Medical News Today: Colorectal cancer: The importance of diet

Colorectal cancer is quite common, especially among the aging population. An important risk factor for colorectal cancer is diet, and dietary choices are also vital during and after treatment. In this Spotlight, we give you an overview of which diets are best, and which are best avoided.
colorful fruit and veg
What does a good diet for preventing colorectal cancer and for aiding cancer treatment look like?

Colorectal cancer is a type of cancer that affects a person’s rectum, colon, or both. This is also known as the large intestine.

According to the American Cancer Society (ACS), 2018 could bring around 97,220 new diagnoses of colon cancer and 43,030 new cases of rectal cancer to the United States.

This type of cancer is more likely to appear in older individuals, but there are many other risk factors associated with its emergence, such as genetic and lifestyle factors.

Of the latter, one of the most cited risk factors is diet — referring specifically to poor dietary habits that often also lead to obesity.

Below, we look at which foods and nutrients have been said to raise the risk of colorectal cancer, and which types of diet have been deemed helpful in its prevention.

We also cover the diets most likely to keep the body resilient during and after treatment for this type of cancer.

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Prevention: What to avoid

Numerous studies have indicated that a diet too rich in red meat is associated with a heightened risk of colorectal cancer. “Red meat” is defined by the World Health Organization (WHO) as “all mammalian muscle meat, including beef, veal, pork, lamb, mutton, horse, and goat.”

A review of the evidence supporting this link notes that “consumption of red meat might be related directly to the incidence of [colorectal cancer] or indirectly because a diet high in meat tends to be low in vegetables, fruit, and fiber.”

red meat
Eating a lot of red meat is known to significantly increase the risk of colorectal cancer.

A study of North Italian populations showed that individuals who eat red meat alongside eggs, cheese, and other fatty foods — as well as refined starches — on a frequent basis had an almost twice higher risk of developing rectal or colon cancer than their peers who favored a plant-based diet.

More recent research also revealed that “a daily increase of 100 [grams] of all meat or red meat is associated with a significant 12–17 percent increased risk of colorectal cancer.”

In 2015, a report published by the International Agency for Research on Cancer made the news by pointing out that every 50-gram portion of processed meat, such as bacon or salami, eaten every day increases a person’s risk of developing colorectal cancer by 18 percent.

This evidence led the WHO to classify processed meats as “carcinogenic to humans.”

The damage caused by unwholesome diets made the headlines again in early 2018, when a study published in The BMJ reported that “ultra-processed foods” might increase the risk of developing various types of cancer.

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Prevention: What to eat

So, if a high intake of red meat and processed foods contributes to the risk of colorectal cancer, what should be eaten to protect our bodies from this outcome?

According to the ACS, a diet high in fruits, vegetables, and fibers could help to minimize the risk, and many existing studies seem to support this advice.

A study from the Loma Linda University in California found that vegetarian-style diets are linked to a decreased risk of colorectal cancer. The researchers studied four types of plant-based diet. These were:

colorful salad
In order to reduce the risk of colorectal cancer, eat a healthful diet that favors fruit and veg.
  • vegan, or strictly no products of animal origin
  • lacto-ovo vegetarian, which includes dairy and eggs but no meat
  • pescovegetarian, which includes fish but no meat
  • semivegetarian, which includes meat and fish infrequently

All four of these plant-based diets were deemed to be less likely to lead to cancer than non-vegetarian diets.

One study from last year also suggests that the more colorful your meal the better, and that individuals should focus on integrating a rainbow of fruit and vegetables into their diets.

More specifically, their experiments on the pig model — which provides the closest resemblance to the human body in terms of metabolic processes — indicated that purple potatoes might protect against colon cancer.

That may be because these root vegetables contain compounds that reduce levels of certain pro-inflammatory proteins in the body, and inflammation is known to contribute to colon cancer risk.

Recently, researchers have also isolated a number of elements typical of Mediterranean-style diets that could help to prevent the onset of colorectal cancer.

People with a low risk of developing this condition ate plenty of fruits, vegetables, nuts, and whole grains, as well as fish and poultry, rather than red meat, and they drank little alcohol and soft drinks.

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What to eat during and after treatment

According to guidelines from the Dana-Farber Cancer Institute in Boston, MA, people undergoing treatment for colorectal cancer should also favor the “rainbow plate” meals and eat a varied array of fruits and vegetables to support their immune system.

Eating small but frequent portions is another approach that specialists at the Dana-Farber Institute suggest that people following treatment may find useful.

bowl of tree nuts
A diet rich in tree nuts could improve the outcomes of cancer treatment.

They advise patients to stay hydrated and avoid alcohol and caffeine, explaining that some types of medication may clash with these beverages.

But a previous study conducted by researchers at the Institute — which we covered on Medical News Today — indicated that those undergoing treatment for colorectal cancer had an almost halved risk of cancer recurrence if they drank four cups of coffee, or 460 milligrams of caffeine, per day.

As lead study author Charles Fuchs explains, “We found that coffee drinkers had a lower risk of the cancer coming back and a significantly greater survival and chance of a cure.”

Research published last year in JAMA Oncology suggests that a diet high in sources of fiber may improve survival rates for patients with stage one colorectal cancer. Eating whole grains was also linked to a better treatment outcome, the researchers noted.

Another study from last year notes that eating a minimum of 2 ounces (approximately 57 grams) of tree nuts — such as cashews, hazelnuts, walnuts, and pistachios — almost halved the risk of colon cancer recurrence for individuals following stage three cancer treatment. Tree nut consumption also reduced the risk of death following treatment by 53 percent.

As for the risk of developing a second cancer following treatment, the ACS say that it can be reduced by making the same healthful diet choices advised for the prevention of a first cancer. These include maintaining a healthy weight, placing “an emphasis on plant foods” in daily meals, and avoiding alcohol intake.

In fact, Dr. Victor Moreno — from the University of Barcelona in Spain — and colleagues found that lifestyle factors are more important than genetic risk factors when it comes to the development of colorectal cancer.

This is important, considering that lifestyle, unlike genetic traits, is somewhat modifiable.”

First study author Dr. Gemma Ibáñez

This suggests that a “revamp” of personal health choices may go a long way toward supporting positive outcomes.

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Medical News Today: Adult brains make no new ‘memory’ cells

New research led by the University of California, San Francisco suggests that the human hippocampus, or the brain region that is important for memory and learning, stops making new cells in childhood.
vibrant brain cell
Researchers find that the hippocampus produces no new brain cells after childhood.

The findings, which have been published in the journal Nature, are likely to fan the flames of an already heated debate about the human brain’s capacity to heal itself through “neurogenesis,” or the birth of new brain cells.

“We find,” explains Arturo Alvarez-Buylla, who is a professor of neurological surgery working at the University of California, San Francisco (UCSF) and the head of the laboratory behind the study, “that if neurogenesis occurs in the adult hippocampus in humans, it is an extremely rare phenomenon, raising questions about its contribution to brain repair or normal brain function.”

The study challenges a growing body of evidence that suggests that it may be possible to treat brain-wasting disorders such as Alzheimer’s disease by promoting neurogenesis to replenish the brain cells, or neurons, that are destroyed by disease.

However, the undaunted authors point instead to the new questions that their findings raise, such as how does the human brain adapt and learn if it cannot make new neurons?

Perhaps the answers to this question will open an even better path to new treatments for brain diseases, they suggest.

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Doubts about neurogenesis in humans

Over the past 30 years, Prof. Alvarez-Buylla and his team have been finding increasing evidence that the brains of songbirds and rodents can make new neurons throughout their lives. However, more recently, they have begun to question whether this is true of the human brain.

For example, the UCSF group has cast doubt on whether neurogenesis in the olfactory bulb — which is an ancient part of the brain that is important for sensing odors — continues into adulthood in humans as it does in rodents.

For their new study, Prof. Alvarez-Buylla and collegues analyzed 59 human hippocampus samples collected from China, Spain, and the United States.

Some of the tissue samples — which ranged from before birth into adulthood — were taken from postmortems, while others were retrieved during surgery on epilepsy patients.

The team carefully analyzed the samples to look for changes in new neurons and stem cells over the lifespan. They focused on an area known as the dentate gyrus, a “simple cortical region” that forms an integral part of the hippocampus and is important for memory formation.

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No evidence of neurogenesis in adult tissue

The researchers found prolific evidence of neurogenesis occurring before birth and right after it. They calculated that the average number of new neurons per square millimeter of dentate gyrus tissue in newborns was 1,618.

However, neurogenesis fell sharply after birth: the number of new neurons per square millimeter had reduced fivefold by age 1.

The evidence also revealed that the decline continued through childhood: there was a 23-fold decrease between the ages of 1 and 7 years, and another fivefold reduction by the age of 13.

At this point, by early adolescence, the concentration of new neurons per square millimeter of brain tissue had fallen to just 2.4.

The researchers found no evidence of neurogenesis in adult dentate gyrus tissue — in neither the 17 postmortem samples nor in those retrieved from 12 adult epilepsy patients.

“In young children,” says Mercedes Paredes, an assistant professor of neurology at UCSF and who co-led the tissue analysis, “we were able to see that substantial numbers of new neurons continue to be made and integrated into the dentate gyrus, but neurogenesis fades away completely by early adolescence.”

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Neurogenesis and hippocampal plasticity

When they analyzed the neural stem cells — which are the precursor cells that spawn new neurons — the researchers discovered that they, too, were abundant in the brain before birth, but by early childhood, they had almost disappeared.

They also found no evidence of early accumulation of neural stem cells in the subgranular zone of the human dentate gyrus.

This is in contrast to mice, where this early concentration does happen. The team suggests that this means that it might be a necessary step for neurogenesis to continue into adulthood.

In conclusion, the investigators accept that, while they searched extensively, they cannot say for certain that the adult human hippocampus never makes new neurons.

“But,” says Dr. Shawn Sorrells, who is a senior researcher in Prof. Alvarez-Buylla’s group, “I think that we need to step back and ask what that means.”

If neurogenesis is so rare that we can’t detect it, can it really be playing a major role in plasticity or learning and memory in the hippocampus?”

Dr. Shawn Sorrells

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Medical News Today: Can you learn in your sleep? Yes, and here’s how

Sleep is known to be crucial for learning and memory formation. What’s more, scientists have even managed to pick out specific memories and consolidate them during sleep. However, the exact mechanisms behind this were unknown — until now.
woman asleep surrounded by books
We may one day be able to induce brain waves that will enable us to learn in our sleep.

Those among us who grew up with the popular cartoon “Dexter’s Laboratory” might remember the famous episode wherein Dexter’s trying to learn French overnight.

He creates a device that helps him to learn in his sleep by playing French phrases to him.

Of course, since the show is a comedy, Dexter’s record gets stuck on the phrase “Omelette du fromage” and the next day he’s incapable of saying anything else.

This is, of course, a problem that puts him through a series of hilarious situations.

The idea that we can learn in our sleep has captivated the minds of artists and scientists alike; the possibility that one day we could all drastically improve our productivity by learning in our sleep is very appealing. But could such a scenario ever become a reality?

New research seems to suggest so, and scientists in general are moving closer to understanding precisely what goes on in the brain when we sleep and how the restful state affects learning and memory formation.

For instance, previous studies have shown that non-rapid eye movement (non-REM) sleep — or dreamless sleep — is crucial for consolidating memories.

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It has also been shown that sleep spindles, or sudden spikes in oscillatory brain activity that can be seen on an electroencephalogram (EEG) during the second stage of non-REM sleep, are key for this memory consolidation.

Scientists were also able to specifically target certain memories and reactivate, or strengthen, them by using auditory cues.

However, the mechanism behind such achievements remained mysterious until now. Researchers were also unaware if such mechanisms would help with memorizing new information.

Therefore, a team of researchers set out to investigate. Scott Cairney, from the University of York in the United Kingdom, co-led the research with Bernhard Staresina, who works at the University of Birmingham, also in the U.K.

Their findings were published in the journal Current Biology.

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Sleep spindles key for memory consolidation

Cairney explains the motivation for the research, saying, “We are quite certain that memories are reactivated in the brain during sleep, but we don’t know the neural processes that underpin this phenomenon.”

“Sleep spindles,” he continues, “have been linked to the benefits of sleep for memory in previous research, so we wanted to investigate whether these brain waves mediate reactivation.”

“If they support memory reactivation, we further reasoned that it could be possible to decipher memory signals at the time that these spindles took place.”

To test their hypotheses, Cairney and his colleagues asked 46 participants “to learn associations between words and pictures of objects or scenes before a nap.”

Afterward, some of the participants took a 90-minute nap, whereas others stayed awake. To those who napped, “Half of the words were […] replayed during the nap to trigger the reactivation of the newly learned picture memories,” explains Cairney.

“When the participants woke after a good period of sleep,” he says, “we presented them again with the words and asked them to recall the object and scene pictures.”

“We found that their memory was better for the pictures that were connected to the words that were presented in sleep, compared to those words that weren’t,” Cairney reports.

Using an EEG machine, the researchers were also able to see that playing the associated words to reactivate memories triggered sleep spindles in the participants’ brains.

More specifically, the EEG sleep spindle patterns “told” the researchers whether the participants were processing memories related to objects or memories related to scenes.

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How to boost memory while we sleep

“Our data suggest that spindles facilitate processing of relevant memory features during sleep and that this process boosts memory consolidation,” says Staresina.

“While it has been shown previously,” he continues, “that targeted memory reactivation can boost memory consolidation during sleep, we now show that sleep spindles might represent the key underlying mechanism.”

Cairney adds, “When you are awake you learn new things, but when you are asleep you refine them, making it easier to retrieve them and apply them correctly when you need them the most. This is important for how we learn but also for how we might help retain healthy brain functions.”

Staresina suggests that this newly gained knowledge could lead to effective strategies for boosting memory while sleeping.

Direct induction of sleep spindles — for example, by stimulating the brain with electrodes — perhaps combined with targeted memory reactivation, may enable us to further improve memory performance while we sleep.”

Bernhard Staresina

So, though learning things from scratch à la “Dexter’s Lab” may take a while to become a reality, we can safely say that our brains continue to learn while we sleep, and that researchers just got a lot closer to understanding why this happens.

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Medical News Today: Vitamin D may protect against cancer

Researchers provide further evidence that vitamin D may protect against cancer, after finding that people from Japan had a lower risk of the disease when they had higher levels of the “sunshine vitamin.”
vitamin D on sand with sunglasses
Researchers suggest that a higher vitamin D level could protect against cancer.

The results of the study — which is one of the first to investigate the link between vitamin D levels and cancer risk in an Asian population — were recently published in The BMJ.

The research was conducted by Taiki Yamaji, of the Center for Public Health Sciences of the National Cancer Center in Japan, and her colleagues.

Vitamin D is an essential vitamin for our bodies. It not only helps to maintain calcium levels for good bone health; it also plays significant roles in immune system functioning, neuronal communication, and muscle functioning.

The National Institutes of Health (NIH) say that adults should aim to get around 600 International Units of vitamin D every day.

The body’s main source of vitamin D is sunlight, which is why it is often referred to as the “sunshine vitamin.” We can also get vitamin D from certain foods, including salmon, tuna, and cheese, as well as from dietary supplements, which are available to purchase online.

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Previous research has suggested that low vitamin D levels are a risk factor for certain cancer types, and that increasing levels of the vitamin could help to protect against the disease.

However, Yamaji and colleagues point out that most research on vitamin D and cancer risk to date has focused on white populations.

“Given that vitamin D concentrations and metabolism vary substantially by race/ethnicity,” note the researchers, “whether similar associations would also be observed in non-Caucasian populations remains to be clarified.”

With this in mind, the researchers sought to determine how vitamin D levels influence the risk of cancer in Japanese adults.

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Overall cancer risk reduced by a fifth

The researchers analyzed the data of 33,736 Japanese people who were a part of the Japan Public Health Center-based Prospective Study. They were between the ages of 40 and 69, and they were followed-up for an average of 16 years.

Blood samples were taken from each participant at study baseline. These were assessed for levels of 25-hydroxyvitamin D, which is the circulating form of vitamin D.

The participants were divided into four groups based on their vitamin D levels, ranging from the lowest to highest.

Information was also gathered on the subjects’ medical history, as well as on their dietary and lifestyle factors.

Over the 16-year follow-up period, a total of 3,301 new cancer cases were identified among the study participants.

Compared with subjects who had the lowest vitamin D levels, those with a higher level had a 20 percent lower risk of cancer overall, the team reports.

This finding persisted after accounting for myriad possible confounding factors, including age, body mass index (BMI), levels of physical activity, smoking status, and alcohol intake.

On looking at specific cancers, the researchers found that a higher vitamin D level was associated with a 30–50 percent lower risk of liver cancer, with this reduced risk being more prominent in men.

Higher vitamin D levels were not linked to a lower risk of lung cancer or prostate cancer, the team reports, and no association was found between higher vitamin D levels and an increase in cancer risk.

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A possible ‘ceiling effect’

Yamaji and colleagues caution that their findings are solely observational, so no conclusions can be made about the link between vitamin D and cancer risk.

Furthermore, the study has some important limitations. For example, they point out that there were only a small number of organ-specific cancers included in their analysis.

Additionally, they note that it is possible that some cancer risk factors that were not accounted for in this study might have influenced the findings.

Still, the researchers say that their findings “support the hypothesis that vitamin D has protective effects against cancers at many sites.”

That being said, the results indicate that there is a “ceiling effect” for vitamin D and cancer risk. In other words, there is an optimal level of vitamin D that protects us against cancer, but going beyond this level offers no further benefit.

“Future studies are needed,” the researchers conclude, “to clarify the dose-response pattern and the optimal [vitamin D] concentrations for cancer prevention.”

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Medical News Today: How to cope with your food allergy

Every year, millions of people in the United States have allergic reactions to food. While some allergies cause minor symptoms, others result in severe reactions. We have researched the best ways to cope with living with food allergies.
food allergies written on a board surrounded by food
Steps can be taken to cut the risk of exposure to food allergens.

Food allergies affect around 4 percent of adults and 5 percent of children in the United States.

A food allergy occurs when the body’s immune system triggers an abnormal response to food.

Symptoms of allergic reaction to a specific food range from sneezing and nasal congestion to anaphylaxis.

Anaphylaxis is a potentially life-threatening response that impairs breathing and sends the body into a state of shock. Anaphylaxis to food leads to around 30,000 visits to the emergency room, 2,000 hospitalizations, and 150 deaths each year in the U.S.

There is currently no cure for food allergies, and avoiding the food to which you are allergic is the only way to prevent a reaction.

However, measures can be taken to reduce the risk of serious health consequences by avoiding food allergens and quickly recognizing and managing allergic reactions to food if they occur.

Here are Medical News Today‘s suggested tips and tools for living well with food allergies.

1. Read food labels

Reading food labels might seem like an obvious way to avoid foods that you are allergic to, but research has indicated that confusing food labels may put consumers with food allergies at an increased risk of facing an allergic reaction.

woman looking at a food label
Avoid foods that may contain the food allergen or are manufactured in the same facility as the allergen.

A study revealed that consumers with concerns about food allergies often misunderstand food labels about food allergen exposure that read “manufactured on shared equipment” or “may contain.”

Individuals with food allergies should stay away from food products with these labels to prevent a severe allergic reaction.

Yet, around 11 percent of the consumers surveyed purchased products with a “may contain” label and 40 percent bought foods with a “manufactured in a facility that also processes” statement on the label.

The Food Allergen Labeling and Consumer Protection Act of 2004 (FALCPA) is a law that requires that all food labels in the U.S. must list ingredients that may cause an allergic reaction.

Though there are at least 160 foods that can lead to allergic reactions in those with food allergies, the act applies to the eight most common allergenic foods that account for 90 percent of all food reactions.

The eight most allergenic foods include:

  • milk
  • eggs
  • fish
  • crustacean shellfish
  • tree nuts
  • peanuts
  • wheat
  • soybeans

The FALCPA enforces that any of these eight foods, or any ingredient that contains protein derived from them, are designated as a “major food allergen.”

Food allergens are identified on food labels in one of three ways:

  1. Ingredient name. For example, the allergen name “milk” may be included in the ingredient name “buttermilk.”
  2. Following the ingredient name. The food allergen may appear after the ingredient, such as “whey (milk),” “lecithin (soy),” and “flour (wheat).”
  3. After the ingredients list. A “contains” statement may appear next to the list of ingredients, such as “contains milk, soy, and wheat.”

The FALCPA’s labeling requirements only apply to foods that “may contain” an allergen and not to the potential presence of major food allergens due to cross-contact during manufacturing.

Including warning labels such as “may be prepared in a facility that also uses nuts” or “may contain trace amounts of nuts” is voluntary.

Always be cautious when buying products without labels — such as a cake from a pastry shop.

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2. Avoid cross-contact and cross-reactivity

Individuals with food allergies must be aware of the potential cross-contact of non-allergenic with allergenic foods, and cross-reactivity among related foods.


Cross-contact occurs when an allergen is unintentionally transferred from a food that contains the allergen to a food that does not contain the allergen.

a cheeseburger being flipped on a grill
Indirect cross-contact can occur when the same utensils used to flip a cheeseburger are used for a hamburger, for example.

Cross-contact could occur when an allergen is applied directly or indirectly to another food.

For example, direct cross-contact is removing cheese from a cheeseburger to make it a hamburger.

Indirect cross-contact would be using the same utensil to turn the hamburger that was used to flip a cheeseburger.

You can avoid cross-contact with the following tips:

Purge your kitchen. Remove all products that you can’t eat from your refrigerator, freezer, and pantry.

Clean all cooking apparatus, including cooking utensils, cookware, stovetop, and oven, with soap and water.

Organize separate food preparation areas if you are sharing a kitchen with roommates or family members who eat foods that you can’t.

Cook allergy-safe foods first if you are cooking a range of foods.

Cover allergy-safe foods to prevent them being spluttered with unsafe foods.

Thoroughly wash your hands with soap and water if you have handled a food allergen. Soap and water and commercial wipes will eliminate food allergens, but water alone or sanitizing gels won’t.

Scrub down tables and counters with soap and water after cooking every meal.

Never share food to ensure that cross-contact does not occur.

When dining out, be sure to discuss cross-contact and procedures for cooking meals that are allergen-free with restaurant personnel.


Cross-reactivity occurs when the proteins in one food are similar to the proteins in another. The immune system may identify the proteins as being the same and cause an allergic reaction.

Some people that are allergic to shellfish or finned fish may need to avoid eating foods from the entire food group due to high levels of cross-reactivity, while others will have an isolated food allergy — to just swordfish, for example.

The rate of cross-reactivity varies among the most common food allergens. The rate between cow’s milk and goat’s milk is a high 90 percent, for example, while the cross-reactivity between peanuts and other legumes is just 5 percent.

If you want to eat foods from the same food group as the food you are allergic to, you might want to consider trying a skin test or oral food challenge to evaluate whether the food may cause a reaction.

3. Recognize your symptoms

If you live with a food allergy, it is crucial that you learn to identify the signs and symptoms of an allergic reaction — particularly anaphylaxis. Being able to spot the early symptoms of a reaction could save your life.

woman with shortness of breath
Learn the early symptoms of an allergic reaction to ensure that you get treated quickly.

An allergic reaction to food can affect the body in the following ways:

  • skin — itching, redness, hives, red bumps, swelling under the skin, rash
  • eyes — itching, tears, redness, swelling around the eyes
  • upper respiratory — runny nose, sneezing, nasal congestion, hoarseness, dry cough, itching
  • lower respiratory — chest tightness, wheezing, shortness of breath, cough
  • mouth — swelling of tongue, palate, or lips, itching
  • gastrointestinal — nausea, reflux, vomiting, diarrhea, abdominal pain, bloody stools
  • cardiovascular — rapid or slow heartbeat, dizziness, fainting, low blood pressure, loss of consciousness
  • other — uterine contractions, sense of “impending doom”

Symptoms of anaphylaxis can be a challenge to recognize. If you’re experiencing any one of the three conditions listed below within minutes to several hours after food exposure, it is likely that you are facing an anaphylactic episode:

  1. Any symptoms that involve your skin, the moist mucosal tissue lining of your nose, mouth, or gastrointestinal tract, impaired breathing or a drop in blood pressure, confusion, or loss of consciousness.
  2. Two or more of the following symptoms: Hives, itchiness, swelling of the tongue or lips, trouble breathing, a drop in blood pressure, abdominal cramps, or vomiting.
  3. A drop in blood pressure that leads to weakness or fainting.

Anaphylaxis can occur as: a single reaction after exposure to allergenic food that improves with or without treatment; two reactions that occur between 8 and 72 hours apart; or a long-lasting reaction that may continue for hours or even days.

An intramuscular injection of epinephrine should be used to treat an anaphylactic reaction as soon as possible after it occurs.

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4. Prepare an emergency action plan

If you have a life-threatening food allergy, it is recommended that everyone you come into contact with knows what to do during an allergic reaction.

blackboard with prepared written in chalk
Be prepared and make sure that you have an anaphylaxis emergency action plan.

An anaphylaxis emergency action plan tells you, your family, friends, co-workers, school staff, or caregivers what to do if you have a severe allergic reaction.

You can download an anaphylaxis emergency action plan from the American Academy of Allergy, Asthma, and Immunology.

This is to be filled in and signed by a doctor. It provides details of your name, age, what you are allergic to, any drugs that you are taking, and a list of the symptoms of anaphylaxis.

Steps on what to do in the event of an allergic reaction — such as the dosage of EpiPen, when to call 911, and your emergency contacts details — are also included in the plan.

5. Know how to use an auto-injector

Anaphylaxis can be treated with epinephrine (also known as adrenaline). Epinephrine works best when injected within minutes of an allergic reaction and rapidly treats throat swelling, impaired breathing, and low blood pressure.

pack of two EpiPens
Learn how to use your epinephrine auto-injector before you have to use it for an allergic reaction.

It is essential that you, your family, teachers, or colleagues learn how to use an epinephrine auto-injector so there is no delay in you receiving the drug.

A delay in using epinephrine is linked with a decline in well-being and even death from anaphylaxis within 30–60 minutes.

Carry your epinephrine auto-injector with you at all times. Make sure that it is easily accessible and can be quickly located by others.

Each time that you receive a refill for your injector, you and a family member should always review the instructions. Instructions sometimes change and may differ between one auto-injector and another.

It can also be helpful to watch videos or view pictures of how to administer the prescribed auto-injector.

Use your epinephrine auto-injector immediately when having an allergic reaction if you have:

  • difficulty breathing
  • trouble swallowing
  • a tight throat
  • repetitive coughing
  • a weak pulse
  • hives, rashes, or swelling of the skin
  • vomiting, diarrhea, or abdominal pain

Once you have administered the epinephrine, call 911 and let the dispatcher know that epinephrine has been used and that more may need to be supplied by the emergency responders.

Make sure that you always wear a medical band or have an anaphylaxis wallet card that notes your allergy, name, and number of your emergency contact.

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Medical News Today: Boosting the brain’s immune cells may stop Alzheimer’s

The results of two new studies — both published in the journal Neuron — suggest that the brain’s immune cells may hold the key to future treatments for Alzheimer’s disease.
brain illustration<!--mce:protected %0A-->
Your brain contains immune cells called microglia, which can be boosted to clear up Alzheimer’s-related brain damage, suggests new research.

Alzheimer’s disease affects more than 5 million people in the United States, and the condition ranks as the 6th leading cause of death in the country.

Among a range of other hallmarks, Alzheimer’s is characterized by neurological damage that is thought to be caused by plaques from a “sticky” protein called beta-amyloid.

Beta-amyloid is normally found in the membrane around nerve cells, but when it clumps together into small lumps or plaques between neurons, it can stop them from communicating with each other and impair brain function.

For years, researchers have been trying to understand exactly how the production of beta-amyloid triggers the symptoms of Alzheimer’s disease. Some researchers have even tried to develop anti-beta-amyloid drugs, but clinical trials of these pharmacological interventions have largely proven unsuccessful.

Now, researchers led by Prof. Huaxi Xu — the director of the Neuroscience Initiative at the Sanford Burnham Prebys Medical Research Institute in La Jolla, CA — offer a potential new strategy for eradicating the excessive buildup of the brain protein.

Prof. Xu and his team studied the behavior of a triggering receptor found on a type of cell called microglia — or the immune cells of the central nervous system — in two mouse studies. Their findings can be accessed here.

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Helping immune cells to fight beta-amyloid

The receptor is called TREM2. As Prof. Xu explains, “Researchers have known that mutations in TREM2 significantly increase Alzheimer’s risk, indicating a fundamental role for this particular receptor in protecting the brain.”

But what the new research reveals is “specific details about how TREM2 works,” adds Prof. Xu. Specifically, the first study shows that amyloid beta binds to the receptor, triggering a chain reaction that may culminate with slowing down the progression of Alzheimer’s.

Once bound to the amyloid beta, the triggering receptor TREM2 then “tells” the immune cells to start breaking down and clearing out amyloid beta, “possibly slowing Alzheimer’s disease pathogenesis,” explains Prof. Xu.

The first study also demonstrates that TREM2 binds to so-called amyloid beta oligomers, which are molecular complexes that have been receiving more and more attention in specialist literature for their role in Alzheimer’s progression.

Also, the study showed that removing TREM2 in mice altogether interfered with the electrical currents that normally activate microglia.

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TREM2 may stop Alzheimer’s progression

The second study strengthened the findings of the first; it showed that “increasing TREM2 levels renders microglia more responsive and reduces Alzheimer’s disease symptoms,” says Prof. Xu.

More specifically, the researchers added TREM2 to mice that had been genetically modified to develop an aggressive form of Alzheimer’s.

More TREM2 signaling stopped the disease from advancing and even reversed some of the cognitive decline, the study authors report.

“These studies are important,” explains Prof. Xu, “because they show that in addition to rescuing the pathology associated with Alzheimer’s disease, we are able to reduce the behavioral deficits with TREM2.”

“To our knowledge,” he continues, “this provides convincing evidence that minimizing amyloid beta levels alleviates Alzheimer’s disease symptoms.” Prof. Xu also emphasizes that these findings offer a new therapeutic avenue.

Going after microglia, rather than amyloid beta generation, may be a new research avenue for Alzheimer’s disease […] We could use brain immune cells to solve what’s becoming a public health crisis.”

Prof. Huaxi Xu

However, he also cautions against potential pitfalls. “It could be beneficial in early stages to activate microglia to eat up amyloid beta […], but if you over-activate them, they may release an overabundance of cytokines (causing extensive inflammation) damaging healthy synaptic junctions as a side effect from over-activation.”

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Medical News Today: Antidepressants: Do they really work?

Recently, there has been one major health issue dominating the mainstream media: antidepressants. More specifically, do they actually work?
A bottle of pills spilling onto a table
Are antidepressants safe and effective? This question has been widely debated in recent years.

The global debate on this issue was kick-started earlier this year, when British author Johann Hari published his book, Lost Connections: Uncovering the Real Causes of Depression — and the Unexpected Solutions.

Hari used antidepressants for 13 years, starting when he was a teenager, and the new book is his attempt to answer some of the questions that had plagued him for years.

In particular, what causes depression? And, why did antidepressants not cure my depression?

Lost Connections was launched to a fanfare of endorsements from celebrities, including musicians Elton John and Brian Eno, political activist Naomi Klein, and even Hillary Clinton. It posed a radical question: “Is everything we know about depression wrong?” It suggested radical solutions.

For these reasons, the work immediately sparked controversy.

The antidepressant debate

Lost Connections surrounds the plentiful claims that antidepressants are mostly ineffective, that this ineffectiveness has been concealed by the pharmaceutical industry thanks to inefficient regulatory systems, and that the physiological mechanisms sometimes suggested as triggering depression are not supported by evidence.

“Telling people, as I was told by my doctor, that depression is caused by a problem in your brain is, firstly, untrue,” said Hari to The Guardian.

“[A]nd,” he adds, “it is also really problematic because it cuts people off from finding the real causes of their depression and anxiety. We’ve been telling ourselves this chemical story for 35 years and every year depression and anxiety gets worse.”

These claims alarmed health professionals and journalists, who are now concerned that the book will prompt mental health patients to stop taking their medication without consulting a doctor.

Meanwhile, others were more worried about the veracity of the claims that Hari used — particularly his soundbite that “between 65 and 80 percent of people on antidepressants are depressed again within a year” — and questioned whether they could be supported by peer-reviewed scientific papers.

Though Lost Connections has definitely struck a populist nerve, critics of Hari are quick to point out that this is only his second major work following a career-threatening plagiarism scandal in 2011, which forced him to withdraw from the public eye for an extended period.

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The Lancet review: The final word?

The debate raged on across social media and in countless editorial columns until last month, when the results of a 6-years-in-the-making systematic review assessing the efficacy of antidepressants was published in The Lancet.

The review assessed all of the scientific data — both published and unpublished — that researchers from Oxford University in the United Kingdom could find. This exhaustively researched analysis was interpreted by some commentators to be the final word on the antidepressant controversy.

For instance, Prof. Carmine Pariante — spokesperson for the Royal College of Psychiatrists in the U.K. — commented:

This meta-analysis finally puts to bed the controversy on antidepressants, clearly showing that these drugs do work in lifting mood and helping most people with depression.”

“Importantly,” Prof. Pariante adds, “the paper analyzes unpublished data held by pharmaceutical companies, and shows that the funding of studies by these companies does not influence the result, thus confirming that the clinical usefulness of these drugs is not affected by pharma-sponsored spin.”

The review does acknowledge that the short-term benefits of antidepressants are, on average, modest, but it concludes that all of the 21 antidepressants studied are more effective than placebo for the treatment of major depressive disorder in adults.

Some drugs were discovered to be more effective than others. Escitalopram (Lexapro), mirtazapine (Remeron), paroxetine (Paxil, Brisdelle, Pexeva), agomelatine (Valdoxan), and sertraline (Zoloft) all had a higher response rate and lower dropout rate than other antidepressants, the researchers report.

The paper’s authors draw particular attention to the global burden of depression; it affects around 350 million people and is becoming more common, with substantial increases in the number of depressed people since 1990 — which are thought to be driven by an expanding and aging population.

In the U.S. alone, the financial burden of depression comes in at $210 billion per year, comprising 50 percent workplace costs, 45 percent direct costs, and 5 percent suicide-related costs.

We don’t know how antidepressants work

Most of the antidepressants that were included the study belong to a class of drugs called selective serotonin reuptake inhibitors (SSRIs).

chemical formula for serotonin
It is believed that antidepressants work by boosting serotonin levels, but this has not been confirmed.

They are thought to work by raising levels of the neurotransmitter serotonin, but the researchers admit that evidence to support this mechanism of action is not definitive. Really, no one quite knows exactly how antidepressants work.

Serotonin has been linked to maintaining mood balance, appetite, and motor, cognitive, and autonomic functions.

Since the late 1980s, low serotonin levels were thought to be a main driver of depression. But this position has been questioned — and not just by Johann Hari.

In 2015, Medical News Today reported on an editorial published in The BMJ from a prominent critic of SSRIs called Prof. David Healy. He argued the idea that depression is caused by low levels of serotonin, and that SSRIs restore serotonin levels is a myth originating in pharma marketing.

The Oxford-based researchers argue that more research and newer, more precise antidepressants are required, admitting that the identification of new molecular targets has been made difficult precisely because of the lack of clear evidence on how antidepressants work.

The lack of research assessing the long-term use of these medicines has led to some concerns that antidepressants may contribute to unacceptably high health risks compared with their modest benefits.

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Can antidepressants raise early death risk?

Recently, MNT looked at a study suggesting that common antidepressants may drastically increase the risk of mortality.

a description of antidepressants and a person holding a pill
Research has suggested that antidepressants may increase the risk of premature death.

The team behind this study, at McMaster University in Ontario, Canada, conducted a meta-analysis of 16 studies involving a total of around 375,000 participants.

They found that people taking antidepressants have a 33 percent higher risk of premature death compared with people who aren’t.

In addition, people using antidepressants were found to be 14 percent more likely to have a stroke, heart attack, or other cardiovascular event.

The meta-analysis did not find a significant difference in outcomes between people taking SSRIs and those using tricyclics, an earlier generation of antidepressants.

However, as this research was an observational study, the scientists were unable to prove that antidepressants cause premature death; they could only record a link between the two.

Speaking to MNT, lead study author Marta Maslej speculated on possible mechanisms that could drive this association.

Antidepressants disrupt the functioning of monoamines (important biochemicals such as serotonin and dopamine), and these monoamines have important functions not only in the brain, but all over the body.”

Marta Maslej

“For example,” she added, “serotonin affects growth, reproduction, digestion, immune function, and many other processes, and it is found in almost every major organ.”

“Disrupting the functioning of serotonin can therefore have different adverse effects, which can contribute to a risk of death in many different ways.”

It is estimated that around 1 in 10 U.S. adults now take antidepressants, and with the incidence of depression on the rise, it seems unlikely that these numbers will reverse any time soon.

It is also unlikely that the intense debate over the role these medicines play in our society will die down or become any less controversial — despite the new data.

But one thing that all voices — from Hari to the research teams — in this debate firmly agree on is that if you are taking antidepressants and you are concerned about their effects, you should not stop taking them without consulting your doctor first.

Always speak to your doctor before making any changes to your medication.

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