English Breakfast Tea: Not Your Typical Morning Tea

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One of the best things about tea is that you’ll never run out of flavors, blends or varieties to choose from. However, if you prefer strong black tea over the mild flavors of white and green tea, or even herbal teas, then there’s one type that you may love to sip on: English breakfast tea.

Despite its name, English breakfast tea is actually a delicious blend that can be enjoyed any time of the day. This robust beverage also delivers a number of health benefits. Here’s what you need to know about English breakfast tea, including its history, preferred brewing methods and other interesting facts.

What Is English Breakfast Tea?

English breakfast tea is a classic black tea that is made from different blends of tea, such as Assam, Kenyan and Ceylon teas.1 These different types of tea come from the Camellia sinensis plant — the same plant from which green, oolong and white teas are made.

Frank Sanchez of Uptown Tea Imports, who says that the English breakfast tea started as a Chinese congou tea, gave a short overview of how this blend came to The Kitchn:2

“The English started importing Chinese tea in the 17th century and then it really kicked into gear in the 18th century.

“Then, during the Opium Wars, China imposed an embargo on tea. Around the same time, the British East India Company started producing tea in Assam, India. For a while, the old stocks of Chinese tea were dwindling and the new stocks of Indian tea started coming in, and they were blended together.

Jump ahead to the end of the 19th century and tea was beginning to be produced in Ceylon (now Sri Lanka). You started to have a stronger and stronger Ceylon component in English breakfast tea.”

You may be wondering how this blend acquired its name. Typically, breakfast teas such as these are created as an accompanying beverage to the traditional English morning meal, which is hearty, rich and often composed of foods like pork, beef and bread.3 It’s said that the strong flavor and the caffeine in the beverage give tea drinkers added mental alertness and helps boost their physical energy in the morning.4

Today, however, English breakfast tea can be enjoyed anytime of the day. It is full-bodied, tangy and rich, with a dark red color and a relaxing fragrance with slight notes of raisins. This drink can be blended with lemon or milk5 (although take note that adding dairy may affect the nutrition profile of the tea).

4 Benefits of English Breakfast Tea

The benefits that English breakfast tea offer are quite similar to those offered by other black teas. These include:

  • Helping eliminate free radicals and slowing aging — This tea comes with natural antioxidants called flavonoids, which are said to help reduce free radicals in the body.6
  • Promoting good circulation — One study published in the journal Circulation found that people struggling with coronary artery problems had better circulation after consuming black tea for four weeks.7
  • Helping promote heart health — Aside from improving cholesterol levels, black tea may also help reduce heart attack risk. A study published in the American Journal of Clinical Nutrition found that an increased intake of black tea may help inhibit ischemic heart disease.8
  • Helping with weight management and optimizing metabolism — A study published in the European Journal of Nutrition found that decaffeinated black tea may stimulate the production of good bacteria in the gut. It also uses and changes our energy metabolism in the liver via gut metabolites.9

English Breakfast Tea Caffeine Content

Since it’s made from black tea, this tea blend has caffeine. But how much caffeine is there in English breakfast tea? According to a study published in the International Journal of Nutrition, Pharmacology, Neurological Diseases, the amount ranges from 60 to 90 milligrams in every 8-ounce cup. This is less than half the amount that you can get from sipping a cup of coffee.10

If you are caffeine-sensitive, you should limit or avoid drinking English breakfast tea, as the caffeine in it could lead to neurological changes,11 rapid heart rate12 and other issues.

How to Make English Breakfast Tea

You can use tea bags or loose leaf tea to create the perfect cup of English breakfast tea. Here’s a simple recipe from SparkRecipe that you can follow:13

Ingredients

  • 3 tablespoons loose leaf English breakfast tea or 2 to 3 teabags
  • Hot water, for cleaning the teapot
  • 20 ounces boiling water, for steeping
  • Lemon wedges

Procedure

  1. Using hot water, warm your clean teapot, and then throw the water away.
  2. Fill the pot again with fresh boiling water.
  3. Add the loose leaves or the teabags to the pot and allow to brew for three to five minutes before serving.
  4. Serve with lemon wedges.

This makes four cups of tea.

How to Store English Breakfast Tea

Similar to wine, tea can become flat and lose its flavor over time. For English breakfast and other black teas, the typical shelf life is around two years — however, if improperly stored, it may become stale much sooner than that.

Ideally, store the tea, whether loose leaf or teabags, in an airtight container. Keep in a cool, dark place, like a pantry, away from other pungent cooking ingredients, as tea can absorb other strong odors. Do not store it in a refrigerator, though, as the moisture can cause it to degrade faster.14

English Breakfast Tea Side Effects

Too much of anything can sometimes cause problems, and this is true even when it comes to a healthy tea like English breakfast tea. This is because the tannins in black tea, which are water-soluble polyphenols,15 may lead to several side effects, such as vomiting, nausea and stomach upset, if consumed in excessive amounts.16

People who are recovering from a heart attack or acute cardiovascular disorders should also refrain from drinking English breakfast tea — or other highly caffeinated beverages — because of the effects of caffeine on heart rate. The same goes for pregnant women and nursing moms, as the caffeine may affect their child’s health.

A 2017 study noted that consuming high amounts of caffeine from coffee and tea during the second trimester of pregnancy may have effects on the brain of the fetus, potentially leading to behavioral disorders later in life.17

Enjoy English Breakfast Tea Any Time of the Day (but Moderate Your Intake)

Just because it’s labeled a breakfast tea doesn’t mean you have to limit yourself to only drinking it in the morning. This is one of the top tea products enjoyed everywhere not only for its health benefits but also its robust flavor. It will certainly wake you up — but that’s most likely because of its caffeine.

If you’re caffeine-sensitive, limit your intake of this tea or avoid it completely — don’t worry, there are other caffeine-free tea varieties out there you can opt for, like matcha, tulsi or ginger tea.

Frequently Asked Questions (FAQs) About English Breakfast Tea

Q: Does English breakfast tea have caffeine?

A: Yes. Every 8-ounce cup can contain 60 to 90 milligrams of caffeine.18

Q: How should you drink English breakfast tea?

A: English breakfast tea is traditionally enjoyed hot. It can be flavored with lemon or milk. Be warned that adding milk may affect the antioxidants in the tea, though.

Note: When buying tea of any kind, make sure that it’s organic and grown in a pristine environment. The Camellia sinensis plant in particular is very efficient in absorbing lead, fluoride and other heavy metals and pesticides from the soil, which can then be taken up into the leaves. To avoid ingesting these dangerous toxins, a clean growing environment is essential, so that you can be sure you’re ingesting only pure, high-quality tea.

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Senoinflammation: an Expanded View of Age-Related Chronic Inflammation

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The ability to selectively destroy a sizable fraction of senescent cells in many tissues in old animals has led to the understanding that these errant cells and their secretions are an important cause of the chronic inflammation characteristic of old age. The accumulation of senescent cells is far from the only mechanism involved, but the contribution is sizable. Removing senescent cells can turn back numerous inflammatory age-related conditions in animal models. The open access paper here proposes a view of age-related chronic inflammation that pulls together this and all of the other discoveries of the past decade related to aging and inflammation into what they term “senoinflammation”.


Age-associated chronic inflammation is characterized by unresolved and uncontrolled inflammation with multivariable low-grade, chronic and systemic responses that exacerbate the aging process and age-related chronic diseases. Currently, there are two major hypotheses related to the involvement of chronic inflammation in the aging process: molecular inflammation of aging and inflammaging. However, neither of these hypotheses satisfactorily addresses age-related chronic inflammation, considering the recent advances that have been made in inflammation research. A more comprehensive view of age-related inflammation, that has a scope beyond the conventional view, is therefore required.

Based on the available findings from biochemical, molecular, and systems analyses, we propose the senoinflammation concept. It provides not only a broader scope, but also creates an intricate network among many inflammatory mediators that can lead to systemic chronic inflammation. When gene regulation is impaired because of constant damage to the genomic DNA by augmented oxidative susceptibility during the aging progresses, several key inflammatory transcription factors, including p53, AP-1, STAT, and NF-κB, that are important in cell survival become over-activated.

The resulting aberrant gene regulation in senescent cells leads them into a proinflammatory state, thereby altering systemic chemokine or cytokine activities. The proinflammatory senescent cell secretome imposes further stresses on the intracellular organelles, as well as tissues, organs, and systems, thus influencing metabolic disorders such as insulin resistance. It seems plausible that a vicious cycle takes place between senescent cell secretome induction and metabolic dysregulation, as proposed in the senoinflammation concept, and this may well be the underpinning of the aging process and age-associated diseases.

It is hoped that a better understanding of the molecular mechanisms involved in senoinflammation will provide a basic platform for the identification of potential targets that can suppress age-related chronic inflammation and thereby lead to the development of effective interventions to delay aging and suppress age-associated diseases.

Link: https://doi.org/10.14336/AD.2018.0324

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Fibrosis as a Consequence of Processes of Aging

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Fibrosis is a malfunction of tissue maintenance and regeneration in which scar-like collagen deposits form, disrupting tissue structure and function. It almost always occurs in later life, even in fibrotic conditions clearly caused by environmental factors, such as smoking in the case of chronic obstructive pulmonary disease. Why is this? The authors of the open access paper noted here consider the mechanistic reasons as to why fibrosis is age-related, enumerating the processes associated with aging that are thought to have the greatest influence over fibrosis.

There is presently little that can be done to turn back fibrosis in established medical practice. That said, clearance of senescent cells has produced promising results in animal studies and an initial human study. That removal of senescent cells appears to reliably produce benefits ties in with the connection of fibrosis to chronic inflammation and its effects on regenerative processes. Senescent cells generate inflammation, and this appears to drive, to a sizable degree, many of the diseases and dysfunctions of aging.


Aging is a predisposing factor for cardiac and pulmonary fibrosis, with the prevalence of heart failure and fibrotic respiratory diseases such as idiopathic pulmonary fibrosis (IPF) increasing dramatically with advancing age. The aging of cardiac and lung tissue ultimately results in structural remodeling of the extracellular matrix (ECM) caused by alterations in the concentration and organization of ECM components such as collagen and elastin. Biological aging is accelerated by the cumulative damage and stress that occurs during a lifetime. This premature aging is particularly pertinent to the pulmonary system, which is subjected to lifelong challenges by airborne pollutants, particulates, and pathogens. Similarly, due to the high metabolic demand of the heart, large mitochondrial population and infrequent cardiomyocyte turnover, the heart is also highly susceptible to cumulative oxidative damage and stress with age. Cellular and immunological changes occur concomitantly with age-related tissue remodeling.

There are a great many hallmarks that represent common denominators of aging, such as stem cell exhaustion, genomic instability, telomere attrition, epigenetic alteration, and loss of proteostasis; in this review we focus on four processes of aging which play an integral role in fibrosis. Senescence, inflammaging, compromised autophagy and mitochondrial dysfunction are interrelated processes, which reduce the regenerative capacity of the aged heart and lung, and have been shown to be involved in cardiac fibrosis and IPF. As a consequence, challenges to an aging heart or lung are more likely to lead to pathological tissue remodeling rather than wound resolution and tissue restitution. This is exemplified in experimental models that show cardiac fibrosis in mice post-myocardial infarction increases with age. Similarly, pulmonary fibrosis in experimental lung injury is exacerbated by aging.

Age-related processes such as senescence and inflammaging diminish the regenerative capacity of damaged cardiac and pulmonary tissue, increasing the likelihood of pathological fibrosis following injury or challenge. What is interesting about these two processes is that at low levels, they mediate beneficial effects, but as you age and the level increases, they become deleterious. This is most evident with senescence, which protects the organism from cancer but which, in excess, can promote aging and the hallmark features of fibrosis. Furthermore, inflammaging and its sustained increase of inflammatory markers, which at normal levels regulate the immune response, contributes to the acquired resistance of myofibroblasts to apoptosis, and the low grade chronic inflammation which sustains the persistent fibrosis of cardiovascular disease and IPF. Given the similarities between cardiac and pulmonary fibrosis, investigating targets and testing future treatments in both organs with a focus on these key age-related processes seems justifiable and may lead to better treatment opportunities.

Link: https://doi.org/10.14336/AD.2018.0601

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Increased Levels of Progerin Observed in Overweight Individuals

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Progerin is the malformed version of LMNA, a protein vital to the structure of the cell nucleus. It is the cause of progeria, a rare condition that has the superficial appearance of greatly accelerated aging. It isn’t aging, however, but rather an enormous burden of cellular damage and dysfunction resulting from structural issues in the cell nucleus that affect near all forms of function. In normal aging, there is also an enormous burden of damage and dysfunction, but this arises from a completely different mix of issues. Some of the end results, such as cardiovascular disease, are somewhat similar, but one can’t compare the two if interested in first causes.

In the case of patients with progeria, the LMNA gene is mutated, resulting in large amounts of progerin. One of the interesting observations made over the past decade is that some tiny fraction of LMNA is malformed in older people without progeria, however, and it has been suggested that this may contribute to the aging progress. As for many such mechanisms, the question is whether or not its contribution is significant in comparison to that resulting from the various other forms of disarray in aging tissues. That question has not been resolved. The easiest way to do so would be to find an efficient way to remove or block the activity of all progerin and observe the results, but that has yet to take place.

In the open access paper noted here, researchers report on the interesting observation that overweight individuals have higher levels of progerin. Being overweight does in fact accelerate most of the processes of aging. Visceral fat tissue is metabolically active, and generates chronic inflammation through a range of different mechanisms, from increased numbers of senescent cells through to inappropriate signaling on the part of normal fat cells. Inflammation drives the progression of many forms of age-related disease. Again we might ask the question: given this sizable contribution, is the presence of progerin in the observed amounts significant? Answers will remain speculative until such time as the progerin can be removed.

High Body Mass Index is Associated with Elevated Blood Levels of Progerin mRNA


Excess weight is growing in frequency globally. Obesity is associated with morbidity and premature mortality and represents a major risk factor for many diseases especially cardiovascular disease. It is linked to a significant decrease in life expectancy of 5-10 years in comparison to persons with Body-Mass-Index (BMI) between 22.5 to 24.9. An elevated BMI, adipose tissue and muscular fat depositions, respectively, have been associated with aging. Aging is defined as deterioration of cellular and organ function with time related to many physiologic and phenotypical changes and represents the strongest risk factor for myocardial infarction, stroke, diabetes, and cancer. Therefore, premature aging-like syndromes such as Hutchinson-Gilford progeria syndrome (HGPS) are of particular interest in exploring pathophysiological changes of aging processes related to cardiovascular disease.

HGPS is based on mutations influencing the precise encoding and processing of lamin A (LMNA) an important filament protein in the nucleus of eukaryotic cells. LMNA is involved in the correct forming of a filamentous meshwork between chromatin and the nuclear membrane, keeping the nuclear envelope upright, which is essential to regulate processes like DNA replication, DNA repair, and RNA transcription. Individuals suffering from HGPS exhibit early cardiovascular atherosclerosis and often die due to heart attack and stroke as teenagers. Toward the end of life, HGPS patients also suffer from heart failure due to cardiac fibrosis and cardiomegaly.

In most HGPS cases, a single point mutation activates a cryptic splicing site causing the production of 50 amino acids truncated prelamin A called progerin. Progerin lacks the cleavage site for zinc-metalloproteinase (ZMPSTE24) resulting in accumulation in the nucleus, leading to disturbed lamina, telomere and DNA damages, apoptosis, early cellular senescence, and finally to deterioration of organ function. Astonishingly, it was shown that low amounts of progerin mRNA derived by alternative splicing are also expressed in healthy individuals leading to the discussion of the role of progerin in normal aging by various groups. Since obesity and premature aging are both accompanied with an increased cardiovascular morbidity and mortality, we aimed to investigate the association of BMI with respect to progerin mRNA expression in the blood of individuals with known cardiovascular disease.

This study shows that mRNA levels of the aging related lamin A splice variant progerin, associated with premature aging in HGPS, were significantly upregulated in subjects with BMI ≥ 25 kg/m2. Moreover, our data revealed a significantly positive correlation of BMI with progerin mRNA. These data provide to our knowledge for the first-time evidence for a possible involvement of progerin in previously observed accelerated aging of overweight and obese individuals potentially limiting their longevity. Our results also showed that progerin mRNA was positively correlated with C-reactive protein (CRP). This might suggest an association of progerin with an inflammatory response triggering accelerated aging. Moreover, we found an increase of the acute phase protein CRP in patients with BMI ≥ 25, indicating a higher systemic inflammatory status in the overweight group. This is consistent with prior findings where obesity was considered to predispose to local and systemic inflammation with ongoing activation of immune cells.

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Chronic Stress Raises Your Risk of Several Types of Cardiovascular Disease

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Stress has enormous implications for your health. From an evolutionary perspective, the stress response is a lifesaving biological function that enables you to instinctively square-off against an assailant, run away from a predator or take down a prey.

However, those of us living in the modern world are now activating this same biological reaction in response to activities and events that have no life-threatening implications whatsoever, from speaking in public to filling out tax forms to sitting in traffic jams.

The sheer number of stress-inducing situations facing us on a daily basis can actually make it difficult to turn the stress response off, and marinating in corrosive stress hormones around the clock can have very serious consequences for your health.

Stress Is ‘Robustly Associated’ With Cardiovascular Disease

Recent research1 again highlights the health risks of chronic stress, as data show people with stress related disorders are 29% more likely to develop cardiovascular disease compared to a sibling without a stress disorder, and 37% more likely compared to the general population.

Cardiovascular diseases included ischemic heart disease, cerebrovascular disease, emboli/thrombosis, hypertensive disease, heart failure and arrhythmia/conduction disorder.

The study, published in the BMJ, compared health data on 136,637 Swedes diagnosed with a stress disorder — including acute stress reaction, post-traumatic stress disorder and adjustment disorder — with 171,314 siblings and 1.3 million people in the general population that did not have a stress-related disorder.

Interestingly, within the first year of a stress diagnosis, the risk for cardiovascular disease was even greater — 64% greater than that of a sibling and 71% greater than the general population. The link was also particularly strong for those under the age of 50. According to the authors:2

“Most people are, at some point during their life, exposed to psychological trauma or stressful life events such as the death of a loved one, a diagnosis of life threatening illness, natural disasters, or violence.

Accumulating evidence suggests that such adversities might lead to an increased risk of several major diseases (including cardiovascular morbidity, injury, infection, and certain autoimmune diseases but not cancer) and mortality, with the largest risk elevations usually noted among people who develop psychiatric disorders as a result of their trauma …

Stress related disorders are robustly associated with multiple types of cardiovascular disease, independently of familial background, history of somatic/psychiatric diseases, and psychiatric comorbidity …

In addition, patients with stress related disorders tended to have a higher burden of somatic diseases at the index date and a lower family income level, and to be more likely to be divorced or widowed, compared with their unaffected siblings or matched unexposed people …

These findings call for enhanced clinical awareness and, if verified, monitoring or early intervention among patients with recently diagnosed stress related disorders.”

How Stress Affects Your Cardiovascular Health

As noted in the featured study3 and elsewhere,4 while there are still unanswered questions, a number of mechanisms have been proposed to explain the link between stress and cardiovascular disease. Among them:

Increased blood pressure caused by acute stress can set the stage for acute cardiovascular events; long term, elevated blood pressure can lead to endothelial dysfunction and arteriosclerosis

Chronically elevated cortisol, released in response to stress, can also raise triglycerides and blood sugar, which like high blood pressure are risk factors for heart disease

Biological stress reactions can also over time trigger other risk factors for cardiovascular disease, such as:

Chronic inflammation

Autonomic dysfunction

Hypothalamic-pituitary-adrenal axis dysregulation

Altered neurochemistry that contributes to negative behavior such as smoking and poor sleep habits

Plaque buildup in your arteries

High-Stress Lifestyle Linked to Higher Risk of Heart Attack and Stroke

There’s no shortage of evidence showing that stress impacts your heart health. Previous research5 has demonstrated that stress increases your risk of heart attack and stroke by causing overactivity in your amygdala.

Known as your brain’s fear center, this brain region, located in your temporal lobe, is activated in response to both real and perceived threats. It’s also involved in the processing of other emotions, including positive ones, as well as emotional memories of all kinds. One of its most basic jobs, though, is to keep you safe by biochemically preparing you to fight or flee as needed.

In this particular study, inflammation levels and brain and bone marrow activity of 293 participants were measured. All were over the age of 30, and none had a diagnosed heart problem. By the end of the observation period, which lasted between two and five years, 22 participants had experienced a serious cardiac event such as heart attack, stroke or angina (chest pain).

Based on brain scans, the researchers were able to conclude that those with higher activity in the amygdala were at an elevated risk of a cardiac event. As it turns out, there appears to be a significant correlation between amygdala activity and arterial inflammation — triggered by immune cell production in your bone marrow — which is a risk factor for heart attack and stroke.

This was confirmed in a sub-study involving 13 patients with a history of PTSD.6 Here, levels of C-reactive protein were also measured, showing those with the highest stress levels also had the highest amygdala activity and higher levels of inflammatory markers. Lead author Dr. Ahmed Tawakol from Massachusetts General Hospital and Harvard Medical School, told Science Daily:7

“Our results provide a unique insight into how stress may lead to cardiovascular disease. This raises the possibility that reducing stress could produce benefits that extend beyond an improved sense of psychological wellbeing. Eventually, chronic stress could be treated as an important risk factor for cardiovascular disease, which is routinely screened for and effectively managed like other major cardiovascular disease risk factors.”

Ilze Bot, Ph.D., a Dutch biopharmaceutical researcher who wrote an accompanying commentary to the study, added:8

“In the past decade, more and more individuals experience psychosocial stress on a daily basis. Heavy workloads, job insecurity, or living in poverty are circumstances that can result in chronically increased stress

These clinical data establish a connection between stress and cardiovascular disease, thus identifying chronic stress as a true risk factor for acute cardiovascular syndromes, which could, given the increasing number of individuals with chronic stress, be included in risk assessments of cardiovascular disease in daily clinical practice.”

Other Ways Stress Can Trigger a Heart Attack

Stress can also promote or trigger a heart attack in other ways. For example, studies9 have shown that as your stress level rises, so does your level of disease-promoting white blood cells, and this is yet another way by which stress can lead to atherosclerosis, plaque rupture and myocardial infarction.

During moments of high stress your body also releases norepinephrine, which researchers claim10 can cause the dispersal of bacterial biofilms from the walls of your arteries. This dispersal can allow plaque deposits to suddenly break loose, thereby triggering a heart attack.

A sudden release of large amounts of stress hormones and rapid elevations in blood pressure may even trigger a heart attack or stroke even if you don’t have an underlying heart problem. In the case of broken heart syndrome, the symptoms of a heart attack occur even though there’s no actual damage to the heart at all.

According to the British Heart Foundation,11 broken heart syndrome — clinically known as Takotsubo cardiomyopathy — is a “temporary condition where your heart muscle becomes suddenly weakened or stunned.” The left ventricle (your heart’s largest chamber) also changes shape, which adds to the temporary dysfunction.

This sudden weakness of the heart is thought to be due to the sudden release of large quantities of adrenaline and other stress hormones. Adrenaline increases your blood pressure and heart rate, and it’s been suggested it may lead to narrowing of the arteries that supply blood to your heart, or even bind directly to heart cells allowing large amounts of calcium to enter and render the cells temporarily unable to function properly.

While most will successfully recover, in some, the change of shape of the left ventricle can trigger a fatal heart attack. Having a history of neurological problems, such as seizure disorders and/or a history of mental health problems is thought to raise your risk.12 On the upside, while the condition can be life-threatening and requires immediate medical attention, it’s usually a temporary condition that leaves no permanent damage.

Sports Fanatics Beware

Another paper13 looking at stress and sudden heart events noted the risk of heart attack and stroke was greater following emotionally intense sporting events, such as European soccer games. As noted by the authors:

“One of the first studies was from the Netherlands, in which mortality from coronary heart disease and stroke was found to be increased in men on the day of an important football match between the Netherlands and France in the 1996 European football championship tournament. There was no similar increase found in women, nor on any of the other days in which the Dutch played a football game in that tournament.

The increase occurred on the day the Dutch played their one game that ended in a penalty shoot-out, a do-or-die situation in which the winner of the game is determined in dramatic fashion. The study investigators proposed that the heightened intensity of the game and resultant outcome (the Dutch lost) may have been responsible for the 14 excess deaths caused by coronary heart disease and stroke in the Netherlands that day …

A subsequent study from England showed that admissions from acute MI were increased by 25% on the day of and two days after England lost to Argentina in the 1998 World Cup in yet another game that ended in a penalty shoot-out.”

The researchers detail several potential mechanisms by which watching sporting events could contribute to cardiac events, including:

  • Sympathetic nervous system stimulation, which can increase coronary vascular tone, thereby reducing your relative oxygen supply. At the same time, your level of circulating catecholamines (“induced by the emotional involvement in the game”) increases, which raises your need for oxygen by raising heart rate and blood pressure
  • Increased ventricular inotropy and changes in coronary tone may alter “the shear stress of blood against a vulnerable atherosclerotic plaque, contributing to plaque fracture”
  • Increased concentrations of catecholamines can also trigger arrhythmias and increase platelet aggregation — a part of the sequence of events that lead to the formation of a blood clot

High Resting Heart Rate Linked to Early Death

In related news, researchers also warn that having a high resting heart rate may affect your longevity. Middle-aged men with a resting heart rate of 75 beats per minute (bpm) were twice as likely to develop heart disease and die early than those with a resting heart rate around 55 bpm.14

They also found that those whose resting heart rate remained stable during the decade between their 50s and 60s had a lower risk of cardiovascular disease than those whose resting heart rate rose over time. As reported by Newsweek:15

“The researchers believe this could be because a high resting heart rate may put the heart under stress and increase oxygen consumption. It has also been linked to sympathetic overactivity where the nervous system works too hard, which is tied to conditions that affect the heart such as high blood pressure and metabolic syndrome.”

Another study found that boosting your cardiorespiratory fitness may reduce your risk of heart attack, especially for women. According to lead author Rajesh Shigdel, the results suggest your cardiorespiratory fitness — which reflects the maximum amount of oxygen your body is able to use during exertion — could be used “as a risk calculator for first heart attacks.”16

Women with the highest cardiorespiratory fitness levels were 25% less likely to have a heart attack than those with low cardiorespiratory fitness. Among men, high levels were slightly less effective for lowering their risk of heart attack at 10%. According to Shigdel, “People who want to increase cardiorespiratory fitness should strive to be physically active at least 150 minutes each week and minimize time spent being sedentary.” 17

Recognizing Signs of Stress

Many have gotten so used to being wound up into a stress-knot, they don’t even realize the position they’re in. So, the first step is to recognize that you’re stressed, and then take steps to address it. Common signs and symptoms of stress include:18

Sleeping poorly; trouble falling asleep; excessive tiredness

Binge drinking

Lack of appetite or overeating

Having a “short fuse” / being quick to anger or losing your temper

Feeling overwhelmed, sad or irritable; frequent crying or quick to tears

Headaches and/or general aches and pains

Lower Acute Stress With Proper Breathing

As mentioned earlier, stress is associated with an overactive amygdala, which when triggered by a real or perceived threat, causes oxygen to be shunted from your internal organs, including your brain, to your extremities. Essentially, your body is prepared for fighting — not thinking.

However, critical thinking is really what’s required when facing a stressful situation in today’s world. Fist-fighting is not the most appropriate solution when faced with traffic jams or interpersonal difficulties, for example, yet because of the stress response, your brain has been largely shut off.

Step 1, then, is to bring oxygen back to your brain, which you can do through some simple breathing exercises. You may want to experiment with a few different ones to see if one works better than another. Following are three variations that can do the trick. Breathing technique No. 1:

  1. Simply breathe in to a count of four
  2. Hold your breath for another count of four
  3. Breathe out to the count of four
  4. Hold again for a count of four

Another one I like is the 4-7-8 breathing exercise taught by Dr. Andrew Weil.

  1. Sit up straight and place the tip of your tongue up against the back of your front teeth. Keep it there through the entire breathing process
  2. Breathe in silently through your nose to the count of four, hold your breath to the count of seven, and exhale through your mouth to the count of eight, making an audible “whoosh” sound. That completes one full breath
  3. Repeat the cycle another three times, for a total of four breaths. After the first month, you can work your way up to a total of eight breaths per session

A third method is the controlled breathing method taught by Patrick McKeown, one of the top teachers of the Buteyko Breathing Method. If you’re experiencing anxiety or panic attacks, or if you feel stressed and your mind can’t stop racing, try the following breathing sequence.

Its effectiveness stems from the fact that it helps retain and gently accumulate carbon dioxide. This not only helps calm your breathing but also reduces anxiety. In short, the urge to breathe will decline as you go into a more relaxed state:

  1. Take a small breath into your nose, followed by a small breath out
  2. Hold your nose for five seconds in order to hold your breath, and then release your nose to resume breathing
  3. Breathe normally for 10 seconds
  4. Repeat the sequence several more times

Counter Stress by Activating Your Body’s Relaxation Response

Once you’ve addressed the oxygenation of your brain, next, engage in some sort of physical relaxation technique, as the stress response causes the muscles in your body to tighten. One simple one that can be done anywhere is to tighten the muscles in an area for a few seconds, and then release; moving from section to section. Start with your feet and legs, and move upward. This may even be done in concert with your breathing exercise of choice.

Visualization techniques such as those taught by Dr. Martin Rossman, author of “The Worry Solution,” can also be helpful. Imagery is the natural language of your brain, which is in part why visualization and guided imagery exercises are so powerful for changing thoughts and behavior.

As noted by Rossman, the three keys to calmness are breathing, relaxation and visualization. Ideally, do all three. Here’s Rossman’s suggestion for pursuing calmness: Breathe and relax your body part by part, then imagine being in a beautiful, peaceful place where you feel safe. This could be either a real or imaginary place. Spend 10 or 20 minutes there, actively visualizing the serenity of your surroundings, to interrupt the stress response.

This will disengage your fight or flight response, allowing your physiology to return to equilibrium, or what is also termed “the relaxation response.” This is a compensatory repair, renew and recharge state that brings you back to balance.

Mindfulness training — which focuses on being present in the moment — is another strategy that can be very helpful. In one study, people who participated in 10 sessions over the course of one month experienced “significantly decreased” stress, anxiety and depression.19 Mindfulness meditation is a more formal practice of mindfulness, in which you consciously zone in on, or focus your attention on, specific thoughts or sensations, then observe them in a nonjudgmental manner.

The Emotional Freedom Techniques for Stress Relief

Last but not least, energy psychology techniques such as the Emotional Freedom Techniques (EFT) can be very effective for reducing stress by helping you to actually reprogram your body’s reactions to the unavoidable stressors of everyday life. This is important as, generally speaking, a stressor becomes a problem when:

  • Your response to it is negative
  • Your feelings and emotions are inappropriate for the circumstances
  • Your response lasts an excessively long time
  • You’re feeling continuously overwhelmed, overpowered or overworked

EFT is not the same thing as mindfulness; it is entirely different and used for different purposes. I regard mindfulness and meditation as tools that are useful for your entire life, like exercise for your mind. Ideally, you should strive to be mindful and use meditation daily.

EFT is different in that it works best for targeted stress relief, such as recovering from an emotional trauma or overcoming an addiction. You might only need to use EFT a few times throughout your life, while mindfulness and meditation are life-long endeavors.

When you use EFT, simple tapping with the fingertips is used to input kinetic energy onto specific meridians on your head and chest while you think about your specific problem and voice positive affirmations.

This combination of tapping the energy meridians and voicing positive affirmation works to clear the “short-circuit” — the emotional block — from your body’s bioenergy system, thus restoring your mind and body’s balance, which is essential for optimal health and the healing of chronic stress.

While the video above will easily teach you how to tap for stress, it is important to realize that self-treatment for more serious issues is not recommended. For serious or complex issues, seek out an experienced practitioner to guide you through the process.

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On Alzheimer's Disease Research, Both Appropriate and Inappropriate Pessimism

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This is a pessimistic popular science article on the state of Alzheimer’s disease research. I think the tone appropriately pessimistic where it examines the present dominant approach to building therapies, which is to say clearing amyloid-β from the brain via immunotherapy. I think it inappropriately pessimistic for the near future, however, given the various projects currently under development. Take, for example, the brace of approaches based on restored drainage of molecular wastes in cerebrospinal fluid, or filtration of cerebrospinal fluid to achieve much the same outcome. Further, and closer to widespread availability in the clinic, senolytic therapies to clear senescent cells have been used to demonstrate that senescent immune cells in the brain, and the neuroinflammation that they cause, are a significant contribution to both Alzheimer’s disease and other neurodegenerative conditions. Removing these cells may well do more for Alzheimer’s patients in the near term than any other approach attempted to date.


Not only have there been more than 200 failed trials for Alzheimer’s, it’s been clear for some time that researchers are likely decades away from being able to treat this dreaded disease. Which leads me to a prediction: There will be no effective therapy for Alzheimer’s disease in my lifetime. Alzheimer’s sits right at the confluence of a number unfortunate circumstances. If you understand why there won’t be much headway on Alzheimer’s, you’ll also understand a bit more why modern medicine has been having fewer breakthroughs on major diseases.

For decades it was widely believed that the cause of Alzheimer’s was the build-up of abnormal proteins called amyloid and tau. These theories dominated the field and led some to believe we were on the verge of effective treatments – through preventing or removing these abnormal proteins. But had the theories been correct we would likely have had at least one or two positive clinical trials. In retrospect, the multi-decade amyloid fixation looks like a mistake that could have been avoided. It was always possible that the classic plaques and tangles were epiphenomena of aging and not the cause of the disease. Epiphenomena are characteristics that are associated with the disease but are not its cause.

But even more convincing that researchers are closer to the beginning than the end in understanding the cause of Alzheimer’s is the long list of alternative theories. This now includes but is not limited to: infection, disordered inflammation, abnormal diabetes-like metabolism, and numerous environmental toxins. And the past few years have seen more evidence for viral, bacterial, and fungal infections. These viral and bacterial hypotheses were portrayed as eureka moments. But this begs the question: How did powerful tools of epidemiology miss associations with things like cold sores and gum disease?

Here’s the thing – regardless of type, Alzheimer’s has a powerful age-related association. This is true even for patients with early-onset inherited form of Alzheimer’s. Give someone the worst possible genome for Alzheimer’s – including the dreaded APOE e4 gene that may be associated with a 10-fold increase in risk – and that person still needs to age a bit before developing the disease. If correct, this conception of the disease means we’re even further away from an effective treatment. Aging is not disease. It is the normal arc of life and an ineluctable part of being human (“dust unto dust”). As such, the biology of aging didn’t get the attention that was bestowed on organ systems and diseases during the golden years of research funding. In retrospect, I think this may have been a grave mistake. If you list the risk factors for the major diseases of modern life – heart disease, diabetes, dementia – the most powerful is almost always age. Bottom line: We also lack an understanding of the basic science of Alzheimer’s most important risk factor.

Link: https://theconversation.com/no-cure-for-alzheimers-disease-in-my-lifetime-114114

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GATA3 Macrophages as a Contributing Cause of Cardiac Fibrosis

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The innate immune cells called macrophages are deeply involved in both inflammation and regeneration. They adopt different phenotypes, or polarizations, depending on circumstances, such as the M1 polarization (inflammatory, aggressive in pursuit of pathogens) and M2 polarization (pro-regenerative, anti-inflammatory). The simple view of macrophage polarization in aging tissues is that problems arise with an excess of M1 macrophages, and this is a part of the chronic inflammation that is characteristic of aging. It is well known that inflammation, when maintained over the long term, is highly disruptive of tissue function, and contributes to the progression of all of the common age-related disease.

The open access commentary here makes the point that this model of polarization and inflammation is overly simplistic, and the reality is much more complex. The researchers illustrate this with data on M2 macrophages expressing GATA3, suggesting that it is these cells, rather than pro-inflammatory M1 macrophages, that are contributing to the fibrosis that appears in cardiac tissue with age. Fibrosis is a disarray of tissue maintenance and regeneration, involving the deposition of scar-like collagen structures that degrade tissue function. The usual view of fibrosis is that it is a consequence of inflammation, very connected to the inflammatory presence of senescent cells, for example. Given that, it is quite interesting to see this sort of contradictory data.


Chronic inflammation is believed to contribute to the pathogenesis of many age-related diseases including cardiovascular disease. Chronic inflammation, particularly from activation of innate immunity, is highly sensitive to changes in the tissue environment that is associated with aging. The immune cell type that is particularly influenced by changes in its microenvironment is the monocyte/macrophage. These cells display a high level of plasticity and heterogeneity in response to their environmental cues. For example, based on the response of cultured macrophages to treatment with IL-4 or interferon γ, cells have been proposed to polarize to either M2 or M1 phenotypes, respectively. Although the M1-M2 polarization concept is useful in describing the two extremes of macrophage phenotypes, the concept does not accurately recapitulate the complex response of cells to their driving tissue microenvironment in vivo.

The plasticity of monocytes/macrophages are determined by the constellation of transcription factors that are activated and expressed in response to environmental cues. To understand the role of GATA3 transcription factor in the pathogenesis of cardiac diseases, we generated myeloid-specific GATA3 knockout mice and found that their cardiac function is significantly improved in response to ischemia or pressure overload compared with the GATA3 sufficient control group. Analysis of the profile of monocytes/macrophages in vivo revealed that GATA3-positive macrophages are not found in the healthy adult tissue. In the setting of a myocardial infarction, however, the deficiency of GATA3-positive macrophages led to a significant improvement of cardiac function compared with the GATA3 sufficient control group.

This improvement was found to be associated with the presence of many pro-inflammatory macrophages, but, few “anti-inflammatory/reparative” macrophages. This was unexpected because the prevailing hypothesis is that controlling the pro-inflammatory pathways may improve cardiac function. Our data suggest that exuberant repair, rather than unrestrained inflammation, may contribute to the excessive and maladaptive remodeling of the myocardium in the post myocardial infarction setting. Extensive evidence suggests that the aging heart undergoes fibrotic remodeling. Although targeting of pro-inflammatory pathways is thought to be an important strategy to control excessive tissue fibrosis, numerous anti-inflammatory drugs have been found to have little or no therapeutic benefit in fibrotic diseases. Our data suggest that GATA3-positive macrophages, which presumably display an M2 phenotype, are highly fibrogenic. It is therefore possible that targeting a subset of inflammatory cells, rather than global inflammation, may be a useful therapeutic strategy to control fibrotic diseases associated with aging.

Link: https://doi.org/10.18632/aging.101929

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Presenting the SASP Atlas for the Senescence-Associated Secretory Phenotype

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The presence of growing numbers of lingering senescent cells is one of the root causes of aging. Vast numbers of cells become senescent every day, but near all are quickly removed, either via programmed cell death or the actions of the immune system. A tiny number survive, however, and that alone would eventually be enough to cause age-related disease and death. While senescent cells never rise to very large fractions of all of the cells in a given tissue, they cause considerable harm via a potent mix of secreted signals known as the senescence-associated secretory phenotype, or SASP. The SASP causes chronic inflammation and destructive remodeling of the nearby extracellular matrix. Further, it changes the behavior of other cells for the worse, including increasing their chances of becoming senescent.

In today’s open access paper, researchers present the start of a new database that will categorize the many molecules making up the SASP for various cell types. Since nothing is simple in biochemistry, the SASP is undoubtedly meaningfully different from tissue to tissue and cell type to cell type. Why does the SASP exist? Senescent cells have important transient roles in wound healing and in regulating the growth of embryonic tissues. Here the signals are beneficial, involved in growth and regeneration, and senescent cells are cleared from the site after they have served their purpose. Further, senescence in response to DNA damage or a toxic environment is a defense against cancer, in that senescent cells cease to replicate, encourage nearby cells to do the same, and rouse the immune system into greater activity – exactly the sort of strategy that should put a halt to cancer in its earliest stages.

Unfortunately, that the clearance of senescent cells is imperfect, and some always linger, ensures that the SASP becomes a cause of aging. Signals that are beneficial in specific contexts in the short term become harmful when continually present. In old tissues, the secretions of senescent cells actively maintain a degraded, dysfunction state of cellular metabolism and tissue function. This is why senolytic treatments capable of selectively removing some fraction of senescent cells are proving to be so very effective for a very wide range of age-related diseases in animal studies. Fortunately, no great understanding of the SASP is needed to make progress in this form of treatment; we know that removing chronic SASP is beneficial, and that should be the primary focus of development.

SASP Atlas


The senescence-associated secretory phenotype (SASP) has recently emerged as both a driver of, and promising therapeutic target for, multiple age-related conditions, ranging from neurodegeneration to cancer. The complexity of the SASP, typically monitored by a few dozen secreted proteins, has been greatly underappreciated, and a small set of factors cannot explain the diverse phenotypes it produces in vivo. Here, we present ‘SASP Atlas’, a comprehensive proteomic database of soluble and exosome SASP factors originating from multiple senescence inducers and cell types. Each profile consists of hundreds of largely distinct proteins, but also includes a subset of proteins elevated in all SASPs. Based on our analyses, we propose several candidate biomarkers of cellular senescence, including GDF15, STC1, and SERPINs. This resource will facilitate identification of proteins that drive specific senescence-associated phenotypes and catalog potential senescence biomarkers to assess the burden, originating stimulus and tissue of senescent cells in vivo.

A Proteomic Atlas of Senescence-Associated Secretomes for Aging Biomarker Development


Cellular senescence is a complex stress response that causes an essentially irreversible arrest of cell proliferation and development of a multi-component senescence-associated secretory phenotype (SASP). The SASP consists of myriad cytokines, chemokines, growth factors, and proteases that initiate inflammation, wound healing, and growth responses in nearby cells and tissues. In young and healthy tissues, the SASP is typically transient and tends to contribute to the preservation or restoration of tissue homeostasis. However, the increase in senescent cells with age and a chronic SASP are now known to be key drivers of many pathological hallmarks of aging, including chronic inflammation, tumorigenesis, impaired stem cell renewal, and others.

Using either or both of two transgenic mouse models that allow the selective elimination of senescent cells, or compounds that mimic the effect of these transgenes, data from several laboratories strongly support the idea that the presence of senescent cells drives multiple age-related phenotypes and pathologies, including age-related atherosclerosis, osteoarthritis, cancer metastasis and cardiac dysfunction, myeloid skewing in the bone marrow, kidney dysfunction, and overall decrements in healthspan.

Several types of stress elicit a senescence and secretory response, which in turn can drive multiple phenotypes and pathologies associated with aging in mammals. Some of these stressors have shared effects. For example, telomere attrition resulting from repeated cell division (replicative senescence), elevated reactive oxygen species, chromatin disruption, and even the activation of certain oncogenes all can cause genotoxic stress, as can a number of therapeutic drug treatments, such as anti-cancer chemotherapies and certain highly active antiretroviral therapies for HIV treatment or prevention. However, whether these stressors produce similar or distinct SASPs is at present poorly characterized. Therefore, a comprehensive characterization of SASP components is critical to understanding how senescent response can drive such diverse pathological phenotypes in vivo. It is also a critical step in clarifying how various stimuli, all acting through senescence, differentially affect health.

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The Trouble With Dentistry

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According to the National Institute of Dental and Craniofacial Research,1 92% of adults aged 20 to 64 have had cavities in their permanent teeth. Interestingly, Caucasian adults and those living in families with higher incomes have had more decay, or at least have been treated for more cavities. Adults in the same age range have an average of 3.28 decayed or missing permanent teeth.

While many believe water fluoridation is an effective way of preventing tooth decay, supporting facts are just not there. According to the World Health Organization (WHO) data reported by the Fluoride Action Network, the U.S., which provides fluoridated water to 74.6% of community water systems,2 has higher rates of tooth decay than many countries that do not fluoridate their water, including Denmark, the Netherlands, Belgium and Sweden.3

If fluoridation were effective, you would expect to see higher numbers of cavities in communities without fluoridated water and the number of cavities to decline when fluoride is introduced. Instead, demographic studies have demonstrated fluoridated water has little to do with cavity prevention.4,5,6

Instead, caries often follow demineralization of the tooth triggered by acids formed during bacterial fermentation of dietary sugars. Just as depression is not triggered by a lack of Prozac, dental caries are not caused by a lack of fluoride — a neurotoxic compound that has no biological benefits. Excess dietary sugar is the most significant factor driving dental decay.7

Dentistry Lacks Sufficient Research to Substantiate Many Procedures

The American Dental Association (ADA) claims the Code on Dental Procedures and Nomenclature (CDT) as their intellectual property.8 In 2000,9 the code was named as a HIPAA standard code set, and any electronic dental claim must use these procedural codes. According to the ADA, there are times when a code is not available and dentists are encouraged to request additions and revisions.

This process is different from the International Classification of Diseases (ICD) based on data developed by WHO,10 which copyrights the information and publishes the classification.11 An adaptation of the classification for use in the U.S. is completed by National Center for Health Statistics (NCHS), and must conform to WHO conventions.

Oftentimes when expensive surgery or a regimen of pills is recommended, most seek a second opinion. However, the same is not true when you’re sitting in the dentist chair. A Cochrane review of dental studies12 finds many of the standard dental and cosmetic treatments are not substantiated by research.

For instance, they could not find enough evidence to support or oppose the surgical removal of asymptomatic impacted wisdom teeth,13 to prove if antibiotic prophylaxis is effective or ineffective in those at risk for bacterial endocarditis before a dental procedure,14 and only three trials were found analyzing the efficacy of filling cavities in primary teeth, none of which were conclusive.15

In other words, much of the research in the field of dentistry is sadly lacking. While the recommendations may be appropriate, they may also not be, and many simply do not have adequate evidenced-based science to warrant their use.

As noted in recent article in The Atlantic,16 “[W]hat limited data we have don’t clearly indicate whether it’s better to repair a root-canaled tooth with a crown or a filling.” Derek Richards, director of the Centre for Evidence-Based Dentistry at the University of Dundee, commented on the gaping hole of evidence in the field of dentistry:17

“The body of evidence for dentistry is disappointing. Dentists tend to want to treat or intervene. They are more akin to surgeons than they are to physicians. We suffer a little from that. Everybody keeps fiddling with stuff, trying out the newest thing, but they don’t test them properly in a good-quality trial.”

Anatomy of a Tooth

According to the Academy of General Dentistry,18 at least 40 million adults in the U.S. suffer from sensitive teeth. They describe the sensitivity as being caused by the movement of fluid within tiny tubes located in the dentin, or the layer of tissue found beneath the hard enamel. When the fluid reaches the nerve, it causes irritation and pain.

These tiny tubules are exposed when your enamel is worn down or the gums have receded. This increases your risk of experiencing pain while eating or drinking hot or cold foods. The Cleveland Clinic19 lists some factors that may lead to sensitivity, including brushing too hard, gum disease, cracked teeth, teeth grinding and acidic foods.

The tubules branch throughout the tooth and are different between peripheral and the inner aspects.20 The branching pattern reveals an intricate and profuse system crisscrossing the intertubular dentin.

Studies demonstrate anaerobic bacteria and gram positive rods, as well as a large number of bacterial species, may be found within this tubule system in those suffering periodontal disease. The researchers concluded:21

“It seems clear that, in more than half of the infected roots, bacteria are present in the deep dentin close to the cementum and that anaerobic culturing of dentin is more sensitive than histology to detect these bacteria.”

Further research finds a necrotic dental pulp may develop unnoticed for years and the course of the disease is modulated by the variance of the microbiota in the root canal space and the capacity of the individual’s immune system.22

Another study23 found the environment of the deep layers of the endodontic dental area is anaerobic, favoring the growth of anaerobes, including Lactobacillus, Streptococcus and Propionibacterium.

Avoid Root Canals Whenever Possible

Root canals are not your only option. Teeth are similar to other systems in your body as they require blood supply, venous drainage and nerve innervations. Teeth that have undergone a root canal are dead and typically become a source of chronic bacterial toxicity in your body. In one study published in 2010, the authors wrote:24

“Root canal therapy has been practiced ever since 1928 and the success rate has tremendously increased over the years owing to various advancements in the field. One main reason is the complete understanding of the microbiology involved in the endodontic pathology.”

If any other organ in your body lost blood supply and lymphatic drainage it would die. Your physician would recommend it being removed so necrosis and bacteria would not kill you. But dead teeth are commonly left in your mouth. Anaerobic bacteria thrive in your dentin tubes and the blood supply surrounding the dead teeth drains the toxicity, allowing it to spread throughout your body.

This toxicity may lead to a number of diseases, including autoimmune diseases, cancer, irritable bowel disease and depression. Dr. George Meinig has a unique perspective on the underlying dangers of root canal therapy as he was one of the founding members of the American Association of Endodontists, root canal specialists.25

When he wasn’t filling canals, he was teaching the technique to dentist across the country. After spending decades practicing endodontics, he retired and began pouring over the detailed research of Dr. Weston Price. He was shocked to find valid documentation of systemic illnesses resulting from the latent infections lingering in the filled canals.

The result was his book “Root Canal Cover Up.” In an interview with me, Meinig describes the result of Price’s research findings and credible reasons why you should avoid a root canal. Price’s work demonstrated that many who suffered chronic degenerative diseases could trace the origins to root canals.

The most frequently reported conditions were heart and circulatory diseases. The next most common diseases were of the joints and those of the brain and nervous system. Meinig assumes all root filled teeth harbor bacteria and other infective agents, but not everyone is made ill since those with strong immune systems may be able to prevent bacterial colonies from taking hold.

Oral Health Inextricably Linked to Your Overall Health

However, Meinig cautions that over time, most who have undergone a root canal seem to develop some type of systemic symptoms. If you choose to have a dead tooth removed, just pulling the tooth is not enough. Price found bacteria in tissue and bone adjacent to the tooth’s root. Consequently, Meinig developed a protocol he describes in his book to ensure no bacterial growth is left.

Historically, dentistry and medicine were separated. It’s unfortunate how many fail to fully appreciate the influence oral health has on overall health. The delicate balance of bacteria in your mouth is as important to your health as your gut microbiome.

Periodontal disease, which affects the soft tissue and bone, is triggered by an increase in Porphyromonas gingivalis,26 a bacteria that impairs your immune response. Dental caries have been causally linked to Streptococcus mutans.27 In turn, your oral health impacts the rest of your body and they have a significant impact on your risk of disease.

For example, Type 2 diabetes and periodontal disease are strongly connected,28 as are cardiovascular disease and periodontal disease.29 Research30 has demonstrated failing to brush on a daily basis may increase your risk of dementia by 22 to 65%, compared to brushing three times a day, and good oral hygiene may lower your risk of pneumonia by 40%.31

When the bacteria causing tooth decay and gum disease enter your circulatory system, your body increases the release of C-reactive protein known to lead to many chronic diseases.32 Therefore it’s only common sense to pay attention to your oral health, and develop good habits that support your oral microbiome.

Seek Out a Biological Dentist for Care

One step toward achieving good oral health is to seek out a biological dentist, also known as a holistic or environmental dentist. These doctors operate according to the belief system that your teeth are an integral part of your body and, hence, your overall health.33 They recognize oral and dental health have a major influence on disease and any medical treatment takes this into account.

While I recommend using a biological dentist for all your dental needs, if you’re considering the removal of dental amalgams, it’s absolutely essential. Most conventional dentists are unaware of the dangers involved and lack the experience to remove amalgam fillings without placing your health at risk in the process. Another strategy biological dentist use is to check the compatibility of dental materials with your body.

What’s in Your Silver Fillings?

The silver fillings in your mouth are dental amalgam. As noted by the U.S. Food and Drug Administration (FDA),34 dental amalgam has been used to fill cavities for more than 150 years in hundreds of millions of patients around the world.

Amalgam is a mixture of metals consisting of elemental mercury and a powdered alloy of silver, tin and copper, 50% of which is elemental mercury by weight. The FDA also admits amalgam fillings release low levels of mercury in vapor form that may be inhaled and absorbed in your lungs.

Mercury is a neurotoxin.35 How your health is affected will depend on the form of mercury, the amount in the exposure and the age at which you’re exposed. Additionally, how long the exposure lasts and your underlying health will determine symptoms you may experience.

Symptoms of prolonged exposure to elemental mercury may include emotional changes, insomnia, headaches and poor performance on mental function tests. In 2009, the FDA issued a final rule on dental amalgams reclassifying mercury from a class I (least risk) device to class II (more risk) and designated a special controls guidance document for dental amalgam.36

The WHO37 found mercury exposure, even in small amounts, may trigger serious health concerns and can have toxic effects on lungs and kidneys, as well as the nervous, digestive and immune systems. It is considered one of the top 10 chemicals or groups of chemicals of major public health concern.

Daily Care May Protect Oral Health

As Meinig discussed in our interview, the only scientifically-proven way to prevent tooth decay is through nutrition. He related how in Price’s travels he found 14 cultural pockets of natives who had no access to “civilization” and ate no refined foods.

While their diets varied, they all ate whole, unrefined foods. Without access to tooth brushes, floss, fluoridated water or toothpaste, each group were almost all 100% free of caries.

For a discussion of how you may integrate holistic and preventive strategies, such as making your own toothpaste, flossing guidelines, and information on oil pulling and nutritional supplements to support your oral health, see my previous article, “Dental Dedication: Improve Your Oral Health.”

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Pericyte Cell Therapy Promotes Muscle Regrowth Following Atrophy in Mice

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Researchers here show that boosting the numbers of the pericyte cell population involved in vascular system growth and activity improves restoration of muscle mass following atrophy. This is particularly interesting in the context of the fact that capillary vessel networks decline in density in tissues with age, the processes of maintenance and blood vessel construction becoming disarrayed, and that this decline is thought to contribute to age-related loss of muscle mass and strength. Muscle is an energy-hungry tissue, and we might thus expect that factors relating to delivery of nutrients and oxygen via the vascular network have some impact on its maintenance and growth. That point is demonstrated here.


By injecting cells that support blood vessel growth into muscles depleted by inactivity, researchers say they are able to help restore muscle mass lost as a result of immobility. The research, conducted in adult mice, involved injections of cells called pericytes, which are known to promote blood vessel growth and dilation in tissues throughout the body. The injections occurred at the end of a two-week period during which the mice were prevented from contracting the muscles in one of their hind legs. “Just as the mice were becoming mobile again, we transplanted the pericytes and we found that there was full recovery of both muscle mass and the vasculature, too.”

The team also observed that muscle immobility itself led to a significant decline in the abundance of pericytes in the affected muscle tissues. “We know that if you are under a condition of disuse – for example, as a result of long-term bed rest, or the immobilization of a body part in a cast – you lose muscle mass. And even when you come out of that state of immobility and you start moving your muscles again, there’s this really long, slow process of recovery. Older adults might never fully rebuild the lost muscle mass after a period of immobility. They can’t recover, they become disabled, and there’s this downward spiral. They may become institutionalized and experience early mortality. To my knowledge, no one has demonstrated that anything has been effective in improving the recovery process. We’re excited by the new findings because we hope to one day use these cells or biomaterials derived from these cells to help restore lost muscle mass.”

Link: https://www.eurekalert.org/pub_releases/2019-04/uoia-iep042319.php

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