Most women will experience hot flashes when going through the menopause.
In the USA, the term hot flashes is used to describe this phenomenon whereas in the UK the term hot flushes is used. Both mean the same thing.
Hot flashes are also known as vasomotor symptoms. The term ‘vasomotor’ refers to the vasomotor center in the brain which plays an important role in regulating peripheral blood flow and blood pressure.
Menopausal hot flashes may be described as a sudden feeling of warmth, that seems to come from nowhere and spreads throughout the body, usually most intense over the face, neck, and chest. Sometimes the hot flashes are accompanied by sweating, palpitations, and reddening of the skin.
Some women only have mild symptoms with occasional hot flashes that don’t really affect their quality of life, while others can have many a day, and find them very uncomfortable, disruptive and sometimes embarrassing.
Hot flashes have been consistently shown to be associated with discomfort, sleep disturbances, fatigue, and decreased quality of life.
Pregnancy and childbirth are pretty rotten jokes to play on the female, but I cannot help suspecting that the menopause may be nature’s last — and most outrageous — grand belly laugh.
― Elizabeth Oakleigh-Walker Buchan, “Rite of Passage,” 1993
1. What Is Menopause?
The natural menopause is the time in a woman’s life when she stops having periods. It occurs when the ovaries naturally begin to decrease their production of the sex hormones estrogen and progesterone. Menopause marks the end of fertility and childbearing years.
Induced menopause occurs if the ovaries are surgically removed or damaged, for example by radiation or drugs.
Menopause is defined as the time when there have been no menstrual periods for 12 consecutive months, and no other biological or physiological cause can be identified (1).
Periods usually start to become less frequent over a few months or years before they stop altogether.
The menopause is a natural part of aging and usually occurs between 45 and 55 years of age. The average age of menopause in the United States is 51.5 years (range, 45-59 y) (2).
Premature menopause (before 40 years of age) occurs in approximately 1 in 100 women. Women who smoke are likely to go into menopause earlier than those who don’t smoke (3)
The term ‘postmenopause’ describes all the years beyond menopause.
2. What Is Perimenopause (Menopause Transition)?
The changes of the menopause transition begin about six years before the natural menopause. This period is called perimenopause.
During perimenopause, the levels of hormones produced by the ovaries fluctuate, resulting in irregular menstrual patterns. Usually, there is an irregularity in the length of the period, the time between periods, and the level of flow.
The average length of perimenopause is four years, but for some women, it may last only a few months or continue for ten years. Perimenopause ends when a woman has gone 12 months without having her period.
Menopausal symptoms usually begin during perimenopause.
3. What Are Menopausal Symptoms?
The most common symptom during the menopausal transition and menopause is hot flashes.
Women may experience a number of other symptoms, including vaginal dryness, sleep disturbances, breast pain, migraines, problems with memory loss and difficulty concentrating, and new-onset depression (4).
Changes in lipids and bone loss often begin to occur during premenopause.
4. What Are Menopausal Hot Flashes?
Hot flashes, also known as vasomotor symptoms, are often described as a sudden sensation of heat in the chest, face, and head that rapidly become generalized.
The sensation of heat usually lasts for two to four minutes and is often associated with profuse sweating and sometimes palpitations (5).
Sometimes hot flashes are followed by chills, shivering, and a sensation of anxiety.
Some women only experience occasional hot flashes while some may have repeated episodes, sometimes every hour during day and night.
Hot flashes may mark adverse underlying vascular changes among midlife women (6). They may also be a marker for risk of bone loss (7).
5. How Common Are Hot Flashes?
Up to 80% of women going through menopause experience hot flashes (8).
However, only approximately 20 to 30 percent of women seek medical attention for treatment (5).
Women with perimenopause shorter than six months (estimated at 10% of women) have lower rates of hot flashes (9).
6. When Do Hot Flashes Begin and How long Do They Last?
Although the average age of menopause is approximately 51 years, hot flashes can start well before the final menstrual period and last for several years after the onset of menopause.
Recent studies have demonstrated that the average duration of menopausal symptoms such as hot flashes is approximately 7 to 9 years (10).
Early evidence suggested that the prevalence of hot flushes accelerates during perimenopause, peaks at about the time of the last menstrual period and declines rapidly after that (11).
However, even though the frequency and severity of hot flashes decrease with age for most women, some continue to report persistent symptoms even into their seventh and eighth decades of life.
A recently published study from the Mayo Clinic showed that flashes may still be disruptive in women over a decade past the natural age of menopause (12).
One study showed that African American women had a longer total duration of hot flashes, whereas Chinese and Japanese women had shorter total duration. (13).
The menopause is a natural part of aging and usually occurs between 45 and 55 years of age. It happens when the ovaries naturally begin to decrease their production of the sex hormones estrogen and progesterone.
7. What Causes Menopausal Hot Flashes?
Menopausal hot flashes are mediated by thermoregulatory dysfunction at the level of the hypothalamus (14). The dysfunction appears to be initiated by low estrogen levels, the hallmark of the menopausal transition. Elevation of luteinizing hormone (LH) co-occurs.
The feeling of heat is caused by peripheral vasodilatation (the widening of blood vessels). Hence, the term ‘vasomotor symptoms’ is often used to describe hot flashes.
When peripheral blood vessels dilate, skin blood flow is increased causing a feeling of warmth.
Perspiration may lead to rapid heat loss. Shivering may then occur to restore the core temperature to normal (5).
8. What Risk Factors Increase the Risk of Hot Flashes?
Several characteristics and health behaviors have been reported to be significantly associated with an increased risk of hot flashes, including cigarette smoking, obesity, and lower levels of education (15).
Obese women have a higher risk of hot flashes (16).
One study showed that among women who were overweight or obese and had bothersome hot flushes, an intensive behavioral weight loss intervention resulted in improvement in flushing (17).
Current smoking may predispose a woman to more severe or frequent hot flashes (18).
Socioeconomic factors and low levels of education are associated with an increased risk of hot flashes (19).
Furthermore, African American women report more frequent hot flashes than Caucasian women (19).
9. Can Hot Flashes Cause Sleep Disturbances?
Sleep disturbances are common during the menopausal transition.
An essential feature of hot flashes is that they are more common at night than during the day and are associated with arousal from sleep. Hence, hot flashes that occur at night (night sweats), may be the underlying cause of disrupted sleep.
One study showed that hot flashes accounted for a significant proportion of time awake during the night in perimenopausal women (20).
However, there are many other possible causes of disrupted sleep in this population. Examples are obstructive sleep apnea (OSA), anxiety, and depression.
10. What Nonmedical Treatments May Be Used to Treat Hot Flashes?
There is considerable interest in the development of effective nonmedical interventions to help women manage hot flashes
Simple measures such as lowering room temperature, using fans, dressing in layers of clothing that can be easily shed, and avoiding triggers (such as spicy foods, too much alcohol, and stressful situations), can help reduce the number of hot flashes (5).
Growing evidence from recent randomized controlled trials suggests that cognitive-behavior therapy (CBT) can effectively reduce the impact of hot flushes (21).
CBT seems to work mainly by changing symptom perception and cognitive appraisal.
Hypnosis may be beneficial for hot flashes (22), but there is limited data available on its efficacy.
Results of one placebo double blind-controlled trial suggest that vitamin E may reduce the frequency and severity of hot flashes (23).
Herbal remedies such as black cohos are used by many postmenopausal women for hot flashes. However, clinical trials have shown that it is not more effective than placebo (24).
There have been concerns that black cohosh could stimulate breast tissue like estrogen, increasing the risk of recurrence in women who have had breast cancer. However, so far, there is no evidence that it is harmful, even in women with breast cancer.
There are a variety of plant-based treatments available for the treatment of hot flashes. Isoflavones and phytoestrogens, found in many plants, fruits, and vegetables, are commonly used.
Phytoestrogens also called ‘dietary estrogens,’ are a diverse group of naturally occurring nonsteroidal plant compounds that have structural similarity with estradiol. They are found in many foods, including soybeans, chickpeas, lentils, flaxseed, lentils, grains, fruits, vegetables, and red clover.
Isoflavone supplements, a type of phytoestrogen, can be purchased in health food stores.
A systematic review of plant-based therapies published 2016 showed that phytoestrogen supplementations were associated with modest reductions in the frequency of hot flashes and vaginal dryness but no significant reduction in night sweats (25)
However, it is still considered uncertain whether phytoestrogens help to reduce hot flashes as most studies have not reported benefit. Furthermore, some phytoestrogens might act like estrogen in some tissues of the body.
Many experts suggest that women who have a history of breast cancer should avoid phytoestrogens.
11. What Is the Role of Hormonal Therapy?
Hormone replacement therapy is effective for the treatment of hot flashes.
Hormone therapy may also help prevent bone loss and reduce the risk of bone fractures in postmenopausal women.
However, there are also risks associated with menopausal hormone therapy. These risks depend on the individual treated, the type of hormone therapy administered, and the dose and length of treatment.
Estrogen is the hormone that provides the most menopausal symptom relief. Progestogen is added to protect women against uterine (endometrial) cancer from estrogen alone.
The general rule is that women with an intact uterus are given both estrogen and a progestin, while those who have undergone hysterectomy may be given estrogen only.
Systemic estrogen (available as pill, skin patch, gel, cream or spray) is the most effective treatment for the relief of hot flashes.
Vaginal preparations of estrogen (available as a cream, tablet or rings) can be effective for vaginal and urinary symptoms but have not been shown to reduce the severity of hot flashes (26).
A combination drug of bazedoxifene with conjugated estrogens (Duavee) has been approved for treating menopausal symptoms. In theory, the risk of uterus and breast cancer might be less with this combination than with estrogen replacement therapy (27).
12. What Are the Risks Associated with Hormonal Therapy?
It is a longheld belief that estrogen may protect against cardiovascular disease. Before the late 1990s, hormone therapy (estrogen with or without progestin) was recommended for both primary and secondary prevention of cardiovascular disease (28).
In 1998 the Heart and Estrogen/ Progestin Replacement Study (HERS) reported an increase in cardiovascular events among women with a history of cardiovascular disease treated with conjugated equine estrogen and medroxyprogesterone acetate (29).
Subsequently, hormone therapy was considered inappropriate for secondary prevention but still retained a role of primary prevention of cardiovascular disease.
In 2002, the Women’s Health Initiative (WHI) investigators (30) reported an increase in the composite outcome, including breast cancer and cardiovascular events, in women without pre-existing cardiovascular disease randomly assigned to receive conjugated equine estrogen and medroxyprogesterone acetate.
Following the publication of the WHI trial, guidelines were revised to recommend against the routine use of hormone therapy for reasons other than treatment of menopausal symptoms, and that treatment should continue for the shortest duration possible.
Today, hormone replacement therapy is believed to be associated with an increased risk of breast cancer, uterine (endometrial) cancer, stroke and blood clots in the veins. These risks are higher in women over age 60.
Hence, in women with a history of breast cancer, coronary heart disease, a previous venous thrombotic event (blood clot in legs or lungs) or stroke, or those at moderate or high risk for these complications, other therapies should be considered first.
A recent meta-analysis suggests that menopausal hormone therapy does not affect the risk of death from all causes, cardiac death, and death from stroke or cancer (31).
13. For How Long Should Menopausal Hormone Therapy Continue?
In most cases, short-term hormone therapy is considered the most sensible option.
Short-term therapy is considered to be less than five years (or not beyond age 60 years) (32).
However, sometimes hot flashes persist after discontinuation of hormonal therapy. In these cases, non-hormonal therapies (see no. 15 below) may be tried.
For women who experience recurrent, bothersome hot flashes after stopping estrogen, and do not get adequate relief with nonhormonal therapies, extended use of hormone therapy may be considered (33).
14. How Difficult Is It to Stop Menopausal Hormone Therapy?
Most women have no trouble stopping menopausal hormone therapy. Studies show that approximately 75% of women who try to stop can do so without significant difficulty (34).
Approximately one-quarter of women who try to stop report that they are unable to discontinue postmenopausal hormone therapy, mainly owing to the development of hot flashes (35).
Some clinicians recommend slowly tapering hormone therapy to avoid withdrawal symptoms. One study suggests that tapering may lessen recurrence of menopausal symptoms after discontinuation (36)
As persistent hot flashes can severely impact quality of life, extended use of hormone therapy may be warranted when the clinician and the patient agree that the benefits outweigh the risk.
15. What Can Nonhormonal Drug Therapy Be Used to Treat Hot Flashes?
Hormone therapy is the most effective therapy for hot flashes. However, non-hormonal drugs are available for the treatment of the condition
Some women are not appropriate candidates for hormone therapy, such as those that have been recently treated for breast cancer.
Non-hormonal therapy may also be tested in women who experience recurrent hot flashes after stopping hormone therapy.
The agents most commonly used include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), antiepileptics, and centrally acting drugs.
Paroxetine (Brisdelle, Paxil), an SSRI that is also used to treat anxiety and depression, is the only nonhormonal medication approved by the Food and Drug Administration for managing hot flashes. However, other related drugs, including SSRIs like fluoxetine (Prozac) as well as norepinephrine reuptake inhibitors like venlafaxine (Effexor), have also shown to be effective.
Gabapentin (Neurontin), a drug also used to treat seizures an nerve pain, may also help against hot flashes.
Bad breath, also called halitosis, is a widespread condition that can affect people of any age. Indeed, about 30% of people may have bad breath.
It has been reported that Americans spend up to 3 billion dollars a year on gum, mints and breath fresheners, in most cases in order to improve their breath (1).
The type and intensity of bad breath may vary depending on the source and the underlying cause.
Although there rarely is a severe underlying disorder, bad breath may negatively affect quality of life and personal relationships. It can be socially embarrassing and may even cause anxiety.
The range of terms used in the scientific literature includes halitosis, bad or foul breath, oral malodor, fetor ex-ore, and fetor oris. These all describe unpleasant breath exhaled from the sufferer’s mouth.
Fortunately, in most cases, halitosis can be controlled, and simple treatment measures have been proven to be very useful.
Good looks aren’t what I look for in a man. That’s way down the list. If a man can make me laugh and stimulate me intellectually, then I wouldn’t mind if he was 4ft 8ins with a huge belly. The only thing that would put me off is bad breath – but even that can be fixed. A bad personality isn’t so easy to fix.
― Olga Kurylenko
1. What Is Bad Breath (Halitosis)?
Halitosis is defined as “oral malodor with intensity beyond a socially acceptable level perceived” (2).
Halitosis is not a disease in itself but a symptom with a variety of underlying causes.
It is important to acknowledge that there is a difference between the occasional and temporary bad breath that most people experience and chronic bad breath.
Temporary halitosis may be caused by tobacco smoking and consumption of aromatic food such as garlic and onion or beverages such as alcohol and coffee.
Chronic halitosis, however, is most often due to microbial degradation in the oral cavity but may sometimes be caused by an underlying disease process.
2. What’s the Difference Between Halitosis, Pseudohalitosis, and Halitophobia?
Halitosis can be classified into three main categories: genuine halitosis, pseudo-halitosis, and halitophobia.
In genuine halitosis, the patient has obvious oral malodor with an intensity beyond socially acceptable levels.
Pseudohalitosis also called subjective halitosis or delusional halitosis (imaginary halitosis), describes a perception by the patient that halitosis is present although there is no objective evidence of bad breath (2).
The term halitophobia describes the persistent fear of having bad breath that other people find offensive. It is estimated that 0.5%–1% of the adult population is affected by this problem in their social life (3).
3. What’s the Difference Between Physiologic and Pathologic Halitosis?
The term physiologic halitosis is used to describe bad breath that does not have a specific underlying cause (4). It is often transient and usually worse in the morning.
The term pathologic halitosis is used when the breath odor is a symptom of a disease or other pathologic condition, or aggravated by it (5).
Most often, physiologic halitosis is attributable to putrefaction processes taking place in the oral cavity, frequently within the white-colored coating found on the posterior portion of the tongue (6).
4. What Causes Foul Morning Breath (Morning Halitosis)?
Bad breath commonly occurs in the morning. This type of bad breath is defined as physiologic halitosis and usually resolves immediately after brushing, flossing, eating, or drinking water.
Foul morning breath is believed to be partly caused by a relatively low flow of saliva during sleep. This may promote bacterial action on entrapped food particles present on the dorsum of the tongue (2).
5. What Causes Bad Breath (Halitosis)?
Microbial degradation in the oral cavity is the primary cause of bad breath.
The primary causative microbes are gram-negative, anaerobic bacteria.
Volatile sulfur compounds (VSCs) are formed via the degradation of methionine and cysteine present in food particles. The most important VSCs involved in halitosis are hydrogen sulfide, methyl mercaptan, and dimethyl sulfide (3).
Other gases that may be responsible for halitosis are skatole, cadaverine, and putrescine (2).
The bacterial action causing oral halitosis most often takes place on material between the teeth and the dorsum of the posterior portion of the tongue (7).
Other causes of halitosis include disorders of the throat and nasal cavity, gastrointestinal disorders, and systemic disorders.
6. What Are the Most Common Causes of Bad Breath (Halitosis)?
In nearly 85% of all halitosis cases, the origin is found in the oral cavity (3).
One study of 2.000 patients showed that 76% of halitosis had oral causes: tongue coating (43%), gingivitis/periodontitis (11%) or a combination of the two (18%) (8).
Tounge coating is the most common cause of bad breath. The dorsum of the tongue is an ideal niche for oral bacteria.
Tounge coating is the most common cause of bad breath. The dorsum (upper surface) of the tongue is an ideal niche for oral bacteria.
Accumulation and putrefaction of food remnants, poor oral hygiene, dental plaque, and dental caries all contribute to bad breath.
It has also been shown that unclean acrylic dentures (worn at night or not regularly cleaned or with rough surfaces) contribute to bad breath (9).
Gingivitis and periodontitis are common causes of the halitosis (10).
Gingivitis is a common form of gum disease that causes irritation, redness, and inflammation of the gingiva, the part of the gum around the base of the teeth.
Periodontitis is a gum infection that damages the soft tissue and destroys the bone that supports the teeth. Periodontitis is common but largely preventable. It’s usually the result of poor oral hygiene (11).
Tonsillitis, an inflammation of the tonsils, may cause halitosis
Dry mouth (xerostomia) is a fairly common condition that may cause bad breath (12). Several commonly used drugs may cause dry mouth (see no. 10 below).
7. Can Bad Breath Originate from the Nose?
Yes, it can.
When halitosis has a nasal cause, nasal exhalation will cause more bad breath than oral expiration (2).
Halitosis originating from the nose may be caused by acute and chronic sinusitis and postnasal drip.
8. What Gastrointestinal Disorders Can Cause Halitosis?
Zenker’s diverticulum may cause halitosis
Volatile substances originating from the stomach or esophagus may sometimes cause bad breath
Zenker’s diverticulum, a pouch of the upper portion of the esophagus, sometimes associated with difficulty swallowing, may cause halitosis. The bad breath is caused by the breakdown of stagnant food in the pouch by microorganisms.
Stomach ulcers and gastroesophageal reflux disease (GERD) may occasionally cause halitosis.
9. What Systemic Disorders Can Cause Halitosis?
Advanced kidney disease, diabetic ketoacidosis, and advanced liver disease may cause bad breath.
Respiratory tract infections such as bronchitis are rare causes of halitosis.
10. Can Drugs Cause Bad Breath (Halitosis)?
Many medications can cause dry mouth which may lead to halitosis. Examples are diuretics, antihistamines, decongestants, tricyclic antidepressants, and amphetamines (2).
The following drugs may be directly responsible for oral malodor: dimethyl sulfoxide, cysteamine, nitrates and nitrites (isosorbide dinitrate), disulfiram, penicillamine (penicillin), chloral hydrate, phenothiazine, suplatast tosilate, and paraldehyde (13).
11. What Should You Look For if You Have Bad Breath (Halitosis)?
Most causes of halitosis may be found in the oral cavity.
Check if there is a coating of the tongue. Look closely at the posterior portion of the upper surface (dorsum)of the tongue.
Check the teeth. Are they in good repair?
Check if the dental floss has a bad smell after it has been used.
Check the gums. Redness or swelling of the gums may indicate gingivitis.
12. How Can Bad Breath (Halitosis) Be Prevented or Cured?
Malodor that arises from the mouth is the consequence of microbial putrefaction of food debris, cells, saliva, and blood. (14).
Hence, good oral hygiene is the first step to prevent halitosis.
Brushing at least twice a day and flossing daily can help to prevent and reverse gingivitis and periodontitis.
If halitosis persists despite good oral hygiene, the tongue may be the likely source of the odor. In such cases, tongue cleaning may be indicated.
Gentle cleaning of the posterior portion of the tongue with a toothbrush or with a plastic tongue cleaner may often be helpful.
Bridges or dentures should clean it thoroughly at least once a day. Dental retainers or mouth guards should be cleaned each time before they are put in the mouth.
Proper hydration may help prevent dry mouth.
Decreasing alcohol and coffee intake may be helpful.
A range of mouthwashes has been suggested for the treatment of bad breath. These act by reducing either the bacterial load or the associated odoriferous compounds (12).
13. Can Mouthwashes Help to Prevent Halitosis?
Studies suggest that mouthwashes containing chlorhexidine gluconate, cetylpyridinum chloride, chlorine dioxide, and zinc chloride can be effective in reducing bad breath (13, 14).
Patients may sometimes be reluctant to use chlorhexidine long term as it has an unpleasant taste and if used too frequently, and can cause reversible staining of the teeth (12).
Triclosan, often used in mouthwashes and toothpaste may also reduce oral malodor. A formulation of triclosan/co-polymer/sodium fluoride seems to be particularly useful in reducing volatile sulfur compounds, oral bacteria, and oral malodor (15).
The best time to use mouthwash is probably before bedtime (2). The bacterial activity leading to bad breath is most significant during sleep, and if taken before sleep, the mouth rinse may remain in the mouth for a longer period, leading to a greater effect.
Mouthwashes should also be used an hour or more after brushing the teeth because detergents in toothpaste may inactivate the antibacterial agents used in mouthwashes (2).
Because much of the bad breath originates from the back of the tongue, it is important to gargle when using mouthwashes.
In the early fall of 1975, two mothers from Old Lyme, Connecticut, desperately sought medical help because of a mysterious outbreak of a strange, unexplainable disease. Both children and adults were affected, and arthritis appeared to be the most prominent symptom.
It was soon discovered that many patients also reported a skin lesion with an expanding bulls-eye pattern a few weeks preceding the onset of arthritis (1).
The lesion matched the description of or erythema migrans, a skin lesion previously reported in Europe and thought to be a result of an infectious agent. However, this was the first time erythema migrans had been associated with arthritis (2).
In December 1975, a surveillance study was carried out in Lyme and surrounding towns on the eastern bank of the Connecticut River. The study was led by Allan C. Steere, MD, and Stephen E. Malawista, MD, from the Rheumatology section of the Yale School of Medicine.
In 1976, Steere and Malawista suggested that Lyme arthritis was a tick-borne disease. They published evidence showing the that the incidence of the disorder was 30 times greater on the east side of the river, where Lyme is located than it was on the west side, similar to the difference in deer and deer tick distribution in the area (3).
Scientists later confirmed that ticks indeed are the transmission vector of the infectious agent in Lyme disease.
The risk of Lyme disease is year round, but the highest risk window is late spring into early summer.
Over 300,000 new cases of Lyme disease are estimated to occur every year in the United States (4). Today, Lyme disease is the most common tick-borne disease in the United States, Canada, and Europe.
Fortunately, Lyme disease is rarely life-threatening.
1. What Is the Cause of Lyme Disease?
Lyme disease is caused by a few different species of the spirochete Borrelia.
Spirochetes are long and slender cork-screw-like bacteria, usually only a fraction of a micron in diameter but 5 to 250 microns long. They are tightly coiled and look like small springs or telephone cords (5).
In North America, Lyme disease is caused primarily by Borrelia Burgdorferi (6). In Europe and Asia, infections caused by Borrelia afzelii, and Borrelia garinii are more common.
Spirochetes are cork-screw-like bacteria that look like miniature springs or telephone cords.
In the northeastern United States, rodents such as the white-footed mouse are the primary reservoir of the Borrelia species.
The spirochetal infection is transmitted by the bite of infected ticks
The risk of exposure to ticks is highest in the woods and the edge area between lawns and woods. Ticks may also be carried by animals and pets onto parks and gardens and into houses. Campers, hikers, and outdoor workers may be exposed in wooded, brushy, and grassy places.
2. How Do Ticks Transmit Lyme Disease?
The spirochetal infection causing Lyme disease is transmitted by the bite of infected ticks of the Ixodes ricinus complex.
There is no evidence that Lyme disease is transmitted from person-to-person through touching, kissing, having sex or sharing silverware or glasses with a person with Lyme disease.
The three tick species that commonly bite people in the eastern United States include the blacklegged tick, the Lone Star tick, and the American dog tick. The blacklegged tick is the only one that transmits Lyme disease in the United States (7).
The blacklegged tick (or deer tick, Ixodes scapularis) spreads the disease in the northeastern, mid-Atlantic, and north-central United States, and the western blacklegged tick (Ixodes pacificus) spreads the disease on the Pacific Coast.
It is believed that ticks need to be attached for 36 to 48 hours before they can transmit Lyme disease bacteria.
Ticks obtain blood by inserting their mouth parts into the skin of a person or animal. As they feed, their bodies slowly enlarge.
Most humans are infected through the bites of immature ticks called nymphs. Nymphs are tiny and often difficult to see. Adult ticks also transmit Lyme disease bacteria, but they are much larger and are more likely to be discovered before they have had time to transfer the bacteria (8).
Ticks obtain blood by inserting their mouth parts into the skin of a person or animal. Ixodes ticks are slow feeders, and one meal can take several days. As they feed, their bodies slowly enlarge.
3. In What Areas Is Lyme Disease Most Common?
For Lyme disease to exist in an area, three environmental elements must be present (8):
animals that are infected with Lyme disease bacteria
ticks that can transmit the bacteria, and
animal hosts (such as mice and deer) that can provide food for the ticks in their various life stages
Lyme Disease is present in North America, Europe, and Asia.
Travelers involved in outdoor activities in forested areas are at risk, including campers, hikers, and hunters. Brushing against vegetation or walking in city parks known to have infected ticks can also put a person at risk.
Risk of Lyme Disease increases during the warmer months when ticks are most active. However, ticks can be found year-round in areas where temperatures are above freezing.
Lyme disease is distributed over a wide geographic area in northern temperate regions of the world.
In the United States, most infections occur in the following areas (8):
Northeast, from Virginia to Maine
North-central states, mostly in Wisconsin and Minnesota
West Coast, mainly northern California
4. What Are the Symptoms of Lyme Disease?
The signs and symptoms of Lyme disease are often divided into three clinical stages. However, the clinical features may overlap and some patients present at a later stage with no history of prior signs of the disease (7).
The first stage is characterized by the occurrence of the red, circular, bulls-eye rash called erythema migrans.
The second stage sometimes called early disseminated disease, is characterized by multiple erythema migrans lesions that occur days to weeks following the tick bite. During this period neurological symptoms may occur, including numbness, pain, nerve paralysis, and meningitis (fever, stiff neck, and severe headache). Although rare, some patients experience cardiac involvement including an irregular heartbeat.
The most common clinical manifestations include fatigue, anorexia, headache, neck stiffness, muscle aches (myalgia), joint pain (arthralgias), enlarged lymph nodes, and fever (6).
It is important to acknowledge that different people exhibit different signs and symptoms of Lyme disease. Some patients never develop erythema migrans, some only develop arthritis, and some patients only have neurological symptoms.
General symptoms such as fever, muscle aches, and fatigue can be mistaken for viral infections such as influenza. Joint pain can be mistaken for other types of arthritis, and neurologic signs may be similar to those experienced by patients with multiple sclerosis or peripheral neuropathy of another origin.
The third stage, late Lyme disease is characterized by arthritis involving one or more large joints, especially the knee. Late Lyme disease may occur months to few years following the tick bite and is not always preceded by a history of early localized or disseminated disease.
Neuropsychiatric manifestations may be present during late Lyme Disease. These may include cognitive disturbances and polyneuropathy. The latter is characterized by pain and paresthesias (9).
In Europe, some patients develop a chronic skin condition called acrodermatitis chronica atrophicans (10). It may appear months to years after the initial infection and is mainly due to Borrelia afzelli. The condition is not known to occur in the United States.
5. What Is Erythema Migrans?
The first stage of Lyme Disease, early localized disease, is characterized by a skin lesion called erythema migrans.
Erythema migrans is a red circular rash that often appears at the site of the tick bite. It usually occurs within a month following the bite, most often within the first 3 to 14 days.
Erythema migrans occurs in 80% of patients with Lyme disease (11).
The rash typically expands slowly over the course of days or weeks. Sometimes many rashes appear, varying in shapes and sizes. They are often found on the thighs, groin, trunk, and armpits.
The center of the rash may clear as it enlarges, resulting in a “bulls-eye” appearance. Although the central clearing is classic for erythema migrans, it is usually not present during the first days of the rash.
Erythema migrans is not particularly painful but may occasionally burn or itch and is usually hot to the touch.
Not all rashes that occur at the site of a tick bite are due to Lyme disease. An allergic reaction to tick saliva can also occur and be confused with the rash of Lyme disease. It most often appears within hours to a few days after the tick bite, usually, do not expand, and disappear within a few days.
The classic bulls-eye rash associated with Lyme disease is called erythema migrans.
6. What Are Post-Lyme Disease Syndrome and Post-Treatment Lyme Disease Syndrome (PTLDS)?
The terms pos”post-Lyme disease syndrome” and post-treatment Lyme Disease Syndrome (PTLDS) are sometimes used to describe general symptoms that may be present for long periods after Lyme disease has been treated.
Examples of such symptoms are headache, fatigue, joint pain (arthralgias), musculoskeletal pain, and cognitive difficulties. In most cases, these symptoms disappear gradually in six to twelve months.
Between 5-15 percent of patients treated for Lyme disease may develop PTLDS. The cause of the disorder is unclear but is not believed to be due to persistent or ongoing infection following treatment.
7. What Is Neuroborreliosis?
The term Neuroborreliosis or Lyme neuroborreliosis (LNB) is sometimes used to describe the neurologic manifestations of Lyme disease (12).
Neuroborreliosis may occur during the early and late stages of Lyme disease.
The nervous system is involved in 10% to 15% of cases early Lyme disease (13)
Early neuroborreliosis may present with facial palsy (inability to control the facial muscles on the affected side of the face), meningitis and painful radiculoneuritis (inflammation of one or more roots of the spinal nerves). It usually occurs within about six to twelve weeks following the infection.
The symptoms of acute neuroborreliosis usually disappear following antibiotic treatment.
Late/chronic Lyme neuroborreliosis is characterized by various neuropsychiatric manifestations (14).
The clinical symptoms include seizures, speech difficulties, ataxia (lack of control of voluntary muscle movements), chronic spastic para- tetra- and hemiparesis, mood disorders, psychosis, visual and auditory hallucinations, paranoia, anorexia nervosa, and obsessive-compulsive disorder (15).
8. What Diseases May Resemble Lyme Disease?
Known as “The Great Imitator,” Lyme disease may mimic many other conditions. This may lead to several difficulties in diagnosis.
Muscle aches, fever, and headache are common symptoms of flu. These are also experienced by many patients with Lyme disease.
Arthritis, a common symptom of Lyme Disease, may have many other causes. It may be mistaken for rheumatoid arthritis, gout, osteoarthritis or degenerative arthritis.
Some patients with Lyme disease suffer from chronic fatigue. This may be mistaken for chronic fatigue syndrome or fibromyalgia.
The neuropsychiatric symptoms of Lyme disease may mimic Parkinson’s disease, multiple sclerosis, Alzheimer’s and depression.
9. How Is Lyme Disease Diagnosed?
The diagnosis of Lyme disease should take into account the patients history and exposure to ticks in areas where Lyme disease is known to occur. Hence, detailed travel and activity history is essential.
The diagnosis of early Lyme disease is made on clinical grounds, primarily based on the presence of erythema migrans. Lab tests are unlikely to support the diagnosis at this stage because the immune system will not have had enough time to produce antibodies.
During early disseminated disease and late Lyme disease, lab testing plays a vital role. For serologic testing, a two-tier conditional strategy is recommended (16):
Enzyme-linked immunosorbent assay (ELISA) test is used most often to detect Lyme disease and detects antibodies to Borrelia burgdorferi. A different type of enzyme immunoassay (immunofluorescent assay or IFA) may be substituted for the ELISA test. However, both these tests can sometimes provide false positive results and are therefore not used as the sole base for diagnosis.
If the ELISA test is positive, the Western blot test is usually done to confirm the diagnosis.
A negative Western blot test supersedes the result of a positive ELISA or IFA, and testing should be considered negative. A positive Western blot test is considered evidence of an encounter with Borrelia burgdorferi (16).
10. How Is Lyme Disease Treated?
Several antibiotics are useful for treating Lyme disease. These are usually given by mouth but may be given intravenously in more severe cases.
Patients treated with antibiotics in the early stages of the infection usually recover rapidly and completely.
Most patients who are treated in later stages of the disease also respond well to antibiotics.
A few patients may have persistent or recurrent symptoms and may require an additional course of antibiotic treatment. Longer courses of antibiotics have not been shown to be beneficial in patients who have been previously treated and have chronic symptoms.
Antibiotics commonly used for oral treatment include doxycycline, amoxicillin, or cefuroxime axetil. People with specific neurological or cardiac forms of illness may require intravenous treatment with antibiotics such as ceftriaxone or penicillin (17).
11. How Is Lyme Disease During Pregnancy Treated?
Untreated Lyme disease during pregnancy may lead to infection of the placenta and possible stillbirth. However, no severe effects on the fetus have been found in cases where the mother receives appropriate antibiotic treatment for her Lyme disease (18).
In general, treatment for pregnant women with Lyme disease is similar to that of non-pregnant adults, although certain antibiotics, such as doxycycline, are not used because they can affect fetal development.
Additionally, there are no reports of Lyme disease transmission from breast milk.
12. How Can Tick Bites Be Prevented?
It is possible to decrease the chances of being bitten by a tick with a few precautions. Avoiding tick-infested areas is the first rule. This is especially important in May, June, and July.
If you live in a risk area, keeping your lawn well manicured and adding a deer fence may be helpful. Because ticks get Lyme disease from mice, eliminating the mouse habitats around your yard is important. This includes removing wood piles and rock piles where the mice tend to live and breed (4).
During outdoor activity, it is important to avoid wooded, overgrown areas and stay out of tall grass and the uncleared regions of the forest. Staying on marked trails is recommended when hiking.
Wearing protective clothing is recommended. That includes long sleeves, long pants and avoid going barefoot or wearing open shoes.
Insect repellant containing DEET, picaridin, IR3535, oil of lemon eucalyptus, para-menthane-diol, or 2-undecanone may be used on the body and Permethrin on clothes. It is imperative always to follow the manufacturer’s instructions when applying these substances.
Permethrin should not be applied to your skin. It is a unique substance and does not need to be reapplied frequently because it stays bound to clothes for several months.
It is a good protective habit to shower immediately or within two hours of coming indoors.
Always check for ticks after being outdoors. Ticks are tiny and sometimes hard to see. By feeling for ticks, they may be found in hidden areas, such as behind your knee or in your armpit
13. How Should Attached Ticks Be Removed From the Skin?
Because ticks must usually be attached for at least a 24 hours before they can transmit the spirochetes causing Lyme disease, early removal reduces the risk of infection.
The quickest way to remove a tick is with tweezers. Grasp the tick between the head of the tick and the skin and to pull softly but securely away.
Sometimes, parts of the mouth of the tick will be left in the skin. However, these small mouthparts do not transmit Lyme disease and should be left alone. Just leave them in place. They will work their way out on their own.
Grasp the tick between the head of the tick and the skin and pull softly but securely away.
14. Is a Lyme Disease Vaccine Available?
LYMErix, a vaccine for Lyme disease, received licensing and approval from the U.S. Food and Drug Administration (FDA) in 1998, but the manufacturers (GlaxoSmithKline — then called SmithKline Beecham) stopped selling it in 2002, due to a lack of demand.
The vaccine was based on a specific part of B. burgdorferi called outer surface protein A (OspA). It was found to be between 49 and 68 percent effective in preventing Lyme disease after two injections, and 76 to 92 percent effective in preventing Lyme disease after three injections
In April 2002, GSK announced that even with the incidence of Lyme disease continuing to rise, sales for LYMErix declined from about 1.5 million doses in 1999 to a projected 10,000 doses in 2002. Although studies conducted by FDA failed to reveal that any reported adverse events were vaccine-associated, GSK discontinued manufacturing the vaccine (19). Since then, a new vaccine has yet to appear on the market.
15. Do Ticks Transmit Other Diseases than Lyme Disease?
Lyme disease is the most common tickborne disease in the United States, Canada, and Europe. However, ticks may carry several other diseases than Lyme disease.
Examples of tickborne diseases in the United States are (20):
Borrelia miyamotoi Disease
Colorado Tick Fever
Heartland and Bourbon Virus Diseases
Powassan Virus Disease
Rocky Mountain Spotted Fever
Rickettsia parkeri Rickettsiosis
Tickborne Relapsing Fever
Examples of tickborne diseases found in other countries are (21)
African Tick Bite Fever (ATBF, found in Sub-Saharan Africa, Caribbean (French West Indies), and Oceania)
Tickborne Encephalitis (TBE, endemic in focal areas of Europe and Asia, extending from eastern France to northern Japan and from northern Russia to Albania)
Mediterranean spotted fever (also known as boutonneuse fever (found in Europe (Mediterranean basin), Middle East, Indian subcontinent,
Crimean-Congo hemorrhagic fever /found in Asia, Africa, and Europe).
Omsk hemorrhagic fever (found in Southwestern Russia)
Kyasanur Forest disease (found in Southern India, Saudi Arabia (aka Alkhurma disease in Saudi
Migraine is characterized by recurrent attacks of headache. The pain is often described as throbbing, and there may be a pulsing sensation, usually on one side of the head. Migraines are commonly accompanied by nausea, vomiting, and sensitivity to light and sound (1).
The exact cause of migraines is unknown, but they’re believed to be the result of abnormal brain activity, partly caused by imbalances in brain chemicals including serotonin. These abnormalities may temporarily affect nerve signals and blood vessels in the brain.
Prodromal symptoms often occur one or two days before the headache (2). These include constipation or diarrhea, mood changes, appetite changes including food cravings, concentration difficulties, cold extremities, increased thirst, frequent urination and constant yawning.
Warning symptoms known as aura may occur before and sometimes together with the attack. Examples are visual disturbances and sensory abnormalities such as a tingling or touching sensation on one side of the face or in an arm or a leg (3). However, 75-80% of patients don’t experience an aura.
There are known environmental factors that we can come across every day that can “trigger” migraine headaches. These include foods and food additives, medications, emotional stress, menstruation, visual stimuli such as bright lights, fasting, wine, physical exertion, sleep disturbances, intake of highly caffeinated beverages and aspartame (4).
10 Everyday Things that May Trigger Migraines
Knowledge of the most common external triggers for migraine attacks is of crucial importance for individuals who suffer from migraine.
Certain foods and food ingredients may trigger migraine attacks. For instance, a very common ingredient in diet and low-calorie foods is the sugar substitute aspartame. This artificial sweetener can affect dopamine and serotonin levels in the brain, which can be a factor in migraine headaches (5).
Another common substance in food that may hasten the onset of a migraine is monosodium glutamate, best known as MSG (6). It’s often used to flavor Chinese food, but can also be found in soups and processed meats.
Nitrites are preservatives frequently found in sausage, beef jerky, hot dogs, deli meats and other meats. Nitrate-containing compounds have been identified as common headache triggers (7).
If you suffer from migraine, the next time you get invited to a wine and cheese party, you may want to RSVP no. Wine contains preservatives called sulfites, which can potentially induce migraines (8). Sulfites can also be found in processed foods, including dried fruits.
As for the cheese plate, aged cheeses have an amino acid called tyramine, which has been associated with migraines (9).
If you think you’ll skip the cheese in favor of the fruit that’s usually paired with it, well, think again. You may be opening yourself up to a migraine attack if you eat apples or pears, which contain tannins. This natural plant substance can also be found in tea, black walnuts, red wine, tea, chocolate, vanilla, raspberries, and many herbal products
Research shows that reducing tannin in the diet may reduce the risk of migraine attacks (10).
Finally, whatever you eat, handle it carefully, especially if you tend to eat leftovers for meals. The same tyramine that can be an issue in certain cheeses can multiply in foods, especially if it’s not properly refrigerated.
In addition to wine, there are other beverages that may cause trouble for you if you are a migraine sufferer. Alcohol is known to trigger a headache if too much is consumed—ask anyone who’s ever had a hangover—and studies suggest that alcohol and migraine symptoms are linked (11).
On the other hand, caffeine has a more mixed effect on migraines—depending on the person, caffeine can lead to a migraine or guard against one. If you note that you experience symptoms after a cup of coffee, you may want to cut back on your consumption (12).
So what can you drink? Water is always a safe, and a healthy choice. In fact, if you don’t drink enough water, you may experience dehydration, and that may lead to a migraine attack.
Identifying Your Migraine Triggers
It may not always be easy to determine what environmental factors are triggering migraines. In fact, migraine attacks may be linked to a number of different things. Furthermore, a potential trigger may not precipitate an attack every time.
Sometimes, trigger factors can influence an attack up to 48 hours before a headache occurs. Such trigger factors may easily be ignored.
One study showed that most patients showed at least one dietary trigger, fasting was the most frequent one, followed by alcohol and chocolate. Hormonal factors appeared in 53% with the pre-menstrual period being the most frequent. Physical activities triggered migraine in 13%, sexual activities in 2.5%, 64% reported emotional stress as a trigger, and 81% related some sleep problem as a trigger factor. Regarding environmental factors, smells were reported by 36.5%.
One of the best ways of identifying triggers is to keep a migraine diary. Such a diary should keep a record of daily activity such as when you get up and go to sleep, what you do during the day, what you eat and drink, the surroundings, the weather, the medication you take, your mood, and the menstrual cycle if you are a woman.
Registering the timing of the attacks is essential. For example, if you suffer at weekends, your headache may be triggered by caffeine withdrawal due to drinking fewer cups at home than at work. It may also be due to more wine or alcohol consumption on the weekends. Some people with migraine find that winding down at the weekend after a stressful week or too much sleep at the weekends can trigger an attack (13).
High blood pressure (BP), also called hypertension, increases the risk of heart disease, stroke, and kidney disease. It is one of the most important causes of premature death worldwide.
In 2025, an estimated 1.56 billion adults will be living with hypertension (1). According to the World Health Organization (WHO), hypertension kills nearly 8 million people every year.
Overall, approximately 20% of the world’s adults are estimated to have hypertension. In 1991, the National High Blood Pressure Education Program (NHBPEP) estimated that 43.3 million adults had hypertension in the United States (2). The prevalence dramatically increases in patients older than 60 years.
It is crucial for health professionals and patients to understand how BP is measured, how hypertension is diagnosed and what are the most common pitfalls to avoid when estimating if hypertension is present or not.
1. The Definition of Blood Pressure
Each time the heart muscle contracts it pumps blood into the arteries to supply the tissues and organs of the body with oxygen-rich blood. BP is the measure of pressure in the arteries. This may be compared to the pressure of water in a garden hose, except that the arterial wall is a living tissue.
BP is recorded as two numbers, e.g., 125/80 millimeters of mercury (mm Hg). The first number is the systolic pressure, that is when the heart muscle contracts and blood is pumped into the arteries. The lower figure, the diastolic pressure, is the pressure when the heart is relaxing and filling up with blood, between strokes.
2. The Definition of Normal Blood Pressure and Hypertension
The following is the most widely used classification of BP and hypertension (3):
Normal: Systolic BP lower than 120 mm Hg, diastolic BP lower than 80 mm Hg
Prehypertension: Systolic BP 120-139 mm Hg, diastolic BP 80-89 mm Hg
Stage 1 hypertension: Systolic BP 140-159 mm Hg, diastolic BP 90-99 mm Hg
Stage 2: Systolic BP 160 mm Hg or greater, diastolic BP 100 mm Hg or greater
In 2017, the American College of Cardiology/American Heart Association (ACC/AHA) updated their guidelines for the prevention, detection, evaluation, and management of high blood pressure in adults by eliminating the classification of prehypertension and dividing it into two levels (4).
Normal: Less than 120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage.
3. Understanding How Blood Pressure Changes With Age
A progressive rise in BP is seen with increasing age.
However, age-related hypertension appears to be predominantly systolic rather than diastolic. The systolic BP rises into the eighth or ninth decade, whereas the diastolic BP remains constant or declines after age 40 years. Hence, pulse pressure, the difference between the systolic and diastolic blood pressure, increases with age
The prevalence of hypertension grows significantly with increasing age in all sex and race groups (5). It has been estimated that the incidence of hypertension increases by approximately 5% for each 10-year interval of age.
4. The Circadian Pattern of Blood Pressure
Blood pressure is typically lower at night, during sleep and then starts to rise a few hours before we wake up. It reaches a peak in the morning shortly after awakening. Then in the late afternoon and evening, BP starts dropping again.
Blood pressure is typically lower at night, during sleep and then starts to rise a few hours before we wake up. It reaches a peak in the morning shortly after awakening.
The onset of many acute cardiovascular and cerebrovascular events shows a daily pattern, with the highest incidence of morbidity and mortality in the early morning hours. Strong, although circumstantial, evidence suggests that the early morning surge in blood pressure may contribute to the onset of acute cardiovascular episodes (6).
5. Understanding How Blood Pressure Is Measured
Correct measurement of BP is essential in the diagnosis of hypertension. BP machines have to be properly calibrated, and appropriate cuff sizes have to be selected.
The patient should be in a seated position with the back supported and legs uncrossed. The diastolic pressure may be higher by 6 mm Hg if the back is unsupported and the systolic pressure may be raised by 2-8 mm Hg if the legs are crossed (7).
The patient should not talk during the procedure as it can raise the measured value by as much as 8-15 mm Hg (8)
Here is what you can do to ensure a correct reading (9):
Don’t drink a caffeinated beverage or smoke during the 30 minutes before the test.
Sit quietly for five minutes before the test begins.
During the measurement, sit in a chair with your feet on the floor and your arm supported so your elbow is at about heart level.
The inflatable part of the cuff should completely cover at least 80% of your upper arm, and the cuff should be placed on the bare skin, not over a shirt.
Don’t talk during the measurement.
Have your blood pressure measured twice, with a brief break in between. If the readings are different by 5 points or more, have it done a third time.
Checking blood pressure at home (JAMA. 2017;318(3):310. doi:10.1001/jama.2017.6670)
6. Different Measurement Strategies For Detecting Hypertension
There are three different measurement strategies to detect hypertension:
Ambulatory BP-monitoring (ABPM)
Home BP monitoring
Although screening for hypertension is often performed at the doctor’s office, many individuals with high BP measurements at the office will not have hypertension upon further testing (10). This is commonly due to white coat hypertension.
ABPM monitoring is the preferred method for detecting hypertension. If ABPM is not feasible, home BP monitoring may be used.
7. White Coat Hypertension
It is essential to understand that BP is not a fixed number. BP varies throughout the day in response to what we are doing and what is happening around us.
Some people with normal BP find that it spikes when they visit the doctor. This condition is called white coat hypertension or the white coat effect (also called isolated clinic or office hypertension).
The white coat effects will often happen because we are nervous about having our BP tested by a doctor or nurse. Most of us tend to feel tenser in medical settings than we do in surroundings that are familiar to us, although we do not always notice it.
Sometimes the white coat effect may be powerful, making it impossible to establish a correct resting blood pressure in the doctor’s office. Hence, it is imperative not to rely on office-based BP measurements when diagnosing hypertension.
People with white coat hypertension may sometimes be at increased risk for cardiovascular events and can go on to develop hypertension. Hence, close follow-up is recommended (11).
The white coat effect may persist for years. It may be avoided by using ABPM or home-based BP-monitoring.
8. Ambulatory Blood Pressure Monitoring (ABPM)
Ambulatory blood pressure monitoring (ABPM) is performed by using a small digital BP machine, usually attached to a belt around the body and connected to a cuff around the upper arm.
ABPM is performed by using a small digital BP machine, usually attached to a belt around the body and connected to a cuff around the upper arm. The device takes BP measurements regularly over a 24-48 hour period, usually every 15-20 minutes during daytime and every 30 to 6 minutes during nighttime.
The BP measurements are recorded on the device, and the average day (diurnal) and night (nocturnal) BPs are determined from the data by a computer.
ABPM has been considered to be the reference standard for the diagnosis of hypertension and is a better predictor of cardiovascular disease risk as compared with conventional office-based measurements (9).
9. Reference Values for Ambulatory Blood Pressure Monitoring (ABPM)
When ABPM is used, hypertension is defined as a 24-hour average BP greater to er equal to 125/75 mm Hg (10).
A 24 hour mean BP during ABPM of 115/75 is considered normal and mean BP higher than 125/75 is considered too high.
When looking at individual measurements, normal ambulatory blood pressure should not be above 135/85 mm Hg during the day and not above 120/70 mm Hg at night. Levels above 140/90 mm Hg during the day and 125/75mm Hg at night should be considered as abnormal (9).
10. Dipping and Non-Dipping
The average nighttime BP is approximately 15 percent lower than daytime values. People who undergo this normal physiological change are described as dippers.
Failure of the blood pressure to fall by at least 10 percent during sleep is called non-dipping.
The underlying mechanisms of non-dipping are unknown, but melatonin may play a role (11).
Non-dipping may be associated with increased cardiovascular risk (12).
11. Home Blood Pressure Measurements
Relatively inexpensive semiautomatic devices may be used for home BP measurements. These measurements correlate more closely with the results of 24-hour ABPM than with BP taken in the clinician’s office (13).
The optimal schedule for home blood pressure measurements is unclear. Evidence suggests that 12-14 measurements should be obtained to assess blood pressure correctly. These should include both morning and evening measurements during one week (14).
While seated, the patient should take two measurements (separated by one to two minutes) in the morning and the evening for at least three, and preferably seven consecutive days. Measurements from the first day should be discarded; the home blood pressure is defined as the average of all remaining measures.
It is important to acknowledge that home BP measurements may vary widely depending on factors such as stress caffeine intake, smoking, exercise and natural circadian variation.
12. Office-Based Blood Pressure Measurements
Despite their limitations, office-based BP measurements continue to be the primary technique used worldwide for the detection and management of hypertension.
Clinicians and patients should be aware of the possibility of white coat hypertension.
Multiple measurements on different days may be necessary. The patient should sit quietly for five minutes before the BP is measured. Patient position, cuff size, and cuff placement are all important.
It is crucial for health professionals and patients to understand how BP is measured, how hypertension is diagnosed and what are the most common pitfalls to avoid when estimating if hypertension is present or not.
Office-based BP measurements are of limited value because of the frequency of white coat hypertension.
Ambulatory blood pressure measurements (ABPM) are considered to be the reference standard for the diagnosis of hypertension and provide a better predictor of cardiovascular disease risk as compared with conventional office-based measurements.
It is important to acknowledge that reference values for ABPM measurements are different from those used for office-based measurements.
If not ABPM is feasible, home BP monitoring may be used. Educating patients about when and how to perform such measurements is of crucial importance.
Major depression affects more than 16 million American adults each year (1). It can occur to anyone, at any age. And, importantly, depression is not a personal weakness but a severe medical illness.
Of course, we all have times when our mood is low. Gloom, heartache, melancholy, woe, desolation. These are all parts of life’s journey and fortunately most often normal temporary reactions to daily events. But, at what stage should such feelings be defined as clinical depression?
The British author and poet, Giles Andreae who himself has battled depression once said: “Thinking you’ve had depression makes about as much sense as thinking you’ve been run over by a bus. Trust me – you know when you’ve got depression (2)”
Although this is not entirely true, it emphasizes the difference between clinical depression and occasional episodes of low mood. However, unfortunately, too many people don’t acknowledge their depression or think it isn’t serious or even believe that it is some personal weakness.
Only about a third (35.3%) of those suffering from severe depression seek treatment from a mental health professional (3). Hence, it is estimated that as many as two-thirds of people with depression do not realize that they have a treatable illness and do not seek treatment.
According to The American Psychiatric Association, “depression (major depressive disorder) is a common and serious medical illness that negatively affects how you feel, the way you think and how you act. Fortunately, it is also treatable. Depression causes feelings of sadness and/or a loss of interest in activities once enjoyed. It can lead to a variety of emotional and physical problems and can decrease a person’s ability to function at work and home” (4).
Hence, we might conclude that depression reflects long and persistent periods of low mood without reason? But, that’s a misinterpretation. The truth is that there is a reason. That reason is the disease we call depression.
The British actor and writer Stephen Fry has talked openly about his depression. He says: “Why should I be depressed? I’ve got enough money. I’ve got a job. People like me. There is no reason to be depressed. That’s as stupid as saying there is no reason to have asthma or there is no reason to have the measles. You know you’ve got it. It’s there. It’s not about reason.
Depression is often considered to be a mood disorder. Fry says: “To me, mood is like the weather. Weather is real. It is absolutely real: when it rains, it rains – you get wet, there is no question about it. It is also true about weather that you can’t control it; you can’t say if I wish hard enough it won’t rain. It is equally true that if the weather is bad one day, it will get better and what I had to learn was to treat my moods like the weather.”
1. Depressive Mood
Persistent sad, anxious or “empty” mood is an essential feature of major depression.
However, frequently those who have suffered from depression describe their depressive mood in a more specific manner. It is not just about feeling sad all the time. It is somewhat different and usually much worse.
In fact, people with depression not always feel sad. They may be able to speak with their friends and have a laugh. On the outside, it may look like there’s nothing wrong. But inside, there is something missing. There is an emptiness, so hard to describe and so hard to understand unless you have experienced it yourself.
Let me quote Stephen Fry again: “There comes a time when the blankness of the future is just so extreme, it’s like such a black wall of nothingness. Not of bad things like a cave full of monsters and so, you’re afraid of entering it. It’s just nothingness, the void, emptiness and it is just horrible.”
Fry even goes further and says: “It’s like contemplating a future-less future and so you just want to step out of it. The monstrosity of being alive overwhelms you.”
Depression is often associated with anxiety. Both are facilitated by stress, either recent or dating back to childhood (5). Up to 70 percent of patients with depression experience anxiety (6).
Anxiety may be described as a feeling of worry, nervousness, or unease about something with an uncertain outcome.
Today, many experts believe that depression and anxiety are not two disorders that coexist but two faces of one disorder (7).
Often, anxiety precedes depression, sometimes by several years. Typically the onset of anxiety is in late childhood or early adolescence. Depression usually begins a few years later with typical onset in the mid-20s (8). But, of course, depression may occur at any age.
One person suffering from depression and anxiety wrote (9): I’ve always lacked self-confidence, even before my anxiety disorder was identified. I try to mingle with the best of them, but at the same time on the inside, I’m an intolerable nervous wreck and always wish I was at home watching repeats of “Friends” with a slab of fudge cake, even when I’m socializing with my nearest and dearest. Sadly, I don’t think this will ever change. So when I’m at that point where I’m trying just to leave the house, let alone do anything adventurous, my fragile mind always says “But, why? Why bother? You’re going to fail at this anyway?”
In fact, isolation may become quite severe. Simple tasks such as going to the supermarket may become a major hurdle.
3. Loss of Interest or Pleasure in Activities Once Enjoyed (Anhedonia)
The word Anhedonia describes the inability to experience pleasure from activities usually found enjoyable, e.g., exercise, hobbies, and social interactions. In Greek, anhedonia directly translates to “without pleasure.”
Most patients with depression have anhedonia. It is a crucial feature of major depression. Events and activities we used to enjoy become less interesting or fun. We may even lose interest in our friends. Libido and interest in sex often decrease as well.
Some experts suggest that anhedonia comes not from a reduced capacity to experience pleasure, but instead from an inability to sustain good feelings over time. In other words, maybe pleasure is experienced fully, but only briefly, not long enough to sustain interest or involvement in life’s good things (10).
In anhedonia, the simple and satisfying sensation of joy seems to be lacking.
Following his experience with depression, Giles Andrea wrote: “And if depression has taught me one thing, it is this: what a rare and beautiful treasure is the simple human gift of joy. For me now, joy – our capacity to delight in one another and the world – is the reason why we are here. It is as simple as that. And I feel compelled to spread the word (2).”
Anhedonia may promote social withdrawal and negative feeling towards yourself and others. Emotional abilities may be reduced, and there may be a tendency to show fake emotions. We may struggle to adjust to social situations and our interest in intimacy may diminish.
Sometimes, anhedonia is divided into social anhedonia (a general disinterest in social contact), and physical anhedonia (an inability to feel pleasure from things likes eating, touching or sex)(11).
4. Fatigue or Loss of Energy
Contrary to many other medical symptoms, fatigue is an entirely normal phenomenon in particular situations. We all become tired, but it usually gets better by rest or sleep. However, chronic fatigue as a medical symptom is typically persistent and not relieved by rest (12).
Chronic fatigue is prevalent among patients with depression. It is often described as feeling tired all the time, exhausted or listless. Some people with depression experience total lack of energy sometimes called ‘anergia’.
Fatigue and depression seem to have a circular relationship. For some, fatigue will come first; for others, depression will come first, but for most, it will probably be unclear (13). The fatigue may lower self-esteem and make the depression worse, leading to more fatigue.
If the fatigue that comes with depression becomes overpowering, basic tasks such as getting out of bed and walking may be exhausting.
The symptoms of fatigue can affect physical, cognitive, and emotional function, impair school and work performance, disturb social and family relationships, and increase healthcare utilization (14).
5. Feelings of Worthlessness or Excessive Guilt
A study of patients with major depression published 2015 showed that self-blaming emotions occurred in more than 80% of patients with self-disgust/contempt being more frequent than guilt, followed by shame (15).
The majority (85% of patients) reported feelings of inadequacy and self-blaming emotions as the most bothering symptoms compared with 10% being more distressed by negative emotions towards others.
Patients with depression often tend to misinterpret events or minor setbacks as evidence of personal failings (16).
A patient with depression has described her feelings in the following manner (17):
“I should be a spy; I am so good at leading a double life. I can put on a smile, muster up a good conversation (after ignoring a few calls and messages), but the reality is, all those “normal,” happy interactions exhaust me, and for that, I feel guilty.
I feel guilty that I want to scream at my boyfriend who is just trying to be understanding. I feel guilty that I cause those closest to me to worry. My parents, my partner, my family, and friends, all of them try to support me, to ensure I don’t get too low. How do I tell them it isn’t them and no matter what they do often I just feel low? I feel guilty that their efforts to help sometimes just make it worse.
I feel guilty for canceling plans last-minute. I mean to go, I want to go, but often I just don’t have the strength. I am brilliant at making excuses, but the shame I feel for letting people down is ever-present.
I even feel guilty for feeling guilty. Maybe some other people understand this warped way of thinking. I would tell anyone else with depression to not be so hard on themselves, to acknowledge their efforts. But to me, I just feel guilty.”
6. Sleep Disturbance (Insomnia and Hypersomnia)
Several types of sleep disorders may occur in patients with depression. The term insomnia is used often used to describe the symptoms associated with these sleep disorders.
Insomnia may be a difficulty falling asleep, waking up frequently during the night with difficulty returning to sleep, waking up too early in the morning, or merely an unrefreshing sleep. It is not defined by the number of hours slept but reflects the satisfaction with sleep. Insomnia is often associated with tiredness, lack of energy, difficulty concentrating, and irritability.
Depression may be associated with difficulty getting to sleep (initial insomnia). Waking in the middle of the night (middle insomnia) or earlier than usual (terminal insomnia) with difficulty turning to sleep is common. Prolonged nighttime sleep or daytime sleeping (hypersomnia) may occur as well.
About three-quarters of depressed patients have insomnia symptoms, and hypersomnia is present in about 40% of depressed young adults and 10% of older patients, with a preponderance of females (18).
Disturbed sleep is a very distressing symptom which has a significant impact on quality of life in depressed patients (19).
Many patients with depression wake up prematurely in the early morning hours, unable to get back to sleep. This early-morning awakening is often associated with dysphoria and depressive thoughts, and sometimes there is an agitated, even a panicky feeling. This may often get better during the day and the evenings are often more comfortable.
7. Neurocognitive Dysfunction (Difficulty Concentrating, Remembering or Making Decisions)
Neurocognitive dysfunction is common in patients with depression (20).
Memory loss and an inability to focus or concentrate may be pronounced. Working memory, fluency, and planning and problem-solving abilities may be impaired.
People with depression often feel like they can’t focus. Comprehending what you are reading may become difficult and affect the ability to store information. This may negatively impact enjoyment when reading for pleasure.
The ability to receive information or directions may be impaired. We may appear easily distracted. This may affect performance at school and work. Sometimes these symptoms may be misinterpreted as lack of interest or consideration.
In most cases, neurocognitive dysfunction in depression is readily distinguished from that caused by dementia.
8. Change in Appetite and Body Weight
Reduced appetite and weight loss are common in patients with depression. However, increased appetite and weight gain may also occur.
Changes in eating habits are often related to other symptoms of depression, such as lack of energy and interest or pleasure from activities.
While a loss of appetite is common in depression, the sadness or worthlessness experienced by many patients may be associated with overeating (emotional eating). Emotional eating is eating in response to emotional rather than physical hunger.
Psychomotor disturbances that are common in depression include both agitation and retardation (16).
Psychomotor agitation is a series of unintentional, nonproductive or purposeless motions. In patients with depression, this may present as hand-wringing, pacing, and fidgeting.
Psychomotor retardation is a slowing down of thought and physical movements and may include slowing of body movements, thinking, and speech.
10. Thoughts of Suicide or Death
Depressed patients often experience recurrent thoughts of death. Suicidal ideation often occurs and there is a risk of suicidal attempt in some patients with depression (21).
Sometimes, suicidal ideation is passive. Patients often consider life not worth living and that their closest family and friends would be better off if the patient were dead.
In contrast, active suicidal ideation is marked by thoughts of wanting to die or commit suicide (16). There may be suicide plans and preparatory acts (e.g., selecting time and location, choice of method, or writing a suicide note). Such behavior indicates the patient is severely ill.
Suicidal ideation is usually preceded by hopelessness and negative expectations for the future. The patient may regard suicide as the only option to escape a never-ending and intense emotional and often physical pain
Alarmingly, many patients with suicidal ideation have not been recognized as having depression. In a large Canadian study, 48% of patients who had suicidal ideation and 24% of those who had made a suicide attempt reported not receiving care or even perceiving the need for care (22). The investigators concluded that future research should be directed toward finding better ways to identify these individuals and address barriers to their care and other factors that may interfere with their receiving help.
The annual suicide rate in the United States is approximately 13 per 100,000 individuals. Suicide is the tenth leading of cause of death. In 2014, the total number of suicide deaths in the United States was 42,773 (23). This equals 117 suicide deaths every day.
It is recognized that certain occupations and professions may be more susceptible to depression and suicide. Occupations that require frequent or difficult interactions with the public or clients, and have high levels of stress and low levels of physical activity seem to be at highest risk (24).
The medical profession has the highest risk of death by suicide of any profession or occupation. Other high control and highly regulated professions such as law enforcement, military, and the legal profession may be more likely to experience depression and suicidal behavior, and less likely to seek intervention because of the associated stigma and possible licensure implications (25).
Recent research suggests that suicide is three times more likely in individuals who have experienced a concussion, so occupations that might result in head injuries may be predisposed to suicide, with or without concomitant depression (26, 27).
Many individuals with depression have described their suicidal thoughts(27). Here are a few examples:
“It feels like you’re all alone and no matter what’s said to you, you feel like it’s not true or doesn’t matter. It feels like you just need to end it all because you’re so tired of fighting every single day.”
“I didn’t realize what I was feeling until I came out of it. It felt like I wasn’t breathing, I was drowning, and someone was holding my head under water. I was lost, alone and there was no other way out. No one understood me and no one ever would. When I finally broke free of the deep suicidal thoughts, I was able to see them for what they were, not before or during. I felt choked by the emotions and blinded by them.”
“A constant ache in my heart, my lungs, my wrists, my legs, my mind and the pit of my stomach. The ache that tells me nothing is sacred; everything is pointless. That nothing ever has or ever will matter. Why must I continue breathing? Why must I keep getting out of bed every day when I am so incredibly tired? Feeling utterly worthless, to the point that you wonder if your own children would be better off without you around.”
“The thought of death formed as a monster in my head. It is after me; I cannot run away from it. I don’t want to die, but I don’t want to live, either. The pain is too much strong, so I desperately think I cannot take another day. But deep down inside of me, I always have a tough wish to see another day — as a human instinct, I guess. I grabbed this very little feeling to go on. I hope everyone else will [too].”
“And if depression has taught me one thing, it is this: what a rare and beautiful treasure is the simple human gift of joy. For me now, joy – our capacity to delight in one another and the world – is the reason why we are here. It is as simple as that. And I feel compelled to spread the word.” Giles Andrea
Symptoms of depression may include the following:
Persistently sad, anxious, or empty moods
Loss of pleasure in usual activities (anhedonia)
Feelings of helplessness, guilt, or worthlessness
Crying, hopelessness, or persistent pessimism
Fatigue or decreased energy
Loss of memory, concentration, or decision-making capability
Poor abstract reasoning
Change in appetite or weight
Physical symptoms that defy diagnosis and do not respond to treatment – (very commonly pain and gastrointestinal complaints)
Thoughts of suicide, death, or suicide attempts
Poor self-image or self-esteem
To establish a diagnosis of major depression, a patient must express two of the first two itemsabove and at least five of the other symptoms listed. Such disturbances must be present nearly daily for at least two weeks (25).
Dear reader. If you have read this article, it may be for general information purposes or because you fear or believe that you may be suffering from symptoms associated with depression. If the latter is true, I want to remind you that depression is not a personal weakness but a serious medical disorder.
Because depression is a disease, it can not be “willed” or “wished away”. Unfortunately, that is a common misperception by the public and some medical professionals.
Patients with depression often feel terrible. The combination of physical and emotional symptoms may be overwhelming. The tiredness, darkness, and emptiness may seem unbearable. However, depression is a treatable disease. Almost all people who have suffered from depression will tell you that things will get better. And that is true.
And, remember; Never be ashamed of your depression. You wouldn’t if you had a brain tumor, heart attack or leukemia.
Oh, and finally; Don’t try to deal with your depression by yourself. Seek professional help.