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What are the health benefits of dark chocolate?

Dark chocolate is rich in minerals, such as iron, magnesium, and zinc. The cocoa in dark chocolate also contains antioxidants called flavonoids, which may provide several health benefits.

Chocolate comes from cacao, which is a plant with high levels of minerals and antioxidants. Commercial milk chocolate contains cocoa butter, sugar, milk, and small quantities of cacao. In contrast, dark chocolate has much larger amounts of cacao and less sugar than milk chocolate.

In this article, we explore some of the potential health benefits of dark chocolate. We also cover nutritional information, risks and considerations, and how much to eat.

Antioxidants dark chocolate benefits
Dark chocolate contains compounds with antioxidant properties.

Dark chocolate contains several compounds that possess antioxidant properties, such as flavanols and polyphenols. Antioxidants neutralize free radicals and prevent oxidative stress.

Oxidative stress refers to the damage that excessive amounts of free radicals can inflict on cells and tissues in the body.

Oxidative stress contributes to the natural aging process. Over time, the effects of oxidative stress may also contribute to the development of a variety of diseases, such as:

Heart disease risk Regularly eating dark chocolate may help reduce a person's likelihood of developing heart disease. Some of the compounds in dark chocolate, specifically flavanols, affect two major risk factors for heart disease: high blood pressure and high cholesterol. We discuss the potential benefits of dark chocolate for these two risk factors and others below: Blood pressure The flavanols in dark chocolate stimulate nitric oxide production in the body. Nitric oxide causes blood vessels to dilate, or widen, which improves blood flow and lowers blood pressure. A 2015 study investigated the effects of chocolate consumption in 60 people with type 2 diabetes and high blood pressure. The researchers found that participants who ate 25 grams (g) of dark chocolate daily for 8 weeks had significantly lower blood pressure than those who ate the same quantity of white chocolate. The findings of a 2017 review showed that the beneficial effects of dark chocolate on blood pressure might be more significant in older people and those with a higher risk of cardiovascular disease, as opposed to younger, healthy individuals. Cholesterol Dark chocolate also contains certain compounds, such as polyphenols and theobromine, that may lower levels of low-density lipoprotein (LDL) cholesterol in the body and increase levels of high-density lipoprotein (HDL) cholesterol. Doctors often refer to LDL cholesterol as "good cholesterol" and HDL cholesterol as "bad cholesterol." A 2017 study reported that eating dark chocolate for 15 days raised HDL cholesterol levels in people living with HIV. However, dark chocolate consumption did not affect LDL cholesterol levels in the study participants. Thank you for supporting Medical News Today Anti-inflammatory effects dark chocolate benefits for arthritis
Eating dark chocolate may help reduce inflammation in the body. Inflammation is part of the body's natural immune response to germs and other harmful substances. However, chronic inflammation can damage cells and tissues and may increase the risk of some health conditions, including type 2 diabetes, arthritis, and certain types of cancer. Dark chocolate contains compounds with anti-inflammatory properties that may help reduce inflammation in the body. A small pilot study from 2018 involving five healthy people examined the effects of dark chocolate on the immune system. The results suggested that consuming large amounts of 70-percent dark chocolate affects the activity of genes that regulate the immune response. However, it remains unclear how this study will be of practical significance. In another study from 2018, researchers found that eating 30 g of 84-percent dark chocolate each day for 8 weeks significantly reduced inflammatory biomarkers in people with type 2 diabetes. The authors of the study concluded that there is a need for additional studies to evaluate the optimal amounts of dark chocolate to use to treat those with diabetes. Insulin resistance Insulin resistance occurs when the body's cells stop responding to the hormone insulin. Insulin resistance can cause abnormally high levels of blood glucose, which can lead to prediabetes and type 2 diabetes. A 6-month study from 2018 examined the relationship between regular dark chocolate consumption and blood glucose levels among Hispanic individuals. The research findings suggest that eating 2 g of 70-percent dark chocolate each day may help lower fasting glucose levels and reduce insulin resistance. Brain function Eating dark chocolate may improve brain function and help prevent neurodegenerative conditions, such as Alzheimer's disease and Parkinson's disease. The findings of a small 2018 study suggest that the flavanols present in dark chocolate may enhance neuroplasticity, which is the brain's ability to reorganize itself, particularly in response to injury and disease. A study from 2016 identified a positive association between regular chocolate consumption and cognitive performance. However, the researchers collected data from surveys and had to rely on self-reported chocolate intake, so they were unable to draw any definitive conclusions from the findings. Thank you for supporting Medical News Today Nutritional information dark chocolate benefits bar
Dark chocolate with 70–85 percent cocoa is a good source of magnesium, zinc, and iron. According to the United States Department of Agriculture, a 101-g bar of dark chocolate with 70–85 percent cocoa solids provides: 604 calories 7.87 g of protein 43.06 g of fat 46.36 g of carbohydrates 11.00 g of dietary fiber 24.23 g of sugar 12.02 milligrams (mg) of iron 230.00 mg of magnesium 3.34 mg of zinc Risks and considerations The health benefits of dark chocolate come primarily from the flavanols present in the cacao solids. However, flavanol content varies among dark chocolate products. Processing methods also differ between manufacturers, and this can affect the flavanol content of the chocolate. There is no legal requirement for chocolate manufacturers to report the flavanol content in their products. However, dark chocolate products with a higher percentage of cacao solids should generally contain more flavanols. Although dark chocolate contains beneficial antioxidants and minerals, it is usually also high in sugar and fat, which makes it a very calorie-dense food. Dark chocolate contains fat in the form of cocoa butter, which mainly consists of unhealthful saturated fats. People should, therefore, try to limit their consumption of dark chocolate to avoid consuming too many calories, fats, and sugars. In general, dark chocolate contains less sugar than milk chocolate and white chocolate. Dark chocolate with higher percentages of cacao solids typically contains even less sugar. Sugar content varies among chocolate manufacturers, so it is advisable to check the nutrition label. How much to eat? Chocolate manufacturers do not have to report the flavanol content of their products. As a result, it is difficult to know how much dark chocolate a person would need to eat to maximize its health benefits. The studies in this article generally used 20–30 g of dark chocolate per day. Dark chocolate with higher percentages of cacao solids typically contains less sugar but more fat. More cacao also means more flavanols, so it is best to choose dark chocolate that includes at least 70 percent cacao solids. Thank you for supporting Medical News Today Summary Dark chocolate is a rich source of antioxidants and minerals, and it generally contains less sugar than milk chocolate. Some research suggests that dark chocolate may help lower the risk of heart disease, reduce inflammation and insulin resistance, and improve brain function. People who are interested in adding dark chocolate to their diet should keep in mind that it is high in fat and calories, so moderation is key.
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Heart disease and depression: Scientists find missing link

Researchers already recognized the link between depression and heart disease. However, until recently, the mechanisms explaining it remained a mystery. A new study reveals that stress-induced inflammation may explain why mental and cardiovascular health are so intimately related.
senior man having his heart examined by doctor
Why are people with depression more likely to have heart disease?

Heart disease is now the leading cause of death both in the United States and worldwide.

Depression, meanwhile, is the "leading cause of disability worldwide," as well as one of the most common mental health conditions in the U.S.

A significant body of research has established a connection between the two conditions.

For example, reviews of existing studies have shown that people with cardiovascular disease are more likely to have depression, and people with depression have a higher risk of developing cardiovascular disease.

Also, those with depression and heart disease are more likely to die from the latter than those who only have heart disease. This relationship is also proportional, meaning that the more severe the depression, the more likely it is that a person will develop heart disease or die from it.

What explains this link? Researchers from the University of Cambridge in the United Kingdom set out to investigate. Golam Khandaker, a Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge, led the new research with his colleague Stephen Burgess.

The researchers published their findings in the journal Molecular Psychiatry.

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Studying heart disease and depression risk

The team examined data on almost 370,000 people aged 40–69. The data were readily available in the UK Biobank database.

They first wanted to see whether having a family history of coronary heart disease also increased the risk of major depression, and they found that it did.

In fact, people who had lost at least one parent to heart disease had a 20 percent higher risk of depression.

Next, the scientists wondered whether genes determined this link. They calculated the genetic risk score for coronary heart disease but found no connection between the genetic predisposition to develop heart disease and the risk of depression.

This suggested to the scientists that depression and heart disease do not share a common genetic predisposition. Instead, they wondered whether there were any environmental factors that may raise the risk of developing both conditions.

To find out, they applied a statistical tool called Mendelian randomization to examine 15 biological markers, or biomarkers, that may affect heart disease risk.

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Scientists use this technique "to assess the causality of an observed association between a [...] risk factor and a clinically relevant outcome."

Their analysis revealed three biomarkers for the risk of heart disease that were also depression risk factors: triglycerides and the inflammation-related proteins IL-6 and CRP.

The scientists explain that our bodies produce the inflammation proteins IL-6 and CRP in response to physiological factors such as infections and lifestyle factors such as smoking, drinking, and physical inactivity, as well as in response to psychological stress.

High inflammation markers are often present in treatment-resistant depression, and high levels of IL-6 and CRP in particular often characterize acute depressive episodes.

Also, previous studies the researchers cited have shown that people with high levels of IL-6 and CRP are more likely to develop depression.

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Inflammation may explain link

"It is possible," Khandaker points out, "that heart disease and depression share common underlying biological mechanisms, which manifest as two different conditions in two different organs — the cardiovascular system and the brain."

"Our work suggests that inflammation could be a shared mechanism for these conditions."

Golam Khandaker

However, the researchers caution that more work is now necessary. They also note that the role of triglycerides in depression risk has yet to be understood.

"Although we don't know what the shared mechanisms between these diseases are, we now have clues to work with that point toward the involvement of the immune system," says Burgess.

"Identifying genetic variants that regulate modifiable risk factors," he goes on, "helps to find what is actually driving disease risk."

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Higher cholesterol, egg consumption linked to heart disease

A recent study has linked higher consumption of eggs or dietary cholesterol to a higher risk of cardiovascular disease and premature death. The finding is likely to rekindle the debate on eggs and heart health.
close-up of hands preparing eggs in a pan
New research suggests that people should restrict their daily egg intake as part of a healthful diet.

For example, the new study seems to contradict the decision in the United States to omit specific limits on daily intakes of dietary cholesterol and eggs from official advice on healthful eating.

Researchers from Northwestern University Feinberg School of Medicine in Chicago, IL, and other institutions pooled and analyzed data from six U.S. cohort studies covering a total of 29,615 people. Of these, 45 percent were male and 31 percent were black.

They compared eating patterns at baseline, when the average participant age was 52 years, with cardiovascular diseases and deaths that occurred during a follow-up that lasted up to 31 years and whose midpoint was 17 years.

The team describes the findings in a JAMA paper.

Co-corresponding study author Norrina B. Allen Ph.D., an associate professor of preventive medicine at Northwestern, says that the "take-home message" of the study "is really about cholesterol, which happens to be high in eggs and specifically yolks."

"People who consume less cholesterol have a lower risk of heart disease," she adds.

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Guidelines do not limit cholesterol or eggs

According to the Centers for Disease Control and Prevention (CDC), heart disease is the "leading cause of death" in the U.S.

For decades there has been a debate about whether consumption of eggs or dietary cholesterol raises the risk of heart disease and early death.

The official recommendation in the U.S. before 2015 was that people should limit their daily egg consumption to no more than 300 milligrams (mg), which is less than two large eggs.

The more recent Dietary Guidelines for Americans 2015–2020, however, no longer provide limits on dietary cholesterol and egg intake. They include weekly intake of eggs as part of a healthful diet.

"Adequate evidence," they claim, "is not available for a quantitative limit for dietary cholesterol specific to the Dietary Guidelines."

The revised guidelines do, however, retain the message that the choice to drop specific limits does "not suggest that dietary cholesterol is no longer important to consider when building health[ful] eating patterns."

Only foods of animal origin — including dairy products, eggs, shellfish, poultry, and meat — contain dietary cholesterol.

Of the foods most typical of the U.S. diet, eggs contain the most cholesterol. There are around 186 mg of cholesterol in the yolk of a large egg.

The average U.S. adult consumes about 300 mg of dietary cholesterol per day and about three or four eggs per week.

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Higher risk of heart disease and death

Dr. Allen believes that the problem with studies that have found no links between egg consumption and higher risk of cardiovascular disease is that they used less diverse samples and shorter follow-ups, and that they were less able to adjust for other items in the diet.

"Our study," she notes, "showed if two people had [the] exact same diet and the only difference in diet was eggs, then you could directly measure the effect of the egg consumption on heart disease."

The dietary data for the new study came either from completion of questionnaires or interviews that took place during a single visit. These yielded details of what each person had eaten either in the previous year or month.

Around 5,400 cardiovascular events and 6,132 deaths from all causes occurred over the follow-up period. Examples of cardiovascular events include diagnoses of heart disease, stroke, and heart failure.

The scientists found that for "each additional" intake of 300 mg of dietary cholesterol per day, there was a significant 17 percent higher risk of cardiovascular disease and 18 percent higher risk of death from any cause.

The team also calculated the "absolute risk differences" for these results. These were 3.24 percent and 4.43 percent, respectively.

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In other words, for every 1,000 participants in their study, there were 32 additional diagnoses of cardiovascular disease and 4 deaths for every extra 300 mg of cholesterol consumed per day.

The analysis also showed that for each additional half egg eaten per day, there was a 6 percent higher risk of cardiovascular disease and an 8 percent higher risk of all-cause death.

The overall quality of people's diet, the type and amount of fat that they ate, and the amount of exercise that they undertook appeared to have no effect on these links.

"These results," explain the study authors, "should be considered in the development of dietary guidelines and updates."

Single snapshot of diet pattern

Among the study's strengths are the fact that it used a large and diverse sample of people from the U.S., and that there was a long follow-up period.

However, one limitation worth noting is that it only used a single snapshot of egg and cholesterol consumption, and that was at the beginning of the follow-up. People can change their eating habits, and 17–31 years offers plenty of opportunity to do so.

Commenting on the findings, Tom Sanders — who is a professor of nutrition and dietetics at King's College London in the United Kingdom — points out that because the study is prospective, it cannot establish cause and effect; it can only suggest links.

"However," he adds, "the take-home message supported by the accompanying editorial would support the view that a typical [U.S.] diet, which contains lots of meat and plenty of eggs, is associated with poor cardiovascular health and that the [country's] dietary guidelines should reinstate its recommendation that cholesterol intake should not exceed 300 mg per day."

"As part of a healthy diet, people need to consume lower amounts of cholesterol."

Norrina B. Allen Ph.D.

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Common blood pressure drug may increase cardiac arrest risk

A preliminary study concludes that a drug that doctors commonly prescribe to treat angina and blood pressure might increase the risk of sudden cardiac arrest.
Woman with chest pain sitting on a bench
A recent study looked at the risk factors behind cardiac arrest.

Cardiac arrest occurs when the heart stops pumping blood around the body. If a person does not receive treatment, cardiac arrest can be lethal within minutes.

According to the American Heart Association (AHA), in the United States, around 475,000 people die from cardiac arrest each year.

It claims more lives than colorectal cancer, breast cancer, prostate cancer, pneumonia, influenza, vehicle accidents, firearms, HIV, and house fires combined.

The AHA describe cardiac arrest "as one of the most lethal public health problems in the U.S." So, because cardiac arrest is both serious and common, understanding the risk factors involved is essential.

To this end, the European Resuscitation Council set up a project that collects data on cardiac arrest, called the European Sudden Cardiac Arrest network (ESCAPE-NET).

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A new risk factor?

A recent study using ESCAPE-NET data investigated whether a common group of drugs might play a role in cardiac arrest.

Healthcare providers use dihydropyridines to treat high blood pressure and angina, which is chest pain related to reduced blood flow to the heart. The project focused on two dihydropyridines: nifedipine and amlodipine.

The scientists had access to data from the Dutch Amsterdam Resuscitation Studies registry and the Danish Cardiac Arrest Registry, both of which form part of ESCAPE-NET.

The researchers presented their findings at EHRA 2019, the annual congress of the European Heart Rhythm Association, which is taking place in Lisbon, Portugal.

In total, they had access to data from more than 10,000 people who were taking dihydropyridines and 50,000 controls.

Their analysis showed that those who took high-dose nifedipine were significantly more likely to have an out-of-hospital cardiac arrest than those who were not taking dihydropyridines or who were taking amlodipine.

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Why might this be happening?

The scientists moved into the laboratory to examine why the actions of the two drugs differed. Both use the same mechanism, so why does one increase the risk of cardiac arrest while the other appears to make no difference?

Dihydropyridines work by blocking L-type calcium channels. When these channels are blocked, the action potential of cardiac cells becomes shorter.

The phrase "action potential" describes a change in the charge of a membrane associated with the transmission of an impulse. They occur in nerves and muscle cells.

This change could, potentially, drive the arrhythmias that lead to cardiac arrests.

Interestingly, these in vitro experiments matched the findings of the population study. High doses of nifedipine shortened action potentials significantly more than high-dose amlodipine.

"Nifedipine and amlodipine are often used by many cardiologists and other physicians, and the choice often depends on the prescriber's preference and personal experience."

ESCAPE-NET project leader Dr. Hanno Tan

Dr. Tan adds, "Both drugs are generally considered to be equally effective and safe and neither has been associated with sudden cardiac arrest."

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"This study suggests that high-dose nifedipine may increase the risk of sudden cardiac arrest due to fatal cardiac arrhythmia while amlodipine does not."

It is important to note that because this is a new line of investigation, it will be vital to replicate the findings using more participants and other demographics.

As Dr. Tan concludes, "If these findings are confirmed in other studies, they may have to be taken into account when the use of either drug is considered."

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Heart failure: New drug could halt disease and improve heart function

Heart failure occurs when the heart loses its ability to pump blood effectively. Current treatments can slow or stop the disease getting worse, but they can't regress it. Now, scientists have designed a molecule that could not only curb heart failure but also improve the heart's blood pumping ability.
a scientist designs a new molecule to treat heart failure
A new molecule could help prevent heart failure.

The researchers in Brazil and the United States who developed and tested the experimental drug have named it "SAMβA," which is short for "selective antagonist of mitofusin 1-β2PKC association."

When the researchers gave it to rats with heart failure, the molecule not only stopped the disease from progressing but also reduced its severity by improving the ability of heart muscle to contract.

The journal Nature Communications has now published a paper on how the researchers developed SAMβA and tested it on heart cells and rodent models of heart failure.

"The drugs in current use," says first study author Julio C. B. Ferreira, who is a professor in the Biomedical Science Institute at the University of São Paulo in Brazil, "halt [the] progression of the disease but never make it regress."

SAMβA works by blocking a specific interaction between the proteins mitofusin 1 (Mfn1) and beta II protein kinase C (β2PKC) whose association impairs mitochondria in heart muscle cells, causing the cells to die. Mitochondria are tiny compartments inside cell bodies that make the chemical energy cells need to function and live.

"We showed that by regulating this specific interaction, we could both halt [the] progression and make the disease regress to a less severe stage," Prof. Ferreira explains.

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Heart failure and causes

According to the most recent figures from the Centers for Disease Control and Prevention (CDC), in 2016 there were around 5.7 million people in the United States living with heart failure.

The body's organs and tissues require a constant supply of oxygen- and nutrient-rich blood to function and stay in good health.

Heart failure arises when the heart's ability to pump blood does not match the body's needs.

In a healthy heart, the heart muscle contracts and pumps freshly oxygenated blood into the aorta from where it travels to the rest of the body.

In a person with heart failure, the heart muscle is weak or damaged and does not fully contract, leaving some blood left to pool inside the organ.

People with heart failure often feel tired and fatigued and may experience shortness of breath as they go about their everyday lives. They can also struggle to breathe when they lie down, and they can put on weight due to swelling in the stomach, ankles, feet, or legs.

The most common causes of heart failure are diseases and conditions that weaken or damage the heart. These include coronary artery disease, heart attacks, high blood pressure, and diabetes.

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SAMβA 'is selective'

Failing hearts overproduce the protein β2PKC. Previous work by some of the researchers in Brazil had shown that blocking the protein improved heart function in people with heart failure.

However, while the β2PKC inhibitor that they used improved heart function, it also stopped the protein from doing other things that help the heart.

What the new study shows is that SAMβA "is more selective." It only blocks one specific interaction, and that is the one that β2PKC has with Mfn1 — the one that affects the function of mitochondria. It does not affect β2PKC's other interactions.

To show this, the team carried out a series of tests in cells, rodents, and samples of heart tissue from people with heart failure.

It reveals that β2PKC builds up on the outer wall of mitochondria and chemically alters the function of Mfn1 by adding a phosphate group to it. This leads to "buildup of fragmented and dysfunctional mitochondria in heart failure," note the study authors.

Scientists call the process through which β2PKC alters Mfn1 phosphorylation, and it is one of the "most common" mechanisms in cells for altering the function of proteins.

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The team experimented with various compounds to find candidate molecules that could block this interaction between β2PKC and Mfn1 to prevent the ensuing damage to mitochondria.

They identified six molecules that could block the β2PKC-Mfn1 interaction, but of these, only SAMβA did it in a way that did not affect β2PKC's other interactions.

Tests using human heart cells showed that, like the drugs already in use for the treatment of heart failure, SAMβA could curb the progression of the disease.

However, unlike conventional treatments, many of which have been around since the 1980s, SAMβA went a step further: it enhanced the ability of heart cells to contract, which is essential for effective pumping of blood.

The researchers observed that SAMβA also reduced a marker of oxidative stress in the heart cells. Oxidative stress can trigger cell death if the cell cannot defend itself against it.

In a final set of tests, the team induced heart failure in rats by provoking a heart attack. Unlike the rats that received a placebo, those that received SAMβA stopped showing signs of heart failure and showed improvement in heart function.

To make progress toward a clinical treatment, other teams now need to test the molecule independently. There is also a need to check its compatibility with other heart failure drugs.

"Validation and reproduction of our findings by other groups are critical to the process of developing SAMβA for use in treating heart failure. We will be seeking partners in the private and public sectors for this purpose."

Prof. Julio C. B. Ferreira

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