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What is aspartame, the additive in your diet cola, which the WHO may declare as ‘possibly carcinogenic’?

The cancer research arm of the World Health Organisation (WHO) will list the popular sugar substitute aspartame as “possibly carcinogenic to humans”, the news agency Reuters reported on Thursday (June 29). The listing by the International Agency for Research on Cancer (IARC) is likely next month, the Reuters report said, quoting unnamed sources.

Aspartame is one of the world’s most common artificial sweeteners and is used in a wide range of diet soft drinks, sugar-free chewing gum, sugar-free ice-cream, sugar-free breakfast cereals, etc.

A number of studies have repeatedly said that aspartame does not pose a risk for cancer. The listing by WHO, if it comes, will break from those earlier findings, “pitting it against the food industry and regulators”, the Reuters report said.

What is this assessment by the WHO?

Two different WHO groups — IARC and the Joint Organization Expert Committee on Food Additives, or JECFA — are currently reviewing the safety of aspartame.

The IARC concluded a meeting in France last week, and JECFA was scheduled to meet from June 27 to July 6 to update its risk assessment of aspartame, including reviewing how much can be safely consumed, The Washington Post reported on June 22.

The result of both evaluations would be announced on July 14, The Post’s report said, and noted that “many in the nutrition world [were] predicting the WHO will convey new concerns about the sweetener”.

The Reuters report published on June 29 said the IARC ruling had been “finalised earlier this month”, based on a review of all published evidence.

It said that the IARC assessment “does not take into account how much of a product a person can safely consume”, and that “this advice for individuals comes from…[the] JECFA, alongside determinations from national regulators”.

And what exactly is aspartame?

Chemically, aspartame is a methyl ester of the dipeptide of two natural amino acids, L-aspartic acid and L-phenylalanine. It was discovered by James M Schlatter, a chemist at the American pharmaceutical company G D Searle & Co. (which is now a subsidiary of Pfizer) in 1965, apparently by accident, when, while researching an anti-ulcer drug, he happened to lick his finger and detected a sweet taste.

According to the US Food and Drug Administration (FDA), aspartame is about 200 times sweeter than table sugar — which makes aspartame far less sweet than other artificial sweeteners like advantame and neotame, but even then, 1 gram of aspartame has the sweetness intensity of roughly 2 teaspoons (about 8 g) of sugar.

Aspartame is preferred by people trying to cut calories or lose weight, or by diabetics, because while 2 teaspoons (8 g) of sugar provides about 32 kcals of energy, 1 g of aspartame is only 4 kcals.

It is often argued that a 12 fl oz (about 350 ml) can of regular cola contains about 10 teaspoonfuls of sugar, while the same quantity of diet cola containing aspartame has only 7 kcals. Indeed, cans/ bottles of diet fizzy drinks often say “zero sugar” or “zero calories” on the packaging.

Aspartame is present in several brands of artificial sweeteners, the most common of which in India are Equal and Sugar-Free Gold.

So is aspartame dangerous?

Over more than 40 years, aspartame has been one of the most widely studied and rigorously tested chemical additives in food, including for its possible links with cancer. More than 100 studies have found no evidence of harm caused by aspartame.

While doubts and concerns have continued to be raised by some critics and a few studies, there is a broad scientific consensus on the safety of aspartame for all groups of people except one — those suffering from phenylketonuria (PKU), a rare inherited disorder in which the patient does not have the enzyme that is needed to break down phenylalanine, one of the two amino acids in aspartame. Foods containing aspartame carry the warning “Not for phenylketonurics”.

The USFDA permitted the use of aspartame in food in 1981, and has reviewed the science of its safety five times since then, The Washington Post report said. Aspartame is also certified as safe for human consumption by the European Food Safety Authority (EFSA), national regulators in Japan, Australia, New Zealand, and Australia, and even the WHO’s JECFA. Around 100 countries around the world, including India, permit the use of aspartame.

The Reuters report noted that past IARC rulings have “raised concerns among consumers about their use, led to lawsuits, and pressured manufacturers to recreate recipes and swap to alternatives”. This, the report said, “has led to criticism that the IARC’s assessments can be confusing to the public.

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New Research Reveals That Junk Food May Disrupt Deep Sleep

Cant Sleep Insomnia Headache

A study by Uppsala University has found that consuming a diet high in junk food negatively impacts the quality of deep sleep. The researchers have hypothesized that dietary habits should potentially be considered important in conditions like insomnia and aging, which affect sleep quality.

Recent research conducted by Uppsala University examined the impact of junk food on sleep. In a randomized sequence, healthy individuals were given both healthier and less healthy diets. The results indicated a decline in the quality of deep sleep for those who consumed the less healthy diet when compared to those who followed a healthier diet.

The findings were recently published in the journal Obesity.

Several epidemiological studies have established a link between diet and alterations in our sleep patterns. However, the direct influence of diet on sleep has been explored by only a few studies. One way to do that is to have the same participant consume different diets in a randomized order.

Jonathan Cedernaes

Jonathan Cedernaes, MD Ph.D. and Associate Professor in Medical Cell Biology at Uppsala University. Credit: Antwon McMullen

“Both poor diet and poor sleep increase the risk of several public health conditions. As what we eat is so important for our health, we thought it would be interesting to investigate whether some of the health effects of different diets could involve changes to our sleep. In this context, so-called intervention studies have so far been lacking; studies designed to allow the mechanistic effect of different diets on sleep to be isolated,” says Jonathan Cedernaes, Physician and Associate Professor in Medical Cell Biology at Uppsala University.

Previous epidemiological studies have shown that diets with greater sugar content, for example, are linked to poorer sleep. Yet sleep is an interplay of different physiological states, as Cedernaes explains: “For example, deep sleep can be affected by what we eat. But no study had previously investigated what happens if we consume an unhealthy diet and then compared it to the quality of sleep after that same person follows a healthy diet. What is exciting in this context is that sleep is very dynamic. Our sleep consists of different stages with different functions, such as deep sleep which regulates hormonal release, for example.”

He adds, “Furthermore, each sleep stage is hallmarked by different types of electrical activity in the brain. This regulates aspects such as how restorative sleep is, and differs across different brain regions. But the depth or integrity of the sleep stages can also be negatively affected by factors such as insomnia and aging. Previously, it has not been investigated whether similar changes in our sleep stages can occur after exposure to different diets.”

Each study session involved several days of monitoring in a sleep laboratory. Therefore, only 15 individuals were included in the study. A total of 15 healthy normal-weight young men participated in two sessions. Participants were first screened for aspects such as their sleep habits, which had to be normal and within the recommended range (an average of seven to nine hours of sleep per night).

In random order, the participants were given both a healthier diet and an unhealthier diet. The two diets contained the same number of calories, adjusted to each individual’s daily requirements. Among other things, the unhealthier diet contained a higher content of sugar and saturated fat and more processed food items. The meals of each diet had to be consumed at individually adjusted times, which were matched across the two dietary conditions. Each diet was consumed for a week, while the participants’ sleep, activity, and meal schedules were monitored at an individual level.

After each diet, the participants were examined in a sleep laboratory. There, they were first allowed to sleep a normal night, while their brain activity was measured to monitor their sleep. The participants were then kept awake in the sleep laboratory, before being allowed to catch up on sleep. Their sleep was recorded in this case, too.

“What we saw was that the participants slept for the same amount of time when they consumed the two diets. This was the case both while they were following the diets, as well as after they had switched to another, identical diet. In addition, across the two diets, the participants spent the same amount of time in the different sleep stages. But we were particularly interested in investigating the properties of their deep sleep,” explains Cedernaes.

He continues, “Specifically, we looked at slow-wave activity, a measure that can reflect how restorative deep sleep is. Intriguingly, we saw that deep sleep exhibited less slow-wave activity when the participants had eaten junk food, compared with the consumption of healthier food. This effect also lasted into a second night, once we had switched the participants to an identical diet. Essentially, the unhealthy diet resulted in shallower deep sleep. Of note, similar changes in sleep occur with aging and in conditions such as insomnia. It can be hypothesized, from a sleep perspective, that greater importance should potentially be attached to diet in such conditions.”

The researchers do not currently know how long-lasting the sleep effects of the unhealthier diet may be. The study did not investigate whether shallower deep sleep may alter functions that are regulated by deep sleep, for example.

“It would also be interesting to conduct functional tests, for example, to see whether memory function can be affected. This is regulated to a large extent by sleep. And it would be equally interesting to understand how long-lasting the observed effects may be. Currently, we do not know which substances in the unhealthier diet worsened the depth of deep sleep. As in our case, unhealthy diets often contain both higher proportions of saturated fat and sugar and a lower proportion of dietary fiber,” states Cedernaes.

“It would be interesting to investigate whether there is a particular molecular factor that plays a greater role. Our dietary intervention was also quite short, and both the sugar and fat content could have been higher. It is possible that an even unhealthier diet would have had more pronounced effects on sleep,” notes Cedernaes.

Reference: “Exposure to a more unhealthy diet impacts sleep microstructure during normal sleep and recovery sleep: A randomized trial” by Luiz Eduardo Mateus Brandão, Alexandru Popa, Erasmus Cedernaes, Christopher Cedernaes, Lauri Lampola and Jonathan Cedernaes, 28 May 2023, Obesity.
DOI: 10.1002/oby.23787

The study was funded by the Swedish Diabetes Foundation, the Forte – Swedish Research Council for Health, Working Life and Welfare, the Swedish Society for Medical Research (SSMF), Göran Gustafsson’s Foundation, and the Swedish Brain Foundation (Hjärnfonden).



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Diet impacts learning in older nematodes

Newswise — A group from Nagoya University in Japan has discovered that when the diet of nematodes, tiny worms measuring about a millimeter or less in length, includes the bacteria Lactobacillus reuteri, the weakening of associative learning ability caused by aging does not occur. These results may suggest ways to use diet to reduce age-related cognitive decline in other animals, including humans. Their findings were published in the journal eLife

“This research is significant in that it established a method for studying the effects of diet on brain function in aging individuals using a combination of nematodes and bacteria as food,” said Associate Professor Kentaro Noma from the Graduate School of Science at Nagoya University. “Taking advantage of the characteristics of nematodes to measure both individual lifespan and aging of brain function, we found dietary conditions that maintain brain function, but not longevity. We usually think that the decline in brain function is caused by aging, but perhaps the processes of aging of brain function and individual lifespan are controlled by different mechanisms.” 

Researchers are interested in how a person can use diet to maintain healthy brain activity. However, since the effects of diet are complex, they remain a difficult topic to study. To get around this problem, researchers study simpler organisms to understand the basic mechanisms behind these processes.  

Such organisms include nematodes, tiny roundworms favored by researchers because of their simple anatomy, short lifespan, and ease of genetic manipulation. The research group used the nematode Caenorhabditis elegans, which has a short lifespan of only two weeks, but uses its simple nervous system to exhibit memory-learning behaviors.  

Noma was especially interested in the behavior known as thermotaxis, which describes the movement of an organism toward a preferred temperature. “Nematodes seem to learn by associating the presence or absence of food with their rearing temperature,” Noma explained. When C. elegans is reared at a certain temperature with food and then placed on a temperature gradient without food, it will move toward the rearing temperature. However, if it is reared at the same temperature without food, it will not demonstrate thermotaxis toward the rearing temperature. “Therefore,” he continued, “we can use thermotaxis as an indicator of associative learning ability.” 

To see whether changing diet influences learning, the researchers screened 35 different strains of lactic acid bacteria owned by Megmilk Snow Brand Co. They sought to identify possible diets that could maintain the associative learning ability of nematodes as they grew older. The researchers identified Lactobaillus reuteri, a probiotic that is studied for its potential health benefits, especially for the management of gastrointestinal disorders. This bacterium was found to be associated with the maintenance of the associative learning ability of the nematodes, while having no effect on their lifespan. 

To understand how L. reuteri affects nematodes, the group identified a key protein, DAF-16 transcription factor, that regulates the functioning of neurons of nematodes fed L. reuteri. This was what they had hoped to find because the DAF-16 gene is involved in the regulation of the processes of aging and longevity. 

“Since our intestines contain a myriad of bacteria, including E. coli and lactobacilli, the balance of these bacteria may also affect our brain function,” Noma said. “Furthermore, genes similar to those found in this study are also present in humans. This suggests that the mechanism that explained the effect of diet on changes in brain function with age may also exist in humans. With further research, it is possible that maintaining high brain function in old age through diet will become a reality.”  



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You’re Stress Eating Because Your Brain Literally Thinks It Isn’t Full Yet

Mice, they’re just like us—they really like fatty foods and sugary drinks. And according to a new study, they want to eat even more of them when they’re stressed out.

Recently, a group of researchers at Australia’s Garvan Institute of Medical Research found that the part of the rodent brain responsible for controlling hunger and fullness essentially logs off when under pressure. Scientists are confident the exact same thing happens in human brains, too.

We’ve long known that stress impacts our food choices—usually in ways harmful to our health. But very little has been understood about what’s actually happening below the surface when we find ourselves ordering Taco Bell or polishing off a sleeve of Oreos before a big deadline. Herbert Herzog, PhD, the lead researcher, says his team found that chronic stress shuts down the brain’s lateral habenula, which is a neural region that prevents overeating in both mice and humans.

The researchers first divided their mischief of mice (yes, that is what you call a bunch of them) into two groups. Both were fed high-fat mouse chow, but one group was exposed to some mild stressors—such as having their bedding replaced with a shallow pool of water—while the other was left alone. That’s when the scientists discovered what was happening in the lateral habenula. Normally, when a mouse is full, this part of the brain “dampens any positive feelings” about the food it’s eating as an effort to prevent overindulging, Herzog says. But in the stressed group, those same neurons were “silent,” allowing reward signals to stay active and encouraging the mice to keep eating.

Next, the scientists let their mice choose between drinking plain water, or water that had been spiked with sugar. The stressed mice on a high-fat diet guzzled three times as much of the sweetened water than those that were on the high-fat diet but unbothered. The findings suggest that stress delivers a kind of one-two punch to the brain: It quiets the brain’s natural response to satiety, leading to non-stop reward signals that make it more enjoyable to eat highly palatable foods—those typically high in sugar, fat, and calories—and creates a preference for those foods in the longer term.

A molecule called Neuropeptide Y (NPY) seems to be the main character in all of these functions. Experts believe the body naturally produces NPY as a way to cope with stress—the molecule has an anxiolytic effect in the brain, meaning it reduces anxiety—but NPY also shuts down the lateral habenula and prompts you to keep eating comfort foods with abandon. The researchers were able to clearly prove this point: When they artificially blocked NPY (with optogenetics, a biological technique that controls neurons), they discovered that stressed mice consumed less comfort food as a result.

Herzog could technically have performed the same study in humans, but it’s not exactly ethical. “People probably don’t like to be remote controlled,” he says. Still, Herzog—who wanted to know why many of us seem to eat foods higher in fat and sugar when we’re stressed—is confident the findings apply to complex human brains as well as tiny rodent ones. That’s because the neural architecture, particularly the lateral habenula and NPY molecule, are virtually identical in humans and mice. “We can safely assume the pathways and control mechanisms are the same, or at least very similar,” says Herzog.

Thanks to this country’s infamous rat race, over half of the American population experiences stress daily, and simply eliminating that feeling altogether is probably not feasible for most of us. (Presumably not for the mice, either.) So, next time you find yourself dissociating and scraping the bottom of the Pringle canister, lick your fingers, remind yourself that your frazzled brain is starving to be soothed…and maybe try meditation.

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3 Reasons to Go on a Good News Diet

Skip the negative news headlines and click on the positive ones.

The other day, buried underneath dozens of unpleasant and scary news stories—about Vladimir Putin, the latest climate disasters, and American politicians competing to be more offensive than the next, I accidentally stumbled upon an uplifting essay. It was titled “The nature of joy,” about how Margaret Renkl woke up to the most beautiful day in the history of the world (which is what her brother calls every day of his life). Renkl described in colorful detail all the delightful animals visiting her garden, including a pair of Carolina wrens, an armadillo, two lizards, robins, earthworms, and a rabbit who seemed to be jumping around for the sheer joy of moving.

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I decided to search for more flowers of positivity hidden under the usual dung pile of threats and abominations in the daily headlines. Good news stories are hard to find, but I came across the article, “What a musician turned cognitive scientist wants you to know about life,” in which Maya Shankar offered lessons from a life filled with unexpected twists (one of her lessons is about the power of “imaginative courage”).

The next day, I decided to completely bypass all the bad news and went straight to an article about how to turn your daily walk into a “micro-adventure” (one suggestion is to take a scent walk, which inspired me to take a stroll and to notice a spot where I get bathed in the scent of lilac every time I walk by).

Today the positive pickings were fewer, but I did click on one about how “six new trail projects in DC get federal grants” and another addressing the mouth-watering question: What’s the best vanilla ice cream? (Some of the entries toward the top of the list surprised me, so I guess I’ll have to do some follow-up research at the local supermarket).

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It’s understandable that we are drawn to bad news. Our attentional systems light up more for bad news than good news (Soroka, Fournier, and Nir, 2019, Soroka and McAdams, 2015), and we are the descendants of people who didn’t ignore potential threats to their lives (a topic we discuss at length in Kenrick and Lundberg-Kenrick, 2022). But there are three reasons we should all change our news diet, to purposefully look for good news, and try to avoid clicking on those stories about things that make us feel scared, angry, or disgusted.

  1. It would be good for your mental health. Bad news is psychologically unhealthy, and a diet of negative news may even make us depressed (Balmas, Atia, and Halperin, 2023). Sure, our ancestors needed to know about real threats in the local environment, but do their descendants benefit from hearing about the worst things happening thousands and thousands of miles away, mostly having no real implications for their everyday lives back in rural Montana or suburban Michigan?
  2. It would be good for society. Balmas and colleagues note that people who read negative news are more likely to feel politically polarized and angry at those nasty people with whom they disagree. Read less bad news, and hate your neighbor less.
  3. If we all started clicking on the positive news, and getting our friends and relatives to develop the same habit, there would be more positive stories in the news. Because people are addicted to negative news, the news media gives us more of it (the ratio of negative news to positive seems to be increasing over time, according to Soroka and colleagues). But the algorithms embedded in the news media are designed to give us more of what we want, so if enough of us boycott the bad news, and reinforce the good news with clicks, it will lead to one of those virtuous cycles, with the result being more positive news stores to choose from.

You may be wondering how you will find out about actual threats if you Pollyannishly only read the good news. Certainly, you want to know if there’s a killer loose in your neighborhood, but do you really need to hear yet another story about the crazy things the most loony politician just said in Washington, or the latest crimes or falsehoods committed by that same guy who hogs the headlines almost every day? You could limit yourself to one day of bad news per week, which in my case, would sure save a lot of time. I could use that time to walk outside to talk face-to-face with my neighbors about how things are going in my neighborhood, or even to just listen to the birds and smell the flowers.

References

Balmas, M., Atia, R., & Halperin, E. (2022). The Mediating Role of Depression in the Relationship Between News Consumption and Interparty Hostility During Covid-19. International Journal of Communication, 17, 304-330.

Kenrick, D.T., & Lundberg-Kenrick, D.E. (2022). Solving Modern Problems with a Stone-Age Brain: Human evolution and the 7 Fundamental Motives. Washington: APA Books

Soroka, S., Fournier, P., & Nir, L. (2019). Cross-national evidence of a negativity bias in psychophysiological reactions to news. Proceedings of the National Academy of Sciences, 116(38), 18888-18892.

Soroka, S., & McAdams, S. (2015). News, politics, and negativity. Political communication, 32(1), 1-22.

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The truth about intermittent fasting: Diet plan no better than calorie counting, study finds

Intermittent fasting isn’t much better than old-fashioned calorie counting, new study reveals. Photo / Getty Images

Tried the intermittent fasting trend? Turns out it’s no better than counting calories if you’re trying to lose weight, according to a new study.

Research published in the Annals of Internal Medicine journal has found that people who followed intermittent fasting and consumed all their calories within eight hours lost the same amount of weight as those who ate as they pleased but counted their calories, according to The New York Post.

University of Colorado conducted a study where 90 adults participated in a trial, divided into three groups, one of which could eat whatever they liked but only between midday and 8pm. The second group could eat whenever they liked, but cut down their calorie intake by a quarter, and a control group did not change their regular routine and was monitored against the other two.

Intermittent fasting is a popular dieting trend, but does it work? Photo / 123RF

Those who restricted their calories but not their eating time frame ate 405 fewer calories each day, losing an average of 5.4kg after one year. Those who took part in intermittent fasting ate 425 fewer calories each day and lost about 4.5kg.

This new study agrees with previous research and suggests that counting calories, as old-fashioned as it sounds, is still the most efficient way to lose weight.

Lead study author and dietitian Shuhao Lin said the rise of intermittent fasting is likely down to “its sheer simplicity and the fact that it does not require persons to count calories to lose weight”.

The intermittent fasting trend, also known as TRE (time restricted eating) has been adopted by the likes of Jennifer Aniston, Cameron Diaz, Nicole Kidman and Mark Wahlberg.

Jennifer Aniston is a known proponent of intermittent fasting. Photo / Getty Images

TRE involved eating during a specific time period, switching between eating on a regular basis and fasting. One example is the 16:8 diet, where you eat throughout eight hours of the day and then fast for 16. The 5:2 diet involves eating as normal for five days of the week and only eating one 500-600 calorie meal on the other two days.

The 16:8 diet is believed by some to improve blood sugar levels, increase lifespan and enhance brain function – but it can also lead people to over-eat during the eight hours, causing weight gain.

One study suggests that while TRE may have weight loss benefits, it can have a negative effect on fertility and reproduction, while a November 2022 study showed that skipping breakfast and intermittent fasting are associated with a higher risk of dying from heart disease.

But does counting your calories help you lose weight? Some dietitians say there’s little proof of this, though research from Johns Hopkins University considers it a better method for weight loss than intermittent fasting.

Lin says this most recent study’s findings could benefit those who fast intermittently, particularly as it can be frustrating to track every calorie consumed throughout the day.

“Evidence shows that when persons with obesity limit their eating window to six to eight hours per day, they naturally reduce energy intake by 350 to 500 calories,” Lin added.

“From a clinical standpoint, these findings are paramount.”

But the study adds that more research is needed to see who would benefit most from intermittent fasting diets.

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Gut health expert shares one food to ‘avoid’ that can cause stomach problems

A nutritional therapist has lifted the lid on the importance of our gut health and what we should be doing in order to improve it.

More and more people are keen to start taking care of this aspect of their health, as the gut is essential to our physical and mental wellbeing.




In fact, 80 percent of the body’s immune system lies within the gut, so it’s vital we keep it in good shape. And one specific type of food should be avoided if you want to maintain a healthy gut, as it can disrupt the bacteria and cause stomach problems.

That’s according to Abir Hamza-Goodacre, registered nutritional therapist at Benenden who has revealed her top tips on taking care of your gut health that everyone can follow.

One of these is making a simple diet swap that can really benefit your gut in the long run – and that’s avoiding artificial sweeteners.

The expert said: “While you may think that opting for ‘sugar free’ or ‘diet’ foods and drinks are better for you, especially if you are trying to lose weight, they can in fact be worse for the gut microbiome.

“Artificial sweeteners can disrupt the balance of beneficial bacteria in your gut. An imbalanced gut flora can lead to stomach disturbances such as gas and bloating as well as more long-term symptoms, for example unintentional weight changes or constant fatigue.

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The Pre-Workout Supplement You Should Avoid

The ketogenic diet is a popular fad diet that gained popularity for its purported ability to help its followers lose weight and achieve mental clarity. Several years ago, it also garnered support in the athletic community as a way to increase performance, particularly in endurance situations. This led to it being used as a pre-workout supplement with the goal of achieving better performance. New research published in the International Journal of Sport Nutrition and Exercise Metabolism, however, suggests the opposite—that ketone supplementation might actually worsen performance.





What Are Ketones?

Let’s start with the basics: Ketones are products created by the body when it doesn’t have enough glucose to burn for energy. Like a well-oiled machine, carbohydrates are broken down in the body into glucose. Glucose is then used as the body’s primary—and preferred—source of energy. The brain particularly likes glucose. When glucose stores diminish, the body begins breaking down fat for energy, leading to a state of ketosis.



What Is Ketosis?

In a nutshell, ketosis is a metabolic state that your body goes into when it uses fat as its main source of fuel. Ketosis can be induced by dietary changes, like fasting or eating a low-carbohydrate diet, or via ketone supplementation. Ketone supplements, in the form of powders, liquids, capsules and so on, contain a type of ketone known as beta-hydroxybutyrate, otherwise known as BHB.


BHB is a ketone that is naturally produced by the liver when the body’s supply of glucose is too low. BHB supplements were manufactured to provide the body with an external source of ketones, even if a person wasn’t eating a low-carbohydrate diet. Maintaining a state of ketosis is what is suggested to lead to weight loss. And, for a myriad of reasons like having to adhere to a strict low-carb diet, maintaining ketosis is challenging. And it can lead to some negative side effects.


Ketone supplements, in that regard, have been thought to provide a “loophole” for athletes who typically would not be eating a low-carbohydrate diet. Using this strategy, athletes could still eat a balanced diet and use the supplements to get into ketosis, giving the body access to an additional source of fuel. The idea is that the body would be able to switch between fats and carbs as its energy source the same ways as a hybrid car engine can switch between gas and electricity.



What Did This Exercise Study Find?

Researchers from McMaster University enlisted highly-trained endurance athletes who cycled at least five or more hours weekly and whose “athletic performance [was] consistent from day to day,” according to a press release in ScienceDaily. The research was structured as a triple-blind study, where neither the participants, the researchers who interacted with the participants, or the researchers who did the data analysis knew whether the ketone supplement or the placebo was provided, ensuring a significantly lower likelihood of bias affecting the outcome.


Participants were required to commit to 4 lab visits. First, to assess the highest amount of oxygen consumed at peak exercise (VO2 Peak), then for a familiarization trial where they learned what the process would be like, and finally for the 2 experimental phases. Participants were asked to maintain their regular nutrition and exercise habits throughout the study and to prepare for a cycling competition as they normally would.


The experiment itself had participants engaged in two separate in-lab cycling exercises that were 7 days apart, structured to mimic race conditions. Each separate “race” accounted for other distinct variables that could have introduced bias, like bike handlebar and seat configuration as well as fan speed and location. They even accounted for the energy changes that could have affected female participants at different phases of their menstrual cycles and ensured that the two experimental races were performed in the same phase of their cycle. The only difference between each race was that the “drinks contained either a ketone supplement or a similar-tasting placebo.”


After ingesting the supplement, participants rested for thirty minutes and had their blood drawn to determine ketone, glucose, lactate, oxygen and pH levels of the blood. Then they did a 15-minute warm-up of their choosing, followed by a 20-minute timed trial which is strongly correlated with their overall cycling ability at a high intensity level. The only feedback provided to participants was how much time had elapsed in their “race”.



So, Were the Ketones Helpful?

As a reminder, BHBs are the ketone bodies that are both produced by our livers when glucose levels are low and can be synthetically manufactured into supplements to put consumers into a state of ketosis. Previous research in the Journal of Phisiology suggested that taking a ketone supplement could enhance athletic performance if the exercise was performed in a way that led to a specific BHB concentration of 1–3 mM. In this study, participants’ BHB levels were around 2 mM, which would have suggested higher performance. But that wasn’t the case at all. The main finding from the study was that the speed participants could sustain during the test was actually lower after drinking the ketone supplement, even when compared to the placebo.


Researchers think this may be due to how ketone ingestion affect pH balance of the blood, heart rate and how tired the cyclists felt during the exercise. It is still not clear how the ketone dose and the corresponding rise in BHBs would affect performance in other endurance tests that require longer exercises at a moderate to high intensity level.



The Bottom Line

More research is needed to fully understand how the body reacts to taking ketone supplements and how these reactions can changes in a person’s ability to exercise. But for now, it’s safe to say that it’s probably not going to improve your workout and it might even make it worse! Instead, focus on fueling your body with whole foods before, during and after a workout to get the most science-backed bang for your buck.

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When It Comes to Immunity, You Are What You Eat

Newswise — The notion that diet and health are inextricably linked is hardly novel. For millennia, people have known that poor nutrition is responsible for many health problems. But the precise mechanisms that explain just how diet alters the function of our cells, tissues, and organs have remained poorly understood. 

Now, a study led by Harvard Medical School researchers sheds light on this process, pinpointing a critical intermediary between food and health — the gut bacteria that make up our microbiome, or the collection of microorganisms that live in symbiosis with humans.

The work, which was conducted in mice and published June 28 in Nature, shows that gut microbes feast on common fatty acids such as linoleic acid and convert them to conjugated linoleic acid (CLA). This byproduct then serves as a signal for a biological cascade that ultimately spurs a specific type of immune system to develop and reside in the small intestine.

In the study, the researchers observed that mice in whom this cascade was interrupted more readily succumbed to a common foodborne pathogen.

The findings, the team said, detail an intricate interplay between gut microbes, food, and immunity. They also underscore the importance of understanding how individual microbial species in the gut could alter specific organ functions and exercise important effects on health.

“The triad of diet-microbes-immune system has attracted considerable attention, with a paucity of detail to demonstrate how these three components work together,” said study senior author Dennis Kasper, the William Ellery Channing Professor of Medicine at Brigham and Women’s Hospital and professor of immunology in the Blavatnik Institute at Harvard Medical School. “We have found one of the clearest demonstrations here of a mechanism underlying how diet and the microbiome build the immune system.”

In the new study, Kasper worked in collaboration with Xinyang Song, a former postdoctoral researcher in the Kasper lab, now a principal investigator at the University of Chinese Academy of Sciences, and colleagues from HMS, Massachusetts General Hospital, Tufts University, and the UMass Chan Medical School.

The team initially noticed that germ-free mice — a common lab model that is not naturally colonized by microorganisms, and thus has no microbiome — were missing a subset of immune cells known as CD4+CD8aa+ intraepithelial lymphocytes (IELs), which normally reside in a specific part of the small intestine.

Interestingly, mice that were not germ-free but ate a minimal diet composed of just the essential nutrients to keep them alive were also deficient in these cells. However, CD4+CD8aa+ IELs were present in non-germ-free mice fed a typical rich commercial diet composed of many different nutrients.

Suspicious that an interplay between diet and the microbiome might be responsible for the presence or absence of CD4+CD8aa+ IELs, the researchers examined which nutrients were lacking from the minimal diet, eventually homing in on various fatty acids. After feeding individual fatty acids to mice on minimal diets with typical microbiomes, they discovered that animals that ate a long-chain fatty acid known as linoleic acid began growing CD4+CD8aa+ IELs in their small intestines.

Kasper explained that many bacteria that reside in the gut produce an enzyme called linoleic acid isomerase (LAI) that converts linoleic acid into a conjugated form, with some linoleic acid double- and single-chemical bonds rearranged. Further investigation showed that CLA — the conjugated form of linoleic acid — was abnormally low both in mice with a typical microbiome fed a minimal diet or in germ-free mice fed a rich diet, suggesting that bacteria were necessary to convert linoleic acid into CLA.

When the researchers colonized germ-free mice with bacteria that produced LAI and fed them a rich diet, these animals developed CD4+CD8aa+ IELs in their small intestines. Conversely, when the researchers colonized them with bacteria that had been genetically modified to not produce LAI, they did not develop these immune cells, showing that CLA produced by this bacterial enzyme was essential for these immune cells to grow.

Further investigation revealed a more complete mechanism behind why CLA spurred CD4+CD8aa+ IEL development: The researchers found that some immune cells in the small intestine produced a protein called hepatocyte nuclear factor 4g (HNF4g) on their surfaces, which serves as a receptor for CLA. When CLA attached to these receptors, the cells produced a different protein called interleukin 18R (IL-18R), which in turn lowered the production of a third protein called ThPOK. The less ThPOK produced, the more CD4+CD8aa+ IELs developed.

This complex pathway has clear implications for immunity to infection, Kasper said. Indeed, when the researchers tampered with any part of the cascade — for example, preventing production of IL-18R or HNF4g— mice in whom the cascade was turned off didn’t produce CD4+CD8aa+ IELs and were unable to fight off infection with Salmonella typhimurium, a bacterial species commonly responsible for cases of food poisoning.

“One of the reasons that more examples of the diet-microbes-immune system triad have not yet come to light is that these pathways are so complicated,” Kasper said. “By investigating these intricate pathways, we will have a better understanding of how our microbiomes keep us healthy and how to intervene when they don’t.”

Authorship, funding, disclosures

Co-authors included Haohao Zhang, Yanbo Zhang, Byongsook Goh, Bin Bao, Suelen S. Mello, Ximei Sun, Wen Zheng, Francesca S. Gazzaniga, Meng Wu, Fangfang Qu, Qiangzong Yin, Michael S. Gilmore, and Sungwhan F. Oh.

This work was supported in part by Department of Defense grants W81XWH1910625 and HT9425-23-0226 and Sponsored Research Agreements with Quark Ventures and Evelo Biosciences; National Key R&D Program of China 2022YFA0807300, NSF of China 32270945, and STCSM 22ZR1468700 and 22140902400; China Postdoctoral Science Foundation 2022M723139; NIH R01-AT010268 and Department of Defense W81XWH1910626; and NIH-NICHD T32:5T32HD55148-10 and Quark Ventures A31696 with additional support from the Harvard-wide Program on Antibiotic Resistance (PO1 AI1083214).

 



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Why is gut health important?

Parkinson’s disease affects millions of people around the world, but it remains unclear exactly what causes it, and there is currently no cure for this condition. In an effort to better understand the mechanisms involved, some researchers are now looking to the gut. Why, and what could this research reveal? In this installment of our In Conversation podcast, we discuss how gut health may play a role in Parkinson’s.

Millions of people around the world live with Parkinson’s disease, a neurological condition that primarily affects mobility, balance, and muscle control, though its symptoms can include many other issues, from mood changes to gastrointestinal issues and a deterioration of memory and other cognitive functions.

According to data from the World Health Organization (WHO), the global prevalence of Parkinson’s has doubled in the past 25 years, and as per the most recent estimates, the disease has resulted in “5.8 million disability-adjusted life years” globally.

While much of this increase is driven by increasing numbers of older adults, there is also some evidence that age-adjusted incidence is also on the rise.

Dopaminergic medication, deep brain stimulation, and speech and occupational therapy are some of the treatments currently available to people with Parkinson’s disease, but researchers are constantly on the lookout for more and better treatments.

In order to pave the way to better treatments, scientists are first seeking to understand more about how Parkinson’s disease works, and what mechanisms in the body might affect its development.

Several studies from the past 12 months have focused on one particular aspect of Parkinson’s disease, namely gut health. But why is gut health important in Parkinson’s, and what could it reveal about the disease?

To find out more about the current research and how the disease can affect individuals, Medical News Today welcomed two guests to the latest installment of our In Conversation podcast: Dr. Ayse Demirkan and Gary Shaughnessy.

Dr. Demirkan is a senior lecturer in AI Multiomics for Health and Wellbeing at the University of Surrey in the United Kingdom, and co-author of a paper about the imprint of the microbiome in Parkinson’s disease, which appeared in Nature Communications in November 2022.

Gary Shaughnessy is the chair of trustees at Parkinson’s UK, a research and support nongovernmental organization. In 2015, Shaughnessy received a diagnosis of Parkinson’s disease, and since then, he has been taking on regular physical challenges to raise money for Parkinson’s research.

Listen to this month’s podcast below, or on your preferred streaming platform:

Over the past few years, an increasing amount of evidence has come to light indicating that there is a two-way communication route between the brain and the gut. Researchers have termed this the gut-brain axis.

The gut-brain axis has been implicated in many health conditions affecting the brain, from dementia to depression. And while the gut-brain connection may be less obvious in other conditions, it is, in fact, clearer in Parkinson’s disease, which, in some people, is also characterized by gastrointestinal symptoms, such as constipation.

One perspective on Parkinson’s disease, known as the Braak hypothesis, suggests that, in many cases, an unknown pathogen can reach the brain via two routes, one of which implicates the gut.

According to this hypothesis, one way for pathogens to reach the brain could be by being swallowed, reaching the gut, and then advancing to the brain via the vagus nerve — the longest cranial nerve that connects the brain with, among others, the intestines. This may then trigger the onset of Parkinson’s disease.

In our podcast, Dr. Demirkan acknowledged that, at first, the notion of looking to the gut to understand more about Parkinson’s disease might seem surprising, but that the Braak hypothesis provides an intriguing lens through which to assess potential mechanisms at play.

“[Through the Braak hypothesis,] there comes the idea that the disease actually starts in the intestines, and then through the vagus nerve, it spreads to the other tissues and toward the brain,” she explained.

According to her, Parkinson’s disease is the neurological condition most interesting to study in relation to gut health for one simple reason: Parkinson’s gut microbiome stands out the most.

Through the recent study they conducted, Dr. Demirkan and her colleagues saw that individuals with Parkinson’s disease had distinct gut microbiomes characterized by dysbiosis — the phenomenon of imbalance between so-called good versus bad bacteria.

Their study suggested that around 30% of the proportion of gut bacteria in people with Parkinson’s disease is different from those without Parkinson’s.

“We found one-third of these microbes [in the gut of people with Parkinson’s] to be different,” Dr. Demirkan said on the podcast.

“So this is a very strong indication of dysbiosis. And also how they [the bacteria] function, what kind of genes they carry, [these aspects were] also different. We found a reduced [amount of] short-chain fatty acid producers, for example, bacteria that [are] known to be gut-friendly […] We found increased pathogenic bacteria […], including Escherichia coli, and we found a lot of bacterial pathways disturbed as well, potentially affecting the well-being of the neuronal tissues.”

– Dr. Ayse Demirkan

Dr. Demirkan and her colleagues found that bacteria such as Bifidobacterium dentium — which can cause infections such as brain abscesses — were at significantly elevated levels in the gut of people with Parkinson’s disease.

Other infection-causing bacteria more abundant in people with Parkinson’s were E. coli, Klebsiella pneumoniae, which can cause pneumonia, and Klebsiella quasipneumoniae, which can cause similar infections.

The study conducted by Dr. Demirkan was not the only recent research to zoom in on the differences in gut bacteria.

Research from the University of Helsinki — published in May 2023 in Frontiers — in animal models of Parkinson’s disease, suggests that Desulfovibrio bacteria may be implicated in this condition. These bacteria produce hydrogen sulfide, which may lead to forms of inflammation.

Desulfovibrio also came up in a study from The Chinese University of Hong Kong, which appeared in May 2023 in Nature Communications. This study, whose aim was to find a method of diagnosing Parkinson’s earlier, identified an “overabundance” of these bacteria in people with REM sleep behavior disorder and early markers of Parkinson’s.

REM sleep behavior disorder is a deep sleep disturbance tied to a higher risk of Parkinson’s disease. In people with this disorder, the usual brain mechanisms that prevent them from “acting out” the content of their dreams no longer work, which means that they perform uncontrolled movements in their sleep.

Shaughnessy told us that he, too, experiences deep sleep disturbances. “[O]ver the last few years, I have very really vivid dreams, and […] I’ve fallen out of bed a few times because I’m turning over doing something, you know, sort of dealing with whatever it is in the dream,” he described.

If gut bacteria do play a role in Parkinson’s disease, the question that arises is: What mechanisms might mediate their impact on neurological health?

One hypothesis hinted at in the studies on the link between the gut and the brain in Parkinson’s is that systemic inflammation may be one of the mechanisms involved, since some of the bacteria that are overabundant in this condition are pro-inflammatory, meaning that they can trigger inflammation.

There is research indicating that immunosuppressant medication is associated with a lower risk of Parkinson’s disease, which suggests that a similar type of medication may also help manage the condition.

Indeed, chronic brain inflammation is an important part of Parkinson’s disease, and some studies seem to indicate that systemic inflammation may worsen brain inflammation and thus contribute to disease progression.

Some inflammatory conditions have actually been linked with a higher risk of Parkinson’s. For example, one Danish study from 2018 suggested that people with inflammatory bowel disease (IBD) have a 22% higher risk of Parkinson’s disease than peers without this inflammatory condition.

In the podcast, Dr. Demirkan agreed that inflammation linked to Parkinson’s disease may start in the gut, caused by “bad” bacteria. However, she emphasized that this potential mechanism is not yet confirmed, and further research on this topic is necessary to draw firm conclusions.

If gut bacteria may play a role in Parkinson’s disease, it may seem reasonable to infer that diet could help fight gut dysbiosis and perhaps provide an easy option for symptom management.

While there are some dietary recommendations and nutritional supplements that may help provide some symptom relief for some people, it remains unclear just how much diet can actually do to alter the course of this disease.

One study from 2022 suggests that diets high in flavonoids — natural pigments found in many fruits — are linked to a lower risk of mortality in Parkinson’s disease.

And an older study, from 2018, argued that a protein found in many types of fish, called “parvalbumin,” may help prevent Parkinson’s disease by stopping alpha-synuclein from collecting into clumps in the brain — which is what happens in the brains of people with Parkinson’s, disrupting signals between brain cells.

However, when asked about the potential of diet and supplements to regulate gut bacteria in people with Parkinson’s, Dr. Demirkan expressed some reservations.

She emphasized that since people have different risk factors for Parkinson’s, as well as different iterations of the disease, it is difficult to make general recommendations that would actually prove helpful:

“It’s very difficult for me to advise anyone anything […] because we are all very individual, our gut microbiome is individual. So prevention [of the condition] is [one thing] I think, and the long-term maintenance is something else, together with the other complications of the disease. So I cannot really advise anything, but studies show there is a problem with increased sugar consumption […] There are some intervention studies on diet indeed, but it’s very difficult [to conclude anything], as the studies are not really […] finalized. [It is difficult to know] how to advise an individual with a certain genetic and lifelong history of exposure to different things, because we don’t know what is in [them].”

There is, nevertheless, some research suggesting that exercise can be an effective means of managing the symptoms of Parkinson’s disease.

One study from 2022, published in Neurology, suggested that participating in regular, moderate-to-vigorous exercise could help slow down the progression of Parkinson’s disease for those in the early stages.

Research from 2017 advised that at least 2 and a half hours of exercise per week could help people with Parkinson’s improve their mobility while slowing down disease progression.

Dr. Demirkan agreed that exercise can be a helpful strategy for managing Parkinson’s disease. “[E]xercise itself is an amazing way of shaping our brain and body,” she said.

“[I]n terms of reversing [Parkinson’s] pathology, there are some large physiological effects that we can think about. If you’re running a marathon, for example, it’s a big thing that your body has to go through. […] [F]or instance, one thing is that your heat increase for a long time in like a […] feverish way, right? There is a long-term increase in the core heat, that’s one thing, and that should definitely have an important effect [on the gut],” she explained.

Indeed, some research suggests that the heat stress taking place during exercise could reduce intestinal blood flow, which eventually may impact the gut microbiome by potentially suppressing some bacteria and making room for others to expand.

As to which form of exercise is best for people with Parkinson’s disease, a Cochrane review published in January 2023 concluded that pretty much all forms of exercise can help improve life quality for those living with this condition.

According to the review authors, existing evidence suggests that aqua-based training “probably has a large beneficial effect” on quality of life. Endurance training is also helpful, both in improving life quality, in general, and in managing motor symptoms, in particular.

When it comes to managing motor symptoms, the authors write that dance, aqua-based exercise, gait/ balance/ functional exercise, and multi-domain training could all be equally helpful.

And some past research — in women with overweight but without Parkinson’s — has suggested that endurance training results in an increase in beneficial bacteria called Akkermansia, which contribute to improved metabolic function.

Shaughnessy, who regularly takes part in demanding and arduous marathons and other sports challenges to raise funds for Parkinson’s research told us that exercise has helped him more than anything in maintaining his well-being.

“[E]xercise has become a big part — was already a part of my life before [the diagnosis], but it’s become […] a big way of helping me to manage and control the condition,” he told us in the podcast.

“I gradually went from, you know, a bit of running to marathons. And then the latest thing I’ve done was a 14-day cycle from Liverpool to Ukraine — 1,400 miles, which was probably a little bit beyond my capability, to be honest,” he mused.

But challenging himself in this way, he said, truly helped him on a mental level. “[W]hile I’m exercising, I don’t feel like I have Parkinson’s, quite often,” Shaughnessy told us.

For him, it is all about focusing on what you are actually able to achieve at any given point in time, and aiming for that.

“[A big part] of managing the condition, I think, is around your mental attitude. Because when I first was diagnosed, I actually found it very difficult, running. And I’d go running as part of being on business trips abroad and so on, I’d run in cities I went to, and I did decline in the first months, quite rapidly in terms of my running. But my wife actually said to me, ‘just focus on what you can do, not what you can’t do.’ And that was a bit of a turning point for me. And, you know, by not worrying about [it], I’ve got to get better and go quicker, and just focus on enjoying my running. And, you know, actually, ironically, I have got better and I ran my personal best in the marathon in May this year — so, 8 years after diagnosis.”

– Gary Shaughnessy

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