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Blood pressure 94 54: Low blood pressure (hypotension) – Symptoms and causes


Low blood pressure (hypotension) – Symptoms and causes


Low blood pressure might seem desirable, and for some people, it causes no problems. However, for many people, abnormally low blood pressure (hypotension) can cause dizziness and fainting. In severe cases, low blood pressure can be life-threatening.

A blood pressure reading lower than 90 millimeters of mercury (mm Hg) for the top number (systolic) or 60 mm Hg for the bottom number (diastolic) is generally considered low blood pressure.

The causes of low blood pressure can range from dehydration to serious medical disorders. It’s important to find out what’s causing your low blood pressure so that it can be treated.

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For some people, low blood pressure signals an underlying problem, especially when it drops suddenly or is accompanied by signs and symptoms such as:

  • Dizziness or lightheadedness
  • Fainting
  • Blurred or fading vision
  • Nausea
  • Fatigue
  • Lack of concentration


Extreme hypotension can result in this life-threatening condition. Signs and symptoms include:

  • Confusion, especially in older people
  • Cold, clammy, pale skin
  • Rapid, shallow breathing
  • Weak and rapid pulse

When to see a doctor

If you have signs or symptoms of shock, seek emergency medical help.

If you have consistently low blood pressure readings but feel fine, your doctor will likely just monitor you during routine exams.

Even occasional dizziness or lightheadedness may be a relatively minor problem — the result of mild dehydration from too much time in the sun or a hot tub, for example. Still, it’s important to see your doctor if you have signs or symptoms of low blood pressure because they can point to more-serious problems. It can be helpful to keep a record of your symptoms, when they occur and what you’re doing at the time.


Blood pressure is a measurement of the pressure in your arteries during the active and resting phases of each heartbeat.

  • Systolic pressure. The top number in a blood pressure reading is the amount of pressure your heart produces when pumping blood through your arteries to the rest of your body.
  • Diastolic pressure. The bottom number in a blood pressure reading refers to the amount of pressure in your arteries when your heart is at rest between beats.

Current guidelines identify normal blood pressure as lower than 120/80 mm Hg.

Blood pressure varies throughout the day, depending on:

  • Body position
  • Breathing rhythm
  • Stress level
  • Physical condition
  • Medications you take
  • What you eat and drink
  • Time of day

Blood pressure is usually lowest at night and rises sharply on waking.

Blood pressure: How low can you go?

What’s considered low blood pressure for you may be normal for someone else. Most doctors consider blood pressure too low only if it causes symptoms.

Some experts define low blood pressure as readings lower than 90 mm Hg systolic or 60 mm Hg diastolic. If either number is below that, your pressure is lower than normal.

A sudden fall in blood pressure can be dangerous. A change of just 20 mm Hg — a drop from 110 systolic to 90 mm Hg systolic, for example — can cause dizziness and fainting when the brain fails to receive enough blood. And big drops, such as those caused by uncontrolled bleeding, severe infections or allergic reactions, can be life-threatening.

Conditions that can cause low blood pressure

Medical conditions that can cause low blood pressure include:

  • Pregnancy. Because the circulatory system expands rapidly during pregnancy, blood pressure is likely to drop. This is normal, and blood pressure usually returns to your pre-pregnancy level after you’ve given birth.
  • Heart problems. Some heart conditions that can lead to low blood pressure include extremely low heart rate (bradycardia), heart valve problems, heart attack and heart failure.
  • Endocrine problems. Parathyroid disease, adrenal insufficiency (Addison’s disease), low blood sugar (hypoglycemia) and, in some cases, diabetes can trigger low blood pressure.
  • Dehydration. When your body loses more water than it takes in, it can cause weakness, dizziness and fatigue. Fever, vomiting, severe diarrhea, overuse of diuretics and strenuous exercise can lead to dehydration.
  • Blood loss. Losing a lot of blood, such as from a major injury or internal bleeding, reduces the amount of blood in your body, leading to a severe drop in blood pressure.
  • Severe infection (septicemia). When an infection in the body enters the bloodstream, it can lead to a life-threatening drop in blood pressure called septic shock.
  • Severe allergic reaction (anaphylaxis). Common triggers of this severe and potentially life-threatening reaction include foods, certain medications, insect venoms and latex. Anaphylaxis can cause breathing problems, hives, itching, a swollen throat and a dangerous drop in blood pressure.
  • Lack of nutrients in your diet. A lack of the vitamin B-12, folate and iron can keep your body from producing enough red blood cells (anemia), causing low blood pressure.

Medications that can cause low blood pressure

Some medications can cause low blood pressure, including:

  • Water pills (diuretics), such as furosemide (Lasix) and hydrochlorothiazide (Microzide, others)
  • Alpha blockers, such as prazosin (Minipress)
  • Beta blockers, such as atenolol (Tenormin) and propranolol (Inderal, Innopran XL, others)
  • Drugs for Parkinson’s disease, such as pramipexole (Mirapex) or those containing levodopa
  • Certain types of antidepressants (tricyclic antidepressants), including doxepin (Silenor) and imipramine (Tofranil)
  • Drugs for erectile dysfunction, including sildenafil (Revatio, Viagra) or tadalafil (Adcirca, Alyq, Cialis), particularly when taken with the heart medication nitroglycerin (Nitrostat, others)

Types of low blood pressure

Doctors often break down low blood pressure (hypotension) into categories, depending on the causes and other factors. Some types of low blood pressure include:

  • Low blood pressure on standing up (orthostatic or postural) hypotension). This is a sudden drop in blood pressure when you stand up from a sitting position or after lying down.

    Gravity causes blood to pool in your legs when you stand. Ordinarily, your body compensates by increasing your heart rate and constricting blood vessels, thereby ensuring that enough blood returns to your brain.

    But in people with orthostatic hypotension, this compensating mechanism fails and blood pressure falls, leading to dizziness, lightheadedness, blurred vision and even fainting.

    Orthostatic hypotension can occur for various reasons, including dehydration, prolonged bed rest, pregnancy, diabetes, heart problems, burns, excessive heat, large varicose veins and certain neurological disorders.

    A number of medications also can cause orthostatic hypotension, particularly drugs used to treat high blood pressure — diuretics, beta blockers, calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors — as well as antidepressants and drugs used to treat Parkinson’s disease and erectile dysfunction.

    Orthostatic hypotension is especially common in older adults, but it also affects young, otherwise healthy people who stand up suddenly after sitting with their legs crossed for long periods or after squatting for a time.

  • Low blood pressure after eating (postprandial hypotension). This drop in blood pressure occurs one to two hours after eating and affects mostly older adults.

    Blood flows to your digestive tract after you eat. Ordinarily, your body increases your heart rate and constricts certain blood vessels to help maintain normal blood pressure. But in some people these mechanisms fail, leading to dizziness, faintness and falls.

    Postprandial hypotension is more likely to affect people with high blood pressure or autonomic nervous system disorders such as Parkinson’s disease.

    Eating small, low-carbohydrate meals; drinking more water; and avoiding alcohol might help reduce symptoms.

  • Low blood pressure from faulty brain signals (neurally mediated hypotension). This disorder, which causes a blood pressure drop after standing for long periods, mostly affects young adults and children. It seems to occur because of a miscommunication between the heart and the brain.
  • Low blood pressure due to nervous system damage (multiple system atrophy with orthostatic hypotension). Also called Shy-Drager syndrome, this rare disorder has many Parkinson disease-like symptoms. It causes progressive damage to the autonomic nervous system, which controls involuntary functions such as blood pressure, heart rate, breathing and digestion. It’s associated with having very high blood pressure while lying down.

Risk factors

Low blood pressure (hypotension) can occur in anyone, though certain types of low blood pressure are more common depending on your age or other factors:

  • Age. Drops in blood pressure on standing or after eating occur primarily in adults older than 65. Neurally mediated hypotension primarily affects children and younger adults.
  • Medications. People who take certain medications, for example, high blood pressure medications such as alpha blockers, have a greater risk of low blood pressure.
  • Certain diseases. Parkinson’s disease, diabetes and some heart conditions put you at a greater risk of developing low blood pressure.


Even moderate forms of low blood pressure can cause dizziness, weakness, fainting and a risk of injury from falls.

And severely low blood pressure can deprive your body of enough oxygen to carry out its functions, leading to damage to your heart and brain.

Sept. 22, 2020

Low Blood Pressure | NHLBI, NIH

Blood pressure is the force of blood pushing against the walls of your arteries as the heart pumps blood. It is usually described as two numbers: systolic and diastolic. The numbers record blood pressure in millimeters of mercury (mm Hg), with systolic listed above diastolic. For most adults, a healthy blood pressure is usually less than 120/80 mm Hg. Low blood pressure is blood pressure that is lower than 90/60 mm Hg.

Some people have low blood pressure all the time, and it is normal for them. Other people experience a sudden drop in blood pressure or have low blood pressure that may be linked to a health problem. Many systems of the body, including organs, hormones, and nerves, regulate blood pressure. For example, the autonomic nervous system sends the “fight-or-flight” signal that, depending on the situation, tells the heart and other systems in the body to increase or decrease blood pressure. Problems with the autonomic nervous system, such as in Parkinson’s disease, can cause low blood pressure.

Other causes of low blood pressure include medicines, bleeding, aging, and conditions such as dehydration, pregnancy, diabetes, and heart problems. Older adults have a higher risk for symptoms of low blood pressure, such as falling, fainting, or dizziness upon standing up or after a meal. Older adults are also more likely to develop low blood pressure as a side effect of medicines taken to control high blood pressure.

For many people, low blood pressure goes unnoticed. Others feel light-headed, confused, tired, or weak. You may have blurry vision, a headache, neck or back pain, nausea, or heart palpitations. Sitting down may relieve these symptoms. If blood pressure drops too low, the body’s vital organs do not get enough oxygen and nutrients. When this happens, low blood pressure can lead to shock, which requires immediate medical attention. Signs of shock include cold and sweaty skin, rapid breathing, a blue skin tone, or a weak and rapid pulse. If you notice signs of shock in yourself or someone else, call 9-1-1.

Your doctor will use a blood pressure test to diagnose low blood pressure. Other tests may include blood, urine, or imaging tests and a tilt table test if you faint often. You may not need treatment for low blood pressure. Depending on your signs and symptoms, treatment may include drinking more fluids, taking medicines to raise your blood pressure, or adjusting medicines that cause low blood pressure. Recommended lifestyle changes include changing what and how you eat and how you sit and stand up. Your doctor may also recommend compression stockings if you have to stand for long periods.

Visit Low Blood Pressure for more information about this topic.

Understanding Blood Pressure [Ultimate BP by Age Chart]

We all know that understanding blood pressure & maintaining healthy readings are important for our overall health and longevity. After all, it’s one of the most talked about indicators of health, particularly when it comes to your heart.

But what exactly is blood pressure? Do you know what your blood pressure numbers mean? Compare your measurements to the charts below and read about understanding blood pressure readings.

Nov. 2017 American Heart Association New Blood Pressure Chart Guidelines and Updates:

The American Heart Association recently released a new set of stricter guidelines. Changing the numbers means that more Americans will now meet the guidelines for high blood pressure, also known as hypertension. Here are some of the changes:

  • Greater Emphasis on Measurements
    • The AHA is putting more pressure on Americans to stay on top of their readings. They recommend that routine measurements are taken on a regular basis at home, and not just at the doctor’s office..
  • Guidelines Remove “Prehypertension”
    • By eliminating the Prehypertension category, more Americans now fall into the range of high blood pressure. The goal behind these changes is to initiate prevention, evaluation, and treatment of higher numbers far sooner than in the past.
  • New “Elevated” Blood Pressure
    • Measurements ranging from 120-129 mm Hg (systolic) and less than 80 mm Hg (diastolic)
  • Hypertension Stage 1
    • Previously defined as greater than 140 to 153 mm Hg (systolic) over 90 to 96 mm Hg (diastolic)
    • New definition = 130 to 139 mm Hg (systolic) over 80 to 89 mm Hg (diastolic)
  • Hypertension Stage 2

    • Previously defined as greater than 160 mm Hg (systolic) over 100 mm Hg (diastolic)
    • New definition = 140/90 mm Hg or greater

General Blood Pressure Ranges

The chart below provides a general overview of blood pressure ranges updated to match the new American Heart Association guidelines. Take your blood pressure and identify your systolic & diastolic readings to compare ranges on the chart, OR enter your results in the blood pressure calculator to learn more about causes, symptoms, and treatment for your blood pressure readings

Keep in mind that it is possible for your readings to be affected by other factors like age, medication, & sometimes even gender. Check out the chart below for a breakdown of blood pressure ranges by age.

Remember, your blood pressure is recorded as two numbers – systolic and diastolic – diagnosing high or low blood pressure only requires one of these numbers to be outside of the healthy range.

Blood Pressure Chart by Category:

The categories above are based off the official American Heart Association blood pressure guidelines, which were recently updated in November of 2017 ( Chart Reference)

*For proper blood pressure diagnosis, talk to your primary care physician or cardiologist

Looking to track your blood pressure? Understand your readings and learn ways you can improve your blood pressure with our FREE PDF. Download it Now!

Blood Pressure Calculator: Understanding your Blood Pressure Numbers

Please remember that for an official blood pressure diagnosis and treatment regimen, you must consult your primary physician or medical care professional  who will do a thorough assessment to determine the proper diagnosis.

Enter both Systolic & Diastolic readings (in mm Hg) below. Results will display the corresponding blood pressure category & information regarding the causes, symptoms, and treatment options for your range of blood pressure.

Normal Blood Pressure Chart by Age

How Age Affects Blood Pressure

For infants, toddlers, and pre-adolescent aged children, doctors follow separate guidelines and standards to define high blood pressure. Average readings tend to be lower at a younger age and increase as you grow older . During late adolescence (around 17-19 yrs old) doctors typically begin to follow the standard adult guidelines for high blood pressure.

As you age, your risk of developing high blood pressure increases.

Click Here for Pediatric Blood Pressure Chart by Age Reference

Charted Blood Pressure Ranges

The following table provides a rough guide to understanding blood pressure as you age. Start by taking your blood pressure to find your systolic (top number) & diastolic (bottom number) pressure. Then, locate your age range in the right-hand column to see where your readings fall.

Age Hypotension (low blood pressure) Normal BP Elevated Hypertension Stage 1 Hypertension Stage 2
17-19 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
20-24 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
25-29 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
30-34 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
35-39 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
40-44 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
45-49 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
50-54 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
55-59 < 90 < 60 <120 < 80 120-129 <80 130-139 80-89 140+ 90+
60+ < 90 < 60 120 <80 120-129 <80 130-139 80-89 140+ 90+

S = Systolic Pressure
D = Diastolic Pressure

Blood pressure charts aren’t commonly broken down by age, however, pediatric charts are often separated into ranges for infants, toddlers, and pre-adolescents. Pediatric standards for high and low blood pressure differ from those used for adults. Sometimes gender can influence readings, but measurements are still compared on the same scale. ( Chart reference)

Click here to download your FREE + PRINTABLE Blood Pressure PDF & make understanding your readings easy. 

Locate your readings on the chart above & Click below to learn more about your blood pressure:

*Remember to always consult with your doctor for an accurate diagnosis and treatment plan when it comes to your blood pressure readings.

What Affects Blood Pressure?

Personal characteristics which play a role in blood pressure readings are:

  • Gender and Blood Pressure

According to the National Institute on Aging, males are more likely to have high blood pressure before age 55,  while normal blood pressure for women tends to rise after menopause. Women are less likely than men to experience complications associated with high blood pressure.

However, regardless of differences in the prevalence and complications of high blood pressure between the sexes, treatment and diagnosis are the same for both men and women.

  • Normal Blood Pressure By Age

As you age, your body goes through many changes that can put you at risk for other conditions. If you’re over 50, having a higher than usual systolic pressure might increase your risk of developing heart disease. Systolic blood pressure tends to increase steadily over time due to stiff arteries, a build-up of plaque, and a higher rate of cardiac and vascular disease. This means older adults need to be even more vigilant about monitoring their blood pressure and practicing heart-healthy self-care.

  • Height and Blood Pressure

Height isn’t a risk factor but taller people tend to have higher blood pressure because this offsets gravity and other factors to ensure the brain – the highest organ – gets enough blood flow and oxygen. However, the effect of height is minor, so it’s not taken into account in blood pressure range guidelines.

Traits can be passed from one generation to the next. This is known as heredity. There is a genetic role in high blood pressure, heart disease, and other heart conditions. However, researchers believe that it may be partly due to sharing common environments and other behaviors that can increase your risk.

  • Normal Blood Pressure and Heart Rate

While a rising heart rate will increase blood flow through the body, it does not necessarily correspond with an increase in the pressure of that blood flow. This is because blood vessels can increase in size (dilate) to facilitate larger quantities of blood. Even if your heart rate were to double, your normal blood pressure & high pulse may only slightly increase blood pressure.

Understanding Blood Pressure Measurements

Understanding blood pressure numbers is a crucial part of overall well-being. When your heart beats, it moves blood through your body to deliver oxygen and other nutrients. The blood pushes on the walls of the blood vessels as it travels through the body. The force of the blood pressing against the vessel walls is known as blood pressure.

Your blood pressure readings consist of two numbers:

Systolic Blood Pressure

Your systolic blood pressure measures the pressure on the walls of the vessel as your heart is contracting or beating. It is recorded as the top number in your blood pressure reading.

Diastolic Pressure

Your diastolic blood pressure is the pressure in the vessels while the heart is relaxed, in between heartbeats. It is recorded as the bottom number in your blood pressure reading.

Your blood pressure is reported by placing the systolic number over the diastolic number. For example, your blood pressure might be reported as 120/80. To be diagnosed with high blood pressure, only one of these numbers must be outside of the normal range. But, remember that one high reading doesn’t mean there’s a problem. High blood pressure is a condition that can only be diagnosed by your doctor.

Normal Blood Pressure

Normal blood pressure can range from 110 to 134 (systolic) over 75 to 87 (diastolic), depending on your age.

Recent updates by the American Heart Association now recognizes normal blood pressure as readings of 90/60 mm Hg or less

If your blood pressure reading is defined as ‘normal,’ that means you’re within the healthy range – which is great news for your arteries, heart, brain, and kidneys!

How to Maintain Normal Blood Pressure Level

Here are some tips to help keep your blood pressure readings within the normal and healthy range:

A diet rich in fresh fruits and vegetables, whole grains, nuts, seeds, and lean protein sources like fish and beans goes a long way toward maintaining normal blood pressure and heart health.

Be sure to avoid processed foods, trans fats, and red meat, and cut down on your intake of sugar and saturated fat.

Season your food with herbs and spices instead of salt – which is known to raise blood pressure. The American Heart Association recommends an ideal limit of no more than 1,500 mg of sodium a day (a little over half a teaspoon of salt). Bear in mind that over 75% of our sodium intake comes from the salt already added to processed foods and restaurant meals, and not from the salt shaker.

A high salt intake throws off the balance of sodium and potassium in the body, increasing fluid retention, and putting excess strain on the kidneys and the blood vessels that serve them. Potassium-rich foods such as potatoes, bananas, avocados, sweet potatos, and dark leafy greens will help lessen the effects of sodium.

  • Exercise Regularly or Stay Active

Make sure to engage in regular activities to keep blood pressure within the normal range. Exercise causes the body to release nitric acid, which helps blood vessels to dilate, reducing blood pressure.

Regular activity also helps with weight loss, stress reduction, and overall heart health.

Resistances bands are simple way to add routine exercise into your daily life & maintain normal readings or lower high blood pressure. ( Find the Best Resistance Band Sets Here)

  • Maintain a Healthy Weight

Staying within a healthy weight range for your height is important to keep blood pressure under control. Excess pounds are a risk factor for heart disease and type 2 diabetes, two conditions associated with high blood pressure.

Control stress levels. Stress causes an increase in blood pressure, so staying cool and calm can help you maintain your healthy blood pressure readings. Relaxation techniques like deep breathing, meditation, and yoga are proven stress-busters.

Too much alcohol increases blood pressure and contributes to weight gain. According to the, Mayo Clinic, women of any age and men over 65 should enjoy no more than one drink a day, and men under 65 should have no more than two drinks daily.

Smoking increases blood pressure and heart rate and raises the risk of heart attack or stroke. Nicotine also leads to narrowing and hardening of the arteries, which can increase your blood pressure readings.

Elevated Blood Pressure (previously labeled Prehypertension)

Recently added by the AHA, Elevated blood pressure is the new “Prehypertension” (so to say)

This range of blood pressure was previously defined as slightly elevated blood pressure that may lead to hypertension if left untreated. Measurements ranged from 130 to 146 (systolic) over 85 to 91 (diastolic), depending on age. New standards now classify Elevated Blood Pressure as:

  • Measurements ranging from 120-129 mm Hg (systolic) and less than 80 mm Hg (diastolic)

Causes of elevated blood pressure are the same as the causes of hypertension, and the treatment options are similar.

At this stage, there may be no noticeable hypertension symptoms , but damage to the body may still be occurring, and your risk of heart attack and stroke is increased.

Click below to learn more about what causes elevated blood pressure, the symptoms & the best treatment methods

Stage 1 Hypertension

Readings in this category range from 130 to 139 mm Hg (systolic) over 80 to 89 mm Hg (diastolic), depending on age.

Recent updates by the American Heart Association now recognizes stage 1 hypertension as readings of 130/80 mm Hg or higher.

Stage 1 hypertension, which can be caused by everything from poor diet to stress, is considered to be mild to moderate high blood pressure.

Many people with stage 1 hypertension don’t experience any noticeable symptoms . However, your doctor may decide that you need treatment, even without symptoms. It’s vital that you follow up with your primary care doctor for any blood pressure concerns.

If not addressed, stage 1 hypertension will increase your risk of heart attack, stroke, and other serious health issues. It may also progress to stage 2 hypertension – a more severe type of high blood pressure.

Click below to learn more about what causes stage 1 hypertension, the symptoms & the best treatment methods

Stage 2 Hypertension

Blood pressure readings higher than 1 40/90 mm Hgindicate stage 2 hypertension, which is considered severe high blood pressure.  This is a serious condition and requires immediate treatment – which includes eliminating the root causes of the condition.

Recent updates by the American Heart Association now recognizes stage 1 hypertension as readings of 140 /9 0 mm Hg or higher

Stage 2 hypertension is severe high blood pressure. 

At this stage, you may be noticing some symptoms of hypertension and your risk of heart attack, stroke, and other serious health issues greatly increase.

Click below to learn more about what causes stage 2 hypertension, the symptoms & the best treatment methods

Hypertensive Crisis:

The term Hypertensive Crisis encompasses both Hypertensive Urgency and Hypertensive Emergency. These conditions are caused by untreated hypertension and require immediate attention.

If your blood pressure reading is 180/120 or higher, wait about five minutes and retake your blood pressure. If you have two readings that are this high, but you aren’t having any other concerning symptoms such as chest pain, back pain, shortness of breath, change in vision, numbness/weakness, or difficulty speaking – you are experiencing hypertensive urgency.

Contact your physician immediately to discuss next steps. This type of blood pressure problem can usually be handled by adjusting your medications, but it is crucial that you speak to your doctor.

If your blood pressure reading is 180/120 or higher and you’re experiencing symptoms such as shortness of breath, back pain, chest pain, numbness/weakness, change in vision, or difficulty speaking – you’re having a hypertensive emergency and need to seek emergency medical attention. Do not wait to see if your blood pressure improves. Call 911 or head to the nearest emergency room. To treat this serious condition, doctors may give you blood pressure medications intravenously (IV),  or other treatments aimed to decrease your risk of long-term effects.

If left untreated, you might begin to experience signs of organ damage that include:

  • Body weakness or numbness
  • Trouble breathing
  • Chest pain
  • Back pain
  • Slurred speech
  • Headache
  • Seizure
  • Changes in vision

Treatment for a Hypertensive Crisis

If you are experiencing a Hypertensive Crisis, never wait for your blood pressure to come back down before seeking medical attention. Treatment options include blood pressure medication administered through IVs and specific therapy treatment for possible organ damage.

Causes of High Blood Pressure

For many people, no one specific factor leads to the development of high blood pressure. It tends to develop gradually over time as a result of age and the build-up of fatty deposits in the arteries.

However, some lifestyle factors can speed up the onset of high blood pressure. A few of these factors include a high-sodium diet, too much alcohol, inactivity, and stress.

Health conditions like thyroid disease, kidney disease, and sleep apnea might increase your risk of high blood pressure. Taking medications such as prescription drugs, decongestants, and pain relievers may also be contributing factors.

Hypertension Symptoms and Risks

Risks associated with high blood pressure can become life-threatening if not adequately monitored or addressed ( Image reference).

Most people with high blood pressure, particularly prehypertension and stage 1 hypertension, don’t experience any symptoms.

Even at stage 2, hypertension may not cause any noticeable effects. Those who do experience symptoms may notice:

  • Headaches
  • Nosebleeds
  • Shortness of breath

However, even in the absence of symptoms, the elevated blood pressure is still damaging your blood vessels and heart and increasing the risk of heart attack, heart disease, stroke, and more.

For these reasons, regular check-ups along with at-home blood pressure monitoring are necessary to stop progression or reverse some of the damage done.

Treatments for High Blood Pressure

Whether you have prehypertension, or full-blown hypertension at any stage, the treatments options are the same. However, those with more severe high blood pressure may need to be more aggressive in their approach than those with blood pressure readings which are close to normal. Common treatment regimen include…

At Home Monitoring

A small, portable, at-home blood pressure monitor cuff is a convenient way to stay on top of your readings throughout the day ( Image Reference).

If you have any of the health conditions associated with high blood pressure, including sleep apnea, kidney problems, or thyroid disease, it’s esstenial to follow the treatment plan you were prescribed. Invest in an at-home blood pressure monitor to help track your readings. Careful monitoring can:

  • Identify abnormal measurements
  • Recognize lifestyle habits that increase your blood pressure
  • Monitor in-between routine doctor visits
  • Keep track of blood pressure while on medication

Healthy Diet

A healthy, balanced, diet helps to keep high blood pressure at bay ( Image Reference).

What you put in your body can have a profound impact on your health. Choose to fill your plate with fresh fruits and vegetables, whole grains, nuts, seeds and lean protein sources like fish and beans. Make sure to incorporate drinks that lower blood pressure and avoid diuretics.

For lower blood pressure and all-around better health, avoid processed foods, trans fats, and red meat, and cut down on your intake of sugar and saturated fat.

Ditch the Salt

Too much dietary salt disturbs the delicate balance of sodium and potassium in the body. This increases fluid retention and puts excess strain on the kidneys and the blood vessels around the kidneys.

The American Heart Association recommends people consume no more than 1,500 mg of sodium a day – which is a little over half a teaspoon of salt. It’s not just the salt in the salt shaker you should be concerned with – research shows that over 75% of our sodium intake comes from the salt already added to processed foods and restaurant meals.

Potassium-rich foods such as potatoes, bananas, avocados, sweet potatos, and dark leafy greens will help lessen the effects of sodium.

Stay Active

Make sure to engage in regular activities to bring your blood pressure back into the normal range.

Exercise causes the body to release nitric acid, which helps blood vessels to dilate, reducing blood pressure. Regular activity also helps with weight loss, stress reduction, and heart health.

Walking, cycling, swimming, water aerobics, golf (without a cart), and yoga are all fantastic exercises for adults of all ages.

Don’t forget that other everyday activities which involve movement – known as incidental physical activities – can contribute to improved fitness levels, at least according to some research. This includes things like moderate intensity gardening, vacuuming, washing the car, or walking around the supermarket.

Maintain a Healthy Weight

Carrying excess weight can be dangerous to your heart health, as it requires your arteries to work harder. Set goals and track progress with a simple at home scale ( See Product on Amazon).

If you are overweight, If you’re overweight, talk to your doctor about a weight loss regimen. Losing as little as 5 pounds can make a difference!

Being overweight or obese is also a risk factor for heart disease and type 2 diabetes, two conditions associated with high blood pressure.

Stop Stressing

Stress and anxiety may be contributing to your elevated blood pressure results. Practice relaxation techniques like deep breathing, meditation, and yoga on a regular basis to lower your blood pressure, and even bring it back within the normal range.

Enjoy Alcohol in Moderation (or Not at All!)

While we’ve all heard the health benefits of a glass of red wine now and then, too much alcohol increases blood pressure, contributes to weight gain, and can cause you to make poor food choices.

For better health, women of any age and men over 65 should enjoy no more than one drink a day, and men under 65 should have no more than two.

Quit Smoking

There are no health benefits to smoking! Nicotine not only increases blood pressure and heart rate, but it also raises the risk of heart attack or stroke, and leads to narrowing and hardening of the arteries.

Discuss Medication with a Doctor

When dealing with high blood pressure readings, it’s necessary to consult with your doctor to find proper ways to manage and prevent hypertension.

Depending on your age, lifestyle, and blood pressure readings, your doctor may recommend medication as part of a treatment program for hypertension.

It’s not clear if medication is beneficial for adults who have prehypertension alone. However, if you have another medical condition along with prehypertension, such as diabetes or kidney disease, your doctor might decide it’s best to start treatment as early as possible.

Those with stage 1 and stage 2 hypertension may be prescribed one or more of the following drugs:

  • ACE inhibitors
  • Aldosterone antagonists
  • Alpha blockers
  • Alpha-beta blockers
  • Angiotensin II receptor blockers (ARBs)
  • Beta-blockers
  • Renin inhibitors
  • Thiazide diuretics
  • Vasodilators

Hypotension (Low Blood Pressure)

While all the focus seems to be on high blood pressure, low blood pressure (hypotension) is also a potentially dangerous condition. In severe cases, it can cause shock – a life-threatening condition that occurs when the body isn’t receiving adequate blood flow.

A reading of less than 90 (systolic) or 60 (diastolic) can indicate low blood pressure, although this may vary from person to person. As a result, you may not experience any symptoms of hypotension even if your blood pressure readings indicate you have it. In cases like this, a doctor may or may not recommend interventions.

Causes of Hypotension

There are several possible causes of low blood pressure, and you must find the root cause raise your readings back to a normal range.

Possible causes include:

  • Anaphylaxis – a severe allergic reaction
  • Blood loss
  • Dehydration
  • Heart problems such as low heart rate, heart attack, or heart failure
  • Low blood sugar or diabetes
  • Medications such as diuretics, alpha blockers, beta blockers, some antidepressants, erectile dysfunction treatments, and drugs for Parkinson’s disease
  • Nutrient deficiencies, particularly a lack of Vitamin B12 and folate
  • Pregnancy
  • Septicemia – a severe infection in the bloodstream
  • Thyroid conditions

Low blood pressure can also be encountered when moving quickly to a standing position after sitting or lying down. Hypotension after meals (postprandial hypotension) is common in older adults.

Symptoms and Risks of Hypotension

If you have low blood pressure, you may experience:

  • Blurred vision
  • Dizziness
  • Extreme tiredness
  • Fainting
  • Inability to concentrate
  • Lightheadedness
  • Nausea

Severe cases of hypotension can result in shock – a life-threatening condition which requires emergency medical intervention. Shock is characterized by:

  • A weak and rapid pulse
  • Cold and clammy skin
  • Confusion, especially in older adults
  • Quick and shallow breathing

Treatments for Hypotension

If your hypotension is just slightly below the healthy range and doesn’t cause you any symptoms, it’s unlikely you need treatment.

Those who do experience symptoms may wish to:

Increase Fluid Intake

Water is a staple in any healthy diet, but maintaining hydration and avoiding diuretics can help to increase low blood pressure ( Image Reference).

Drinking more water will help to raise blood volume and prevent dehydration. Steer clear of coffee, tea, and alcohol – which are diuretics – and can increase your risk of becoming dehydrated.

Eat a Balanced Diet with Regular Meals

A diet rich in fresh fruits and vegetables, whole grains, nuts, seeds and lean protein sources like fish and beans is important for blood pressure and heart health. Avoid processed foods, trans fats, and red meat, and cut down on your intake of sugar and saturated fat.

As blood pressure tends to drop after eating, several smaller, low-carb meals spaced throughout the day may help ease symptoms. It can also be helpful to reduce your intake of high-carbohydrate foods like potatoes, white pasta, and white bread.

Add More Salt

People with low blood pressure may actually benefit from a little extra dietary sodium, which can help to raise blood pressure.

However, it’s important to discuss this with your doctor first, because too much salt can cause heart failure, especially in older adults or those with underlying health conditions.

Invest in Compression Stockings

These stockings – which are often used to treat varicose veins – help those with hypotension by preventing blood from pooling in the legs.

Discuss Medication with a Doctor

Some medications are available to help those with hypotension – a doctor will be able to advise you of your options.

Slowly Change Body Positions

Hypotension which causes symptoms from quickly changing body positions can be remedied by slowing down and noticing how you move.

Be sure to move from a sitting position to a standing one gently. Before getting out of bed in the morning, practice some deep breathing exercises, and slowly move from a horizontal position to a sitting one, before gently standing upright.

If you notice symptoms while standing by crossing your legs and squeezing your thighs.

Good Practices for Taking Your Blood Pressure

While monitoring your blood pressure at home is a great way to keep your health on track, it’s cruical that you use the device properly. For accurate readings, follow these good practice guidelines:

Next time you have a doctor’s appointment, bring along your home monitor and have your doctor compare readings between your device and theirs. You should re-test for accuracy in this manner if you drop or damage the device.

To confirm that you are using your device properly, ask your doctor to watch you take a reading. For the greatest accuracy, take two or three readings each time, leaving two minutes between results.

When taking your blood pressure, it’s imperative that the cuff is put on correctly before starting the measurment. Be sure to refer to your device’s manual for specifications and instructions on proper placement. Also, ensure that the cuff is appropriately sized for your arm. Universal cuff sizes work for most, but custom small or large cuffs are available.

You should measure your blood pressure in the morning, but not immediately after waking. Make sure to take a reading before you exercise, eat, or take medications.

In the evening, take a second reading, ensuring it’s not within 30 minutes of eating, smoking, or consuming caffeine or alcohol.

Use the same arm each time you take your blood pressure. Prop up the arm, at heart level, on a steady surface, using a cushion if necessary. You should place the cuff against your bare skin rather than your clothing.

  1. Be sure to sit in a comfortable and upright position throughout the measurement
  2. Do not cross your legs
  3. Avoid talking until results are displayed

Stress can cause your blood pressure to shoot up, which can leave you feeling even more stressed! Stay Zen-like before taking your daily readings for a more accurate result.

If your device doesn’t automatically log your results, write them down on a dedicated notepad. It’s normal for there to be some variation in readings. For example, your blood pressure numbers are often higher in the morning or when taken at the doctor’s office.

However, if you have concerns about any of your blood pressure readings, contact your doctor.

Understanding Blood Pressure Infographic – Know Your Numbers

Having blood pressure outside the normal range puts your health in jeopardy. If it’s too high, you’re at risk of serious medical conditions, including heart attacks and stroke. Blood pressure that’s too low can be life-threatening in severe cases.

Regardless, ALWAYS discuss readings and health conditions with your physician to ensure accurate results and the safest actions for your health.

Keep in mind that you can have high blood pressure and not even know it. This silent condition might be doing untold harm to your body. Knowing your numbers is the only way to find out for sure if your blood pressure readings fall within the optimal range, and making smart lifestyle choices is the only way to keep them there!

Stay consistent with your health. Use the infographic below as a reminder and helpful guide to understanding your blood pressure readings. View below or click image for free PDF 🙂



New blood pressure guidelines put half of U.S. adults in unhealthy range

Chart Reference

Socioeconomic inequalities in blood pressure: co-ordinated analysis of 147,775 participants from repeated birth cohort and cross-sectional datasets, 1989 to 2016 | BMC Medicine

  • 1.

    Bundy JD, Li C, Stuchlik P, Bu X, Kelly TN, Mills KT, He H, Chen J, Whelton PK, He J. Systolic blood pressure reduction and risk of cardiovascular disease and mortality: a systematic review and network meta-analysis. JAMA Cardiol. 2017;2:775–81.

    PubMed Central 

    Google Scholar 

  • 2.

    Lopez AD, Adair T. Is the long-term decline in cardiovascular-disease mortality in high-income countries over? Evidence from national vital statistics. Int J Epidemiol. 2019;48(6):1815–23.

  • 3.

    Gottesman RF, Schneider AL, Zhou Y, Coresh J, Green E, Gupta N, Knopman DS, Mintz A, Rahmim A, Sharrett AR. Association between midlife vascular risk factors and estimated brain amyloid deposition. JAMA. 2017;317:1443–50.

    PubMed Central 

    Google Scholar 

  • 4.

    Lane CA, Barnes J, Nicholas JM, Sudre CH, Cash DM, Parker TD, Malone IB, Lu K, James SN, Keshavan A, Murray-Smith H. Associations between blood pressure across adulthood and late-life brain structure and pathology in the neuroscience substudy of the 1946 British birth cohort (Insight 46): an epidemiological study. Lancet Neurol. 2019;18(10):942–52.

    PubMed Central 

    Google Scholar 

  • 5.

    Sharp SI, Aarsland D, Day S, Sønnesyn H, Group AsSVDSR, Ballard C: Hypertension is a potential risk factor for vascular dementia: systematic review. Int J Geriatr Psychiatry 2011, 26:661–669.

  • 6.

    Shah K, Qureshi SU, Johnson M, Parikh N, Schulz PE, Kunik ME. Does use of antihypertensive drugs affect the incidence or progression of dementia? A systematic review. Am J Geriatr Pharmacother. 2009;7:250–61.


    Google Scholar 

  • 7.

    Carter AR, Gill D, Davies NM, Taylor AE, Tillmann T, Vaucher J, Wootton RE, Munafò MR, Hemani G, Malik R. Understanding the consequences of education inequality on cardiovascular disease: Mendelian randomisation study. BMJ. 2019;365:l1855.

    PubMed Central 

    Google Scholar 

  • 8.

    Colhoun HM, Hemingway H, Poulter N. Socio-economic status and blood pressure: an overview analysis. J Hum Hypertens. 1998;12:91–110.


    Google Scholar 

  • 9.

    Davies NM, Dickson M, Smith GD, van den Berg GJ, Windmeijer F. The causal effects of education on health outcomes in the UK Biobank. Nat Hum Behav. 2018;2:117.

    PubMed Central 

    Google Scholar 

  • 10.

    Hardy R, Kuh D, Langenberg C, Wadsworth ME. Birthweight, childhood social class, and change in adult blood pressure in the 1946 British birth cohort. Lancet. 2003;362:1178–83.


    Google Scholar 

  • 11.

    Grotto I, Huerta M, Sharabi Y. Hypertension and socioeconomic status. Curr Opin Cardiol. 2008;23:335–9.


    Google Scholar 

  • 12.

    Scholes S, Bajekal M, Love H, Hawkins N, Raine R, O’Flaherty M, Capewell S. Persistent socioeconomic inequalities in cardiovascular risk factors in England over 1994-2008: a time-trend analysis of repeated cross-sectional data. BMC Public Health. 2012;12:129.

    PubMed Central 

    Google Scholar 

  • 13.

    Leng B, Jin Y, Li G, Chen L, Jin N. Socioeconomic status and hypertension: a meta-analysis. J Hypertens. 2015;33:221–9.


    Google Scholar 

  • 14.

    Zhou B, Bentham J, Di Cesare M, Bixby H, Danaei G, Cowan MJ, Paciorek CJ, Singh G, Hajifathalian K, Bennett JE. Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19·1 million participants. Lancet. 2017;389:37–55.

    Google Scholar 

  • 15.

    He F, Brinsden H, MacGregor G. Salt reduction in the United Kingdom: a successful experiment in public health. J Hum Hypertens. 2014;28:345.


    Google Scholar 

  • 16.

    Zhou B, Danaei G, Stevens GA, Bixby H, Taddei C, Carrillo-Larco RM, Solomon B, Riley LM, Di Cesare M, Iurilli ML, Rodriguez-Martinez A. Long-term and recent trends in hypertension awareness, treatment, and control in 12 high-income countries: an analysis of 123 nationally representative surveys. The Lancet. 2019;394(10199):639–51.

  • 17.

    Bann D, Johnson W, Li L, Kuh D, Hardy R. Socioeconomic inequalities in body mass index across adulthood: coordinated analyses of individual participant data from three British birth cohort studies initiated in 1946, 1958 and 1970. PLoS Med. 2017;14:e1002214.

    PubMed Central 

    Google Scholar 

  • 18.

    Jokela M. Are neighborhood health associations causal? A 10-year prospective cohort study with repeated measurements. Am J Epidemiol. 2014;180:776–84.


    Google Scholar 

  • 19.

    Galobardes B. Socioeconomic inequalities in health: individual or area level; does it matter? BMC Public Health. 2012;12:171.

    PubMed Central 

    Google Scholar 

  • 20.

    Falaschetti E, Mindell J, Knott C, Poulter N. Hypertension management in England: a serial cross-sectional study from 1994 to 2011. Lancet. 2014;383:1912–9.


    Google Scholar 

  • 21.

    Power C, Atherton K, Strachan DP, Shepherd P, Fuller E, Davis A, Gibb I, Kumari M, Lowe G, Macfarlane GJ. Life-course influences on health in British adults: effects of socio-economic position in childhood and adulthood. Int J Epidemiol. 2007;36:532–9.


    Google Scholar 

  • 22.

    Murray ET, Mishra GD, Kuh D, Guralnik J, Black S, Hardy R. Life course models of socioeconomic position and cardiovascular risk factors: 1946 birth cohort. Ann Epidemiol. 2011;21:589–97.

    PubMed Central 

    Google Scholar 

  • 23.

    Strand B, Murray ET, Guralnik J, Hardy R, Kuh D. Childhood social class and adult adiposity and blood-pressure trajectories 36-53 years: gender-specific results from a British birth cohort. J Epidemiol Community Health. 2012;66:512–8.


    Google Scholar 

  • 24.

    Atherton K, Power C. Health inequalities with the National Statistics-Socioeconomic classification: disease risk factors and health in the 1958 British birth cohort. Eur J Public Health. 2007;17:486–91.


    Google Scholar 

  • 25.

    Rose G. Sick individuals and sick populations. Int J Epidemiol. 2001;30:427–32.


    Google Scholar 

  • 26.

    Bann D, Fitzsimons E, Johnson W. Determinants of the population health distribution: an illustration examining body mass index. Int J Epidemiol. 2020;49:731–7.

    PubMed Central 

    Google Scholar 

  • 27.

    Li L, Hardy R, Kuh D, Power C. Life-course body mass index trajectories and blood pressure in mid life in two British birth cohorts: stronger associations in the later-born generation. Int J Epidemiol. 2015;44:1018–26.

    PubMed Central 

    Google Scholar 

  • 28.

    Li L, Law C, Power C. Body mass index throughout the life-course and blood pressure in mid-adult life: a birth cohort study. J Hypertens. 2007;25:1215–23.


    Google Scholar 

  • 29.

    Wills AK, Lawlor DA, Matthews FE, Aihie Sayer A, Bakra E, Ben-Shlomo Y, Benzeval M, Brunner E, Cooper R, Kivimaki M, et al. Life course trajectories of systolic blood pressure using longitudinal data from eight UK cohorts. PLoS Med. 2011;8:e1000440.

    PubMed Central 

    Google Scholar 

  • 30.

    Phelan JC, Link BG, Tehranifar P. Social conditions as fundamental causes of health inequalities: theory, evidence, and policy implications. J Health Soc Behav. 2010;51:S28–40.

    Google Scholar 

  • 31.

    Corraini P, Olsen M, Pedersen L, Dekkers OM, Vandenbroucke JP. Effect modification, interaction and mediation: an overview of theoretical insights for clinical investigators. Clin Epidemiol. 2017;9:331.

    PubMed Central 

    Google Scholar 

  • 32.

    Kuh D, Pierce M, Adams J, Deanfield J, Ekelund U, Friberg P, Ghosh AK, Harwood N, Hughes A, Macfarlane PW, Mishra G. Cohort profile: updating the cohort profile for the MRC National Survey of Health and Development: a new clinic-based data collection for ageing research. Int J Epidemiol. 2011;40(1):e1–9.

  • 33.

    Wadsworth M, Kuh D, Richards M, Hardy R. Cohort profile: The 1946 National Birth Cohort (MRC National Survey of Health and Development). Int J Epidemiol. 2006;(35):49–54.

  • 34.

    Power C, Elliott J. Cohort profile: 1958 British birth cohort (National Child Development Study). Int J Epidemiol. 2006(35):34–41.

  • 35.

    Elliott J, Shepherd P. Cohort profile: 1970 British birth cohort (BCS70). Int J Epidemiol. 2006;35:836–43.


    Google Scholar 

  • 36.

    Wadsworth M: The origins and innovatory nature of the 1946 British national birth cohort study. Longitudinal and Life Course Studies 2010, 1:121–136.

  • 37.

    Wadsworth ME, Bynner J. A companion to life course studies: the social and historical context of the British birth cohort studies: Taylor & Francis; 2011.

  • 38.

    Wadsworth M. The imprint of time: childhood, history and adult life. Oxford: Clarendon Press; 1991.

    Google Scholar 

  • 39.

    Stafford M, Black S, Shah I, Hardy R, Pierce M, Richards M, Wong A, Kuh D. Using a birth cohort to study ageing: representativeness and response rates in the National Survey of Health and Development. Eur J Ageing. 2013;10:145–57.

    PubMed Central 

    Google Scholar 

  • 40.

    Mostafa T, Wiggins D. The impact of attrition and non-response in birth cohort studies: a need to incorporate missingness strategies. Longitudinal and Life Course Studies. 2015;6:131–46.

    Google Scholar 

  • 41.

    Atherton K, Fuller E, Shepherd P, Strachan D, Power C: Loss and representativeness in a biomedical survey at age 45 years: 1958 British birth cohort. J Epidemiol Community Health 2008, 62:216–223.

  • 42.

    Wadsworth ME, Mann SL, Rodgers B, Kuh DJ, Hilder WS, Yusuf EJ. Loss and representativeness in a 43 year follow up of a national birth cohort. J Epidemiol Community Health. 1992;46:300–4.

    PubMed Central 

    Google Scholar 

  • 43.

    Sterne JA, White IR, Carlin JB, Spratt M, Royston P, Kenward MG, Wood AM, Carpenter JR. Multiple imputation for missing data in epidemiological and clinical research: potential and pitfalls. BMJ. 2009;338:b2393.

    PubMed Central 

    Google Scholar 

  • 44.

    Stang A, Moebus S, Möhlenkamp S, Dragano N, Schmermund A, Beck E-M, Siegrist J, Erbel R, Jöckel K-H. Algorithms for converting random-zero to automated oscillometric blood pressure values, and vice versa. Am J Epidemiol. 2006;164:85–94.


    Google Scholar 

  • 45.

    Moody A, Mindell J, Faulding S: Health Survey for England 2016: Prescribed medicines LONDON: NHS England: The Health and Social Care Information Center 2017.

  • 46.

    Mindell J, Biddulph JP, Hirani V, Stamatakis E, Craig R, Nunn S, Shelton N. Cohort profile: the health survey for England. Int J Epidemiol. 2012;41:1585–93.


    Google Scholar 

  • 47.

    Gordon P, Lawton D. Dictionary of British education: Psychology Press; 2003. https://books.google.co.uk/books?hl=en&lr=&id=MGL4ocnnkrwC&oi=fnd&pg=PP9&dq=Gordon+P,+Lawton+D.+Dictionary+of+British+education:+Psychology+Press&ots=rqS25pxj8z&sig=jZ1aFBGepA_HX0Voex_UiOSMXV8#v=onepage&q&f=fal.

  • 48.

    National Institute for Health Care Excellence: Hypertension: clinical management of primary hypertension in adults (update). 2019.

  • 49.

    Law M, Wald N, Morris J, Jordan R. Value of low dose combination treatment with blood pressure lowering drugs: analysis of 354 randomised trials. BMJ. 2003;326:1427.

    PubMed Central 

    Google Scholar 

  • 50.eds.). City; 2015. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/417897/Indicators_acc.pdf.

  • 53.

    Heckman JJ, MaCurdy TE. A simultaneous equations linear probability model. Can J Econ. 1985:28–37.

  • 54.

    Koenker R, Bassett G Jr. Regression quantiles. Econometrica. 1978:1;33–50.

  • 55.

    Hypertension in adults: diagnosis and management. [https://www.nice.org.uk/guidance/ng136/resources/hypertension-in-adults-diagnosis-and-management-pdf-66141722710213]. Published 28 August 2019.

  • 56.

    Kanjilal S, Gregg EW, Cheng YJ, Zhang P, Nelson DE, Mensah G, Beckles GL. Socioeconomic status and trends in disparities in 4 major risk factors for cardiovascular disease among US adults, 1971-2002. Arch Intern Med. 2006;166:2348–55.


    Google Scholar 

  • 57.

    Kim YJ, Lee JS, Park J, Choi DS, Kim DM, Lee K-H, Kim HY, Kim SG, Lee J. Trends in socioeconomic inequalities in five major risk factors for cardiovascular disease in the Korean population: a cross-sectional study using data from the Korea National Health and Nutrition Examination Survey, 2001–2014. BMJ Open. 2017;7:e014070.

    PubMed Central 

    Google Scholar 

  • 58.

    Ernstsen L, Strand BH, Nilsen SM, Espnes GA, Krokstad S. Trends in absolute and relative educational inequalities in four modifiable ischaemic heart disease risk factors: repeated cross-sectional surveys from the Nord-Trøndelag Health Study (HUNT) 1984–2008. BMC Public Health. 2012;12:266.

    PubMed Central 

    Google Scholar 

  • 59.

    Eriksson M, Carlberg B, Pennlert J, Söderberg S, Eliasson M. Time trends and socioeconomic differences in blood pressure levels: the Northern Sweden MONICA study 1994–2014. Eur J Prev Cardiol. 2017;24:1473–81.


    Google Scholar 

  • 60.

    Murphy A, Palafox B, O’Donnell O, Stuckler D, Perel P, AlHabib KF, Avezum A, Bai X, Chifamba J, Chow CK. Inequalities in the use of secondary prevention of cardiovascular disease by socioeconomic status: evidence from the PURE observational study. Lancet Glob Health. 2018;6:e292–301.

    PubMed Central 

    Google Scholar 

  • 61.

    Scholes S, Conolly A, Mindell JS. Income-based inequalities in hypertension and in undiagnosed hypertension: analysis of Health Survey for England data. J Hypertens. 2020;38:912–24.


    Google Scholar 

  • 62.

    Serumaga B, Ross-Degnan D, Avery AJ, Elliott RA, Majumdar SR, Zhang F, Soumerai SB. Effect of pay for performance on the management and outcomes of hypertension in the United Kingdom: interrupted time series study. BMJ. 2011;342:d108.

    PubMed Central 

    Google Scholar 

  • 63.

    Chang KC, Vamos EP, Palladino R, Majeed A, Lee JT, Millett C. Impact of the NHS Health Check on inequalities in cardiovascular disease risk: a difference-in-differences matching analysis. J Epidemiol Community Health. 2019;73:11–8.


    Google Scholar 

  • 64.

    Sun D, Zhou T, Heianza Y, Li X, Fan M, Fonseca VA, Qi L. Type 2 diabetes and hypertension: a study on bidirectional causality. Circ Res. 2019;124:930–7.

    PubMed Central 

    Google Scholar 

  • 65.

    McDoom MM, Palta P, Vart P, Juraschek SP, Kucharska-Newton A, Roux AVD, Coresh J. Late life socioeconomic status and hypertension in an aging cohort: the Atherosclerosis Risk in Communities Study. J Hypertens. 2018;36:1382.

    PubMed Central 

    Google Scholar 

  • 66.

    Virdis A, Giannarelli C, Neves MF, Taddei S, Ghiadoni L. Cigarette smoking and hypertension. Curr Pharm Des. 2010;16:2518–25.


    Google Scholar 

  • 67.

    Taylor B, Irving HM, Baliunas D, Roerecke M, Patra J, Mohapatra S, Rehm J. Alcohol and hypertension: gender differences in dose–response relationships determined through systematic review and meta-analysis. Addiction. 2009;104:1981–90.


    Google Scholar 

  • 68.

    Barberio AM, Sumar N, Trieu K, Lorenzetti DL, Tarasuk V, Webster J, Campbell NR, McLaren L. Population-level interventions in government jurisdictions for dietary sodium reduction: a Cochrane Review. Int J Epidemiol. 2017;46:1551–405.

    PubMed Central 

    Google Scholar 

  • 69.

    Mackenbach JP. The persistence of health inequalities in modern welfare states: the explanation of a paradox. Soc Sci Med. 2012;75:761–9.


    Google Scholar 

  • 70.

    Hoffmann R, Kröger H, Geyer S. Social causation versus health selection in the life course: does their relative importance differ by dimension of SES? Soc Indic Res. 2019;141:1341–67.

    Google Scholar 

  • 71.

    Connelly R, Gayle V. An investigation of social class inequalities in general cognitive ability in two British birth cohorts. Br J Sociol. 2019;70:90–108.


    Google Scholar 

  • 72.

    VanderWeele TJ, Vansteelandt S, Robins JM. Effect decomposition in the presence of an exposure-induced mediator-outcome confounder. Epidemiology (Cambridge, Mass). 2014;25:300.

    Google Scholar 

  • 73.

    Capewell S, Graham H. Will cardiovascular disease prevention widen health inequalities? PLoS Med. 2010;7:e1000320.

    PubMed Central 

    Google Scholar 

  • 74.

    Alsabbagh MW, Lemstra M, Eurich D, Lix LM, Wilson TW, Watson E, Blackburn DF. Socioeconomic status and nonadherence to antihypertensive drugs: a systematic review and meta-analysis. Value Health. 2014;17:288–96.


    Google Scholar 

  • Blood Pressure Range Chart – Vaughn’s Summaries

    1. Why did I do this? I searched
    high and low on the Internet, and I could find nothing like
    this in one place – a Summary of human BP range, the
    Averages, and the Comments relating to each BP level.

    2. How did I get the numbers? I started with the
    commonly seen “Systolic/ Diastolic pairs” seen in the
    literature – 200/120, 160/100, 140/90, 120/80 and 90/60.
    From there, I interpolated and extrapolated all the other
    numbers. Note that these are AVERAGE relationships. For
    instance, instead of 140/90, your BP may be 140/100, or
    140/80. Each individual will have a unique
    systolic-diastolic relationship. If your S/D difference
    varies significantly from the averages shown above, this can
    be helpful in assessing your particular cardiovascular

    3. Fairly recently, the difference between Systolic
    and Diastolic pressure, named “Pulse
    “, has been gaining
    interest in the research community. This Pulse Pressure has
    been found to correlate linearly with heart attack risk –
    the higher the number, the higher the risk. According to
    this theory, a BP of 140/ 90 (PP=50) is more desirable than
    a BP of 140/ 80 (PP=60).
    This PP relationship at each pressure appears to be almost

    4. As for the comments, I have “averaged” the
    references made in the literature, since not all doctors
    agree upon the pressures at which to treat, and how
    aggressively to treat (multiple medications, type of meds,
    etc.). You can rest assured that the pharmaceutical
    companies prefer that you take medication at 135/80, since
    they sell the meds. Most doctors are not so aggressive.
    Remember that ALL medications have side effects.
    have more serious
    side effects than any other class of prescription drugs.

    5. Be aware of the “Circadian Rhythm” cycle.
    Your Blood Pressure is highly influenced by the time of day.
    For normal people, the highest BP occurs about midday, and
    the lowest at about 3-4 AM in the morning. For some people,
    described as “non-dippers”, this early morning BP dip does
    not occur. For these people, highest blood pressure usually
    occurs around 6 AM to 9 AM in the morning. Some doctors are
    not aware of this, and make erroneous assumptions. A
    non-dipper may see 150/95 in the morning, and 130/85 in the
    evening. Non-dipping is usually associated with abnormal
    sleep conditions, such as sleep apnea, heavy snoring, drug
    and alcohol abuse, etc.

    6. One blood pressure reading means very little. The
    advice to “Have your blood pressure checked once a year” is
    useless. What time of day? Had you eaten less salty foods
    recently? Were you relaxed that day, when you are usually
    much more stressed? Had you recently exercised vigorously?
    You must check your BP far more often than once a year,
    especially if you show “borderline” readings. I can produce
    a very low, or very high blood pressure AT WILL, based upon
    what I do during the 24 hours prior to the measurement.

    7. Beware of “white coat syndrome”, which
    results in a much higher BP reading than normal, due to the
    authoritative doctor, the foreboding, sterile exam room, and
    the smells such as alcohol and disinfectant. All this is not
    relaxing. Some unaware doctors may prescribe medication,
    when in fact, you don’t need it at all. As soon as you leave
    the office, your BP returns to normal. This is another great
    reason to use your own automatic BP wrist monitor, so that
    you come to know your own body, and the effects of stress,
    food, mood, sleep, and time of day.

    8. MAP = Mean Arterial Pressure. Three formulas are
    used to compute MAP. All three produce very similar
    Above, I used Method #1 –
    MAP = DP + (1/3 (SP – DP))
    Ideal Mean Arterial Pressure is defined as 93 mm of
    mercury, which corresponds to 120/80.

    Alternative Method #2 –
    Also, MAP = (2/3 DP) + (1/3 SP)

    Alternative Method #3
    MAP = ((2*DP) + SP) / 3

    where SP= Systolic Pressure,
    and DP= Diastolic Pressure

    This is the average blood pressure for men and women by age

    IT’S important to keep an eye on your blood pressure.

    If you want to keep track of how your blood’s pumping… here’s all you need to know.


    Use our guide for checking your blood pressure from homeCredit: Getty Images

    What is the average blood pressure for men and women?

    The average blood pressure differs depending on your age.

    • 1 – 12 months 90/60
    • 1 – 5 years 95/65
    • 6 – 13 years 105/70
    • 14 – 19 years 117/77
    • 20 – 24 years 120/79
    • 25 – 29 years 121/80
    • 30 – 34 years 122/81
    • 35 – 39 years 123/82
    • 40 – 44 years 125/83
    • 45 – 49 years 127/84
    • 50 – 54 years 129/85
    • 55 – 59 years 131/86
    • 60 – 64 years 134/87

    What is a normal blood pressure reading?

    The ideal blood pressure should be below 120 and over 80 (120/80) and most UK adults have blood pressure in the range 120 over 80 (120/80) to 140 over 90 (140/90).

    The higher number is the systolic pressure, which is the force at which your heart pumps blood around your body, and the lower number is the diastolic pressure, the resistance to the blood flow in the blood vessels.

    You can request a blood pressure reading at your local GP – it only takes a minute or so.

    Blood pressure is measured with an instrument called a sphygmomanometer, where a a cuff is placed around your arm and inflated with a pump until the circulation is cut off.

    Then, a small valve slowly deflates the cuff, and the doctor measures blood pressure.


    Symptoms of high blood pressure include severe headaches and fatigueCredit: Getty – Contributor

    How can I monitor my blood pressure at home?

    If you want to measure your blood pressure at home, you will need to a buy a blood pressure monitor.

    It’s particularly important if a doctor has told you to monitor your blood pressure regularly.

    If you are about to check your levels, avoid smoking, exercise, caffeine and stress directly before as these can affect your blood pressure.

    Roll up your sleeve and sit with your arm resting palm-up on the arm of the chair.

    Make sure you’re relaxed, in a quiet space and you don’t need to use the bathroom – as this can change the reading.

    Then follow these simple steps:

    1. Locate your pulse on the inside of your elbow with your index and middle finger
    2. Secure the cuff of the monitor onto your arm using the fabric fastener to make sure it’s in place
    3. Inflate and deflate the cuff using the instructions on the monitor – machines can differ
    4. Keep your arm straight for the most accurate reading
    5. Record the reading from the machine, as well as any special circumstances at the time (meals, stress, exercise etc.)

    What are the risks if your blood pressure is too high or too low?

    If your blood pressure is too high (know as hypertension), it puts extra strain on your arteries (and your heart) and this may lead to heart attacks and strokes.

    For the most part, the lower your blood pressure the better.

    However, if you experience symptoms of dizziness, nausea, fainting and dehydration, then low blood pressure may be a problem.

    If you experience any of those symptoms, it’s best to see your GP.

    High blood pressure ‘hypertension’ raises the risk of heart attacks and strokes

    Frontiers | The Role of Metabolic Syndrome in Endometrial Cancer: A Review


    Endometrial cancer is one of the most common gynecological malignancies. The latest cancer statistics from the American Cancer Society showed that in 2018, the number of new cases of endometrial cancer in the United States was 63,230, and the number of deaths was 11,350. The incidence of malignant endometrial tumors in women ranked fourth, and the incidence of death from endometrial cancer ranked sixth (1). With the increasing incidence of metabolic diseases (obesity, diabetes and hypertension), the incidence of endometrial cancer is increasing, and affecting younger populations worldwide. It is estimated that the incidence of endometrial cancer will increase to 42.13 per 100,000 people in the United States by 2030 (2). In recent years, early diagnosis, surgery, radiotherapy and chemotherapy can significantly improve the therapeutic effect of patients, but the treatment of early lesions and the need to retain fertility, late and recurrent patients is still limited. A clinical analysis of 276 patients with endometrial cancer showed that the 5-year disease-free survival rate and the 5-year overall survival rate were 82.3 and 81%, respectively, and the recurrence rate and the cancer-related mortality rate were 14.5 and 15.9%, respectively (3).

    Regarding the pathogenesis of endometrial cancer, the traditional view is that long-term non-progesterone estrogen overstimulation of the endometrium is the main cause of endometrial hyperplasia and endometrial cancer. Estrogen can bind with nuclear estrogen receptor (ER) and play a “genotype”-regulatory effect by regulating the transcription of specific target genes. Additionally, our previous studies have found that estrogen can also induce Ca2+ influx by binding to the G protein-coupled estrogen receptor (GPER) on the cell membrane surface, activating the calcium channel Cav1.3, and activating the downstream signal transduction pathway (MAPK/Erk) rapidly, thereby promoting the proliferation of endometrial cancer. This process does not involve gene transcription and protein synthesis; therefore, it is called the “non-gene-transcription effect” (4). At present, long-term progesterone is commonly used in the clinical treatment of endometrial cancer. However, the overall effective rate of progesterone therapy for primary endometrial cancer is only 50–70%, and the recurrence rate is as high as 40% (5, 6). The objective response rate of progesterone therapy for advanced and recurrent endometrial cancer is only 15–20% (7). Interestingly, recent studies have shown that serum estrogen levels in patients with endometrial hyperplasia and endometrial cancer are not elevated compared with those in the normal control group (8). Moreover, epidemiological studies have shown that long-term estrogen exposure in post-menopausal women does not increase the risk of endometrial cancer (9). Traditional views do not explain why endometrial cancer still occurs in post-menopausal women with low estrogen levels. These studies suggest that local estrogen sensitivity, rather than increased circulating estrogen, may drive the occurrence and development of endometrial cancer. At the same time, other factors besides estrogen may also induce the occurrence and development of endometrial cancer.

    Endometrial cancer is often associated with obesity, diabetes, and hypertension. These conditions are commonly known as the metabolic triad of endometrial cancer. Epidemiological studies showed that the risk of endometrial cancer in diabetic patients was 2.12 times higher than that in normal patients, while the risk of endometrial cancer in those who were overweight (BMI ≥ 25 kg/m2) was 2.45 times higher than that in the control group. The risk of endometrial cancer in obese patients with hypertension was 3.5 times higher than that in the control group. Additionally, endometrial cancer is one of the cancers most closely related to metabolic diseases (10). Several studies have shown that metabolic syndrome caused by obesity, diabetes and hypertension is closely related to the incidence and adverse prognosis of endometrial cancer. A meta-analysis of six studies reported that metabolic syndrome is closely associated with increased risk of endometrial cancer in women (relative risk: 1.89, 95% CI 1.34–2.67) (11). A new research reported that there was a very high prevalence of metabolic syndrome in women newly diagnosed with endometrial cancer (12). A prospective case control study reported that women newly diagnosed with endometrial cancer have a higher prevalence of incident hyperglycemia, total: HDL cholesterol ratio, and three or more cardiovascular risk factors than women without endometrial cancer (13). All these studies suggest that metabolic syndrome is closely related to the incidence of endometrial cancer. However, the exact mechanism of metabolic syndrome affecting the occurrence and development of endometrial cancer has not been determined to date, which may be related to the elevation of such metabolites as blood sugar, insulin, insulin-like growth factor and triglyceride in serum (14, 15). The dynamic interaction between cells and the cell microenvironment plays an important role in regulating the growth of normal tissues and cancer cells. The tumor cell microenvironment includes tumor cells and other cells, such as fibroblasts, lymphocytes, macrophages, adipocytes, and other secreted factors, to form a unique tumor microenvironment system. An abnormal imbalance of the cell microenvironment often leads to tumorigenesis (16). It is suggested that molecules related to metabolic syndrome can accelerate the progression of endometrial cancer not only by acting directly on tumor cells but also by further remodeling the immune microenvironment of tumors.

    In this review, we focus on the metabolic microenvironment of endometrial cancer and summarize the key molecular signaling pathways of obesity, diabetes and hypertension-related metabolic syndrome affecting the occurrence, development and prognosis of endometrial cancer, aiming to explore new methods of early prevention, and targeted treatment of endometrial cancer.

    Molecular And Metabolic Mechanisms Underlying the Obesity-Endometrial Cancer Link

    Epidemiological data showed that obesity is closely related to the increase in the incidence of various cancers. Some scholars have confirmed the causal relationship between obesity and breast cancer by constructing a genetically engineered mouse model and have shown that obesity is closely related to the increase in the survival rate of residual cancer cells (17). A meta-analysis of 26 studies in the United States showed that every five units increase in body mass index (BMI) increased the risk of endometrial cancer by 50% [relative risk [RR], 1.50; 95% CI, 1.42–1.59] (18). A study reported that a history of bariatric surgery and maintained normal weight after surgery is associated with a 71 and 81% reduced risk for uterine malignant tumors (19). These findings suggest that obesity may be a modifiable risk factor related to development of endometrial cancer. However, the mechanism by which obesity increases the risk of endometrial cancer has not been elucidated. At present, the possible mechanisms are as follows: obese patients are often accompanied by insulin resistance (hyperinsulinemia), abnormal fat metabolism (leptin, adiponectin disorders), hyperglycemia, hyperlipidemia, and chronic inflammation. These factors may promote the occurrence and development of tumors (Figure 1). To explore the key mechanism of obesity-induced endometrial cancer occurrence and development, it is helpful to provide a new intervention target for the treatment of patients with metabolic syndrome.

    Figure 1. Dysfunctional adipose tissue in obesity.

    Adipocyte-Derived Estrogen Signaling

    Endometrium is a highly dynamic tissue controlled by ovarian steroids, estrogen and progesterone. Long-term estrogen stimulation without progesterone antagonism is a key factor in the occurrence of endometrial cancer. The decline of ovarian function in post-menopausal women is accompanied by a decrease in hormone levels. However, post-menopausal women are still prone to endometrial cancer. It has been reported that adipose-derived aromatase converts circulating androstenedione into estradiol, leading to elevated serum estradiol levels, which binds to estrogen receptors α and β (ERα and ERβ), eventually leading to recruitment of transcription factors, and gene transcription may be activated or repressed (20). Thus, in post-menopausal women, adipose tissue is the main source of estrogen biosynthesis. In addition, obesity can lead to hyperinsulinemia, which can reduce the synthesis of sex hormone binding protein (SHBG) by increasing the bioavailability of insulin-like growth factor-1 (IGF-1), thereby leading to an increase in estrogen levels. Therefore, obesity increases the risk of endometrial cancer, possibly by indirectly affecting estrogen levels. A meta-analysis showed that hormone replacement therapy (HRT) could modified the BMI-endometrial cancer risk association, however, menopausal status and histologic subtype did not significantly impact upon these associations (21). These findings support the hypothesis that hyperestrogenia is an important mechanism underlying the BMI-endometrial cancer association. Additional studies are needed to explore the exact mechanism mediating the link between body adiposity and endometrial cancer.

    Adipocyte-Derived Insulin Resistance

    In obese patients, excessive accumulation of adipose tissue leads to elevated levels of circulating free fatty acids and increased expression of serum adipokines, such as leptin, visfatin, and cytokines, which ultimately leads to insulin resistance. Hyperinsulinemia with a decrease in the serum level of IGF-1 binding protein and an increase in IGF-1 is most often caused by insulin resistance. Obesity-induced chronic low-grade inflammation is an important factor leading to insulin resistance. Obesity-related inflammation is characterized by increased macrophage infiltration and increased expression of inflammatory cytokines in adipose tissue (22). Recently, studies have reported that endoplasmic reticulum chaperone 78 (GRP78) plays an important role in obesity-induced insulin resistance by regulating macrophages (23). The level of the proinflammatory cytokine TGF-α in adipose tissue of obese mice was significantly increased, which was closely related to insulin resistance (24). There are a large number of inflammatory mediators, such as C-reactive protein (CRP), interleukin-6 (IL-6), and plasminogen activator inhibitor-1 (PAI-1), that are elevated in the plasma of obese patients or animals and are closely related to insulin resistance (25). The obesity-induced inflammatory response inhibits insulin signaling in adipocytes and hepatocytes through a variety of signaling pathways, including inhibition of the expression of insulin receptor substrate 1 (IRS-1) and insulin receptor (IR) in insulin signaling pathways and inhibition of PPAR gamma function, and ultimately leads to insulin resistance (26, 27). Increased insulin and IGF-1 can stimulate the proliferation of endometrial cancer cells by binding to IR and IGF-1 receptors (IGF-1R) and activating downstream signaling pathways (28).

    Synergistic Interaction of Estradiol and Insulin Signaling

    There are both genotypic transcriptional and non-transcriptional effects in estrogen signal transduction: estrogen binds to ERα in the nucleus to exert genotypic effects, and the estrogen receptor GPER is located on the cell membrane to exert non-genotypic transcriptional effects. Studies have shown that estrogen combined with insulin can significantly promote the proliferation of endometrial cancer cells compared with estrogen or insulin alone (29). The combination of estrogen and a high-fat diet (mimic insulin resistance) could significantly stimulate the increase of endometrial glands in C57BL/6 mice. The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), peroxisome proliferator activated receptor (PPAR) and LXR/RXR signaling pathways may be involved in this process (30). Insulin upregulates TET1 and then upregulates GPER expression, which enhances the sensitivity of endometrial cancer cells to estrogen (31). Studies have found that estrogen and IGF-1 can synergistically promote the development of tumors in mice by activating MAPK and AKT signaling pathways (32). Other studies have found that estrogen may bind to IGF-1R and exert non-genetic transcriptional effects through the Ras/MAPK signaling pathway (33). How insulin and IGF-1 interact with estrogen in signaling pathways to promote the development of endometrial cancer warrants further investigation.

    Adipose-Derived mTOR Signaling

    Compared with non-obese patients, the activity of VEGF-mTOR in obese endometrial cancer patients increased significantly, suggesting that adipocyte-derived VEGF-mTOR signaling is a potential target for the treatment of obese women with endometrial cancer (34). Adipose tissue mesenchymal stem cell-derived medium can activate Akt/mTOR and promote the proliferation and invasion of cancer cells (35). A new bidirectional inhibitor of PI3K and mTOR is more effective than a simple inhibitor of mTOR (rapamycin) in inhibiting endometrial cancer (36). It is suggested that mTOR signaling may be a key pathway connecting obesity and endometrial cancer, which needs to be verified in a clinical trial.

    Adipose-Derived Stem Cells

    Adipose-derived stem cells play an important role in the tumor microenvironment. Obesity can promote the transformation of adipose-derived stem cells (ASCs) into cancer-related fibroblasts (CAFs), thereby promoting the proliferation and invasive phenotype of cancer cells (37). In addition, adipose-derived stem cells can promote ER + breast cancer cell metastasis independently of estrogen signaling (38). Leptin secreted by adipose-derived stem cells promotes the growth and metastasis of ER + breast cancer by increasing the expression of ER receptor and aromatase (39). It has been reported that ASCs can fuse with endometrial cancer cells, and the fused endometrial cancer cells present a fibroblast-like appearance of mesenchymal phenotype accompanied by downregulation of E-cadherin expression and upregulation of Vimentin expression (40). Further study of the role of ASCs in the occurrence of endometrial cancer will help to elucidate how obesity increases the risk of endometrial cancer.

    Adipose-Derived Adipokines


    Adiponectin is a cytokine secreted mainly by adipocytes. Epidemiological studies have shown that adiponectin levels in the blood circulation of patients with endometrial cancer are decreased (41). Serum low adiponectin levels are closely related to insulin resistance, hyperinsulinemia, obesity, and hypertension (42). A meta-analysis showed that serum adiponectin levels were negatively correlated with the risk of endometrial cancer, especially in post-menopausal women who did not receive HRT (43). In a meta-analysis of 26 studies, for each 1 μg/ml increase of adiponectin, there was a 3% reduction of summary relative risk (SRR) in endometrial cancer risk, and a 14% reduction for each increase of 5 μg/ml (44). Abnormal expression of serum adiponectin is also closely related to the occurrence and development of prostate cancer, breast cancer and colon cancer (45–47). However, the antitumor effect of adiponectin on endometrial cancer mainly depends on the alteration of systemic metabolic state or the direct interaction with tumor cells warrants further study.

    Adiponectin exerts its biological effects mainly by binding to adiponectin receptors. Three types of adiponectin receptors have been identified: adiponectin receptor 1 (AdipoR1), adiponectin receptor 2 (AdipoR2), and T-cadherin. AdipoR1 is mainly expressed in skeletal muscle and epithelial cells, and AdipoR2 is most abundant in the liver (48). AMPK is an important signaling pathway downstream of adiponectin. The adiponectin/AdipoR1 signaling axis can promote the phosphorylation of the AMPK Thr172 site by inducing phosphorylation of the tumor suppressor gene LKB1. AMPK phosphorylation also plays an important role in energy metabolism by activating the TSC2 tumor suppressor (49, 50). Studies have shown that there is no significant difference in the expression of AdipoR1 and AdipoR2 in normal endometrial tissues. In endometrial cancer tissues, the expression of AdipoR1 is higher than that of AdipoR2. Adiponectin/AdipoRs can inhibit the proliferation, adhesion and invasiveness of endometrial cancer cells by activating the downstream LKB1-AMPK/S6 signal axis (51). Adiponectin can not only inhibit the proliferation and migration of endometrial cancer cells through the AMPK/mTOR/S6K1 signaling pathway but can also enhance the sensitivity of endometrial cancer cells to insulin through the AMPK/S6K1/IRS1 signaling pathway (52). Adiponectin increases insulin sensitivity mainly by activating p38MAPK activity. It has been reported that the highly conserved 13-residue segment (ADP-1) of adiponectin can promote the translocation of glucose transporter 4 (GLUT4) to the cell membrane, reduce the blood sugar level of db/db mice and promote the secretion of insulin by pancreatic beta cells, thereby improving the metabolism of glucose and fatty acids (53). In addition, the anti-proliferative effect of adiponectin is related to a variety of cell cycle regulators, cyclin D1, D2, ERK1/2, and Akt.

    It is worth noting that adiponectin not only affects the tumor cells themselves but also regulates the tumor immune microenvironment. In contrast, it has been reported that the deletion of adiponectin may promote the transformation of M2 tumor-associated macrophages to M1 type through the p38MAPK signaling pathway, thereby inhibiting the growth of tumors (54). Therefore, on the one hand, adiponectin can reduce the occurrence of endometrial cancer by changing the metabolic state of the whole body; on the other hand, it can directly inhibit the proliferation of endometrial cancer cells. The decrease in serum adiponectin levels in obese patients is closely related to the increased risk of endometrial cancer (44).


    Visfatin is an insulin-like adipokine identified in recent years. Visfatin is highly expressed in many metabolically related tumors, and its increased expression is closely related to the increased risk of cancer (55). It has been reported that decreased serum adiponectin or increased visfatin levels are independent risk factors for endometrial cancer. The visfatin:adiponectin ratio in the endometrial cancer was significantly higher than the control, which has certain reference value for the diagnosis of endometrial cancer (56). With the increase of BMI, the level of visfatin in obese patients increases significantly. The increase in serum visfatin level is closely related with risk of myometrial invasion (OR: 1.091; 95%CI:1.021–1.166) and lymph node metastasis (OR: 1.018; 95%CI:1.000–1.035) of endometrial cancer. A high level of visfatin suggests poor prognosis in patients with endometrial cancer, which may be a potential therapeutic target for endometrial cancer (57, 58). Studies have shown that visfatin can upregulate the expression of IR and insulin receptor substrate (IRS) 1/2, and it can coactivate the PI3K/Akt and MAPK/ERK1/2 signaling pathways with insulin to promote the proliferation and inhibit apoptosis of endometrial cancer cells (59). Exogenous visfatin can promote the proliferation of breast cancer cells by promoting ERα phosphorylation and activating estrogen response element (ERE)-dependent signaling pathways (60). However, it has not been reported whether visfatin can also enhance estrogen-dependent ER signaling and accelerate the development of endometrial cancer. In addition, visfatin has been reported to be abnormally expressed in a variety of tumors, which can increase the risk of multiple tumors and become a potential molecular marker for the early detection of tumors (55). Therefore, the combination of visfatin and adiponectin may be a marker for the early clinical diagnosis of endometrial cancer and may provide new targets for clinical intervention.


    Leptin is an important adipokine encoded by the obesity gene. Leptin plays an important role in regulating food intake, energy consumption and promoting cell growth by combining with leptin receptor (ObR). Recent studies have found that abnormal expression of leptin and leptin receptor signaling related to obesity plays an important role in the development of breast, colon and endometrial cancer (61, 62). A meta-analysis showed that high levels of leptin can significantly increase the risk of endometrial cancer (risk ratio, RR = 2.55) and that high levels of leptin are an independent risk factor for endometrial cancer (63). The expression of leptin and ObR is positively correlated with the invasiveness of tumors and BMI of patients but is negatively correlated with histological grade. The elevated expression of leptin and ObR is closely related to lymph node metastasis and poor survival prognosis, as well as the positive expression of ERs (64). However, whether the leptin signaling pathway can influence the development of endometrial cancer by affecting the classical estrogen signaling pathway remains to be further confirmed. Studies have shown that the expression of ObR in poorly differentiated endometrial cancer tissues is significantly higher than that in well-differentiated endometrial cancer tissues, and leptin can inhibit the apoptosis of endometrial cancer cells by activating the NIK/IKK signaling pathway. Elevated leptin levels can influence epithelial polarity and promote malignant transformation through overactivation of the PI3K/Akt signaling pathway (65). Leptin also promotes the proliferation and invasion of endometrial cancer cells by activating STAT3 and ERK1/2, JNK signaling pathways. Correspondingly, this proliferation is inhibited when the JAK/STAT3 pathway is blocked (66). Other studies have reported that the leptin-2548 G/A SNP may be involved in the occurrence and development of endometrial cancer (67). It has been reported that leptin can upregulate the expression of STAT3-CPT1B and plays an important role in maintaining the stem and drug resistance of breast cancer cells (68). However, the role of leptin in the maintenance stem cell of endometrial cancer has not been determined to date and requires further study. Elevated leptin levels suggest the presence of endometrial cancer, and serum leptin levels may be an effective tool for assessing the clinical staging of endometrial cancer (69). Although elevated leptin level is a high-risk factor for endometrial cancer, whether it is the most critical molecule associated with obesity and endometrial cancer warrants further investigation.

    Adipose-Derived Inflammatory Cytokines

    Inflammation is the core stage of tumorigenesis and development. It has been reported that 18% of cancer cases worldwide are related to chronic infection, which implies a potential relationship between cancer and inflammation. In a lean state, a balance between adipocytes and immune cells can maintain normal metabolism throughout the body. However, in obese people, this balance translates into a markedly inflammatory adipose tissue microenvironment. Obesity-related adipose inflammation can increase the secretion of pro-inflammatory factors, cause systemic metabolic disorders, and change the microenvironment of tumors, thereby significantly increasing the risk of cancer in obese people. Several studies have confirmed that obesity-related inflammatory cytokines are involved in tumorigenesis.


    IL-6 is an inflammatory cytokine that plays an important role in many physiological and pathological processes. IL-6 is closely associated with a three times increased risk of mortality in overweight/obese patients (70). Studies have confirmed that IL-6 is closely related to the occurrence of a variety of tumors, including endometrial cancer. Adipose-derived IL-6 can promote the proliferation, invasion and angiogenesis of endometrial cancer cells by activating the JAK/STAT3 signaling pathway (71). The elevated plasma level of IL-6 is closely related to the poor prognosis of tumors (72). In addition, estrogen can promote the expression of IL-6 in endometrial cancer cells by binding to GPER on the cell surface (73). It has been reported that estrogen (E2) can promote the expression of IL-6 by binding with nuclear receptor ERα, and IL-6 can promote the synthesis of aromatase by binding with IL-6R of basal cells, thereby accelerating the synthesis of estrogen and forming a positive feedback loop (74). A new study confirms that blocking IL-6-driven inflammatory signaling can inhibit the spread of cancer cells to the liver (75). IL-6 is likely to play a prominent role in the development of endometrial cancer, and it appears to be one of the major mechanisms involved in the obesity-cancer link.


    TNF-α is an inflammatory cytokine secreted by macrophages and adipocytes. It is an important regulator of adipose tissue metabolism and plays an important role in immune regulation, inflammatory response and anti-tumor response. However, recent studies have found that TNF-α is also an endogenous tumor-promoting factor that can promote the proliferation, invasion and metastasis of cancer cells. The level of TNF-α in circulating blood of obese patients is increased, and the increased level of TNF-α is closely related to the poor prognosis of endometrial cancer patients (76). In addition, studies have reported that 11 cancer markers in overweight patients are significantly higher than those in normal weight patients, including ANG-2, sFASL, HB-EGF, IL-8, PLGF, TGF-α, TNF-α, uPA, VEGF-A, VEGF-C, and VEGF-D (77). Compared with lean mice, C57BL/6 mice induced by a high-fat diet had higher levels of serum free fatty acids and TNF-α and higher accumulation of macrophages in adipose tissue (78). A case-control study showed that elevated levels of TNF-α and its soluble receptors (sTNFR1 and sTNFR2) were associated with an increased risk of endometrial cancer [TNF-α-odds ratio [OR]: 1.73; sTNFR1-[OR]:1.68; sTNFR2-[OR]:1.53] (79). Regarding the mechanism of TNF-α in promoting tumorigenesis and development, it has been reported that chronic inflammation induced by obesity promotes the accumulation of macrophages in adipose tissue. TNF-α released by M1 macrophages can promote metastasis and inhibit apoptosis of ovarian cancer cells by activating the signaling pathway of NF-κB (80). TNF-α is also a key factor driving the expression of the aromatase gene, and IL-10 can regulate the expression of aromatase in adipose tissue by inhibiting the TNF-α signaling pathway (81). Moreover, TNF-α could induce serine phosphorylation of IRS-1 and inhibit its triggering of downstream signals, leading to insulin resistance. Insulin resistance-induced hyperinsulinemia and IGF-1 can further enhance the biological effects of TNF-α by activating the TNF-α signaling pathway (80). TNF-α inhibited apoptosis in cancer cells by activating the NF-κB signaling pathway. Although several pathways between TNF-α and tumors have been identified, the precise mechanism of obesity-related TNF-α involved in the development of endometrial cancer remains to be further investigated.


    Plasminogen activator inhibitor-1 (PAI-1) is a protease inhibitor produced by vascular endothelial cells, stromal cells and adipocytes in adipose tissue. Recent studies have found that PAI-1 not only plays an important role in influencing insulin signaling but also plays an important biological role in influencing the invasion, invasion and metastasis of obesity-related tumors (82). PAI-1 is highly expressed in endometrial cancer tissues and is closely related to the poor prognosis of endometrial cancer (83). Studies have reported that PAI-1 may mediate the transcriptional regulation of adipose-derived stem cells in endometrial cancer (84). Therefore, PAI-1 represents a potential therapeutic target.

    Effect of Obesity on the Tumor Immune Microenvironment

    Obesity can promote adipocytes to secrete pro-inflammatory factors, such as TNF-α, IL-6, and IL-18. These pro-inflammatory cytokines can further enhance the infiltration of inflammatory cells, mainly macrophages and T lymphocytes, thereby promoting abnormal proliferation and transformation of normal cells (85). Studies have shown that 16 weeks of aerobic and endurance training can reduce the expression of inflammatory cytokines (IL-6 and TNF-α) in adipose tissue and induce the transformation of inflammatory M1 macrophages into anti-inflammatory M2 macrophages (86). It has been found that adipose tissue-derived leptin can promote the differentiation of Th27 cells and promote T cell function by regulating cell metabolic reprogramming (87). Recent studies have shown that obesity can increase the infiltration of tumor-related macrophages, upregulate the production of IL-1β, and promote angiogenesis and tumor progression (88). It has been reported that M2 macrophages infiltrated in the microenvironment of endometrial cancer can enhance the sensitivity of endometrial cancer cells to estrogen by releasing cytokine IL17A and upregulating the expression of ERα through TET1-mediated epigenetics (8). These studies indicated that obesity may further promote the occurrence and progression of endometrial cancer by affecting the immune microenvironment of tumors.

    Type 2 Diabetes And Endometrial Cancer

    Most epidemiological studies suggested that diabetes is a risk factor for endometrial cancer incidence; for example, a meta-analysis of 16 studies showed that diabetes was statistically significantly associated with an increased risk of endometrial cancer (summary RR 2.10, 95% CI 1.75–2.53), and there was a stronger association with a adjusting for age (RR 2.74, 95% CI 1.87–4.00) (89). Also, diabetes is closely related to increased cancer-specific mortality (HR 2.09, 95% CI 1.31–3.35) and mortality from non-cancer related causes in women with endometrial cancer (90). Therefore, these studies show that diabetes increases both the risk and mortality rates of endometrial cancer.

    Effect of Hyperglycemia on Endometrial Cancer

    Hyperglycemia is an important clinical characteristic of type 2 diabetes mellitus. Systemic hyperglycemia provides favorable conditions for energy metabolism of cancer cells. Previous studies have confirmed that elevated serum glucose can directly regulate cancer-related signaling pathways, especially to meet the needs of rapid proliferation of cancer cells, and can promote the process of glycometabolism reprogramming (91). Metabolic reprogramming is one of the important hallmarks of tumor cells, which are different from normal cells. Even in the presence of abundant oxygen, ~80% of tumor cells metabolize glucose and produce ATP mainly through aerobic glycolysis, also known as the Warburg effect. In addition to the rapid production of energy, glycolysis can also produce a large number of metabolic intermediates, which can be used to synthesize biological macromolecules needed for the rapid growth of tumors, including nucleotides, fatty acids, and proteins.

    Glucose transporter (GLUT) is the main carrier of glucose uptake by cells. When glucose enters the cell, GLUT transports allosteric to transport glucose into the cell to support the high glycolysis rate. It has been reported that high glucose could promote the expression of vascular endothelial growth factor (VEGF)/VEGFR and the process of (epithelial-mesenchymal transition) EMT by regulating the expression of ERα/GLUT4, thereby promoting the proliferation and invasion of endometrial cancer cells (92). In addition, high glucose can increase the activity of glucose uptake and glycolysis by regulating AMPK/mTOR/S6 and MAPK pathways, thereby leading to increased invasiveness of endometrial cancer cells. Moreover, high glucose can promote the proliferation of endometrial cancer cells by activating STAT3 expression, which can be inhibited by metformin (93). The activity of glucose metabolism is closely related to the concentration of glucose outside the cell. However, it is not clear how cells perceive external glucose levels and regulate glycolysis pathway activity. AMPK, an adenylate-activated protein kinase, is a key protein for the perception of extracellular glucose concentration (94). It was reported that high extracellular glucose levels regulate the protein level of CARM1 by reducing AMPK phosphorylation, thereby inhibiting GAPDH methylation, which further promotes the activity of the GAPDH enzyme and glycolysis pathway (95). This study reveals the mechanism by which cells perceive extracellular glucose levels and regulate the rate of glycolysis, helping to elucidate the mechanism by which cancer cells perceive and utilize glucose.

    Pyruvate kinase isozymes M2 (PKM2) is a key metabolic enzyme that promotes glycolysis and plays an important role in tumorigenesis through the Warburg effect. It has been reported that high glucose could promote the abnormal expression of PKM2. Overexpression of PKM2 could promote the accumulation of glycolysis intermediates (pyruvate and lactic acid), provide precursors for the synthesis of biomacromolecules, and lead to cell proliferation and tumorigenesis (96). Lactic acid is a key metabolite of glycolysis in cancer cells. The accumulation of extracellular lactic acid has an important impact on the metabolism of cancer cells and the transformation of non-cancer cells into cancer cells, including metabolic reprogramming, tumor inflammation, and angiogenesis. Recent studies have found that lactic acid produced by glycolysis of cancer cells can inhibit the function of macrophages through a hypoxia-inducible factor-mediated mechanism, induce the transformation of anti-tumor type M1 macrophages into M2, and promote the invasion and migration of cancer cells (97). Interestingly, M2 macrophages are the predominant tumor-associated macrophages in endometrial cancer and play an important role in the occurrence and development of endometrial cancer (98). Monocarboxylate Transporter 1 (MCT1) is an important protein for lactic acid and pyruvate uptake by cells, while MCT4 is an important protein for cell transport of lactic acid and pyruvate, which play an important role in regulating lactic acid metabolism. It has been reported that MCT1 was an independent prognostic biomarker in endometrial cancer (99). A recent study reported that the use of monocarboxylic acid transporter (MCT) inhibitors can reverse the inhibition of lactic acid on macrophage lysosomes (100). Therefore, MCT1 inhibition may have potential as a treatment for endometrial cancer. It is suggested that the enhancement of glycolysis activity and metabolites, such as lactic acid, in endometrial cancer under a high glucose environment may lead to acidification of the tumor microenvironment. The acidic environment may be perceived by tumor-related macrophages, which depend on the monocarboxylic acid transporter 1 (MCT1) pathway to induce macrophage transformation from M1 to M2, thus accelerating the progress of endometrial cancer. These studies suggested that managing hyperglycemia or targeting glycometabolism may be a potential therapeutic strategy for endometrial cancer.

    Effect of Insulin Resistance on Endometrial Cancer

    Insulin resistance and hyperinsulinemia are important characteristics of obesity and diabetes. The expression of insulin and IGF-1 was significantly increased in diabetic patients, and high insulin levels were an independent factor of endometrial cancer (28, 101, 102). High insulin and IGF-1/2 levels in diabetic patients can accelerate the transformation of androstenedione into estrogen by aromatase and increase estrogen levels by inhibiting the synthesis of SHBG. Long-term estrogen stimulation without progesterone antagonism can cause endometrial dysplasia or even malignant transformation (103). It has been reported that after adjusting for BMI, age and histological type, the high expression of IR/IGF-1R is closely related to prognostic high-risk factors, such as the progression of endometrial cancer and lymph node infiltration (104).

    Insulin can activate the phosphoinositide 3-kinase (PI3K)/AKT or mitogen-activated protein kinase (MAPK)/extracellular signaled regulated kinase ERK signaling pathway through binding to IR/IGF-1R to promote EMT of endometrial cancer, which leads to increased proliferation and invasion of endometrial cancer cells, inhibits apoptosis of cancer cells and promotes angiogenesis of tumors (105). In addition, insulin could upregulate the expression of vascular endothelial growth factor, thereby stimulating angiogenesis, which is closely related to the occurrence and development of tumors (106). Recent studies have reported that insulin signal-dependent phosphorylation initiates glucose metabolism prior to glucose transport; thus, the metabolism of glucose is diverted to a specific direction of glycolysis (107). In this way, insulin signaling plays a key role in glycometabolism reprogramming, and insulin resistance can promote the occurrence and development of endometrial cancer through an indirect pathway or ligand-receptor direct pathway.

    IR-A has high affinity for insulin and IGF-II but binds IGF-I with low affinity. IGF-1R has high affinity for IGFs. However, blocking IGF-IR and IR does not completely prevent the growth stimulation of insulin-like growth factor or insulin on cancer cells, suggesting that other receptors may be involved in complex signal transduction systems. Our previous studies found and confirmed for the first time the expression of Hybrid-R in endometrial cancer, which can promote the proliferation and inhibit apoptosis of endometrial cancer cells through the MAPK/ERK signaling pathway (22). Hybrid-R is expected to provide a new therapeutic target and strategy for the precise treatment of endometrial cancer patients with insulin resistance and hyperinsulinemia.

    Metformin in the Treatment of Endometrial Cancer

    Metformin, an insulin sensitizer, is considered a potential anticancer drug. Our previous clinical studies have found that metformin combined with progesterone treatment can significantly improve the efficacy of endometrial cancer patients with poor progesterone treatment (108). It has been reported that plasma hyperglycemia and high levels of IGF-1 in patients with endometrial cancer can be reversed by conventional doses of metformin (109). Metformin can significantly inhibit the proliferation of endometrial cancer cells, which may be related to the activation of AMPK signaling and the inhibition of the mTOR signaling pathway (110). In contrast, some studies have shown that metformin does not reduce the risk of endometrial cancer, nor can it improve the overall survival of patients (111). Correspondingly, studies have found that metformin does not affect the PI3K-Akt-mTOR and insulin signaling pathways and has no effect on weight loss (112). It is of great clinical significance to further study the mechanism of abnormal glucose metabolism promoting endometrial cancer, reveal the key molecule of endometrial cancer caused by metabolic diseases, and find new effective preventive or anti-cancer drugs that can replace metformin.

    Other Types OF Diseases OF Metabolic Syndrome And Endometrial Cancer

    Dyslipidemia is closely related to the incidence of various cancers (113). It was reported that patients with hyperglycemia, hyperlipidemia and hypertension are twice as likely to develop endometrial cancer as normal people (114). The BMI of patients was positively correlated with serum palmitic acid, oleic acid and stearic acid levels. The increase of free fatty acids in obese patients can indirectly promote the proliferation of endometrial cancer cells by increasing the level of estradiol (115). The BMI of patients with endometrial cancer was significantly higher than that of normal controls. At present, there are many studies on the relationship between endometrial cancer and obesity and diabetes, but there are few studies on the relationship between endometrial cancer and hypertension and lipid disorders. The possible mechanisms of abnormal blood lipids associated with the risk of endometrial cancer are as follows: activation of fatty acid and amino hexose pathways leads to the production of reactive oxygen species (ROS) in mitochondria, which induces oxidative stress in cells. Excessive aggregation of ROS clusters interacts with lipids, proteins and DNA in cells, causing changes in membrane and enzyme functions, inducing cell damage, and ultimately leading to tumorigenesis (116). Recent studies have reported that serum cholesterol is elevated in obese people. Cholesterol activates the transcriptional activity of endometrial cancer cells through an ER-dependent pathway and promotes the proliferation of endometrial cancer cells (117). Moreover, recent studies have found that elevated circulating free fatty acids may be an important factor in linking obesity and tumorigenesis, which can promote the proliferation and invasion of breast cancer cells through ERα signaling and the mTOR signaling pathway (118). It has been reported that A-FABP released from adipose tissue can promote the dryness and invasiveness of breast cancer cells (119). Taken together, abnormal lipid metabolism, especially elevated free fatty acids, is closely related to the progression of endometrial cancer. Can fatty acids participate in the occurrence and development of endometrial cancer through an ER-dependent pathway remains to be thoroughly characterized.

    Hypothyroidism is a type of reduced metabolic syndrome caused by a decrease in thyroid hormone synthesis and secretion or by inadequate physiological effects. Brinton et al. indicated that EC is related to previous diagnoses of thyroid diseases (RR = 1.52, 95% CI 1.17–1.98) (120). It has been reported that the incidence of hypothyroidism in EC patients is significantly increased. Serum TSH level before treatment is an independent risk factor for poor prognosis of EC (121). Additionally, elevated TSH levels have been reported to increase the incidence of MS (122). At present, there are few studies on thyroid function and endometrial cancer. Several studies have shown that hypothyroidism is closely related to MS, PCOS, elevated serum leptin levels, and dyslipidemia. Hypothyroidism may promote the occurrence and development of endometrial cancer by indirectly increasing the risk factors of endometrial cancer or through direct interaction (123). Studies examining the relationship between thyroid function (TSH level) and endometrial cancer will provide new insights into the mechanism of endometrial cancer.


    Metabolic syndrome is a complex disorder defined by a cluster of metabolic risk factors that includes insulin resistance, hyperinsulinemia, impaired glucose tolerance, type 2 diabetes mellitus, dyslipidemia, and visceral obesity. Obesity, diabetes and hypertension are the metabolic triad of endometrial cancer. There was a very high prevalence of metabolic syndrome in women newly diagnosed with endometrial cancer. In this article, we review potential pathways directly linking metabolic syndrome with cancer (Figure 2). Obesity-related insulin resistance, leptin and lactone levels are closely related to the occurrence and development of endometrial cancer. Decreased serum adiponectin levels and increased chronic inflammation in obese patients are important factors for increasing the risk of endometrial cancer. Obesity and diabetes have many common pathological characteristics: insulin resistance (hyperinsulinemia), abnormal fat metabolism (elevated leptin, decreased adiponectin), hyperglycemia, hyperlipidemia and chronic inflammation. Many studies have reported that these characteristics can promote the occurrence and development of endometrial cancer by directly acting on tumor cells or regulating the tumor microenvironment. Therefore, there is an urgent need to intervene in chronic diseases related to metabolic syndrome to reduce the incidence of endometrial cancer. A commentary by MacKintosh et al. indicated obese undergoing bariatric surgery or medical weight loss management could reduce the risk of endometrial cancer and hyperplastic abnormalities of the endometrium may be reversible through weight loss (124). Studies have assessed the effects of obesity and weight-loss surgery on endometrial morphology and molecular signaling pathways in endometrial cancer. It was found that insulin resistance (HbA1c, HOMA-IR) and inflammation (hsCRP, IL-6) circulating biomarkers decreased, while reproductive biomarkers (LH, FSH, SHBG) increased significantly (125). C-peptide, insulin, C-reactive protein, leptin, IL-1Ralpha, and IL-6 decreased significantly, while SHBG, IGFBP1, and adiponectin increased significantly in weight-loss interventions in endometrial cancer (126). Thus, bariatric surgery may reduce the risk of endometrial cancer by improving obesity-induced inflammation. However, the role of bariatric surgery in the treatment of endometrial hyperplasia still need conclusive or convincing evidence. Recently, seven markers based on the BMI-sensitive pathway of insulin resistance, adipoR1, adipoR2, ObR, IRβ, IRS-1, IGF-1R, and IGF-2R, have been proposed to develop a new molecular typing system for endometrial cancer. However, no effective molecular typing system and molecular typing markers have been found for endometrial cancer (127). A research proposed a pragmatic endometrial cancer risk prediction model, which included obesity, reproduction, insulin resistance, and genetic risk. This model plays an important role in identifying individuals at high risk of endometrial cancer and guiding preventive treatment of specific disease targets (128). Except for obesity, reproduction, insulin resistance, and genetic risk, the other metabolic syndrome related high risk factors for endometrial cancer as mentioned in the text should also be considered and a large prospective cohort of asymptomatic women is required. Similarly, studies incorporating biomarkers (adiponectin, estradiol, interleukin-1 receptor antagonist, tumor necrosis factor-and triglyceride) into the risk prediction model of endometrial cancer have found that they can modestly improve the predictive ability of endometrial cancer (129). Despite different studies, new molecular markers have been reported, but to date, no reliable molecular markers have been applied to clinical molecular typing. Our recent study found that serum total calcium may be a more sensitive metabolic syndrome parameter than hyperlipidemia in patients with endometrioid cancer (130).

    Figure 2. Potential pathways directly linking metabolic syndrome with endometrial cancer.

    Therefore, it is necessary to screen new markers based on systemic metabolomic changes and to reveal new molecular typing methods and risk prognostic models of endometrial cancer based on serum metabolomic changes. With the frequent application of proteomics, metabolomics, and transcriptomes, the role of key molecules in identifying metabolic syndrome-related diseases in endometrial cancer is of great significance for the early prevention and treatment of endometrial cancer. In conclusion, endometrial cancer is a type of metabolic disease-related tumor. Elucidating the specific roles and mechanisms of metabolic syndrome-related diseases in endometrial cancer is expected to provide a new target for the early prevention and treatment of endometrial cancer. Although the study of the association between metabolic syndrome and cancer may provide an effective therapeutic target for endometrial cancer, improving lifestyle is still the most important component in preventing the morbidity and mortality of endometrial cancer associated with metabolic syndrome. Further in vivo and clinical studies are needed to investigate the therapeutic targeting of the metabolic microenvironment in metabolic syndrome-related endometrial cancer.

    Author Contributions

    XY and JW wrote and approved the final version of this manuscript.


    This work was supported by the National Natural Science Foundation of China (grant nos. 81672571 and 81874108), Special Projects for Strengthening Basic Research of Peking University (grant no. BMU2018JC005), and National Key Technology Research and Development Program (grant no. 2015BAI13B06).

    Conflict of Interest Statement

    The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


    2. Sheikh MA, Althouse AD, Freese KE, Soisson S, Edwards RP, Welburn S, et al. USA endometrial cancer projections to 2030: should we be concerned? Future Oncol. (2014) 10:2561–8. doi: 10.2217/fon.14.192

    PubMed Abstract | CrossRef Full Text | Google Scholar

    3. Tejerizo-Garcia A, Jimenez-Lopez JS, Munoz-Gonzalez JL, Bartolome-Sotillos S, Marqueta-Marques L, Lopez-Gonzalez G, et al. Overall survival and disease-free survival in endometrial cancer: prognostic factors in 276 patients. Onco Targets Ther. (2013) 9:1305–13. doi: 10.2147/OTT.S51532

    PubMed Abstract | CrossRef Full Text | Google Scholar

    4. Hao J, Bao X, Jin B, Wang X, Mao Z, Li X, et al. Ca2+ channel subunit alpha 1D promotes proliferation and migration of endometrial cancer cells mediated by 17beta-estradiol via the G protein-coupled estrogen receptor. FASEB J. (2015) 29:2883–93. doi: 10.1096/fj.14-265603

    PubMed Abstract | CrossRef Full Text | Google Scholar

    7. Thigpen JT, Brady MF, Alvarez RD, Adelson MD, Homesley HD, Manetta A, et al. Oral medroxyprogesterone acetate in the treatment of advanced or recurrent endometrial carcinoma: a dose-response study by the Gynecologic Oncology Group. J Clin Oncol. (1999) 17:1736–44. doi: 10.1200/JCO.1999.17.6.1736

    PubMed Abstract | CrossRef Full Text | Google Scholar

    8. Ning C, Xie B, Zhang L, Li C, Shan W, Yang B, et al. Infiltrating macrophages induce ERalpha expression through an IL17A-mediated epigenetic mechanism to sensitize endometrial cancer cells to estrogen. Cancer Res. (2016) 76:1354–66. doi: 10.1158/0008-5472.CAN-15-1260

    PubMed Abstract | CrossRef Full Text | Google Scholar

    9. Cherry N, McNamee R, Heagerty A, Kitchener H, Hannaford P. Long-term safety of unopposed estrogen used by women surviving myocardial infarction: 14-year follow-up of the ESPRIT randomised controlled trial. BJOG. (2014) 121:700–5. Discussion 5. doi: 10.1111/1471-0528.12598

    PubMed Abstract | CrossRef Full Text | Google Scholar

    11. Esposito K, Chiodini P, Capuano A, Bellastella G, Maiorino MI, Giugliano D. Metabolic syndrome and endometrial cancer: a meta-analysis. Endocrine. (2014) 45:28–36. doi: 10.1007/s12020-013-9973-3

    PubMed Abstract | CrossRef Full Text | Google Scholar

    12. Kitson SJ, Lindsay J, Sivalingam VN, Rutter MK, Crosbie EJ. High prevalence of metabolic syndrome in women newly diagnosed with endometrial cancer. Gynecol Oncol Rep. (2018) 26:109–10. doi: 10.1016/j.gore.2018.08.006

    PubMed Abstract | CrossRef Full Text | Google Scholar

    13. Kitson SJ, Lindsay J, Sivalingam VN, Lunt M, Ryan NAJ, Edmondson RJ, et al. The unrecognized burden of cardiovascular risk factors in women newly diagnosed with endometrial cancer: a prospective case control study. Gynecol Oncol. (2018) 148:154–60. doi: 10.1016/j.ygyno.2017.11.019

    PubMed Abstract | CrossRef Full Text | Google Scholar

    14. Trabert B, Wentzensen N, Felix AS, Yang HP, Sherman ME, Brinton LA. Metabolic syndrome and risk of endometrial cancer in the United States: a study in the SEER-medicare linked database. Cancer Epidemiol Biomarkers Prev. (2015) 24:261–7. doi: 10.1158/1055-9965.EPI-14-0923

    PubMed Abstract | CrossRef Full Text | Google Scholar

    15. Nead KT, Sharp SJ, Thompson DJ, Painter JN, Savage DB, Semple RK, et al. Evidence of a causal association between insulinemia and endometrial cancer: a mendelian randomization analysis. J Natl Cancer Inst. (2015) 107:djv178. doi: 10.1093/jnci/djv178

    PubMed Abstract | CrossRef Full Text | Google Scholar

    16. Cuny T, de Herder W, Barlier A, Hofland LJ. Role of the tumor microenvironment in digestive neuroendocrine tumors. Endocr Relat Cancer. (2018) 25:R519–44. doi: 10.1530/ERC-18-0025

    PubMed Abstract | CrossRef Full Text | Google Scholar

    17. Ecker BL, Lee JY, Sterner CJ, Solomon AC, Pant DK, Shen F, et al. Impact of obesity on breast cancer recurrence and minimal residual disease. Breast Cancer Res. (2019) 21:41. doi: 10.1186/s13058-018-1087-7

    PubMed Abstract | CrossRef Full Text | Google Scholar

    18. World Cancer Research Fund/American Institute for Cancer Research. Continuous Update Project Report. Food, Nutrition, Physical Activity, and the Prevention of Endometrial Cancer. (2013). Available online at: http://www.dietandcancerreport.org (accessed August 1, 2019).

    Google Scholar

    19. Ward KK, Roncancio AM, Shah NR, Davis MA, Saenz CC, McHale MT, et al. Bariatric surgery decreases the risk of uterine malignancy. Gynecol Oncol. (2014) 133:63–6. doi: 10.1016/j.ygyno.2013.11.012

    PubMed Abstract | CrossRef Full Text | Google Scholar

    21. Crosbie EJ, Zwahlen M, Kitchener HC, Egger M, Renehan AG. Body mass index, hormone replacement therapy, and endometrial cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev. (2010) 19:3119–30. doi: 10.1158/1055-9965.EPI-10-0832

    PubMed Abstract | CrossRef Full Text | Google Scholar

    22. Ye J, McGuinness OP. Inflammation during obesity is not all bad: evidence from animal and human studies. Am J Physiol Endocrinol Metab. (2013) 304:E466–77. doi: 10.1152/ajpendo.00266.2012

    CrossRef Full Text | Google Scholar

    23. Kim JH, Lee E, Friedline RH, Suk S, Jung DY, Dagdeviren S, et al. Endoplasmic reticulum chaperone GRP78 regulates macrophage function and insulin resistance in diet-induced obesity. FASEB J. (2018) 32:2292–304. doi: 10.1096/fj.201701017R

    PubMed Abstract | CrossRef Full Text | Google Scholar

    24. Szeto HH, Liu S, Soong Y, Alam N, Prusky GT, Seshan SV. Protection of mitochondria prevents high-fat diet-induced glomerulopathy and proximal tubular injury. Kidney Int. (2016) 90:997–1011. doi: 10.1016/j.kint.2016.06.013

    PubMed Abstract | CrossRef Full Text | Google Scholar

    26. Perrotta F, Nigro E, Mollica M, Costigliola A, D’Agnano V, Daniele A, et al. Pulmonary hypertension and obesity: focus on adiponectin. Int J Mol Sci. (2019) 20:E912. doi: 10.3390/ijms20040912

    PubMed Abstract | CrossRef Full Text | Google Scholar

    27. Liu Z, Wang N, Ma Y, Wen D. Hydroxytyrosol improves obesity and insulin resistance by modulating gut microbiota in high-fat diet-induced obese mice. Front Microbiol. (2019) 10:390. doi: 10.3389/fmicb.2019.00390

    PubMed Abstract | CrossRef Full Text | Google Scholar

    29. Tian W, Teng F, Zhao J, Gao J, Gao C, Sun D, et al. Estrogen and insulin synergistically promote type 1 endometrial cancer progression. Cancer Biol Ther. (2017) 18:1000–10. doi: 10.1080/15384047.2017.1394547

    PubMed Abstract | CrossRef Full Text | Google Scholar

    30. Cheng Y, Lv Q, Xie B, Yang B, Shan W, Ning C, et al. Estrogen and high-fat diet induced alterations in C57BL/6 mice endometrial transcriptome profile. Endocr Connect. (2018) 7:36–46. doi: 10.1530/EC-17-0315

    PubMed Abstract | CrossRef Full Text | Google Scholar

    31. Xie BY, Lv QY, Ning CC, Yang BY, Shan WW, Cheng YL, et al. TET1-GPER-PI3K/AKT pathway is involved in insulin-driven endometrial cancer cell proliferation. Biochem Biophys Res Commun. (2017) 482:857–62. doi: 10.1016/j.bbrc.2016.11.124

    PubMed Abstract | CrossRef Full Text | Google Scholar

    32. Tang H, Liao Y, Xu L, Zhang C, Liu Z, Deng Y, et al. Estrogen and insulin-like growth factor 1 synergistically promote the development of lung adenocarcinoma in mice. Int J Cancer. (2013) 133:2473–82. doi: 10.1002/ijc.28262

    PubMed Abstract | CrossRef Full Text | Google Scholar

    33. Kamanga-Sollo E, White ME, Hathaway MR, Chung KY, Johnson BJ, Dayton WR. Roles of IGF-I and the estrogen, androgen and IGF-I receptors in estradiol-17beta- and trenbolone acetate-stimulated proliferation of cultured bovine satellite cells. Domest Anim Endocrinol. (2008) 35:88–97. doi: 10.1016/j.domaniend.2008.02.003

    PubMed Abstract | CrossRef Full Text | Google Scholar

    34. Sahoo SS, Lombard JM, Ius Y, O’Sullivan R, Wood LG, Nahar P, et al. Adipose-derived VEGF-mTOR signaling promotes endometrial hyperplasia and cancer: implications for obese women. Mol Cancer Res. (2018) 16:309–21. doi: 10.1158/1541-7786.MCR-17-0466

    PubMed Abstract | CrossRef Full Text | Google Scholar

    35. Ko JH, Um JY, Lee SG, Yang WM, Sethi G, Ahn KS. Conditioned media from adipocytes promote proliferation, migration, and invasion in melanoma and colorectal cancer cells. J Cell Physiol. (2019) 234:18249–61. doi: 10.1002/jcp.28456

    PubMed Abstract | CrossRef Full Text | Google Scholar

    36. Chen J, Zhao KN, Li R, Shao R, Chen C. Activation of PI3K/Akt/mTOR pathway and dual inhibitors of PI3K and mTOR in endometrial cancer. Curr Med Chem. (2014) 21:3070–80. doi: 10.2174/0929867321666140414095605

    PubMed Abstract | CrossRef Full Text | Google Scholar

    37. Strong AL, Pei DT, Hurst CG, Gimble JM, Burow ME, Bunnell BA. Obesity enhances the conversion of adipose-derived stromal/stem cells into carcinoma-associated fibroblast leading to cancer cell proliferation and progression to an invasive phenotype. Stem Cells Int. (2017) 2017:9216502. doi: 10.1155/2017/9216502

    PubMed Abstract | CrossRef Full Text | Google Scholar

    38. Sabol RA, Beighley A, Giacomelli P, Wise RM, Harrison MAA, O’Donnnell BA, et al. Obesity-altered adipose stem cells promote ER(+) breast cancer metastasis through estrogen independent pathways. Int J Mol Sci. (2019) 20:E1419. doi: 10.3390/ijms20061419

    PubMed Abstract | CrossRef Full Text | Google Scholar

    39. Strong AL, Strong TA, Rhodes LV, Semon JA, Zhang X, Shi Z, et al. Obesity associated alterations in the biology of adipose stem cells mediate enhanced tumorigenesis by estrogen dependent pathways. Breast Cancer Res. (2013) 15:R102. doi: 10.1186/bcr3569

    PubMed Abstract | CrossRef Full Text | Google Scholar

    40. Li M, Li X, Zhao L, Zhou J, Cheng Y, Xu B, et al. Spontaneous formation of tumorigenic hybrids between human omental adipose-derived stromal cells and endometrial cancer cells increased motility and heterogeneity of cancer cells. Cell Cycle. (2019) 18:320–32. doi: 10.1080/15384101.2019.1568743

    PubMed Abstract | CrossRef Full Text | Google Scholar

    41. Rzepka-Gorska I, Bedner R, Cymbaluk-Ploska A, Chudecka-Glaz A. Serum adiponectin in relation to endometrial cancer and endometrial hyperplasia with atypia in obese women. Eur J Gynaecol Oncol. (2008) 29:594–7.

    PubMed Abstract | Google Scholar

    42. Aggeloussi S, Theodorou AA, Paschalis V, Nikolaidis MG, Fatouros IG, Owolabi EO, et al. Adipocytokine levels in children: effects of fatness and training. Pediatr Exerc Sci. (2012) 24:461–71. doi: 10.1123/pes.24.3.461

    PubMed Abstract | CrossRef Full Text | Google Scholar

    43. Zeng F, Shi J, Long Y, Tian H, Li X, Zhao AZ, et al. Adiponectin and endometrial cancer: a systematic review and meta-analysis. Cell Physiol Biochem. (2015) 36:1670–8. doi: 10.1159/000430327

    PubMed Abstract | CrossRef Full Text | Google Scholar

    45. Karnati HK, Panigrahi MK, Li Y, Tweedie D, Greig NH. Adiponectin as a potential therapeutic target for prostate cancer. Curr Pharm Des. (2017) 23:4170–9. doi: 10.2174/1381612823666170208123553

    PubMed Abstract | CrossRef Full Text | Google Scholar

    47. Nigro E, Schettino P, Polito R, Scudiero O, Monaco ML, De Palma GD, et al. Adiponectin and colon cancer: evidence for inhibitory effects on viability and migration of human colorectal cell lines. Mol Cell Biochem. (2018) 448:125–35. doi: 10.1007/s11010-018-3319-7

    PubMed Abstract | CrossRef Full Text | Google Scholar

    48. Panno ML, Naimo GD, Spina E, Ando S, Mauro L. Different molecular signaling sustaining adiponectin action in breast cancer. Curr Opin Pharmacol. (2016) 31:1–7. doi: 10.1016/j.coph.2016.08.001

    PubMed Abstract | CrossRef Full Text | Google Scholar

    50. Wang Y, Xu W, Yan Z, Zhao W, Mi J, Li J, et al. Metformin induces autophagy and G0/G1 phase cell cycle arrest in myeloma by targeting the AMPK/mTORC1 and mTORC2 pathways. J Exp Clin Cancer Res. (2018) 37:63. doi: 10.1186/s13046-018-0731-5

    PubMed Abstract | CrossRef Full Text | Google Scholar

    51. Moon HS, Chamberland JP, Aronis K, Tseleni-Balafouta S, Mantzoros CS. Direct role of adiponectin and adiponectin receptors in endometrial cancer: in vitro and ex vivo studies in humans. Mol Cancer Ther. (2011) 10:2234–43. doi: 10.1158/1535-7163.MCT-11-0545

    PubMed Abstract | CrossRef Full Text | Google Scholar

    52. Cai ZF, Deng L, Wang MM, Zhang JQ, Li L. [Effect of AMPK/mTOR/S6K1 pathways and the insulin-sensitizing effect for adiponectin in endometrial cancer cells]. Zhonghua Fu Chan Ke Za Zhi. (2018) 53:554–60. doi: 10.3760/cma.j.issn.0529-567x.2018.08.008

    PubMed Abstract | CrossRef Full Text | Google Scholar

    53. Sayeed M, Gautam S, Verma DP, Afshan T, Kumari T, Srivastava AK, et al. A collagen domain-derived short adiponectin peptide activates APPL1 and AMPK signaling pathways and improves glucose and fatty acid metabolisms. J Biol Chem. (2018) 293:13509–23. doi: 10.1074/jbc.RA118.001801

    PubMed Abstract | CrossRef Full Text | Google Scholar

    54. Peng J, Tsang JY, Ho DH, Zhang R, Xiao H, Li D, et al. Modulatory effects of adiponectin on the polarization of tumor-associated macrophages. Int J Cancer. (2015) 137:848–58. doi: 10.1002/ijc.29485

    PubMed Abstract | CrossRef Full Text | Google Scholar

    55. Mohammadi M, Mianabadi F, Mehrad-Majd H. Circulating visfatin levels and cancers risk: a systematic review and meta-analysis. J Cell Physiol. (2019) 234:5011–22. doi: 10.1002/jcp.27302

    PubMed Abstract | CrossRef Full Text | Google Scholar

    56. Wang Z, Gao S, Sun C, Li J, Gao W, Yu L. Clinical significance of serum adiponectin and visfatin levels in endometrial cancer. Int J Gynaecol Obstet. (2019) 145:34–9. doi: 10.1002/ijgo.12772

    PubMed Abstract | CrossRef Full Text | Google Scholar

    57. Ilhan TT, Kebapcilar A, Yilmaz SA, Ilhan T, Kerimoglu OS, Pekin AT, et al. Relations of serum visfatin and resistin levels with endometrial cancer and factors associated with its prognosis. Asian Pac J Cancer Prev. (2015) 16:4503–8. doi: 10.7314/APJCP.2015.16.11.4503

    PubMed Abstract | CrossRef Full Text | Google Scholar

    58. Cymbaluk-Ploska A, Chudecka-Glaz A, Pius-Sadowska E, Sompolska-Rzechula A, Machalinski B, Menkiszak J. Circulating serum level of visfatin in patients with endometrial cancer. Biomed Res Int. (2018) 2018:8576179. doi: 10.1155/2018/8576179

    PubMed Abstract | CrossRef Full Text | Google Scholar

    59. Wang Y, Gao C, Zhang Y, Gao J, Teng F, Tian W, et al. Visfatin stimulates endometrial cancer cell proliferation via activation of PI3K/Akt and MAPK/ERK1/2 signalling pathways. Gynecol Oncol. (2016) 143:168–78. doi: 10.1016/j.ygyno.2016.07.109

    PubMed Abstract | CrossRef Full Text | Google Scholar

    60. Zangooei M, Nourbakhsh M, Ghahremani MH, Meshkani R, Khedri A, Shadboorestan A, et al. Investigating the effect of visfatin on ERalpha phosphorylation (Ser118 and Ser167) and ERE-dependent transcriptional activity. EXCLI J. (2018) 17:516–25. doi: 10.17179/excli2018-1299

    PubMed Abstract | CrossRef Full Text | Google Scholar

    61. Zahid H, Subbaramaiah K, Iyengar NM, Zhou XK, Chen IC, Bhardwaj P, et al. Leptin regulation of the p53-HIF1alpha/PKM2-aromatase axis in breast adipose stromal cells: a novel mechanism for the obesity-breast cancer link. Int J Obes. (2018) 42:711–20. doi: 10.1038/ijo.2017.273

    PubMed Abstract | CrossRef Full Text | Google Scholar

    62. Song NY, Lee YH, Na HK, Baek JH, Surh YJ. Leptin induces SIRT1 expression through activation of NF-E2-related factor 2: implications for obesity-associated colon carcinogenesis. Biochem Pharmacol. (2018) 153:282–91. doi: 10.1016/j.bcp.2018.02.001

    PubMed Abstract | CrossRef Full Text | Google Scholar

    63. Wang PP, He XY, Wang R, Wang Z, Wang YG. High leptin level is an independent risk factor of endometrial cancer: a meta-analysis. Cell Physiol Biochem. (2014) 34:1477–84. doi: 10.1159/000366352

    PubMed Abstract | CrossRef Full Text | Google Scholar

    64. Zhang Y, Liu L, Li C, Ai H. Correlation analysis between the expressions of leptin and its receptor (ObR) and clinicopathology in endometrial cancer. Cancer Biomark. (2014) 14:353–9. doi: 10.3233/CBM-140415

    PubMed Abstract | CrossRef Full Text | Google Scholar

    65. Tenvooren I, Jenks MZ, Rashid H, Cook KL, Muhlemann JK, Sistrunk C, et al. Elevated leptin disrupts epithelial polarity and promotes premalignant alterations in the mammary gland. Oncogene. (2019) 38:3855–70. doi: 10.1038/s41388-019-0687-8

    PubMed Abstract | CrossRef Full Text | Google Scholar

    66. Liu Y, Lv L, Xiao W, Gong C, Yin J, Wang D, et al. Leptin activates STAT3 and ERK1/2 pathways and induces endometrial cancer cell proliferation. J Huazhong Univ Sci Technolog Med Sci. (2011) 31:365. doi: 10.1007/s11596-011-0382-7

    PubMed Abstract | CrossRef Full Text | Google Scholar

    67. Bienkiewicz J, Romanowicz H, Malinowski A, Smolarz B. Association of Single Nucleotide Polymorphism−2548 G/A (rs12112075) of leptin gene with endometrial cancer and uterine leiomyomas. Eur J Obstet Gynecol Reprod Biol. (2017) 218:113–8. doi: 10.1016/j.ejogrb.2017.09.022

    PubMed Abstract | CrossRef Full Text | Google Scholar

    68. Wang T, Fahrmann JF, Lee H, Li YJ, Tripathi SC, Yue C, et al. JAK/STAT3-regulated fatty acid beta-oxidation is critical for breast cancer stem cell self-renewal and chemoresistance. Cell Metab. (2018) 27:136–50 e5. doi: 10.1016/j.cmet.2017.11.001

    CrossRef Full Text | Google Scholar

    69. Cymbaluk-Ploska A, Chudecka-Glaz A, Jagodzinska A, Pius-Sadowska E, Sompolska-Rzechula A, Machalinski B, et al. Evaluation of biologically active substances promoting the development of or protecting against endometrial cancer. Onco Targets Ther. (2018) 11:1363–72. doi: 10.2147/OTT.S155942

    PubMed Abstract | CrossRef Full Text | Google Scholar

    70. Dibaba DT, Judd SE, Gilchrist SC, Cushman M, Pisu M, Safford M, et al. Association between obesity and biomarkers of inflammation and metabolism with cancer mortality in a prospective cohort study. Metabolism. (2019) 94:69–76. doi: 10.1016/j.metabol.2019.01.007

    PubMed Abstract | CrossRef Full Text | Google Scholar

    71. Chu Y, Wang Y, Peng W, Xu L, Liu M, Li J, et al. STAT3 activation by IL-6 from adipose-derived stem cells promotes endometrial carcinoma proliferation and metastasis. Biochem Biophys Res Commun. (2018) 500:626–31. doi: 10.1016/j.bbrc.2018.04.121

    PubMed Abstract | CrossRef Full Text | Google Scholar

    73. He YY, Cai B, Yang YX, Liu XL, Wan XP. Estrogenic G protein-coupled receptor 30 signaling is involved in regulation of endometrial carcinoma by promoting proliferation, invasion potential, and interleukin-6 secretion via the MEK/ERK mitogen-activated protein kinase pathway. Cancer Sci. (2009) 100:1051–61. doi: 10.1111/j.1349-7006.2009.01148.x

    PubMed Abstract | CrossRef Full Text | Google Scholar

    74. Che Q, Liu BY, Liao Y, Zhang HJ, Yang TT, He YY, et al. Activation of a positive feedback loop involving IL-6 and aromatase promotes intratumoral 17beta-estradiol biosynthesis in endometrial carcinoma microenvironment. Int J Cancer. (2014) 135:282–94. doi: 10.1002/ijc.28679

    PubMed Abstract | CrossRef Full Text | Google Scholar

    75. Lee JW, Stone ML, Porrett PM, Thomas SK, Komar CA, Li JH, et al. Hepatocytes direct the formation of a pro-metastatic niche in the liver. Nature. (2019) 567:249–52. doi: 10.1038/s41586-019-1004-y

    PubMed Abstract | CrossRef Full Text | Google Scholar

    76. Smith HO, Stephens ND, Qualls CR, Fligelman T, Wang T, Lin CY, et al. The clinical significance of inflammatory cytokines in primary cell culture in endometrial carcinoma. Mol Oncol. (2013) 7:41–54. doi: 10.1016/j.molonc.2012.07.002

    PubMed Abstract | CrossRef Full Text | Google Scholar

    77. Ku SC, Ho PS, Tseng YT, Yeh TC, Cheng SL, Liang CS. Benzodiazepine-associated carcinogenesis: focus on lorazepam-associated cancer biomarker changes in overweight individuals. Psychiatry Investig. (2018) 15:900–6. doi: 10.30773/pi.2018.05.02.1

    PubMed Abstract | CrossRef Full Text | Google Scholar

    78. Ahmad R, Al-Roub A, Kochumon S, Akther N, Thomas R, Kumari M, et al. The synergy between palmitate and TNF-alpha for CCL2 production is dependent on the TRIF/IRF3 pathway: implications for metabolic inflammation. J Immunol. (2018) 200:3599–611. doi: 10.4049/jimmunol.1701552

    PubMed Abstract | CrossRef Full Text | Google Scholar

    79. Dossus L, Becker S, Rinaldi S, Lukanova A, Tjonneland A, Olsen A, et al. Tumor necrosis factor (TNF)-alpha, soluble TNF receptors and endometrial cancer risk: the EPIC study. Int J Cancer. (2011) 129:2032–7. doi: 10.1002/ijc.25840

    PubMed Abstract | CrossRef Full Text | Google Scholar

    80. Alipourfard I, Datukishvili N, Mikeladze D. TNF-alpha downregulation modifies Insulin Receptor Substrate 1 (IRS-1) in metabolic signaling of diabetic insulin-resistant hepatocytes. Mediat Inflamm. (2019) 2019:3560819. doi: 10.1155/2019/3560819

    PubMed Abstract | CrossRef Full Text | Google Scholar

    81. Martinez-Chacon G, Brown KA, Docanto MM, Kumar H, Salminen S, Saarinen N, et al. IL-10 suppresses TNF-alpha-induced expression of human aromatase gene in mammary adipose tissue. FASEB J. (2018) 32:3361–70. doi: 10.1096/fj.201700938RRR

    PubMed Abstract | CrossRef Full Text | Google Scholar

    82. Vousden KA, Lundqvist T, Popovic B, Naiman B, Carruthers AM, Newton P, et al. Discovery and characterisation of an antibody that selectively modulates the inhibitory activity of plasminogen activator inhibitor-1. Sci Rep. (2019) 9:1605. doi: 10.2210/pdb6i8s/pdb

    PubMed Abstract | CrossRef Full Text | Google Scholar

    83. Steiner E, Pollow K, Hasenclever D, Schormann W, Hermes M, Schmidt M, et al. Role of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor type 1 (PAI-1) for prognosis in endometrial cancer. Gynecol Oncol. (2008) 108:569–76. doi: 10.1016/j.ygyno.2007.11.025

    PubMed Abstract | CrossRef Full Text | Google Scholar

    84. Polusani SR, Huang YW, Huang G, Chen CW, Wang CM, Lin LL, et al. Adipokines deregulate cellular communication via epigenetic repression of gap junction loci in obese endometrial cancer. Cancer Res. (2019) 79:196–208. doi: 10.1158/0008-5472.CAN-18-1615

    PubMed Abstract | CrossRef Full Text | Google Scholar

    86. Dieli-Conwright CM, Parmentier JH, Sami N, Lee K, Spicer D, Mack WJ, et al. Adipose tissue inflammation in breast cancer survivors: effects of a 16-week combined aerobic and resistance exercise training intervention. Breast Cancer Res Treat. (2018) 168:147–57. doi: 10.1007/s10549-017-4576-y

    PubMed Abstract | CrossRef Full Text | Google Scholar

    87. Saucillo DC, Gerriets VA, Sheng J, Rathmell JC, Maciver NJ. Leptin metabolically licenses T cells for activation to link nutrition and immunity. J Immunol. (2014) 192:136–44. doi: 10.4049/jimmunol.1301158

    PubMed Abstract | CrossRef Full Text | Google Scholar

    88. Kolb R, Kluz P, Tan ZW, Borcherding N, Bormann N, Vishwakarma A, et al. Obesity-associated inflammation promotes angiogenesis and breast cancer via angiopoietin-like 4. Oncogene. (2019) 38:2351–63. doi: 10.1038/s41388-018-0592-6

    PubMed Abstract | CrossRef Full Text | Google Scholar

    90. Nagle CM, Crosbie EJ, Brand A, Obermair A, Oehler MK, Quinn M, et al. The association between diabetes, comorbidities, body mass index and all-cause and cause-specific mortality among women with endometrial cancer. Gynecol Oncol. (2018) 150:99–105. doi: 10.1016/j.ygyno.2018.04.006

    PubMed Abstract | CrossRef Full Text | Google Scholar

    92. Gu CJ, Xie F, Zhang B, Yang HL, Cheng J, He YY, et al. High glucose promotes epithelial-mesenchymal transition of uterus endometrial cancer cells by increasing ER/GLUT4-mediated VEGF secretion. Cell Physiol Biochem. (2018) 50:706–20. doi: 10.1159/000494237

    PubMed Abstract | CrossRef Full Text | Google Scholar

    93. Wallbillich JJ, Josyula S, Saini U, Zingarelli RA, Dorayappan KD, Riley MK, et al. High glucose-mediated STAT3 activation in endometrial cancer is inhibited by metformin: therapeutic implications for endometrial cancer. PLoS ONE. (2017) 12:e0170318. doi: 10.1371/journal.pone.0170318

    PubMed Abstract | CrossRef Full Text | Google Scholar

    95. Zhong XY, Yuan XM, Xu YY, Yin M, Yan WW, Zou SW, et al. CARM1 methylates GAPDH to regulate glucose metabolism and is suppressed in liver cancer. Cell Rep. (2018) 24:3207–23. doi: 10.1016/j.celrep.2018.08.066

    PubMed Abstract | CrossRef Full Text | Google Scholar

    96. Wei Y, Wang D, Jin F, Bian Z, Li L, Liang H, et al. Pyruvate kinase type M2 promotes tumour cell exosome release via phosphorylating synaptosome-associated protein 23. Nat Commun. (2017) 8:14041. doi: 10.1038/ncomms14041

    PubMed Abstract | CrossRef Full Text | Google Scholar

    97. Bohn T, Rapp S, Luther N, Klein M, Bruehl TJ, Kojima N, et al. Tumor immunoevasion via acidosis-dependent induction of regulatory tumor-associated macrophages. Nat Immunol. (2018) 19:1319–29. doi: 10.1038/s41590-018-0226-8

    PubMed Abstract | CrossRef Full Text | Google Scholar

    98. Gu S, Ni T, Wang J, Liu Y, Fan Q, Wang Y, et al. CD47 blockade inhibits tumor progression through promoting phagocytosis of tumor cells by M2 polarized macrophages in endometrial cancer. J Immunol Res. (2018) 2018:6156757. doi: 10.1155/2018/6156757

    PubMed Abstract | CrossRef Full Text | Google Scholar

    99. Latif A, Chadwick AL, Kitson SJ, Gregson HJ, Sivalingam VN, Bolton J, et al. Monocarboxylate Transporter 1 (MCT1) is an independent prognostic biomarker in endometrial cancer. BMC Clin Pathol. (2017) 17:27. doi: 10.1186/s12907-017-0067-7

    PubMed Abstract | CrossRef Full Text | Google Scholar

    100. Liu N, Luo J, Kuang D, Xu S, Duan Y, Xia Y, et al. Lactate inhibits ATP6V0d2 expression in tumor-associated macrophages to promote HIF-2alpha-mediated tumor progression. J Clin Invest. (2019) 129:631–46. doi: 10.1172/JCI123027

    PubMed Abstract | CrossRef Full Text | Google Scholar

    101. Friedenreich CM, Langley AR, Speidel TP, Lau DC, Courneya KS, Csizmadi I, et al. Case-control study of markers of insulin resistance and endometrial cancer risk. Endocr Relat Cancer. (2012) 19:785–92. doi: 10.1530/ERC-12-0211

    PubMed Abstract | CrossRef Full Text | Google Scholar

    102. Kabat GC, Kim MY, Lane DS, Zaslavsky O, Ho GYF, Luo J, et al. Serum glucose and insulin and risk of cancers of the breast, endometrium, and ovary in postmenopausal women. Eur J Cancer Prev. (2018) 27:261–8. doi: 10.1097/CEJ.0000000000000435

    PubMed Abstract | CrossRef Full Text | Google Scholar

    104. Joehlin-Price AS, Stephens JA, Zhang J, Backes FJ, Cohn DE, Suarez AA. Endometrial cancer Insulin-Like Growth Factor 1 Receptor (IGF1R) expression increases with body mass index and is associated with pathologic extent and prognosis. Cancer Epidemiol Biomarkers Prev. (2016) 25:438–45. doi: 10.1158/1055-9965.EPI-15-1145

    PubMed Abstract | CrossRef Full Text | Google Scholar

    105. Wang C, Su K, Zhang Y, Zhang W, Zhao Q, Chu D, et al. IR-A/IGF-1R-mediated signals promote epithelial-mesenchymal transition of endometrial carcinoma cells by activating PI3K/AKT and ERK pathways. Cancer Biol Ther. (2019) 20:295–306. doi: 10.1080/15384047.2018.1529096

    PubMed Abstract | CrossRef Full Text | Google Scholar

    106. Zhang H, Fagan DH, Zeng X, Freeman KT, Sachdev D, Yee D. Inhibition of cancer cell proliferation and metastasis by insulin receptor downregulation. Oncogene. (2010) 29:2517–27. doi: 10.1038/onc.2010.17

    PubMed Abstract | CrossRef Full Text | Google Scholar

    107. Krycer JR, Yugi K, Hirayama A, Fazakerley DJ, Quek LE, Scalzo R, et al. Dynamic metabolomics reveals that insulin primes the adipocyte for glucose metabolism. Cell Rep. (2017) 21:3536–47. doi: 10.1016/j.celrep.2017.11.085

    PubMed Abstract | CrossRef Full Text | Google Scholar

    108. Zhou R, Yang Y, Lu Q, Wang J, Miao Y, Wang S, et al. Prognostic factors of oncological and reproductive outcomes in fertility-sparing treatment of complex atypical hyperplasia and low-grade endometrial cancer using oral progestin in Chinese patients. Gynecol Oncol. (2015) 139:424–8. doi: 10.1016/j.ygyno.2015.09.078

    PubMed Abstract | CrossRef Full Text | Google Scholar

    109. Kheirandish M, Mahboobi H, Yazdanparast M, Kamal W, Kamal MA. Anti-cancer effects of metformin: recent evidences for its role in prevention and treatment of cancer. Curr Drug Metab. (2018) 19:793–7. doi: 10.2174/1389200219666180416161846

    PubMed Abstract | CrossRef Full Text | Google Scholar

    110. Cantrell LA, Zhou C, Mendivil A, Malloy KM, Gehrig PA, Bae-Jump VL. Metformin is a potent inhibitor of endometrial cancer cell proliferation–implications for a novel treatment strategy. Gynecol Oncol. (2010) 116:92–8. doi: 10.1016/j.ygyno.2009.09.024

    PubMed Abstract | CrossRef Full Text | Google Scholar

    111. Nevadunsky NS, Van Arsdale A, Strickler HD, Moadel A, Kaur G, Frimer M, et al. Metformin use and endometrial cancer survival. Gynecol Oncol. (2014) 132:236–40. doi: 10.1016/j.ygyno.2013.10.026

    PubMed Abstract | CrossRef Full Text | Google Scholar

    112. Kitson SJ, Maskell Z, Sivalingam VN, Allen JL, Ali S, Burns S, et al. PRE-surgical Metformin In Uterine Malignancy (PREMIUM): a multi-center, randomized double-blind, placebo-controlled phase III trial. Clin Cancer Res. (2019) 25:2424–32. doi: 10.1158/1078-0432.CCR-18-3339

    PubMed Abstract | CrossRef Full Text | Google Scholar

    113. Arthur R, Moller H, Garmo H, Haggstrom C, Holmberg L, Stattin P, et al. Serum glucose, triglycerides, and cholesterol in relation to prostate cancer death in the Swedish AMORIS study. Cancer Causes Control. (2019) 30:195–206. doi: 10.1007/s10552-018-1093-1

    PubMed Abstract | CrossRef Full Text | Google Scholar

    114. Arthur RS, Kabat GC, Kim MY, Wild RA, Shadyab AH, Wactawski-Wende J, et al. Metabolic syndrome and risk of endometrial cancer in postmenopausal women: a prospective study. Cancer Causes Control. (2019) 30:355–63. doi: 10.1007/s10552-019-01139-5

    PubMed Abstract | CrossRef Full Text | Google Scholar

    115. Bruning PF, Bonfrer JM. Free fatty acid concentrations correlated with the available fraction of estradiol in human plasma. Cancer Res. (1986) 46:2606–9.

    PubMed Abstract | Google Scholar

    116. Schmandt RE, Iglesias DA, Co NN, Lu KH. Understanding obesity and endometrial cancer risk: opportunities for prevention. Am J Obstet Gynecol. (2011) 205:518–25. doi: 10.1016/j.ajog.2011.05.042

    PubMed Abstract | CrossRef Full Text | Google Scholar

    117. Gibson DA, Collins F, Cousins FL, Esnal Zufiaurre A, Saunders PTK. The impact of 27-hydroxycholesterol on endometrial cancer proliferation. Endocr Relat Cancer. (2018) 25:381–91. doi: 10.1530/ERC-17-0449

    PubMed Abstract | CrossRef Full Text | Google Scholar

    118. Madak-Erdogan Z, Band S, Zhao YC, Smith BP, Kulkoyluoglu-Cotul E, Zuo Q, et al. Free fatty acids rewire cancer metabolism in obesity-associated breast cancer via estrogen receptor and mTOR signaling. Cancer Res. (2019) 79:2494–510. doi: 10.1158/0008-5472.CAN-18-2849

    PubMed Abstract | CrossRef Full Text | Google Scholar

    119. Hao J, Zhang Y, Yan X, Yan F, Sun Y, Zeng J, et al. Circulating adipose fatty acid binding protein is a new link underlying obesity-associated breast/mammary tumor development. Cell Metab. (2018) 28:689–705 e5. doi: 10.1016/j.cmet.2018.07.006

    PubMed Abstract | CrossRef Full Text | Google Scholar

    120. Brinton LA, Sakoda LC, Frederiksen K, Sherman ME, Kjaer SK, Graubard BI, et al. Relationships of uterine and ovarian tumors to pre-existing chronic conditions. Gynecol Oncol. (2007) 107:487–94. doi: 10.1016/j.ygyno.2007.08.002

    PubMed Abstract | CrossRef Full Text | Google Scholar

    121. Seebacher V, Hofstetter G, Polterauer S, Reinthaller A, Grimm C, Schwameis R, et al. Does thyroid-stimulating hormone influence the prognosis of patients with endometrial cancer? A multicentre trial. Br J Cancer. (2013) 109:215–8. doi: 10.1038/bjc.2013.282

    PubMed Abstract | CrossRef Full Text | Google Scholar

    122. Shinkov A, Borissova AM, Kovatcheva R, Atanassova I, Vlahov J, Dakovska L. The prevalence of the metabolic syndrome increases through the quartiles of thyroid stimulating hormone in a population-based sample of euthyroid subjects. Arq Bras Endocrinol Metabol. (2014) 58:926–32. doi: 10.1590/0004-2730000003538

    PubMed Abstract | CrossRef Full Text | Google Scholar

    125. MacKintosh ML, Derbyshire AE, McVey RJ, Bolton J, Nickkho-Amiry M, Higgins CL, et al. The impact of obesity and bariatric surgery on circulating and tissue biomarkers of endometrial cancer risk. Int J Cancer. (2019) 144:641–50. doi: 10.1002/ijc.31913

    PubMed Abstract | CrossRef Full Text | Google Scholar

    126. Linkov F, Goughnour SL, Ma T, Xu Z, Edwards RP, Lokshin AE, et al. Changes in inflammatory endometrial cancer risk biomarkers in individuals undergoing surgical weight loss. Gynecol Oncol. (2017) 147:133–8. doi: 10.1016/j.ygyno.2017.07.144

    PubMed Abstract | CrossRef Full Text | Google Scholar

    127. Busch EL, Crous-Bou M, Prescott J, Downing MJ, Rosner BA, Mutter GL, et al. Adiponectin, leptin, and insulin-pathway receptors as endometrial cancer subtyping markers. Horm Cancer. (2018) 9:33–9. doi: 10.1007/s12672-017-0318-1

    PubMed Abstract | CrossRef Full Text | Google Scholar

    128. Kitson SJ, Evans DG, Crosbie EJ. Identifying high-risk women for endometrial cancer prevention strategies: proposal of an endometrial cancer risk prediction model. Cancer Prev Res. (2017) 10:1–13. doi: 10.1158/1940-6207.CAPR-16-0224

    PubMed Abstract | CrossRef Full Text | Google Scholar

    129. Fortner RT, Husing A, Kuhn T, Konar M, Overvad K, Tjonneland A, et al. Endometrial cancer risk prediction including serum-based biomarkers: results from the EPIC cohort. Int J Cancer. (2017) 140:1317–23. doi: 10.1002/ijc.30560

    PubMed Abstract | CrossRef Full Text | Google Scholar

    130. Lin Y, Zhou J, Cao L, Xu Q, Hao J, Zhao L, et al. Serum calcium is a novel parameter to assess metabolic syndrome in endometrial carcinoma. J Gynecol Oncol. (2019) 30:e12. doi: 10.3802/jgo.2019.30.e12

    PubMed Abstract | CrossRef Full Text | Google Scholar

    Hypertension and hypotension – treatment with osteopathy

    Osteopathic treatment is a special branch of medicine, which uses both an independent therapeutic approach and a complex one in conjunction with medical treatment, depending on the severity of the patient’s symptoms, as well as the degree of complexity of his disease.

    A distinctive feature of osteopathy is that the specialist perceives the patient’s body as a single whole, a system in which everything is interconnected.

    The osteopathic doctor diagnoses the root cause of the disease, which saves time for the patient.The accompanying symptoms disappear unnoticed and the patient has no cause for concern.

    When starting the examination of a patient, an osteopathic doctor assesses the physical and emotional state. If there are problem areas, a specialist identifies them. Further, the doctor conducts careful work to place the displaced bones in place, to relax the muscles, the tone of which is increased. Using special techniques of osteopathy, the specialist restores the normal blood supply to the body. The consequence of this effect is the improvement of lymph flow.Fascia (connective tissue covering organs, blood vessels, nerves), muscle tissues are being worked out. The joints return to their normal position for proper functioning.

    Osteopath gives the necessary recommendations, answers all questions of interest. After each osteopathy session, the body starts self-regulation and healing. The metabolism is normalized, the work of the nervous and endocrine systems is restored, psychoemotional stress goes away. After a course of osteopathy, headache, irritability, apathy or aggression, pain in the back, joints and muscles disappear, and the correct beautiful posture gradually returns.

    An osteopathic doctor always monitors and, if necessary, corrects all processes. The number of sessions is purely individual for each patient. We are interested in your speedy recovery. Osteopathy sessions can significantly improve your well-being, a sense of your own body and the quality of life in general.

    Her name is HYPOTONIA – articles and news PharmacyMos

    Is It Safe?

    Hypotension (hypotension) is a violation of blood pressure, its insufficiency.Blood is not pumped as intensively as it should, slower than necessary for the normal functioning of the body. Reduced pressure is considered to be below 100/60 mm Hg. Art., and for young people under 25 years old – already 105/60.

    Most often, hypotension occurs from a violation of vascular tone. When the blood vessels are healthy, they can quickly narrow and widen as the heart contracts. In a hypotonic person, the vessels are sluggish, they work slowly and do not keep up with the rhythm of the heart. Therefore, the blood moves sluggishly. In fact, there is stagnation of blood in the arteries.To remove this stagnation, the heart is forced to work harder – and at low pressure, a faster pulse is most often observed.

    Between the upper systolic pressure (when the heart is in maximum contraction) and the lower diastolic (when the heart is in maximum relaxation) there should be a difference (pulse pressure) of no more than 40 mm Hg. Art. And no less. Any deviations from this figure lead to damage to the cardiovascular system.

    With hypotension, the heart is forced to work hard to provide the body with a normal blood supply.

    With a constant deficit in the supply of oxygen to the organs, blood disrupts the work of organs and a disease occurs.

    Many people do not realize that low blood pressure provokes insufficient blood supply to all internal organs and tissues, and, what is most dangerous, to the brain. Against this background, oxygen starvation occurs. This is why fatigue, decreased performance, headaches, dizziness occur!

    Therefore, it is important to diagnose hypotension in a timely manner and carefully treat it

    Low blood pressure and high pulse rates can lead to serious cardiovascular problems such as arrhythmias.A high pulse diagnoses the intense work of the heart, which is forced to quickly pump large volumes of blood. Flaccid vessels do not allow blood to move at a normal rate. The load on the heart increases many times over.

    A low pulse at normal pressure is not hypotension. If a low pulse is observed with hypotension, this is a symptom of very serious diseases such as coronary heart disease.

    How to recognize the “hypo” prefix

    Hypotension has many faces.For example, you might feel overwhelmed after a good night’s sleep. You can always be in a zero mood. Hands and feet may be cold. Pale skin. In the head there are often incomprehensible sensations – compressed, crushed, spinning, hurting. These are all signs of hypotension.

    In addition to the above, hypotension manifests itself in many other features.

    You should be alert if someone close to you have the following symptoms:

    • dizziness, dull, pressing or throbbing headaches in the temples, often on the forehead, on the back of the head, fainting – especially in a stuffy room;
    • apathy, lethargy, drowsiness, decreased performance, weakness, weakness;
    • memory impairment, absent-mindedness;
    • meteorological dependence.At low atmospheric pressure – headache, body aches;
    • 90,049 people practically turn into an “owl”. He gets up hard in the morning, working capacity appears only in the afternoon;

    • rapid pulse, shortness of breath in the absence of heart disease, sleep disturbance;
    • 90,049 people often yawn – this is from lack of oxygen, and not from the desire to sleep;

    • pale skin, cold extremities – impaired thermoregulation, increased sweating;
    • irritability, emotional instability.

    People with low blood pressure can hardly tolerate any changes in the environment – changes in air temperature, humidity, stuffiness, especially emotional stimuli. Often, hypotensive patients cannot stand bright light; a sunny day is painful for them. They practically cannot stand loud sounds. They are irritable, almost always in a bad mood. Depression is often accompanied by hypotension.

    In past centuries, hypotension was considered a female disease. Indeed, the weaker sex is sick with it more often than the strong.Typically, hypotension affects women between the ages of thirty and forty, sometimes from nineteen to thirty.

    Absolutely healthy people, for example, athletes, can also get hypotension. The cause of hypotension in athletes is constant intense physical activity. In such cases, the human body simply begins to respond to bodily fatigue and works in a more economical mode. This hypotension is called “fitness hypotension.”

    “Root” of the disease

    Low blood pressure arises from a variety of reasons: psychological, emotional, with severe physical exertion, as a consequence of the underlying disease.And also – against the background of prolonged psycho-emotional stress, panic attacks, depression, stress, neuroses.

    Sometimes the symptoms of hypotension occur in healthy people as well as a reaction to climate change, to increased physical activity. This reaction of the body is called adaptive hypotension. It often (but not always!) Goes away on its own.

    There is also symptomatic hypotension, which develops as a concomitant ailment against the background of infectious and non-infectious diseases (heart, lungs, liver).Treatment of hypotension in this case will be aimed at eliminating the underlying disease.

    There is also neurocirculatory hypotension. This independent disease, as a rule, occurs against the background of nervous stress, psychological overload, mental fatigue, negative psycho-emotional background and other types of imbalance of the nervous system. In this case, they speak of primary hypotension, which requires targeted treatment to restore the balance of the nervous system and eliminate the symptoms of low blood pressure.

    Hypotension can be caused by the influence of climatic conditions, i.e. if a person moved to a city with a different climate. And the adaptation period will be held under the banner of “HYPOTONIA”. The body can react with reduced pressure to radiation, electromagnetic fields, high humidity. Hypotension can also develop as an allergic reaction to certain sound or color stimuli.

    Broad Spectrum

    Reduced pressure is primary and secondary.

    Primary hypotension is an independent disease. Its cause is often the low activity of the autonomic nervous system – psychoemotional stress. Sometimes primary hypotension is called idiopathic.

    The most common secondary hypotension occurs as a reaction of the body to the underlying disease. It can occur for the following reasons:

    • blood loss, especially in women with heavy menstruation;
    • dehydration;
    • diseases of the heart and blood vessels – atherosclerosis, arrhythmia, circulatory disorders, heart failure, poor vascular tone, vegetative-vascular dystonia;
    • diseases of the gastrointestinal tract – peptic ulcer, hepatitis, pancreatitis;
    • diseases of the urinary system – cystitis;
    • endocrine diseases – diabetes, more often – decreased adrenal function, hypothyroidism;
    • respiratory diseases – pneumonia, bronchitis, tuberculosis;
    • brain trauma, osteochondrosis of various localization;
    • diet abuse, vitamin deficiency E, C, group B;
    • neurosis, depression, lack of sleep, chronic fatigue;
    • intoxication.

    Hypotension is acute and chronic

    Acute form can be perceived as collapse – a sharp drop in vascular tone, as shock – paralytic vasodilation. There is a sharp decrease in the supply of oxygen to the brain, hypoxia occurs, and the functions of vital organs decrease. In acute hypotension, urgent medical attention is needed. The severity of the disease is determined not by the height of the pressure, but by the speed and degree of its decrease.

    Acute hypotension occurs as a concomitant disease in severe diagnoses – appendicitis, heart attacks, thromboembolism, arrhythmias and cardiac dysfunction, severe allergic reactions, large blood loss, severe intoxication, sepsis, dehydration, infections.Acute hypotension is a complication of another disease.

    Chronic low blood pressure is often called physiological. It is often found in athletes, residents of the High North, mountainous regions or the tropics. Chronic hypotension increases the risk of coronary heart disease and ischemic stroke. In young people, it reduces the ability to work, worsens the quality of life.

    Got up, fell … gypsum

    Orthostatic hypotension also happens – a sharp decrease in pressure when changing body position, getting out of bed, chair, chair.It is more common during adolescence. If the body is in a lying position for a long time (with prolonged illnesses) or a sitting position (lessons, lectures, travel), then when standing up, blood cannot immediately flow to the brain in sufficient quantities, the pressure drops, the eyes darken, the head is dizzy, the legs become cottony … Even fainting occurs.

    The reasons are the main diseases – atherosclerosis, anemia, diabetes, taking antidepressants and simply dehydration.It is more common in the morning, sometimes leads to fainting, falling, fortunately, the attack lasts 1-3 minutes. But during this time, you can suffer a lot.


    Hypotension is most often diagnosed by accident. The doctor offers a patient with fatigue and dizziness several times a day for several days to measure the pressure – the so-called pressure profile. After a few days, a person is surprised to learn about the presence of hypotension.

    Cunning, not love

    Hypotension can provoke the development of serious diseases: nervous, cardiovascular, digestive and other systems.

    Hypotension is especially dangerous for expectant mothers. Because with poor blood supply, the fetus begins to experience oxygen starvation. When the placenta is poorly supplied with oxygen, blood, the development of the child can be disrupted.

    And in pregnant women with hypotension, toxicosis often develops at a later date.Therefore, hypotension is not as safe as many people think.

    Treat? Treat!

    It is imperative to treat hypotension. With the right approach and complex treatment, it passes quickly and without consequences.

    Treatment of hypotension should be individualized, based on the causes of the disease. Medical treatment will be prescribed by a doctor, traditional medicine methods are chosen in accordance with the causes of hypotension. There are general guidelines that will always help you recover faster.For hypotensive patients, prevention can completely replace treatment.

    Hypotonic patients are prohibited from low physical activity, work in hazardous work, professional sports. Do not abuse caffeine. The body quickly gets used to it. And instead of a cup of coffee, you will have to consume more than 5 cups a day. And this will lead to health problems.

    With reduced pressure, it is necessary to be in the air more often – at least 30 minutes a day. Go in for sports, temper, visit the pool.Physical activities in the fresh air are useful – without fanaticism, to slight fatigue. Various types of massage help well.

    Since the most common cause of the disease is the wrong way of life, then the method of treatment is clear – to correct the way of life, to observe the daily regimen. For example, if there is sleepiness, sleep more. A rested body will quickly cope with other symptoms.

    So, the normalization of the way of life (work, rest, sleep). It is imperative to include rest in the daily routine, get enough sleep.Hypotensives need more time to sleep than all other people!

    First, it is necessary to restore the balance of the nervous system, eliminate chronic fatigue, increase vitality, improve sleep, improve psycho-emotional state. You need to start by adjusting emotions: react less to unpleasant words, manifestations of hostility. Maintain a good mood, do not worry about trifles.

    Closing in four walls is contraindicated! You need an active emotional life: meeting interesting people, concerts, exhibitions, hobbies.Try to participate in social life, find a balance between openness and excessive emotional sensitivity. That is, do not be sad, do not yearn, do not be “bummer”.

    Don’t overeat. Include potassium-rich foods in your diet – potatoes, eggplants, apricots, dried apricots, and prunes. Add to your daily menu food containing calcium, vitamin D, B vitamins. Bread, milk, nuts, honey, beets, beet juice are very useful.

    These simple recommendations, oddly enough, help to improve the blood supply to the brain and the whole body, to improve the work of blood vessels.When the blood vessels are in order, the level of vitality in the body rises, the body’s ability to recuperate improves, and the effects of stress are eliminated.

    Source: Altai Ekaterina, journalist

    Hypotension – low blood pressure


    Photo: FA Bobo / PIXSELL / PA Images

    What does low blood pressure mean?

    Elena Kovalenko

    March 11, 2016 11:00

    Blood pressure is the pressure exerted by blood moving along the walls of blood vessels.It depends on the resistance of blood vessels, the amount of blood and the strength of the heartbeat. Any jump or drop in pressure affects breathing rate, body temperature, and heart rate. Most often, such a difference hides a disturbance in the work of internal organs and does not pass without a trace.

    Pressure below 90 to 60 is considered to be reduced pressure. It is important to understand that even if one of the indicators is below normal, then you should think about visiting a doctor.

    Symptoms of low blood pressure:

    • Pulsating headache (most often in the temporal or occipital regions)
    • Sudden onset of nausea and vomiting
    • A sharp deterioration in well-being during a change of weather
    • Darkening in the eyes
    • Fainting
    • Weakness and fatigue
    • Feeling of lack of air
    • Coldness of hands and feet, acute sensitivity to temperature changes

    Types of low pressure:

    1.Orthostatic hypotension

    The main symptom of this disease is a decrease in pressure with a sharp rise. For example, a person lay on the bed for a long time, got up and immediately experienced dizziness or even loss of coordination when lifting. Causes of orthostatic hypotension include pregnancy, fever, and neurological diseases. The key risk group is people over 65.

    2. Shay-Drager syndrome

    This syndrome is also called multisystem atrophy with orthostatic hypotension or myeloencephalopathy.

    The cause of the disease lies in disorders of the nervous system and begins to manifest itself in acute vascular insufficiency. The syndrome is currently incurable. The average life expectancy after diagnosis is 10 years.

    3. Postprandial hypotension

    The first sign is a sharp drop in blood pressure immediately after eating. The risk group is people with Parkinson’s disease.

    4. Dystonia or vegetative-vascular hypotension

    A pressure jump occurs after a long standing in one place.Most often, people who are in stuffy and hot rooms suffer from this type of low pressure. This disease is caused by a disruption in the blood communication between the brain and heart. Blood rushes to the lower extremities, and the brain decides that the pressure is increasing, sends a signal to the heart to lower the heart rate, thereby lowering the pressure even more. The risk group includes adolescents aged 12 to 18 years.

    5. Accelerated pulse at low pressure

    If you know that you have problems with low blood pressure, and the pulse at rest has jumped above 80 beats per minute, you should immediately consult a doctor in order to avoid serious consequences for the whole body.

    What is the threat of low blood pressure?

    It is generally accepted to consider hypotension as a less dangerous disease in comparison with the disease of high blood pressure – hypertension, but one should not assume that these problems can be solved on their own and will not bring harm to health.

    Hypotension causes a sharp decrease in blood flow to the brain and heart, causing sudden fainting and dizziness. Such situations can lead to physical injury and loss of performance.

    Most often, hypotension occurs in the elderly, children and adolescents suffer from vegetative-vascular dystonia.It can also occur as a concomitant disease with Parkinson’s disease or diseases of the cardiovascular system.

    How to normalize low blood pressure?

    1. Ambulance drugs

    The most common drugs for low blood pressure are citramone, tinctures of Eleutherococcus and ginseng, pantocrine, Chinese magnolia vine. These drugs should be taken systematically, since the full effect will manifest itself only after their accumulation in the body.

    2. Visit a doctor

    A general practitioner will select the best combination of medications for you based on blood tests, age and concomitant diseases. Remember, an individual approach can significantly shorten the duration of treatment.

    3. Don’t drink coffee.

    Avoid caffeine and caffeine-containing products. It is he who first of all contributes to an increase in heart rate.

    4. Drink plenty of water

    Large amounts of fluid thin the blood and improve its circulation throughout the body.

    5. Rest

    Yes, the world is fast and cruel, but remember that first of all you need to take care of yourself. Take time to rest and recuperate.

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    24-hour central aortic pressure and arterial stiffness monitoring in women with postmenopausal osteoporosis | Tsaren


    Recently, the attention of researchers is directed to the study of the parameters of the central pressure in the aorta, measured by a non-invasive method, as well as related indicators reflecting arterial stiffness.This interest is explained by the fact that central aortic pressure and vascular stiffness parameters are better predictors of cardiovascular events than blood pressure measured at the periphery [1]. The development of cardiovascular diseases is associated with an increase in arterial stiffness [2–4]. This integral indicator is used to analyze the hemodynamic changes observed in various clinical conditions. Arterial stiffness is influenced by age, arterial hypertension, smoking, etc.etc. [5,6]. As the stiffness of the arteries increases, the pulse wave velocity increases and the reflected wave returns to the aorta during systole, which leads to an increase in pulse pressure and augmentation pressure. These central pressure readings can be used to assess vascular stiffness. In addition, central pressure reflects blood flow in the coronary and cerebral arteries in the aorta and is a more significant predictor of cardiovascular events.

    The problems of the late postmenopausal period are cardiovascular diseases and osteoporosis, leading to premature death.Not manifesting itself clinically at the early stages of development, subsequently lead to an increase in morbidity, mortality and require significant material costs [7]. The general pathogenetic mechanisms of the development of cardiovascular diseases and osteoporosis are discussed. In turn, osteoporosis is considered as one of the risk factors for cardiovascular events and a component of the cardiovascular continuum [7]. Thus, it has been demonstrated that women with low bone mineral density are more likely to develop severe coronary atherosclerosis, and the risk of heart attacks and strokes increases [8, 9].There are studies devoted to arterial stiffness in women with osteoporosis, where the authors studied the pulse wave velocity (PWV) and the thickness of the intima-media complex [10]; women with postmenopausal osteoporosis. In recent years, it has become possible to measure central pressure and PWV indicators during the day using the Vasotens technology.It has been shown that a sphygmogram recorded on the brachial artery, as an input signal, also allows the reconstruction of indicators of central aortic pressure by means of mathematical processing. In the software of the BPLab apparatus, which is used for this study, PWV is calculated using the propagation time of the pulse wave reflected from the aortic bifurcation so that it coincides with PWV in the carotid-femoral segment. This calculation allows comparison of arterial stiffness values ​​obtained by means of BPLab with measurements on Sphigmocor.The literature contains data on the high comparability of these methods [11].


    To evaluate indicators of central aortic pressure and arterial stiffness during 24-hour monitoring in postmenopausal women, depending on the presence of osteoporosis.


    Study design

    An observational one-stage continuous single-center uncontrolled study was carried out.

    Compliance Criteria

    Criteria for inclusion in the study were: female gender, age over 50 years, the presence of menopause.Exclusion criteria: endocrine system disease, severe heart failure, respiratory failure, secondary osteoporosis.


    The study was carried out on the basis of the National Healthcare Institution “Road Clinical Hospital at st. Chita-2 “

    Study duration

    The study was conducted from September 2011 to May 2012.

    Description of medical intervention

    To verify osteoporosis, all women underwent anamnesis to identify risk factors for osteoporosis and low-energy fractures, X-ray osteodensitometry in two areas – the lumbar vertebrae and the femoral neck.The diagnosis of postmenopausal osteoporosis was made in accordance with the 2012 Clinical Guidelines for the Prevention and Management of Patients with Osteoporosis [12]. In addition, the absolute ten-year risk of fractures was calculated for all patients – major osteoporotic (MO) – the risk of osteoporotic fractures of any localization and hip fracture (HF) – the risk of hip fracture. All women underwent 24-hour blood pressure monitoring (ABPM). ABPM was performed before the appointment of antihypertensive drugs or 2 days after their withdrawal.

    Main study outcome

    The end points of the study were indicators of central aortic pressure: systolic pressure in the aorta (SADao), diastolic pressure in the aorta (DADao), mean pressure in the aorta (Cp ADao), pulse pressure in the aorta.

    Additional study outcomes

    Additionally, the following parameters were analyzed: the absolute ten-year risk of osteoporotic fractures, the presence of osteoporotic fractures, the number of fractures in history, as well as additional parameters of arterial stiffness: augmentation index (Alxao), pulse pressure amplification (PPA), – calculated as the ratio of the pulse pressure of the brachial artery to the central pulse rate, pulse wave velocity (PWV), arterial stiffness index (ASI), ambulatory stiffness index (AASI), augmentation index per day (Alxao avg.), average augmentation index per day, reduced to heart rate (Alxao avg. to heart rate), average daily pulse blood pressure (pulse blood pressure average). The daily central pressure profiles for SBP and DBP were determined.

    Subgroup analysis

    All women participating in the study were divided into two groups. The division into groups was carried out depending on the established diagnosis of osteoporosis. The first group consisted of postmenopausal women with an established diagnosis of osteoporosis, 36 people, the second group – 43 women was the comparison group.

    Methods of registration of outcomes

    To identify risk factors for osteoporosis and osteoporotic fractures, a questionnaire from the online FRAX program was used and anamnesis was collected to determine the number of osteoporotic fractures. X-ray densitometry was performed on a Challenger apparatus, France. The absolute ten-year risk of osteoporotic fractures was assessed using the FRAX program posted on the website www.shef.ac.uk/FRAX, Russian version, Russian model based on the assessment of clinical factors and the index of bone mineral density of the femoral neck.24-hour monitoring of central aortic pressure and arterial stiffness parameters was performed using the BPLab v. 3.2 (“Petr Telegin”, Russia).

    Ethical review

    The study was approved by the local ethics committee at the State Budgetary Educational Institution of Higher Professional Education ChGMA (protocol No. 20 of 22.03.2011).

    Statistical Analysis

    Statistical processing was performed using the Statistica 6.0 software using nonparametric criteria since the distribution of features was asymmetric: Walda-Wolfowitz, chi-square.Correlation analysis was performed using Spearman’s rank correlation (for quantitative values) and gamma correlation to establish the relationship between a history of low-energy fractures (taken into account as a qualitative sign) and parameters of central pressure and arterial stiffness. Differences were considered significant at p <0.05.


    Objects (participants) of research

    The first group consisted of patients with an established diagnosis of osteoporosis – 36 women, the second group was a comparison group – 43 women.The groups were matched for age, weight, and BMI. The absolute ten-year risk of osteoporotic and hip fractures was statistically significantly higher in the first group. The average number of fractures in the first group was 1.6 ± 0.96. The clinical characteristics of the groups are presented in Table 1.

    Table 1. Clinical characteristics of patients


    Women with osteoporosis, n = 36

    Comparison group, n = 43


    Age, years

    69.4 ± 9.1

    66.7 ± 9.5


    Height, cm

    159.4 ± 6.3

    155.23 ± 7.05


    Weight, kg

    69.6 ± 10.9

    68.5 ± 13.6



    27.1 ± 3.89

    27.9 ± 4.1


    History of osteoporotic fractures

    1.6 ± 0.96

    0.0 ± 0



    20.1 ± 7.82

    8.5 ± 4.59



    7.98 ± 7.27

    2.53 ± 3.05


    24-hour central pressure and arterial stiffness parameters were monitored in 79 women; daily central pressure profiles were determined based on the degree of nighttime decrease in systolic and diastolic pressures.

    Main results of the study

    When analyzing the indicators of central aortic pressure given in Table 2, in women with osteoporosis, there is an increase in average daily SBP by 4.52%, DBP by 8.3%, mean BP in the aorta by 5.24%, amplification pressure in the aorta ( PPA) by 6.7% compared to the control group (see Table 2).

    Table 2. Parameters of central aortic pressure and arterial stiffness during 24-hour monitoring in women with osteoporosis


    Women with osteoporosis, n = 36

    Comparison group, n = 43


    SAD jsc

    123.23 ± 11.45

    117.66 ± 10.05



    77.17 ± 9.19

    70.73 ± 9.98


    Wed AD jsc

    99.47 ± 10.41

    94.26 ± 9.47


    Pulse blood pressure jsc

    46.05 ± 8.31

    46.04 ± 9.43



    31.75 ± 10.43

    34.9 ± 13.28



    118.7 ± 4.41

    110.73 ± 22.57


    SRPV, m / s

    8.4 ± 1.62

    8.24 ± 0.9


    ASI, mm Hg.st

    164.64 ± 32.79

    162.06 ± 32.53


    Alxao av.,%

    1.64 ± 18.06

    5.12 ± 18.03


    Alxao av. to heart rate,%

    -6.11 ± 25.20

    -13.13 ± 27.73


    Average pulse blood pressure

    52.87 ± 10.05

    52.16 ± 10.67


    AASI, conventional units

    0.54 ± 0.23

    0.40 ± 0.22


    The main marker that determines arterial stiffness is the pulse wave velocity (PWV), which can be investigated in various ways. Currently, the reference method is the measurement on the carotid-femoral segment using applanation tonometry. In this case, sphygmograms are recorded from the carotid and femoral arteries with simultaneous recording of an ECG.At present, it is possible to measure this indicator during the day when performing ABPM with the BPLab apparatus, but the two-point method is not applicable for daily monitoring. At the same time, as indicated in the literature, the propagation time of the pulse wave reflected from the aortic bifurcation can be used to assess PWV [13].

    In the group of women with osteoporosis, the average PWV per day was 2% higher than in the control. In previous publications, we have shown that in women with osteoporosis, PWV, measured on the carodid-femoral segment, using applanation tonometry also showed a statistically significant excess compared with the group without osteoporotic fractures and BMD reduction [14].In addition to the increase in PWV, we analyzed other indicators of arterial stiffness. So it was found that in the group of women with osteoporosis, the arterial stiffness index (ASI) was 1.6% higher compared to the control. Studies have shown a direct relationship between the arterial stiffness index and the risk of developing coronary artery disease [15]. In 2006, the concept of the ambulatory arterial stiffness index (AASI) was introduced, which is determined by calculation by the level of SBP and DBP [16]. In the first group, this indicator was 25.9% higher.

    Additional research results

    To establish the relationship between the parameters of central pressure and arterial stiffness and the presence of osteoporotic fractures in the history (taken into account as a qualitative sign), a correlation analysis was performed using the γ-correlation, and also the correlation relationships between the number of osteoporotic fractures in history, the ten-year absolute risk of osteoporotic fractures were assessed. fracture of the femoral neck and parameters of central pressure and stiffness of the arteries.Since in this case the relationship was determined between quantitative values, Spearman’s rank correlation was used. The data are presented in Table 3.

    Table 3. Correlation relationships between the parameters of central pressure, arterial stiffness and the presence of osteoporotic fractures in the anamnesis, their number, the risk of fractures according to FRAX




    Wed ADao

    Alxao av.to heart rate



    Wed PAD

    History of fractures

    γ = 0.45, p = 0.00075

    γ = 0.43, p = 0.0024

    γ = 0.46, p = 0.0002

    γ = 0.37, p = 0.0021


    γ = 0.37, p = 0.0021


    Number of fractures

    r = 0.33 p = 0.0016

    r = 0.34 p = 0.002

    r = 0.33 p = 0.0018

    r = 0.33 p = 0.0016


    r = 0.36 p = 0.0012



    r = 0.33 p = 0.004

    r = 0.27 p = 0.018

    r = 0.35 p = 0.003

    r = 0.29 p = 0.0012


    r = 0.27 p = 0.018



    r = 0.25 p = 0.02


    r = 0.3 p = 0.0042

    r = 0.38 p = 0.0002

    r = 0.28 p = 0.016

    r = 0.25 p = 0.02

    r = 0.27 p = 0.018

    Gamma-correlation revealed a positive relationship between the levels of SBP, DBP, mean blood pressure, augmentation index reduced to heart rate in the aorta, outpatient stiffness index and the presence of osteoporotic fractures in the patient’s history.As a result of the rank correlation, a direct relationship was established between the levels of SBP, DBP, mean blood pressure, mean augmentation index reduced to heart rate in the aorta, outpatient stiffness index and absolute ten-year risk of osteoporotic fractures, as well as the number of osteoporotic fractures in history. The absolute ten-year risk of hip fracture was positively associated with SBP levels, mean blood pressure, mean aortic heart rate-normalized augmentation index, mean pulse pressure, stiffness index, and outpatient stiffness index.

    A study of the degree of nocturnal decrease in central SBP in patients with postmenopausal osteoporosis revealed that only 16.4% of women in this group had a dipper profile (with a sufficient decrease in SBP at night) versus the control group, in which this profile was found in 23.5 % of patients. Regarding pathological profiles, it should be noted that in women with osteoporosis, the hyperdipper type (with an excessive decrease in SBP) was more common (Fig. 1).

    Fig. 1. Profiles of central systolic aortic pressure.

    Diastolic pressure profiles showed the opposite trend. Thus, in women with osteoporosis, the normal dipper DADao daily profile was more common than in the control group, 47.4% versus 26.5% (Fig. 2). Among the pathological profiles in the control group, the nightpicker type prevailed (increase in DADao at night) 1.85 times more often.

    Fig. 2. Profiles of central diastolic aortic pressure.

    The hyperdipper type was found with the same frequency, the nondipper type prevailed in the comparison group.

    Adverse events

    Not recorded during the study.


    Summary of the main research result

    As a result of our study, for the first time it was found that women with postmenopausal osteoporosis with daily monitoring have higher central pressure in the ascending part of the aorta and parameters of arterial stiffness.

    Discussion of the main research result

    It is known that indicators of central pressure to one degree or another depend on the stiffness of the arteries.Thus, the statistically significant increase in the amplification pressure in the aorta revealed by us may indicate that the increase in systolic pressure in the aorta is associated with the phenomenon of pressure augmentation, which may be associated with a higher rigidity of the arteries in the group of patients with osteoporosis. The physiological meaning of pulse wave amplification is to prevent its extinction at the periphery, ie, the descending pulse wave is “fed” with energy, as a result of which SBP increases at the periphery [17].On the other hand, the reflected waves generated in high impedance zones, propagating in the upward direction, are summed up, return to the aortic orifice and superimposed on the central wave, its diastolic part. However, with rigid arteries, the speed of reflected pulse waves increases and, returning to the center, they are superimposed on the systolic part of the central wave, which leads to an increase in SBP in the aorta. This in turn increases left ventricular afterload.

    A marker of arterial stiffness is such an indicator as PWV.Our study revealed an increase in this indicator in the group of women with osteoporosis. In the work of Skripnikova I.A. et al., 2015 demonstrated that in women with low bone mass compared with the control group, PWV, measured by applanation tonometry, was also higher [10].

    In addition, in the course of our study, relationships were established between some parameters of central pressure, arterial stiffness and the presence of fractures, their number and the risk of their occurrence, which may indirectly indicate the presence of a possible pathogenetic relationship between cardiovascular diseases and osteoporosis, which is widely discussed in recent times.

    Study Limitations

    The true reliability of the statistically significant results obtained may not be high due to the small sample of patients. To confirm the identified relationships, studies are required using a similar protocol with a large number of participants.


    In conclusion, it should be noted that women with osteoporosis showed an increase in average daily SBP, DBP and average aortic pressure.It was found that in this group of patients the main indicators of arterial stiffness were increased: PWV, ASI, AASI, PPA. A direct correlation was found between the parameters of central pressure, arterial stiffness and the presence of fractures in the anamnesis, their number, as well as indicators of the absolute ten-year risk of osteoporotic fractures and hip fracture. In patients with osteoporosis, pathological profiles of systolic pressure in the aorta are more often revealed, the predominant type of which was the hyperdipper type.


    Funding source . FSBEI HE Chita State Medical Academy

    Conflict of interest . The authors declare no obvious and potential conflicts of interest related to the publication of this article.

    Acknowledgments . The authors are grateful to the radiologists of the NUZ Road Clinical Hospital at st. Chita-2 for densitometry.

    1.Davies JI, Struthers AD. Pulse wave analysis and pulse wave velocity: a critical review of their strengths and weaknesses. J Hypertens. 2003; 21 (3): 463-472. doi: 10.1097 / 01.hjh.0000052468.40108.43.

    2. Lopatin Yu.M., Ilyukhin O.V., Ilyukhina M.V., Ivanenko V.V. Elasticity of arteries and pulse wave velocity in patients with chronic heart failure of various etiologies // Heart failure.- 2004. – T. 4. – No. 5. – S. 130-131. [Lopatin YM, Ilyuhin OV Ilyuhina MV, Ivanenko VV. Elastichnost ‘arteriy i skorost’ pul’sovoy volny u bol’nykh s khronicheskoy serdechnoy nedostatochnost’yu razlichnoy etiologii. Zhurnal serdechnaia nedostatochnost ‘2004; 4 (5): 130-131 (In Russ.)].

    3. Nedogoda SV, Lopatin Yu.M., Chalyabi TA, et al. Change in the velocity of pulse wave propagation in hypertension // South-Russian medical journal.2002. – No. 3. – S. 39-43. [Nedogoda SV, Lopatin YM, Chalyabi TA, et al. Izmenenie skorosti rasprostraneniya pul’sovoy volny pri arterial’noy gipertenzii. Yuzhno-Rossiyskiy meditsinskiy zhurnal. 2002; (3): 39-43. (In Russ.)].

    4. Orlova Ya.A., Ageev F.T. Arterial stiffness as an integral indicator of cardiovascular risk: physiology, methods of assessment and drug correction // Heart. – 2006. – T. 5. – No. 2.- S. 65-68. [Orlova YA, Ageev FT. Zhestkost ‘arteriy kak integral’nyy pokazatel’ serdechnososudistogo riska: fiziologiya, metody otsenki i medikamentoznoy korrektsii. Serdce. 2006; 5 (2): 65-69 (In Russ.)].

    5. Milyagin VA, Filichkin DE, Shpynev KV, et al. Contour analysis of central and peripheral pulse waves in healthy people and patients with arterial hypertension. // Arterial hypertension. – 2009.- T. 15. – No. 1. – S. 78-85. [Milyagin VA, Filichkin DE, Shpynev KV, et al. Countour analysis of central and peripheral pulse waves in healthy subjects and in hypertensive. Arterial’naia gipertenziia. 2009; 15 (1): 78-85. (In Russ.)]

    6. Aksenova T.A., Gorbunov V.V., Parkhomenko Yu.V., Tsarenok S.Yu. 24-hour monitoring of central aortic pressure and arterial stiffness indicators in combination of hypertension with chronic obstructive pulmonary disease.// Transbaikal Medical Bulletin. – 2012. – No. 2. – S. 9-16. [Aksenova TA, Gorbunov VV, Parkhomenko YV, Tsarenok SY. Daily monitoring of the central aortic pressure and arterial stiffness in combination with hypertension and chronic obstructive pulmonary disease. Zabajkal’skij medicinskij vestnik. 2012; (2): 9-16 (In Russ.)].

    7. Chazova IE, Smetnik VP, Balan VE, et al. Management of women with cardiovascular risk in peri- and postmenopausal women: consensus of Russian cardiologists and gynecologists.// Systemic hypertension. – 2008. – No. 3. – S. 26-39. [Chazova IE, Smetnik VP, Balan VE, et al. Vedenie zhenshchin s serdechno-sosudistym riskom v peri- i postmenopauze: konsensus rossiyskikh kardiologov i ginekologov. Sistemnye gipertenzii. 2008; (3): 26-39 (In Russ.)].

    8. Vogt MT, Valentin RS, Forrest KYZ, et al. Bone Mineral Density and Aortic Calcification: The Study of Osteoporotic Fractures. J Am Geriatr Soc.1997; 45 (2): 140-145. doi: 10.1111 / j.1532-5415.1997.tb04498.x.

    9. Hak AE, Pols HAP, van Hemert AM, et al. Progression of Aortic Calcification Is Associated With Metacarpal Bone Loss During Menopause: A Population-Based Longitudinal Study. Arterioscler Thromb Vasc Biol. 2000; 20 (8): 1926-1931. doi: 10.1161 / 01.atv.20.8.1926.

    10.Skripnikova IA, Alikhanova NA, Tkacheva ON, et al. Bone mineral density and the state of the vascular wall depending on the status of replicative cellular aging in postmenopausal women // Osteoporosis and Osteopathy. – 2015. – T. 18. – No. 3. – C. 13-17. [Skripnikova IA, Alikhanova NA, Tkacheva ON, et al. Mineral’naya plotnost ‘kosti i sostoyanie sosudistoy stenki v zavisimosti ot statusa replikativnogo kletochnogo stareniya u zhenshchin v postmenopauzal’nom periode. Osteoporosis and Bone Diseases.2015; 18 (3): 13-17. (In Russ.)] Doi: 10.14341 / osteo2015313-17.

    11. Rogoza A, Kuznetsov. Central aortic blood pressure and augmentation index: comparison between Vasotens & reg; and SphygmoCor® technology. Research Reports in Clinical Cardiology. 2012: 27. doi: 10.2147 / rrcc.s30994.

    12. Alekseeva LI, Baranova IA, Belova KYu, etc.Clinical guidelines for the prevention and management of patients with osteoporosis. – Yaroslavl: Litera, 2012. [Alekseeva LI, Baranova IA, Belova KY, et al. Klinicheskie rekomendacii po profilaktike i vedeniyu bol’nyh s osteoporozom. Yaroslavl: Litera; 2012 (In Russ.)].

    13. London G, Guerin A, Pannier B, et al. Increased systolic pressure in chronic uremia. Role of arterial wave reflections. Hypertension. 1992; 20 (1): 10-19.doi: 10.1161 / 01.hyp.20.1.10.

    14. Tsarenok S.Yu., Gorbunov V.V. Contour analysis of the central pulse wave and elastic properties of arteries in women with coronary artery disease and a high risk of osteoporotic fractures. // Transbaikal Medical Bulletin. – 2014. – No. 4. – S. 159-163. [Tsarenok SY, Gorbunov VV Contour analysis of the central pulse wave and elastic properties of arteries in women with CHD and high risk of osteoporotic fractures.Zabajkal’skij medicinskij vestnik. 2014; (4): 159-163 (In Russ.)].

    15. Cardio Vision Featuring The Arterial Stiffness Index (ASI) Selected Papers, Letters, and Pertinent Information. Cardio Vision is Distributed by: IMDP [electronic resource] access mode: http://www.imdp.com/media/pdf/imdpcvbrochure.pdf (24/07/2012)

    16.Dolan E, Thijs L, Li Y, et al. Ambulatory Arterial Stiffness Index as a Predictor of Cardiovascular Mortality in the Dublin Outcome Study. Hypertension. 2006; 47 (3): 365-370. doi: 10.1161 / 01.HYP.0000200699.74641.c5.

    17. Nichols WW, O’Rourke MF, Vlachopoulos C. McDonald’s Blood Flow in Arteries, Sixth Edition: Theoretical, Experimental and Clinical Principles. London: CRC Press; 2011.

    Just about health: what the blood pressure signals

    What is this indicator and why do we need it? It’s simple.Oxygen from the air dissolves in water and under a certain physiological pressure (it is determined by two numbers and is written through a fraction, it is considered to be the norm of 120/80) enters the blood. Red blood cells are transported by red blood cells to every cell in the body.

    Arterial pressure is systolic (cardiac, “upper”) – it denotes the upper number in the indicator and diastolic (renal, “lower”) – the lower number. High, low and unstable blood pressure can be recorded.

    Difference between “upper” and “lower” pressure

    A rise in blood pressure can be a symptom of many diseases. Sometimes a high difference between “top” and “bottom” pressure is a natural response to stress, exercise, hunger. But when such leaps are observed in the “state of rest”, this is a reason to sound the alarm.

    The difference between “high” and “low” pressure (called “pulse pressure”) should ideally be 40-50 units. If the indicators differ significantly from each other up or down, this condition is difficult not to notice: a person will immediately feel a headache, weakness, drowsiness, impaired attention and irritability.

    When the difference between the “upper” and “lower” pressure significantly exceeds the normal 40-50 units, it can be symptoms of atherosclerosis, pathologies of the aorta, arteries, left ventricle of the heart.

    Small difference between “upper” and “lower” pressure

    If the tonometer shows too little difference between systolic and diastolic pressure, you should immediately consult a doctor and take an examination: this is fraught with hypoxia, loss of vision, and sometimes can lead to cardiac arrest.The minimum difference between systolic and diastolic pressure is considered to be less than 25%.

    What does the small difference between top and bottom pressure indicate? This may be evidence of left ventricular stroke, myocarditis, tachycardia, aortic stenosis, heart failure, cardiosclerosis … There can be many pathologies, and such tonometer readings are no less dangerous than the big difference.

    If the “upper” pressure is much higher than the “lower”

    The difference between “upper” and “lower” pressure is too high – more than 50 units.And the main reason for such deviations is, first of all, age, when the heart and blood vessels wear out and perform their functions poorly. Among the common causes, doctors also distinguish problems with the digestive organs, gallbladder, kidneys, disorders in the vessels and the brain center. But only a doctor can identify the causes of the pathology.

    In any case, you cannot self-medicate here, you should undergo an examination and receive competent doctor’s appointments. There are many reasons that affect pressure, we will consider the main ones that we can correct without causing harm to the body.

    How pressure rises due to stress

    The root cause of increased blood pressure is stress, namely the hormone adrenaline, which is released during stress or fear. It has a powerful vasoconstrictor effect. It is a mobilizing hormone. Nature provides that if someone angered you, frightened you, you are preparing either to attack, or to run away – the vessels are strongly narrowed in order to avoid large blood loss in case of injury or injury.

    But an adrenaline rush is good at critical moments in life.It is desirable that this hormone leaves the body in the next hour after stress. Otherwise, its spasmodic effect will cause a lot of harm to a person.

    This state is familiar to everyone – you received, for example, unpleasant news, and suddenly something hit your head sharply, your heart ached, and after measuring the pressure it turns out that it is at “high” numbers.

    If nothing is done, it will lead to a heart attack. When a vessel is severely narrowed in the heart muscle, the cells that it serves do not receive enough oxygen.When this happens for a long time, the oxygen demand of heart cells increases, long oxygen starvation leads to necrosis (death) of tissues around this vessel. If you add physical activity at this moment, the leaky muscle from disproportionate loads can rupture.

    The very state of the heart has nothing to do with it. Such situations can happen to young people as well. It’s all about thick blood, and the reasons for its thickening lie in improper diet, a sedentary lifestyle, lack of proper physical activity, and non-compliance with the water-drinking balance.

    Clinical and 44-hour ambulatory blood pressure, as well as indicators of central hemodynamics in patients on programmed hemodialysis | Trukhanov

    1. Tomilina N.A., Andrusev A.M., Peregudova N.G., Shinkarev M.B. Replacement therapy of end-stage chronic renal failure in the Russian Federation in 2010-2015. Report on the data of the Russian register of renal replacement therapy.Part one. Nephrology and dialysis. 2017; 19 (4 Suppl): 195. DOI: 10.28996 / 1680-4422-2017-4Suppl-1-95

    2. Bansal N, McCulloch CE, Rahman M, Kusek JW, Anderson AH, Xie D et al. Blood Pressure and Risk of All-Cause Mortality in Advanced Chronic Kidney Disease and Hemodialysis: The Chronic Renal Insufficiency Cohort Study. Hypertension. 2015; 65 (1): 93–100. DOI: 10.1161 / HYPERTENSIONAHA.114.04334

    3.Zoccali C, Mallamaci F, Tripepi G, Benedetto FA, Cottini E, Giacone G et al. Prediction of left ventricular geometry by clinic, pre-dialysis and 24-h ambulatory BP monitoring in hemodialysis patients: CREED investigators. Journal of Hypertension. 1999; 17 (12 Pt 1): 1751–8. PMID: 10658942

    4. Ataş N, Erten Y, Okyay GU, İnal S, Topal S, Onec K et al. Left Ventricular Hypertrophy and Blood Pressure Control in Automated and Continuous Ambulatory Peritoneal Dialysis Patients.Therapeutic Apheresis and Dialysis. 2014; 18 (3): 297-304. DOI: 10.1111 / 1744-9987.12104

    5. Kulakov V.V., Villevalde S.V., Kobalava Zh.D. Prevalence of markers of chronic kidney disease in patients with arterial hypertension and diabetes mellitus in real practice. Difficult patient. 2017; 3 (15): 49-53

    6. Kobalava J. D., Villevalde S.V., Efremovtseva M.A.Cardiorenal interactions in decompensation of chronic heart failure. Rational pharmacotherapy in cardiology. 2016; 12 (2): 138-46. DOI: 10.20996 / 1819-64462016-12-2-138-146

    7. Agarwal R, Flynn J, Pogue V, Rahman M, Reisin E, Weir MR. Assessment and Management of Hypertension in Patients on Dialysis. Journal of the American Society of Nephrology. 2014; 25 (8): 1630–46. DOI: 10.1681 / ASN.2013060601

    8. Tanner RM, Shimbo D, Dreisbach AW, Carson AP, Fox ER, Muntner P. Association between 24-hour blood pressure variability and chronic kidney disease: a cross-sectional analysis of African Americans participating in the Jackson heart study. BMC Nephrology. 2015; 16 (1): 84. DOI: 10.1186 / s12882-015-0085-6

    9. Agarwal R.Volume-Associated Ambulatory Blood Pressure Patterns in Hemodialysis Patients. Hypertension. 2009; 54 (2): 241-7. DOI: 10.1161 / HYPERTENSIONAHA.109.136366

    10. da Silva GV, de Barros S, Abensur H, Ortega KC, Mion D, Cochrane Renal Group Prospective Trial Register: CRG060800146. Home blood pressure monitoring in blood pressure control among haemodialysis patients: an open randomized clinical trial. Nephrology Dialysis Transplantation.2009; 24 (12): 3805-11. DOI: 10.1093 / ndt / gfp332

    11. Jekell A, Malmqvist K, Wallen NH, Mortsell D, Kahan T. Markers of Inflammation, Endothelial Activation, and Arterial Stiffness in Hypertensive Heart Disease and the Effects of Treatment: Results from the SILVHIA Study. Journal of Cardiovascular Pharmacology. 2013; 62 (6): 559–66. DOI: 10.1097 / FJC.0000000000000017

    12.Minutolo R, Gabbai FB, Agarwal R, Chiodini P, Borrelli S, Bellizzi V et al. Assessment of Achieved Clinic and Ambulatory Blood Pressure Recordings and Outcomes During Treatment in Hypertensive Patients With CKD: A Multicenter Prospective Cohort Study. American Journal of Kidney Diseases. 2014; 64 (5): 744–52. DOI: 10.1053 / j.ajkd.2014.06.014

    13. Liu W, Niu J, Dai C, Yang J. Poor Agreement Between Dialysis Unit Blood Pressure and Interdialytic Ambulatory Blood Pressure.The Journal of Clinical Hypertension. 2014; 16 (10): 701-6. DOI: 10.1111 / jch.12395

    14. Solak Y, Kario K, Covic A, Bertelsen N, Afsar B, Ozkok A et al. Clinical value of ambulatory blood pressure: Is it time to recommend for all patients with hypertension? Clinical and Experimental Nephrology. 2016; 20 (1): 14-22. DOI: 10.1007 / s10157-0151184-1

    15.Zoccali C, Tripepi R, Torino C, Tripepi G, Mallamaci F. Moderator’s view: Ambulatory blood pressure monitoring and home blood pressure for the prognosis, diagnosis and treatment of hypertension in dialysis patients. Nephrology Dialysis Transplantation. 2015; 30 (9): 1443–8. Doi: 10.1093 / ndt / gfv241

    16. Mancia G, Verdecchia P. Clinical Value of Ambulatory Blood Pressure: Evidence and Limits. Circulation Research. 2015; 116 (6): 1034–45.DOI: 10.1161 / CIRCRESAHA.116.303755

    17. Agarwal R. Longitudinal Study of Left Ventricular Mass Growth: Comparative Study of Clinic and Ambulatory Systolic Blood Pressure in Chronic Kidney Disease. Hypertension. 2016; 67 (4): 710-6. DOI: 10.1161 / HYPERTENSIONAHA.115.07052

    18. Agarwal R. Pro: Ambulatory blood pressure should be used in all patients on hemodialysis.Nephrology Dialysis Transplantation. 2015; 30 (9): 1432-7. Doi: 10.1093 / ndt / gfv243

    19. Drawz PE, Alper AB, Anderson AH, Brecklin CS, Charleston J, Chen J et al. Masked Hypertension and Elevated Nighttime Blood Pressure in CKD: Prevalence and Association with Target Organ Damage. Clinical Journal of the American Society of Nephrology. 2016; 11 (4): 642–52. DOI: 10.2215 / CJN.08530815

    20.Wang C, Zhang J, Liu X, Li C, Ye Z, Peng H et al. Reversed Dipper Blood-Pressure Pattern Is Closely Related to Severe Renal and Cardiovascular Damage in Patients with Chronic Kidney Disease. PLoS ONE. 2013; 8 (2): e55419. Doi: 10.1371 / journal.pone.0055419

    21. Chazova I. Ye., Oshchepkova E. V., Zhernakova Yu. V., Karpov Yu. A., Arkhipov M. V., Barbarash O. L. et al. Clinical guidelines. Diagnostics and treatment of arterial hypertension.Cardiology Bulletin 2015; 10 (1): 3-30

    22. Herbert A, Cruickshank JK, Laurent S, Boutouyrie P. Establishing reference values ​​for central blood pressure and its amplification in a general healthy population and according to cardiovascular risk factors. European Heart Journal. 2014; 35 (44): 3122–33. Doi: 10.1093 / eurheartj / ehu293

    23.Hannedouche T, Roth H, Krummel T, London GM, Jean G, Bouchet J-L et al. Multiphasic effects of blood pressure on survival in hemodialysis patients. Kidney International. 2016; 90 (3): 674–84. DOI: 10.1016 / j.kint.2016.05.025

    24. Stern A, Sachdeva S, Kapoor R, Singh J, Sachdeva S. High Blood Pressure in Dialysis Patients: Cause, Pathophysiology, Influence on Morbidity, Mortality and Management. Journal of clinical and diagnostic research.2014; 8 (6): ME01 – ME04. DOI: 10.7860 / JCDR / 2014 / 8253.4471

    25. Nemati E, Ghanbarpour F, Taheri S, Einollahi B. Prevalence of hypertension among Iranian hemodialysis patients and associated risk factors: a nationwide multicenter study. Pakistan journal of biological sciences: PJBS. 2008; 11 (6): 910-4. PMID: 18814655

    26. Abbasi M-R, Lessan-Pezeshki M, Najafi M-T, Gatmiri S-M, Karbakhsh M, Mohebi-Nejad A.Comparing the frequency of hypertension determined by peri-dialysis measurement and ABPM in hemodialysis patients. Renal Failure. 2014; 36 (5): 682-6. DOI: 10.3109 / 0886022X.2014.883933

    27. Taniyama Y. Management of hypertension for patients undergoing dialysis therapy. Renal Replacement Therapy. 2016; 2 (1): 21. DOI: 10.1186 / s41100-016-0034-2

    28.Agarwal R, Pappas MK, Sinha AD. Masked Uncontrolled Hypertension in CKD. Journal of the American Society of Nephrology. 2016; 27 (3): 924–32. DOI: 10.1681 / ASN.2015030243

    29. Gorostidi M, Sarafidis PA, de la Sierra A, Segura J, de la Cruz JJ, Banegas JR et al. Differences Between Office and 24-Hour Blood Pressure Control in Hypertensive Patients With CKD: A 5,693-Patient Cross-sectional Analysis From Spain. American Journal of Kidney Diseases.2013; 62 (2): 285–94. DOI: 10.1053 / j.ajkd.2013.03.025

    30. Mnif K, Jarraya F, Chaker H, Mahfoudh H, Feki S, Charfeddine S et al. PP.28.14. Benefit of forty-eight-hour ambulatory blood pressure monitoring in hemodialysis population. Journal of Hypertension. 2016; 34: e298. DOI: 10.1097 / 01.hjh.00004


    31. Cunha C, Pereira S, Fernandes JC, Dias VP.24-hour ambulatory blood pressure monitoring in chronic kidney disease and its influence on treatment. Portuguese Journal of Nephrology and Hypertension. 2017; 31 (1): 31–6

    32. Velasquez MT, Beddhu S, Nobakht E, Rahman M, Raj DS. Ambulatory Blood Pressure in Chronic Kidney Disease: Ready for Prime Time? Kidney International Reports. 2016; 1 (2): 94-104. DOI: 10.1016 / j.ekir.2016.05.001

    33.Bangash F, Agarwal R. Masked Hypertension and White-Coat Hypertension in Chronic Kidney Disease: A Meta-analysis. Clinical Journal of the American Society of Nephrology. 2009; 4 (3): 656–64. DOI: 10.2215 / CJN.053

    34. Zoccali C, Benedetto FA, Tripepi G, Cambareri F, Panuccio V, Candela V et al. Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients. Kidney International.1998; 53 (4): 1078–84. DOI: 10.1111 / j.15231755.1998.00853.x

    35. Agarwal R, Light RP. The Effect of Measuring Ambulatory Blood Pressure on Nighttime Sleep and Daytime Activity — Implications for Dipping. Clinical Journal of the American Society of Nephrology. 2010; 5 (2): 281-5. DOI: 10.2215 / CJN.07011009

    36. Covic A, Goldsmith DJ, Covic M.Reduced blood pressure diurnal variability as a risk factor for progressive left ventricular dilatation in hemodialysis patients. American Journal of Kidney Diseases: The Official Journal of the National Kidney Foundation. 2000; 35 (4): 617-23. PMID: 10739781

    37. Verdecchia P. Prognostic Value of Ambulatory Blood Pressure: Current Evidence and Clinical Implications. Hypertension. 2000; 35 (3): 844-51. DOI: 10.1161 / 01.HYP.35.3.844

    38. Mojon A, Ayala DE, Pineiro L, Otero A, Crespo JJ, Moya A et al. Comparison of Ambulatory Blood Pressure Parameters of Hypertensive Patients with and Without Chronic Kidney Disease. Chronobiology International. 2013; 30 (1–2): 145–58. DOI: 10.3109 / 07420528.2012.703083

    39. Farmer C. An investigation of the effect of advancing uraemia, renal replacement therapy and renal transplantation on blood pressure diurnal variability.Nephrology Dialysis Transplantation. 1997; 12 (11): 2301-7. DOI: 10.1093 / ndt / 12.11.2301

    40. Pogue V, Rahman M, Lipkowitz M, Toto R, Miller E, Faulkner M et al. Disparate Estimates of Hypertension Control from Ambulatory and Clinic Blood Pressure Measurements in Hypertensive Kidney Disease. Hypertension. 2009; 53 (1): 20-7. DOI: 10.1161 / HYPERTENSIONAHA.108.115154

    41.Agarwal R, Peixoto AJ, Santos SFF, Zoccali C. Out-of-office blood pressure monitoring in chronic kidney disease: Blood Pressure Monitoring. 2009; 14 (1): 2-11. DOI: 10.1097 / MBP.0b013e3283262f58

    42. Amar J, Vernier I, Rossignol E, Bongard V, Arnaud C, Conte JJ et al. Nocturnal blood pressure and 24-hour pulse pressure are potent indicators of mortality in hemodialysis patients. Kidney International. 2000; 57 (6): 2485–91.DOI: 10.1046 / j.15231755.2000.00107.x

    43. Klassen PS. Association Between Pulse Pressure and Mortality in Patients Undergoing Maintenance Hemodialysis. JAMA. 2002; 287 (12): 1548–55. DOI: 10.1001 / jama.287.12.1548

    44. Agarwal R, Peixoto AJ, Santos SFF, Zoccali C. Preand Postdialysis Blood Pressures Are Imprecise Estimates of Interdialytic Ambulatory Blood Pressure.Clinical Journal of the American Society of Nephrology. 2006; 1 (3): 389–98. DOI: 10.2215 / CJN.018

    45. Trukhanova MA, Orlov AV, Tolkacheva VV, Villevalde SV, Kobalava Zh. D. Influence of the duration of programmed hemodialysis on the parameters of central and peripheral hemodynamics in patients with end-stage renal failure. Clinical pharmacology and therapy. 2018; 27 (1): 22-6

    46.Trukhanova M.A., Tolkacheva V.V., Orlov A.V., Villevalde S.V., Kobalava Zh.D. Daily parameters of peripheral and central blood pressure in patients with different etiology of end-stage renal failure. Complex problems of cardiovascular diseases. 2018; 7 (1): 61-6. DOI: 10.17802 / 2306-1278-2018-7-1-61-66

    90,000 Assessment of the circadian rhythm of blood pressure in children

    Ministry of Health of the Russian Federation Moscow Research Institute of Pediatrics and Pediatric Surgery

    St. Petersburg, 2000

    Development organizations:

    Moscow Research Institute of Pediatrics and Pediatric Surgery, Ministry of Health of the Russian Federation. Authors: MD I.V. Leontieva, Doctor of Medical Sciences, Professor Yu.M. Belozerov, L.I. Agapitov.

    Volgograd Medical Academy. Authors: Corresponding Member of the Russian Academy of Medical Sciences, Professor V. I. Petrov, Ph.D. M.Ya. Ledyaev.

    Reviewers: Academician of the Russian Academy of Medical Sciences A.B. Zborovsky, Professor V.N. Chernyshov, Professor E.V. Neudakhin.

    The manual was approved by the Pediatrics Section of the Academic Council of the Ministry of Health of Russia on October 18, 1999, protocol No. 2.

    PDF file

    Carrying out ambulatory blood pressure monitoring with an assessment of a 24-hour rhythm is increasingly being used in therapeutic practice for diagnosing conditions with high and low blood pressure in adults, choosing treatment tactics and monitoring therapy. At the same time, there are no unified approaches to performing ABPM in children and assessing the results obtained. The manual discusses the issues of daily monitoring of blood pressure in children and provides practical advice on performing ABPM and assessing the circadian rhythm of blood pressure.Nomograms are given for determining some parameters of daily monitoring of blood pressure in children.

    The manual is intended for pediatricians, pediatric cardio-rheumatologists, clinical residents, interns, students of pediatric faculties.


    AH – arterial hypertension
    HELL – arterial pressure
    HELL – mean hemodynamic pressure
    DBP – diastopic arterial pressure
    IV – time index
    PI – area index
    KV – coefficient of variation
    PAP – pulse arterial pressure
    SBP – systolic arterial pressure
    SI – daily index
    ABPM – daily monitoring of blood pressure
    SD – standard deviation
    Wed – average value
    HR – heart rate
    ECG – electrocardiogram.

    The origins of hypertension in adults, according to many authors, are in childhood, but the nature and timing of the development of hypertension in children is not well known. In addition, the proportion of children with low blood pressure has been increasing recently. In this regard, the urgent task of pediatrics is to improve the quality of early diagnosis of hyper- and hypotensive conditions.

    In order to adequately assess the level of blood pressure, it must be correctly measured and compared with the standard values.The method of N.S. Korotkov, proposed in 1905 by our compatriot, has historically proven its clinical significance for the diagnosis and prognosis of the course of arterial hypertension. However, the accumulated experience shows that one-time measurements do not always reflect the true blood pressure, do not take into account the effect of the “white coat hypertension”, do not give an idea of ​​the daily rhythm of blood pressure.

    The possibility of continuous 24-hour registration of blood pressure in patients has long attracted doctors of various specialties.The invasive intra-arterial method (Oxford system through a catheter in the brachial artery), despite its high accuracy and continuity of measurement, is not widely used due to the high risk of complications.

    Non-invasive intermittent, but repeated measurement of blood pressure using the Korotkoff auscultatory method, oscillometric method, or a combination thereof, has been used for about 30 years.

    The oscillometric method used in most blood pressure monitors has been known for a long time: one of the first devices for recording arterial oscillograms was designed by L.Uskov in 1904. However, the widespread practical use of this method in medicine became possible in the 80s due to advances in computer technology. Numerous semi-automatic and automatic devices for one-time measurements of blood pressure and monitors for daily monitoring of blood pressure have appeared.

    Self-measurement of blood pressure by patients has become widespread. Numerous studies have confirmed that blood pressure measured by nurses, by the patient himself or by an automated device is lower than that measured by a doctor.Comparison of 24-hour blood pressure monitoring data with the results of random measurements showed that about 40% of patients receive excessive antihypertensive treatment.

    According to many authors, in about a third of adolescents with arterial hypertension detected by random blood pressure measurement, increased blood pressure was also recorded during ABPM.

    If in adults ABPM has been used for a long time and seriously to diagnose hypertension and control antihypertensive therapy, then in children it is a relatively new direction.


    FORMULA OF THE METHOD: a method is proposed for assessing the circadian rhythm of blood pressure in children in vivo using wearable blood pressure monitors in order to improve the quality of diagnosis of hypertensive and hypotensive conditions in pediatrics.

    The novelty of the proposed method lies in the fact that for the first time standards of parameters of daily monitoring of blood pressure are proposed for children of different ages with the allocation of 5, 90, 95 percentiles of blood pressure for adolescents 13–15 years old.For the first time, for calculating the ABPM parameters, the values ​​of the 95th percentile of blood pressure are proposed individually for each child, taking into account gender, age and height.


    The main indications for ABPM are:

    1. Arterial hypertension.

    2. Arterial hypotension.

    3. Syncope conditions.

    4. Short-term, difficult to register with random measurements, fluctuations in blood pressure.

    5. White coat hypertension.

    6. AH refractory to drug therapy.

    There are no absolute contraindications to the use of the ABPM method in pediatrics. Possible complications include:

    1. Edema of the forearm and hand.

    2. Petechial hemorrhages.

    3. Contact dermatitis.

    In order to prevent the appearance of petechial hemorrhages, ABPM should not be performed in children with thrombocytopenia, thrombocytopathy and other disorders of vascular platelet hemostasis during an exacerbation.To prevent the development of edema of the distal part of the limb and contact dermatitis, the cuff should be applied not to the bare shoulder, but to the sleeve of a thin shirt.


    1. Apparatus for daily monitoring of blood pressure and pulse:

    1.1. Ambulatory blood pressure monitor Meditech ABPM-02 (Meditech, Hungary), registered in the Ministry of Healthcare of the Russian Federation under No. 95/192.

    1.2. The system of daily blood pressure and ECG monitoring MEDSET with SCANLIGHT-recorder and CARDIOLIGHT-recorder, SCANLIGHT-CARDIOLIGHT PC-Software programs, patient cable, SCANLIGHT cuff and Medset Battary Changer-Set, (by MEDSET Medizintechnik GmbH, Germany) registered in the MZMP RF No. 97/323.

    1.3. System of daily monitoring of ECG and blood pressure “Cardiotechnika – 4000 AD” (company “INCART”, St. Petersburg, Russia), registered by the Ministry of Health of the Russian Federation under No. 95 / 311-51.

    2. Personal computer with a printer.

    Characteristics of monitors and methods for studying the circadian rhythm of blood pressure in children

    Currently, for daily monitoring of blood pressure in children, monitors are used that use various methods of measuring blood pressure: auscultatory, oscillometric, with a combination of these methods, as well as synchronization with an ECG.More accurate, but also much more expensive, are devices with a combination of auscultatory and oscillometric methods, as well as using synchronization with an ECG: when each vibration in the air in the cuff is correlated with an ECG.

    In auscultatory monitors, a miniature microphone mounted above the brachial artery captures Korotkoff’s tones. In this case, it is necessary to accurately position the microphone, which is often difficult for children. The sensor is very sensitive to external noise and even the slightest displacement.The patient or his parents will not be able to accurately position the microphone on their own, therefore it is undesirable to remove the cuff and sensor. In addition, in children, the hyperkinetic type of blood circulation prevails, in which the phenomenon of “infinite tone” is often observed, which makes it difficult to determine diastolic blood pressure by auscultatory method.

    Currently, monitors with oscillometric measurement of blood pressure are most widely used in terms of price / accuracy.

    The ABPM-02 (AVRM-02, AVRM-02 / M and AVRM-02/0) and SCANLIGHT-II devices use an oscillometric method for measuring blood pressure.The entire cuff is the sensor, therefore, the method is insensitive to noise, to cuff displacements, which can even be removed between measurements by the patient or parents and put on again without compromising the measurement accuracy.

    The device automatically pumps air into the cuff with a built-in compressor to a pressure of 20-30 mm Hg. above the systolic blood pressure and then slowly, stepwise, decreases the pressure below the diastolic. Arterial pulse waves are transmitted through the cuff and recorded by a capacitive or piezoelectric pressure transducer.

    The new blood pressure registration algorithm used in the AVRM-02 / M and AVRM-02/0 devices has a new, higher degree of resistance to external mechanical disturbances arising, for example, due to involuntary hand movements. The essence of the algorithm is stepwise decompression and registration of several fluctuations at each level of pressure in the cuff. In case of unsuccessful registration of oscillations at any level, the apparatus returns to it and repeats the measurement.

    While the pressure in the cuff decreases, the first recorded fluctuations are estimated as systolic blood pressure.The maximum oscillation corresponds to the mean hemodynamic blood pressure. The last recorded oscillation is considered as diastolic blood pressure. The blood pressure values ​​are related by the formula:

    MAP = DBP + 1/3 (SBP – DBP)

    Programming monitors (measurement plan)

    The measurement plan provides for the establishment of day and night periods: as a rule, 06.00–24.00 – day, 00.00–06.00 – night. Frequency rate of measurements in the daytime: 1 time in 15 minutes, in the nighttime: 1 time in 30 minutes.(more rare measurements will not give an idea of ​​the high variability of blood pressure in children, and more frequent measurements during the day do not increase the accuracy of the study, and at night can cause sleep disturbance).

    To check the sleep time, the child should be encouraged to press the “event” button on the monitor when he goes to bed and when he wakes up. According to our observations, the beginning of the night period is about 1 hour after, and the daytime period is 1 hour before the “event”. You can focus on the heart rate graph: at the time of falling asleep, there is a sharp decrease in heart rate, and upon waking up – an increase.According to the heart rate graph, it is possible to indirectly control the depth of sleep: if there was a significant increase in heart rate at night, then the sleep was restless. During statistical processing of data, a shift of the day period by ± 1 hour does not affect the average. Editing the duration of the day and night intervals is possible after entering data from the monitor into the computer.

    When programming monitors, it is necessary to select the appropriate cuff size, turn off the warning sound signal, turn off the display so that the results of scheduled measurements are not displayed, – to reduce the increased attention of children to the device and prevent anxiety from high blood pressure values.

    Procedure for installing the monitor on the patient

    The monitor fits into a case and straps to the patient using two straps, one over the shoulder and the other around the waist. Some guidelines recommend removing the monitor from the patient at night and placing it side-by-side with a longer tube connected to the cuff. However, babies sleep more restlessly than adults and often the tube is wrapped around the baby and kinked, disrupting the measurement process. In our opinion, during the study, the child should not take off the monitor even at night.

    The cuff is selected in accordance with the child’s shoulder circumference, measured at the midpoint of the distance between the olecranon and humeral processes (table 1). The use of cuffs on the forearm or finger is not adequate and cannot yet be recommended for widespread use in pediatric practice.

    Table 1. Selection of the cuff depending on the size of the child’s shoulder

    Shoulder circumference (cm) Dimensions of cuff rubber balloon (cm) Dimensions of the cuff cover (cm)
    91,323 Less than 24


    9 x 41

    24 – 32


    16 x52

    More than 32

    14.5 x 32

    16 x70

    To prevent discomfort associated with the duration of measurements (sweating, chafing, etc.)it is allowed to put a cuff over a thin shirt, a T-shirt with a sleeve. This does not affect the measurement accuracy. The cuff is secured so that the tube fitting or “arteria” mark is approximately over the brachial artery. The exit tube should point upwards so that the patient can wear other clothing over the cuff if necessary.

    After installing the monitor, it is necessary to explain to the child the rules of behavior at the time of measurement and demonstrate one measurement.The child learns about the beginning of the measurement by squeezing the shoulder due to an increase in pressure in the cuff. At this moment, it is necessary to avoid sudden movements: stop if the child was walking or running, lower the arm with the cuff along the body, relax the muscles of the arm as much as possible, do not move your fingers. If the child was sitting or lying, it is necessary to leave the hand in the position in which it was located (it is desirable that the cuff is at the level of the heart).

    As a rule, scheduled measurements are accompanied by a smooth injection of air into the cuff and a stepwise decrease in pressure.Sometimes, in case of unsuccessful measurements, the monitor, after decreasing the pressure, again pumps air into the cuff. It is necessary to explain to the child that until there is a quick and complete release of air from the cuff, it is necessary to remain calm.

    The monitors are equipped with an “extraordinary measurement” button, which you can recommend the child to press when a headache, pain in the heart, dizziness, etc. occurs. At this moment, an extraordinary measurement of blood pressure and heart rate will occur with recording in memory and indication of the results on the display for taking urgent measures, if necessary.

    It should be explained to the child that he should not think about the monitor, listen to his work, worry about night measurements. At the same time, the child must exercise certain caution: avoid intense physical exertion, sudden movements. The monitors are equipped with safety systems: in case of sudden overpressure, the emergency valve will release air. In addition, there is a button to interrupt the measurement. As a rule, children, especially adolescents, are very responsible for monitoring blood pressure.According to our data, the percentage of measurements available for calculations usually exceeds 95%. Nighttime blood pressure monitoring usually does not bother children.

    For diagnostic purposes, it is important that the child, when conducting daily monitoring of blood pressure, is in his usual rhythm of life, and with intense physical, emotional or mental stress, he (or his parents) makes a corresponding entry in the diary (Appendix 1). When evaluating the effectiveness of therapy, a child during ABPM should be in approximately the same conditions before and during treatment.

    Evaluation of monitoring data

    A wide range of modern computer programs provides great opportunities for editing and evaluating monitoring results. These data can be presented in graphical form (graphs, histograms) or in the form of a statistical report. It should be emphasized that editing data in accordance with the patient’s diary is an important preparatory procedure to exclude possible measurement artifacts.

    The graphical form is most convenient for visual assessment of the daily profile and variability of blood pressure.To smooth out random fluctuations of blood pressure, graphs of average values, Fourier transforms, polynomial analysis (polynomial of 5-6 degrees), cosinor analysis are used. ABPM data can be transposed into Excel (Windows) and analyzed by this program.

    When analyzing the data obtained during daily monitoring of blood pressure, the most informative are the following groups of parameters: mean blood pressure values, indices of the time of hypertension and hypotension, indices of the area under the blood pressure curve, indicators of blood pressure variability.For all parameters, the values ​​are calculated both for 24 hours and for separate periods of time (day, night or arbitrary intervals).

    Average values ​​of blood pressure (systolic, diastolic, mean hemodynamic, pulse) give the main idea of ​​the blood pressure level in the patient, more accurately reflect the true level of hypertension than single measurements.

    Until recently, Russia has not established normal limits for daily monitoring of blood pressure in the pediatric population, based on a sufficient number of studies.More attention is paid to this problem abroad. In 1997, M.S. Soergel et al. Determined the proper mean values ​​of blood pressure in children and adolescents based on 24-hour monitoring data as a result of a multicenter study involving 1141 children. Considering that BP values ​​correlate better with body length than with age, the 50th and 95th percentiles of BP were given taking into account the child’s height (Table 2).

    Table 2. Values ​​of the 50th and 95th percentile of blood pressure according to daily monitoring data in children and adolescents, depending on height (M.S. Soergel et al., 1997)

    Height (CM) / n Percentile HELL
    Percentile HELL
    Percentile HELL








    120 (33)







    130 (62)







    140 (102)







    150 (105)







    160 (115)







    170 (83)







    180 (69)








    120 (40)







    130 (58)







    140 (70)







    150 (111)







    160 (56)







    170 (105)







    180 (25)







    Based on a survey of 240 adolescents aged 13–15 years, we obtained standard values ​​of ABPM indicators.The highlighted blood pressure values ​​corresponding to the 5th, 90th and 95th percentile. The data are presented in Table 3.

    Values ​​between the 90th and 95th percentiles should be considered “high normal BP”. The definition of the concept of “high normal blood pressure”, on the one hand, allows avoiding hyperdiagnosis of hypertension and does not cause mental trauma to the child and his parents, on the other hand, it presupposes the identification of a risk group, if possible, of the formation of hypertension, requiring preventive measures and dynamic observation. BP values ​​above the 95th percentile were taken for arterial hypertension.BP values ​​below the 5th percentile were taken as arterial hypotension.

    The index of time (TI) of hypertension or “the proportion of high blood pressure” allows you to estimate the time of the increase in blood pressure during the day. This indicator is calculated by the percentage of measurements that exceed normal blood pressure values ​​in 24 hours or separately for each time of day. For the maximum allowable blood pressure in children during the daytime, we took the 95th percentile values ​​for the corresponding gender, age and height, calculated from our own nomograms (Appendix 2).The maximum permissible blood pressure value in the night time period was taken as a value 10% less than during the day.

    Table 3. Indicators of daily monitoring of blood pressure in adolescents 13-15 years old

    Time Parameters Percentiles Maximum Minimum Average s
    5 90 95
    91,323 Girls (mean age 14.3 years)










    (24 hours)









































    91 233 74




    Boys (mean age 14.1)










    (24 hours)









































    91 233 74




    Time index exceeding 25% for SBP is clearly considered pathological.In this case, the diagnosis of hypertension is made. With stable hypertension, IV hypertension approaches 100% and loses its information content. In this case, the area index or pressure load is determined. The area index is calculated as the area of ​​the figure bounded by the high blood pressure curve and the level of normal blood pressure (in mm Hg * hour / day). The area index reflects the hypertensive load acting on the patient’s body, that is, how long in 24 hours (or day, night) and, on average, by what value, the blood pressure exceeded the upper permissible limit.

    When calculating the “hypotension index”, the percentage of time when BP was below the 5th percentile for age and sex is calculated.

    The normative values ​​of IV and PI obtained in our study with daily monitoring of blood pressure are presented in Table 4.

    Table 4. Standards for time index and area index for adolescents 13-15 years old

    Parameters Day Night


    IO (%)
    Less than







    PI less than 91,232 Mm Hg.st. * hour








    IO (%)
    Less than







    PI less than 91,232 Mm Hg.st. * hour








    Blood pressure is one of more than 300 physiological processes in the body, subject to circadian rhythms. Registration of blood pressure, provided that pressure is measured at intervals of 15-30 minutes during the day, gives a fairly accurate idea of ​​the variability of blood pressure.To assess variability, use:

    1. Determination of the daily index.

    2. Calculation of the standard deviation or coefficient of variability of blood pressure.

    The daily index (SI) shows the difference between the average day and night values ​​of blood pressure as a percentage of the daily average value and is calculated by the formula:

    SI = (Avg. ADd. – Avg. ADn. Night): Avg. BP days x 100%.

    Average SI values ​​obtained in our study with daily monitoring of blood pressure are presented in Table 5.

    Table 5. Average values ​​of the daily index in healthy adolescents (13–15 years old) according to the results of ABPM

    Parameters Boys Girls








    Most people experience a 10–20% decrease in blood pressure at night compared to daytime levels.According to the value of the daily index, four groups of patients are distinguished:

    “dippers” – SI 10 – 20%,

    “non-dippers” – SI 0 – 10%,

    “over-dippers” – SI> 20%,

    “night-peakers” – SI <0.

    According to our data, in 85% of healthy children, the SI for SBP and DBP exceeds 10% “dippers”. “Night-peakers” children are not normally found. with nighttime blood pressure exceeding the average daytime values.

    The coefficient of variation (KB) is a calculated indicator and is determined by the formula:

    kb = CO: Cp x 100

    where KB is the coefficient of variation,

    SD – standard deviation,

    Wed – average value of the parameter.

    KB values ​​obtained in our study with daily monitoring of blood pressure are presented in Table 6.

    Table 6. Standard values ​​of the coefficient of variation in healthy adolescents

    Indicator Day Night

















    Fig.1 shows the daily profile of mean hemodynamic blood pressure, built on the basis of polynomial analysis of data obtained during daily monitoring of blood pressure in adolescents of both sexes (polynomial of the 6th degree). According to our data, healthy children have minimal blood pressure cf. at 2 am. In the future, blood pressure rises and reaches the first peak by 10-11 am, moderately decreases by 16 hours and the second peak is noted at 19-20 hours.

    Fig. 1. Daily profile of mean hemodynamic blood pressure in healthy adolescents.

    In modern conditions, early detection of changes in blood pressure levels in children is extremely important. Daily monitoring of blood pressure makes it possible to verify the initial deviations in the circadian rhythm and the value of blood pressure. Currently, there are no normative data for ABPM for children. This manual summarizes the first experience in the conduct and analysis of ABPM in children. The departure of the ABPM parameters beyond the indicated limits is not unambiguously pathological, but should be considered as a risk factor for the development of hypertension in adulthood.

    Like adults, children with hypertension, as a rule, do not have any external manifestations and signs that clearly distinguish between essential and symptomatic hypertension. Further accumulation of experience on daily monitoring of blood pressure in children with renal, endocrine pathology, essential hypertension, will provide new criteria for the differential diagnosis of these diseases.


    24-hour BP monitoring diary

    F.And O. of the child _________________________________________________

    Date of birth _________________ Age (years) ____________________

    Weight ___________ Height __________ Body mass index (kg / m 2 ) __________

    Full name mother of the child ____________________________________________

    Address: ________________________________________________________

    Phone: ______________________________________________________

    Start date of the study ________ Start time of the study ________

    Cuff: on the right arm on the left arm.

    Appointments (drug, dose) – _____________________________________

    Time Type of activity Complaints
    (hours) 1 2 3 4 5 6 7 8 9 10 Notes

























    where, types of activity: 1 – sleep, 2 – eating, 3 – taking medications, 4 – lying down, 5 – emotional stress, 6 – physical activity;
    complaints: 7 – headaches, 8 – dizziness, 9 – palpitations, 10 – fatigue


    Nomograms for determining the 95th percentile of blood pressure taking into account age and height (according to ABPM data)