscle atrophy. Within 24 hours, atrogin-1 increased, followed by a decrease in muscle fiber diameter over 48 hours. In LPS-injected, statin-fed wild-type (WT) mice, fluvastatin reduced grip strength even though muscle mass did not decrease significantly, resembling the mild weakness experienced by many statin users. Human-derived muscle cells exposed to LPS and fluvastatin showed a reduction in actin alpha 1, skeletal muscle (ACTA1)-positive areas, indicating muscle-cell atrophy.

To investigate whether the muscle-related problems were due to cholesterol reduction or isoprenoid loss, the team added back an isoprenoid, geranylgeranyl pyrophosphate (GG). They then used 25-hydroxycholesterol to restore cellular cholesterol levels. They also used small interfering ribonucleic acid (siRNA) to reduce NLRP3 expression and MCC950 to inhibit NLRP3 inflammasome activity. The researchers compared the findings in WT mice, mice lacking the NLRP3 gene, and human-induced pluripotent stem cell (hiPSC)-derived myoblasts. Most mechanistic experiments focused on fluvastatin, although atorvastatin and cerivastatin supported a broader statin-class effect in LPS-primed muscle cells.

Results

The team found that statins block the mevalonate pathway that produces cholesterol, but this pathway also produces important molecules such as isoprenoids. A decrease in isoprenoid levels also reduces protein prenylation. These alterations lead to metabolic stress and act as danger signals that activate NLRP3 inflammasomes. Upon activation, the NLRP3 inflammasome initiates inflammatory signaling that contributes to muscle atrophy and cell death. Therefore, some side effects might arise from the loss of isoprenoids rather than from cholesterol reduction itself.

Statin-fed WT mice exhibited more damaged muscle fibers, including centrally nucleated fibers, a hallmark of muscle injury and repair. These animals also contained necrotic myofibers. Mice lacking NLRP3 contained about 50% fewer abnormal muscle fibers and showed fewer signs of muscle damage and repair. These findings suggest that NLRP3 contributes considerably to statin-induced muscle injury.

Restoring isoprenoid levels with GG and inhibiting NLRP3 signaling in cellular models reduced muscle atrophy-related changes, further implicating these pathways in statin-associated muscle injury. Likewise, genetic deletion of NLRP3 protected mice from statin-induced muscle abnormalities. Upon GG addition, atrogin-1 levels decreased, and the reduction in phosphorylated FOXO was prevented, improving muscle-cell size.

Reduced protein prenylation impaired YAP, a protein that helps maintain muscle mass and function in skeletal muscles. Statins also altered muscle-cell metabolism by reducing glycolysis, a process that generates energy from glucose in cells. Reduced glycolysis may act as a metabolic danger signal capable of activating the NLRP3 inflammasome. Experiments using hiPSC-derived myoblasts supported the pathway changes observed in mouse cells and mice.

Conclusions

The findings suggest that statins may contribute to muscle weakness and atrophy by reducing isoprenoid levels and protein prenylation and activating NLRP3 inflammasome signaling. Statins also altered proteins involved in muscle growth and function and reduced glycolysis.

The findings suggest that the muscle-related effects are linked to impaired prenylation and inflammatory signaling rather than cholesterol reduction itself. If confirmed in future human studies, including research on inflammatory priming and gut-barrier-related signals, scientists could develop strategies to block NLRP3 inflammasome activation, modulate YAP-linked pathways, or carefully evaluate isoprenoid-related rescue approaches. These approaches could help mitigate muscle-related side effects without compromising statins' cholesterol-lowering benefits.

Download your PDF copy by clicking here.

Drug-induced ‘brain freeze’ could slow stroke damage, study finds

 

Have your competent? doctor and hospital initiate research that finishes the job and delivers 100% recovery protocols! Why can't that be done?

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!

Drug-induced ‘brain freeze’ could slow stroke damage, study finds

Drug-induced hypometabolism may slow stroke-related brain damage, according to early research involving animals and people.

The experimental treatment uses two existing medicines to reduce metabolism and create a state resembling hypothermia.

Tests in mice and rhesus monkeys found that the approach protected brain tissue, while an early trial involving 32 stroke patients reported no notable side effects.

The treatment combined chlorpromazine, an antipsychotic medicine, with the sedative promethazine. The combination was known as C+P.

The small human trial found no significant improvements in the amount of brain damage or participants’ ability to carry out daily activities independently.

Further studies will be needed to establish what benefits the treatment might offer people who have experienced strokes.

The research also provided more information about the role of hypometabolism, when the body uses less energy, in the protective effects associated with hypothermia.

Dr Eric Landsness, assistant professor of neurology at Washington University School of Medicine in St Louis, was not involved in the research.

He said: “What’s exciting about this study is that it’s clear that it’s not just the hypothermia, but it’s the hypometabolism.”

The researchers tested C+P as a treatment for acute ischaemic stroke, which occurs when blood flow to the brain is suddenly blocked.

Ischaemic strokes account for more than 85 per cent of strokes. The acute form is a medical emergency involving the sudden loss of blood flow and neurological function.

Restoring blood flow through reperfusion treatment can cause further damage through processes that began while the brain was deprived of blood.(That's called the neuronal cascade of death and will kill off hundreds of millions of neurons in the first week!; noted by Rockefeller University back in 2008! And you incompetently don't know that?)

Dr Patrick Lyden, professor of physiology and neuroscience, neurology and neurosurgery at the University of Southern California Keck School of Medicine, was not involved in the study.

He said: “You can get significant injury from a lot of processes that were set in motion during the ischaemia.”

Researchers have previously examined whether hypothermia could protect brain tissue from damage caused by both ischaemia and the return of blood flow.

Lyden described hypothermia as “one of the most powerful ways of protecting the brain that we’ve ever studied in lab animals”.

He added: “It’s the standard by which all other brain protectants are measured.”

Hypothermia occurs when body temperature falls below 35°C.

Under normal circumstances, it can be dangerous because the cold may slow the heart and nervous system enough to cause cardiac and respiratory failure.

One theory behind its therapeutic effects is that cooling slows metabolism in a similar way to hibernation.

Lyden said slowing metabolism could also delay the process of brain-cell death.

Therapeutic hypothermia can protect the brain following cardiac arrest and is sometimes used to treat newborn babies with hypoxic-ischaemic encephalopathy.

This is a brain injury caused by reduced oxygen and blood flow around the time of birth.

However, studies of hypothermia in adults who have experienced strokes have produced less encouraging results.

The researchers suggested C+P might provide a more effective way to slow metabolism in stroke patients.

Earlier experiments found that the combination reduced inflammation in the nervous system in rodent stroke models, possibly through metabolic changes that were independent of hypothermia.

In the new study, researchers compared C+P with two other ways of lowering body temperature in mice: adenosine 5’-monophosphate and surface cooling using cold water and ice packs.

All three approaches caused hypothermia, but only C+P reduced overall oxygen consumption and energy expenditure, two signs of slower metabolism.

Landsness said the findings suggested metabolism was more than a secondary effect of hypothermia and should be studied in its own right.

In mice, C+P reduced the burning of sugar by the brain and brown fat, tissue that burns fuel to produce heat.

The treatment was also linked to less brain tissue damage and lower lactate accumulation after stroke. Lactate can build up and contribute to cell death.

Similar effects were observed in rhesus monkeys treated with C+P.

The small human trial suggested that the metabolic effects could also occur in people.

Patients given the highest dose had lower levels of metabolism-related proteins in their blood.

They were also the only participants to experience a significant fall in body temperature four hours after treatment, although their temperatures did not reach the level defined as hypothermia.

Temperatures did fall to that level in the mice and monkeys.

The participants also received standard treatments to restore blood flow to the brain.

C+P did not reduce the amount of brain damage detected 72 hours after treatment or improve independence in daily activities after 90 days.

The study authors, based at Capital Medical University in Beijing, did not respond to a request for comment.

They said future trials could establish whether C+P protects the brain following a stroke.

Although the treatment caused no notable side effects in the early human trial, Lyden said the medicines could potentially interact and cause muscle spasms, seizures or changes in heart rhythm.

He suggested that researchers may need to find other medicines capable of slowing metabolism without these potential risks.

Landsness said: “The new paper happened to fall upon a drug [combo] that happens to induce hypothermia and hypometabolism, but we don’t necessarily know why.”

Further research will be needed to understand how the drugs produce these effects.

Landsness’s laboratory is studying the neural circuits involved in hypothermia and hypometabolism, which could identify other targets for treatment.

This everyday drink is linked to an 18% lower risk of dementia, according to a 43-year study

 Gee, this as been known for years and YOUR INCOMETENT? DOCTOR STILL HASN'T INSTALLED A 24-HOUR COFFEE STATION!

How did you manage to miss that caffeine is likely not the beneficial compound?

The coffee benefits have been out there for years!     IF YOUR DOCTOR WAS COMPETENT AT ALL A 24 HOUR COFFEE STATION WOULD HAVE ALREADY BEEN INSTALLED! Since nothing was done your board of directors is so incompetent they don't know they have incompetent persons working for them?


I do coffee all day, takes that long to get in a 12 cup pot of coffee. This won't change my habit, it's mainly to reduce my dementia and Parkinsons risk and no one knows the amounts for that.

I'm still doing a 12 cup pot of coffee daily to prevent Parkinsons and frailty! Much more important than any problems it can cause.

How coffee protects against Parkinson’s Aug. 2014 

Coffee May Lower Your Risk of Dementia Feb. 2013

Coffee drinkers rejoice! Drinking coffee could lower the risk of Alzheimer’s disease 

And this: Coffee's Phenylindanes Fight Alzheimer's Plaque December 2018

New research suggests drinking coffee may reduce the risk of frailty May 2025

I think I'm in this category:  I never get the jitters or flushed skin.

Genetics determine how much coffee you can drink before it goes wrong

I'm doing a 12 cup pot of coffee a day with full fat milk to lessen my chances of dementia and Parkinsons. Tell me EXACTLY how much coffee to drink for that and I'll change. Yep, that is a lot more than the 400mg. suggested limit, I don't care! Preventing dementia and Parkinsons is vastly more important than whatever problems it can cause! 

Of course, your fuckingly incompetent? doctor did nothing with this from 2+ years ago! And still hasn't created a 24 hour coffee station

This line is great: The findings indicate that even the Espresso Martini cocktail contains the espresso's beneficial compounds - and can contribute to staving off dementia.

The latest here: 

This everyday drink is linked to an 18% lower risk of dementia, according to a 43-year studyResearchers followed nearly 132,000 adults for decades, tracking diet and health outcomes to uncover patterns in long-term cognitive decline.

Key Points

  • A decades-long study of nearly 132,000 people found that higher consumption of caffeinated coffee and tea was associated with an 18% lower risk of dementia, along with better cognitive performance. No similar benefits were observed among decaf drinkers.
  • Experts say the link may be due to caffeine and other compounds in coffee and tea, which are associated with lower inflammation and reduced oxidative stress.
  • The FDA recommends that generally healthy adults limit caffeine intake to no more than 400 milligrams per day, or about four-and-a-half eight-ounce cups of coffee.

Many people rely on a cup of coffee to wake up in the morning, and new research suggests the daily habit could offer more than just a pick-me-up. The study, which analyzed 43 years of data, found that a daily coffee habit is linked to a significantly reduced risk of dementia.

“Dementia is a growing public health concern, and coffee and tea are things many people drink every day,” said Yu Zhang, MBBS, the lead study author and a researcher at the Harvard University T.H. Chan School of Public Health. “We wanted to see whether these common habits might be linked to better brain health over the long term.”

It’s important to stress that the study found a link — it doesn’t definitively prove that your daily cup will ward off dementia. But doctors said the findings are worth paying attention to. “It’s useful information, and it helps us to know that having a caffeinated beverage or two each day may be in our best interests,” said Anna Hohler, MD, director of neurology for Northwell’s Westchester Region. Here’s why. 

What a decades-long study reveals about coffee, tea, and brain health

The study, published in JAMA, analyzed data from nearly 132,000 people who participated in the Nurses’ Health Study and the Health Professionals Follow-Up Study, both of which are long-term biomedical databases. 

Each participant answered questions about their diet every two to four years, and their health data was tracked for up to 43 years. During the study, 11,033 people were diagnosed with dementia. After analyzing dietary and health data, the researchers found that participants who consumed higher levels of caffeinated coffee and tea had an 18% lower risk of developing dementia than those who consumed little to no caffeine. 

Related: No Amount of Alcohol Is Safe for Your Brain, New Landmark Study Finds

Consuming caffeinated coffee and tea was also linked to a lower risk of developing cognitive decline, a gradual worsening of mental function usually associated with age. Coffee-drinking participants also performed better on cognitive function tests. 

The researchers didn’t observe the same benefits among decaf coffee drinkers, suggesting the benefits were related to caffeine, though it's unclear whether caffeine was the only factor at work.

How coffee and tea could support brain health over time

This isn’t the only study linking coffee to a lower risk of dementia. A scientific review and data analysis published in the Journal of Lifestyle Medicine in 2023 found that people who regularly drank one to four cups of coffee a day had a “significantly” lower risk of developing Alzheimer’s disease. However, those who drank more than four cups of coffee a day had an increased risk of developing the disease. 

Related: Regularly Eating Breakfast Could Shield You Against Age-Related Brain Changes, Study Finds

Doctors suggest there are likely a few reasons for this association. “It could be that caffeine is lowering the levels of harmful proteins—amyloid—in the brain, reducing inflammation, or helping brain cells be more adaptable,” said Amalia Peterson, MD, a behavioral neurologist and assistant professor of Neurology at Vanderbilt University Medical Center. “Caffeine is also linked to a reduced risk of type 2 diabetes, which is a risk factor for dementia, and this could help explain this association.”

Coffee may also contain compounds that can help reduce oxidative stress, an imbalance between free radicals and the body’s ability to eliminate them that’s linked to a range of chronic illnesses, Zhang said.

“Caffeine is probably one important part of the story, especially since we saw benefits with caffeinated coffee and tea but not decaf,” Zhang continued. “But it’s likely not just one compound. Coffee and tea also contain polyphenols and other bioactive compounds, so it may be a combination working together rather than one single ingredient.”

What are the other benefits of caffeine?

Caffeine may have many benefits when used in moderation. “Caffeine can improve reaction time, attention, and perceived energy, which has practical benefits for daily functioning,” Keatley says. “It is also associated with improved exercise performance and may support metabolic rate modestly.”

Caffeinated coffee could potentially help you live longer, too. A 2025 study published in The Journal of Nutrition found a link between drinking caffeinated coffee and a lower risk of death over the 11-year study period. The benefits were limited to black coffee and coffee with just a little added sugar. 

Can other sources of caffeine provide the same perks?

The study didn’t investigate beverages outside of coffee and black tea, but Scott Keatley, RD, co-founder of Keatley Medical Nutrition Therapy, said it’s possible that other caffeinated beverages, such as matcha, may offer similar benefits. “Matcha and [black] tea contain caffeine, along with catechins like EGCG and the amino acid L-theanine, which may support attention and reduce neural stress,” he said. “The profile is different from coffee, but the combination of mild stimulation and high antioxidant content could produce similar long-term effects.”

Hohler agrees. “Theoretically, we would expect matcha to have the same properties,” she said. It’s unclear how more-processed caffeinated beverages, such as energy drinks, would affect dementia risk.

“Different beverages have very different overall compositions — things like sugar content, processing, and what other compounds come along with the caffeine all matter,” Zhang said.

The recommended daily limit for caffeine, explained

According to the U.S. Food and Drug Administration, it’s recommended that generally healthy individuals consume no more than 400 milligrams of caffeine per day. 

The amount of caffeine in a cup of coffee varies by type and brew strength. However, this roughly translates to limiting yourself to four-and-a-half eight-ounce cups of coffee, or up to three 12-ounce cups. Ultimately, the study makes the case for enjoying coffee as part of a balanced diet. “It’s not a reason to overdo it, but it is reassuring for people who already enjoy these drinks,” Zhang said.

Reviewed by

Lauren Manaker MS, RDN, LD, CLEC: Lauren is an award-winning registered dietitian and three-time book author, with more than 22 years in the field.

Read the original article on Food & Wine

MMH recognized for its commitment to excellence in cardiovascular care for 6 years in a row

 Two absolute stupidities here: 

  1. Stroke has been called neurological disease by the WHO since 2006 not cardiovascular, once again proving our medical 'professionals' don't keep up to date in their field! Why would your trust anything coming out of such incompetence?
  2. And 'care'; Survivors don't care about 'care; THEY WANT 100% RECOVERY! ARE YOU THAT FUCKING STUPID?

MMH recognized for its commitment to excellence in cardiovascular care for 6 years in a row


  • Midland Memorial Hospital has received two American Heart Association Get With The Guidelines achievement awards for following evidence-based treatment guidelines to improve patient outcomes and reduce hospital readmissions.

Midland Memorial Hospital (MMH) has received two American Heart Association Get With The Guidelines achievement awards for demonstrating a commitment to following up-to-date, research-based guidelines for the treatment of heart disease and stroke, helping save lives, support recovery and reduce hospital readmissions.

Heart disease and stroke are the No. 1 and No. 4 causes of death in the United States, respectively, according to the American Heart Association's 2026 Heart Disease and Stroke Statistics Report.

Studies show patients can experience better outcomes when care(NOT RECOVERY!) teams consistently follow evidence-based treatment guidelines.

Get With The Guidelines puts the expertise of the American Heart Association and American Stroke Association to work for hospitals nationwide, helping ensure patient care(NOT RECOVERY!) is aligned with the latest science-backed guidelines. As a participant in the Get With The Guidelines programs, MMH qualified for the awards by demonstrating a sustained commitment to improving the quality of cardiovascular care(NOT RECOVERY!).

"MMH is committed to delivering high-quality care(NOT RECOVERY!) by adhering to the latest treatment guidelines and streamlining processes to ensure timely, appropriate care(NOT RECOVERY!) for heart attacks and strokes," Stephen Bowerman, president/chief executive officer, said in a news release. "Get With The Guidelines programs help our teams put proven science into practice every day, supporting better outcomes so more people in the greater Midland area can live longer, healthier lives."

This year, Midland Memorial Hospital received these achievement awards:

* Get With The Guidelines-Coronary Artery Disease STEMI Receiving Gold with Target: Type 2 Diabetes

* Get With The Guidelines-Coronary Artery Disease NSTEMI Gold with Target: Type 2 Diabetes

"These awards reflect MMH's commitment to caring for people in their community who need cardiovascular care(NOT RECOVERY!)," said Karen E. Joynt Maddox, M.D., MPH, chair of the American Heart Association Quality Oversight Committee. "By following the American Heart Association's quality improvement protocols, MMH can help advance our shared vision of better patient outcomes, fewer readmissions and lower mortality rates — a win for patients, families and health care(NOT RECOVERY!) systems.

The post MMH recognized for its commitment to excellence in cardiovascular care(NOT RECOVERY!) for 6 years in a row appeared first on Odessa American.(So 6 years of incompetence in not knowing shit about stroke!)

Friday, June 26, 2026

The best vegetable for metabolic health, according to an endocrinologist

 Of course your incompetent? doctor hasn't had the dietician create any form of diet protocol for you, right? So this won't show up in your hospital food or your suggested diet at home!

The best vegetable for metabolic health, according to an endocrinologist

One vegetable that checks all the boxes for metabolic health is broccoli.

Reviewed by Dietitian Jane Leverich, M.S., RDN

Key Points

  • Metabolic health consists of how well our cells are process glucose and inflammatory compounds.
  • According to an endocrinologist, broccoli is the best vegetable to support metabolic health.
  • Broccoli delivers antioxidants that help combat inflammation and fiber that supports gut health.

Unlike heart health or gut health, metabolic health can feel a bit more abstract. “When we talk about metabolic health, we’re really talking about how efficiently our body’s cellular engines are functioning,” says Chhaya Makhija, M.D., DipABLM, a triple-board certified endocrinologist.  Another way to think about it, she says, is how well our cells process glucose, fats, cholesterol and inflammatory compounds and carry out the many functions required to maintain energy and overall health.

One of the best ways to support those cellular engines is by eating more vegetables. “Different vegetables provide different fibers, antioxidants, phytonutrients, vitamins and minerals that work together to support our health,” says Makhija. But one vegetable that may be particularly beneficial for metabolic health is broccoli. Read on to learn why broccoli earned an endocrinologist’s top pick.

Related: I Test Kitchen Gear for a Living—These Are the Amazon Deals I’d Never Pass Up, and You Have Hours to Grab Them

Why Broccoli Tops the List for Metabolic Health

It Contains Compounds That Fight Inflammation

Oxidative stress and chronic inflammation are two factors that can interfere with metabolic health. Though inflammation progresses quietly, it is linked to various chronic diseases and can make it more difficult for the body to regulate blood sugar, cholesterol and blood pressure. The good news is that eating broccoli may help keep inflammation in check. 

Broccoli contains a variety of bioactive compounds—including sulforaphane, quercetin and flavonoids—that have been associated with antioxidant and anti-inflammatory benefits, says Lauren Harris-Pincus, M.S., RDN. This mighty green veggie is also a surprisingly rich source of vitamin C, another potent antioxidant. In fact, a ½-cup serving of cooked broccoli provides more than half of the Daily Value for vitamin C.,

It Supports a Healthy Gut Microbiome

“The gut microbiome plays a much larger role in metabolism than many people realize, influencing everything from glucose regulation to inflammation and overall health,” says Makhija.

Eating more veggies like broccoli is one of the best ways to support gut health. For starters, broccoli is a good source of fiber, which supports digestive health and helps maintain a healthy gut microbiome—creating a more favorable metabolic environment, according to Makhija.

In fact, 1 cup of cooked broccoli provides an impressive 5 grams of fiber. What’s more, research suggests that eating broccoli may positively influence the composition of the gut microbiome. Because broccoli contains prebiotic fiber, it may help support the growth of beneficial gut bacteria.

It’s a Great Choice for Heart Health

When metabolic health is impaired, it can create a domino effect that increases the likelihood of high blood pressure, low HDL (“good”) cholesterol, high triglycerides and elevated blood sugar levels, all of which are associated with a greater risk of heart disease. Broccoli provides several nutrients and compounds that may help support these aspects of cardiometabolic health.

For starters, the fiber in broccoli may help lower cholesterol and support healthy blood sugar levels. The glucosinolates and polyphenols in broccoli also have antioxidant and anti-inflammatory properties, which may help protect blood vessels from oxidative stress. Finally, this cruciferous vegetable naturally contains nitrates, compounds that can help support healthy blood flow and blood pressure. In other words, adding broccoli to your plate may offer multiple benefits for heart health.

It Supports a Balanced Plate

Another reason to add broccoli to your plate is that it can help create a more balanced eating pattern. “I frequently encourage patients to build their plates around vegetables first, because doing so naturally helps reduce reliance on highly processed foods, refined carbohydrates and foods with hidden sugars,” says Makhija. 

One helpful rule of thumb is to fill at least half of your plate with nonstarchy vegetables like broccoli. “In many ways, vegetables are foundational to metabolic health because they nourish both our cells and our gut while supporting healthier eating patterns overall,” she adds. 

Ways to Enjoy Broccoli

Ready to add more broccoli to your plate? Here are some delicious ways to enjoy it: 

  • Toss it into a salad. Broccoli makes a sturdy, fiber-rich base for salads and holds up well in the fridge without getting soggy. Pair it with a creamy or savory dressing and plenty of toppings, like nuts and cheese. 
  • Mix it into pasta or casseroles. If broccoli’s strong flavor has been holding you back, try adding it to mixed dishes like pasta or casseroles instead of serving it as a stand-alone side.
  • Roast it. Toss raw broccoli florets with olive oil and seasonings, then roast until tender with crispy edges and deeper flavor. For an easy dinner, roast broccoli on the same sheet pan as potatoes and your protein of choice.
  • Blend it into soups. Steam broccoli until soft and blend it into soups and stews. You can also blitz it in a food processor to make a higher-fiber broccoli pesto for pasta.

Other Tips for Supporting Metabolic Health

Eating more broccoli—and more vegetables in general—is a great first step toward supporting metabolic health. Here are a few other habits that may help:

  • Focus on fiber. “Approximately 95% of Americans miss the mark on fiber intake, which is an important factor in gut health and the prevention of lifestyle diseases like heart disease, diabetes and cancer. Focus on fiber-rich plant foods, including produce, whole grains, beans/pulses, nuts and seeds,” says Harris-Pincus.
  • Prioritize sleep. Diet isn’t the only factor that influences metabolic health—sleep matters too. “Sleep disruption affects multiple hormonal pathways and can contribute to insulin resistance, higher cortisol spikes, increased appetite, blood pressure changes and greater glucose variability,” says Makhija. She recommends maintaining a consistent sleep schedule with regular bedtimes and wake-up times to help support adequate rest.
  • Manage stress. Don’t overlook the negative health effects of chronic stress. Like inadequate sleep, ongoing stress can affect many of the same hormonal pathways involved in metabolism, says Makhija. “This doesn’t mean eliminating stress—which is impossible—but rather building tools to manage it more effectively.”

Our Expert Take

If there’s one vegetable that stands out for metabolic health, it’s broccoli. This tasty and versatile veggie delivers antioxidants that help combat inflammation, fiber that supports a healthy gut and key nutrients that promote heart health. Still, as much as broccoli has to offer, it’s important to keep in mind that no single food can transform your metabolic health on its own. “Metabolic health is not built through one food, one supplement or one exercise program. It is the result of daily habits that support our hormones, our metabolism and our overall well-being,” says Makhija.

Read the original article on EatingWell