Regularly eating a high fat/calorie diet could reduce the brain’s ability to regulate calorie intake, according to a study published in The Journal of Physiology. Rat studies revealed a signalling pathway which causes a quick response to high fat/high calorie intake, reducing food and calorie intake. But continuously eating a high fat/calorie diet seems to disrupt this signalling pathway, sabotaging this short-term protection.
Senior author Dr Kirsteen Browning said, “Calorie intake seems to be regulated in the short-term by astrocytes. We found that a brief exposure (three to five days) of high fat/calorie diet has the greatest effect on astrocytes, triggering the normal signalling pathway to control the stomach. Over time, astrocytes seem to desensitise to the high fat food. Around 10–14 days of eating high fat/calorie diet, astrocytes seem to fail to react and the brain’s ability to regulate calorie intake seems to be lost. This disrupts the signalling to the stomach and delays how it empties.”
Astrocytes initially react when high fat/calorie food is ingested, triggering the release of gliotransmitters, chemicals (including glutamate and ATP) that excite nerve cells and enable normal signalling pathways to stimulate neurons that control stomach function. This ensures the stomach contracts correctly to fill and empty in response to food passing through the digestive system. When astrocytes are inhibited, the cascade is disrupted. The decrease in signalling chemicals leads to a delay in digestion because the stomach doesn’t fill and empty appropriately.
The vigorous investigation used behavioural observation to monitor food intake in rats which were fed a control or high fat/calorie diet for one, three, five or 14 days. This was combined with pharmacological and specialist genetic approaches (both in vivo and in vitro) to target distinct neural circuits, which enabled the researchers to specifically inhibit astrocytes in a particular region of the brainstem. In this way, they assessed the response of individual neurons.
Human studies will need to be carried out to confirm if the same mechanism occurs in humans. If this is the case, further testing will be required to assess if the mechanism could be safely targeted without disrupting other neural pathways.
The researchers have plans to further explore the mechanism. Dr Browning said, “We have yet to find out whether the loss of astrocyte activity and the signalling mechanism is the cause of overeating or that it occurs in response to the overeating. We are eager to find out whether it is possible to reactivate the brain’s apparent lost ability to regulate calorie intake. If this is the case, it could lead to interventions to help restore calorie regulation in humans.”
Researchers have found new evidence that vitamin D may be metabolised differently in people with high body mass index (BMI), who don’t benefit as greatly from supplements of the nutrient. The study, published in JAMA Network Open, is a new analysis of data from the large-scale VITAL trial, which investigated the effect of vitamin D or marine omega-3 supplements on reducing the risk of developing cancer, heart disease, or stroke.
“The analysis of the original VITAL data found that vitamin D supplementation correlated with positive effects on several health outcomes, but only among people with a BMI under 25,” said first author Deirdre K. Tobias, ScD, an associate epidemiologist in Brigham’s Division of Preventive Medicine. “There seems to be something different happening with vitamin D metabolism at higher body weights, and this study may help explain diminished outcomes of supplementation for individuals with an elevated BMI.”
Vitamin D is an essential nutrient involved in many biological processes, most notably for mineral absorption. While some vitamin D is generated in the body from sunlight, vitamin D deficiencies are often treated with supplementation. Evidence from laboratory studies, epidemiologic research and clinical research has also suggested that vitamin D may play a role in the incidence and progression of cancer and cardiovascular disease, and it was this evidence that prompted the original VITAL trial.
The VITAL trial was a randomised, double-blind, placebo-controlled trial in 25,871 U.S. participants, which included men over the age of 50 and women over the age of 55. All participants were free of cancer and cardiovascular disease at the time of enrolment. While the trial found little benefit of vitamin D supplementation for preventing cancer, heart attack, or stroke in the overall cohort, there was a statistical correlation between BMI and cancer incidence, cancer mortality, and autoimmune disease incidence. Other studies suggest similar results for type 2 diabetes.
The new study aimed to investigate this correlation. The researchers analysed data from 16 515 participants from the original trial who provided blood samples at baseline, as well as 2742 with a follow-up blood sample taken after two years. The researchers measured the levels of total and free vitamin D, as well as many other novel biomarkers for vitamin D, such as its metabolites, calcium, and parathyroid hormone, which helps the body utilise vitamin D.
“Most studies like this focus on the total vitamin D blood level,” said senior author JoAnn E. Manson, MD, DrPH, chief of the Division of Preventive Medicine at the Brigham and principal investigator of VITAL. “The fact that we were able to look at this expanded profile of vitamin D metabolites and novel biomarkers gave us unique insights into vitamin D availability and activity, and whether vitamin D metabolism might be disrupted in some people but not in others.”
The researchers found that vitamin D supplementation increased most of the biomarkers associated with vitamin D metabolism in people, regardless of their weight. However, these increases were significantly smaller in people with elevated BMIs.
“We observed striking differences after two years, indicating a blunted response to vitamin D supplementation with higher BMI,” Tobias said. “This may have implications clinically and potentially explain some of the observed differences in the effectiveness of vitamin D supplementation by obesity status.”
“This study sheds light on why we’re seeing 30–40 percent reductions in cancer deaths, autoimmune diseases, and other outcomes with vitamin D supplementation among those with lower BMIs but minimal benefit in those with higher BMIs, suggesting it may be possible to achieve benefits across the population with more personalised dosing of vitamin D,” said Manson. “These nuances make it clear that there’s more to the vitamin D story.”
The authors conclude that the VITAL findings are a call to action for the research community to continue exploring the potential benefits of vitamin D supplementation for preventing cancer and other diseases and to take BMI into account when evaluating the supplement’s health impacts.
Melanoma cells. Source: National Cancer Institute.
Fewer cases of melanoma were observed among regular users of vitamin D supplements than among non-users, researchers in Finland found. People taking vitamin D supplements regularly also had a considerably lower risk of skin cancer, according to a study of nearly 500 people with increased skin cancer risk, which was published in Melanoma Research.
A key micronutrient, vitamin D may play a role in many diseases. Previous studies investigating the link between vitamin D and skin cancers, have been inconclusive or contradictory, but they mainly focussed on serum levels of calcidiol, which is a metabolite of vitamin D. Serum calcidiol levels have been associated with both a slightly higher or lower risk of different skin cancers. This may be partly due to the fact that serum calcidiol analyses do not provide information on vitamin D metabolism in the human skin, which can express enzymes that generate biologically active vitamin D metabolites or inactivate them.
The new study took a different approach: 498 adult patients with an increased risk of a skin cancer, such as basal cell carcinoma, squamous cell carcinoma or melanoma, were recruited and classified into low risk, moderate risk and high risk. Based on their use of oral vitamin D supplements, the patients were divided into three groups: non-users, occasional users and regular users. Serum calcidiol levels were analysed in half of the patients and found to correspond to their self-reported use of vitamin D.
A key finding of the study is that there were considerably fewer cases of melanoma among regular users of vitamin D than among non-users, and that the skin cancer risk classification of regular users was considerably better than non-users’. Logistic regression analysis showed that melanoma risk among regular users was more than halved compared to non-users.
The findings suggest that even occasional users of vitamin D may have a lower risk for melanoma than non-users. However, there was no statistically significant association between the use of vitamin D and the severity of photoaging, facial photoaging, actinic keratoses, nevus count, basal cell carcinoma and squamous cell carcinoma. Serum calcidiol levels were not significantly associated with these skin changes, either. Since the research design was cross-sectional, the researchers were unable to demonstrate a causal relationship.
Other relatively recent studies, too, have provided evidence of the benefits of vitamin D in melanoma, such as of the association of vitamin D with a less aggressive melanoma.
“These earlier studies back our new findings from the North Savo region here in Finland. However, the question about the optimal dose of oral vitamin D in order to for it to have beneficial effects remains to be answered. Until we know more, national intake recommendations should be followed,” Professor of Dermatology and Allergology Ilkka Harvima of the University of Eastern Finland notes.
With an emphasis on fruits, vegetables and legumes, the Mediterranean diet has long been applauded for its multiple health benefits. Now, new research shows that it may also help overcome infertility, making it a non-intrusive and affordable strategy for couples trying to conceive.
Specifically, researchers identified that the anti-inflammatory properties of a Mediterranean diet can improve couples’ chances of conception.
Infertility is a global health concern affecting 48 million couples and 186 million individuals worldwide.
UniSA researcher, Dr Evangeline Mantzioris, says modifying preconception nutrition is a non-invasive and potentially effective means for improving fertility outcomes.
“Deciding to have a baby is one of life’s biggest decisions, but if things don’t go as planned, it can be very stressful for both partners,” Dr Mantzioris says.
“Research shows inflammation can affect fertility for both men and women, affecting sperm quality, menstrual cycles, and implantation. So, in this study we wanted to see how a diet that reduces inflammation – such as the Mediterranean diet – might improve fertility outcomes.
“Encouragingly, we found consistent evidence that by adhering to an anti-inflammatory diet – one that includes lots of polyunsaturated or ‘healthy’ fats, flavonoids (such as leafy green vegetables), and a limited amount of red and processed meat – we can improve fertility.”
The Mediterranean diet is primarily plant-based, and includes whole grains, extra virgin olive oil, fruits, vegetables, beans and legumes, nuts, herbs, and spices. Yoghurt, cheese, and lean protein sources such as fish, chicken, or eggs; red and processed meats are only eaten in small amounts.
In comparison, a western diet comprises excessive saturated fats, refined carbohydrates, and animal proteins, making it energy-dense and lacking dietary fibre, vitamins, and minerals. Typically, a western diet is associated with higher levels of inflammation.
Florida State University College of Medicine researchers have linked aspartame, an artificial sweetener found in nearly 5000 diet foods and drinks, to anxiety-like behaviour in mice.
Along with producing anxiety in the mice who consumed aspartame, the effects extended up to two generations from the males exposed to the sweetener. The study is published in the Proceedings of the National Academy of Sciences.
“What this study is showing is we need to look back at the environmental factors, because what we see today is not only what’s happening today, but what happened two generations ago and maybe even longer,” said co-author Pradeep Bhide, the Jim and Betty Ann Rodgers Eminent Scholar Chair of Developmental Neuroscience in the Department of Biomedical Sciences.
The study came about, in part, because of previous research from the Bhide Lab on the transgenerational effects of nicotine on mice. The research showed temporary, or epigenetic, changes in mice sperm cells. Unlike genetic changes (mutations), epigenetic changes are reversible and don’t change the DNA sequence; however, they can change how the body reads a DNA sequence.
“We were working on the effects of nicotine on the same type of model,” Bhide said. “The father smokes. What happened to the children?”
Aspartame received FDA approval as a sweetener in 1981. Today, nearly 5000 tonnes are produced each year. When consumed, aspartame becomes aspartic acid, phenylalanine and methanol, all of which can have potent effects on the central nervous system.
Led by doctoral candidate Sara Jones, the study involved providing mice with drinking water containing aspartame at approximately 15% of the FDA-approved maximum daily human intake. The dosage, equivalent to six to eight cans of diet fizzy drink a day for humans, continued for 12 weeks in a study spanning four years.
Pronounced anxiety-like behaviour was observed in the mice through a variety of maze tests across multiple generations descending from the aspartame-exposed males.
“It was such a robust anxiety-like trait that I don’t think any of us were anticipating we would see,” Jones said. “It was completely unexpected. Usually you see subtle changes.”
When given diazepam, a drug used to treat anxiety disorder in humans, mice in all generations ceased to show anxiety-like behaviour.
Researchers are planning an additional publication from this study focused on how aspartame affected memory. Future research will identify the molecular mechanisms that influence the transmission of aspartame’s effect across generations.
Potatoes have long been perceived as having negative health impacts, such as possibly increasing the likelihood of developing Type 2 diabetes. New research published in Diabetes Care has shown while spuds may not have all the same benefits as some other vegetables – such as lowering risk of Type 2 diabetes – health issues associated with potatoes may actually be due to their preparation.
In the long-term Danish Diet, Cancer and Health study, more than 54 000 people reported their dietary intake.
A recent analysis of this study led by Dr Nicola Bondonno from ECU’s Nutrition and Health Innovation Research Institute, found people who consumed the most vegetables had a 21% lower risk of developing Type 2 diabetes than those who consumed the least amount of vegetables.
PhD candidate Pratik Pokharel carried out work on the analysis and said while potatoes didn’t have the same impact on Type 2 diabetes, they also didn’t have any negative effect.
“In previous studies, potatoes have been positively linked to incidence of diabetes, regardless of how they’re prepared – but we found that’s not true,” Mr Pokharel said.
“When we separated boiled potatoes from mashed potatoes, fries or crisps, boiled potatoes were no longer associated with a higher risk of diabetes: they had a null effect.”
Mr Pokharel said underlying dietary patterns were the key.
“In our study, people who ate the most potatoes also consumed more butter, red meat and soft drink – foods known to increase your risk of Type 2 diabetes,” he said.
“When you account for that, boiled potatoes are no longer associated with diabetes. It’s only fries and mashed potatoes, the latter likely because it is usually made with butter, cream and the like.”
Eat your veggies
Mr Pokharel said findings from the study indicate vegetables could play a key role in reducing Type 2 diabetes, as people who ate a lot of leafy greens and cruciferous vegies such as spinach, lettuce, broccoli and cauliflower had a significantly lower risk of developing the condition.
He said the relationship between vegetables and diabetes should be incorporated into public dietary guidelines – as should the benefits of eating potatoes.
“The finding that vegetables lower diabetes risk is crucial for public health recommendations, and we shouldn’t ignore it,” he said.
“Regarding potatoes, we can’t say they have a benefit in terms of type 2 diabetes, but they also aren’t bad if prepared in a healthy way.
“We should separate potatoes and other vegetables in regard to messaging about disease prevention but replacing refined grains such as white rice and pasta with potatoes can improve your diet quality because of fibre and other nutrients found in potatoes.”
Putting it into practice in the kitchen
Mr Pokharel said people should be advised to increase their vegetable intake – and they could include potatoes, so long as they left out some of the unhealthy extras such as butter, cream and oil.
“Potatoes have fibre and nutrients, which are good for you,” he said.
“People talk about carbs being bad, but it’s more about the type of carbs you’re having; compared to something like white rice, boiled potatoes are a good quality of carbohydrate.”
Many people struggle with feeling groggy in the morning until they get their first coffee, but those who wake up feeling refreshed each day is not just merely a fluke of genetics. Scientists report in the journal Nature Communications that people can wake up each morning without feeling sluggish by paying attention to three key factors: sleep, exercise and the nutritional composition of their breakfast.
The findings come from a study of 833 participants who, over a two-week period, were given a variety of breakfast meals; wore wristwatches to record their physical activity and sleep quantity, quality, timing and regularity; kept diaries of their food intake; and recorded their alertness levels from the moment they woke up and throughout the day. The study included both fraternal and identical twins to disentangle the influence of genes from environment and behaviour.
The researchers found that the secret to alertness is a three-part prescription requiring substantial exercise the previous day, sleeping longer and later into the morning, and eating a breakfast high in complex carbohydrates, with limited sugar. The researchers also discovered that a healthy controlled blood glucose response after eating breakfast is key to waking up more effectively.
“All of these have a unique and independent effect,” said UC Berkeley postdoctoral fellow Raphael Vallat, first author of the study. “If you sleep longer or later, you’re going to see an increase in your alertness. If you do more physical activity on the day before, you’re going to see an increase. You can see improvements with each and every one of these factors.”
Morning grogginess is more than just an annoyance. It has major societal consequences: Many auto accidents, job injuries and large-scale disasters are caused by people who cannot shake off sleepiness. The Exxon Valdez oil spill in Alaska, the Three Mile Island nuclear meltdown in Pennsylvania and an even worse nuclear accident in Chernobyl, Ukraine, are well-known examples.
“Many of us think that morning sleepiness is a benign annoyance. However, it costs developed nations billions of dollars every year through loss of productivity, increased health care utilisation, work absenteeism. More impactful, however, is that it costs lives – it is deadly,” said senior author Matthew Walker, UC Berkeley professor of neuroscience and psychology. “From car crashes to work-related accidents, the cost of sleepiness is deadly. As scientists, we must understand how to help society wake up better and help reduce the mortal cost to society’s current struggle to wake up effectively each day.”
Personalised approach to eating
Walker and Vallat teamed up with researchers in the UK, the US and Sweden to analyse data acquired by a UK company, Zoe Ltd., that has followed hundreds of people for two-week periods in order to learn how to predict individualised metabolic responses to foods based on a person’s biological characteristics, lifestyle factors and the foods’ nutritional composition.
The participants were given pre-prepared meals, with different amounts of nutrients incorporated into muffins, for the entire two weeks to see how they responded to different diets upon waking. A standardised breakfast, with moderate amounts of fat and carbohydrates, was compared to a high protein (muffins plus a milkshake), high carbohydrate or high sugar (glucose drink) breakfast. The subjects also wore continuous glucose monitors to measure blood glucose levels throughout the day.
The worst type of breakfast, on average, contained high amounts of simple sugar; it was associated with an inability to wake up effectively and maintain alertness. When given this sugar-infused breakfast, participants struggled with sleepiness.
In contrast, the high-carbohydrate breakfast was linked to individuals revving up their alertness quickly in the morning and sustaining that alert state.
“A breakfast rich in carbohydrates can increase alertness, so long as your body is healthy and capable of efficiently disposing of the glucose from that meal, preventing a sustained spike in blood sugar that otherwise blunts your brain’s alertness,” Vallat said
“We have known for some time that a diet high in sugar is harmful to sleep, not to mention being toxic for the cells in your brain and body,” Walker added. “However, what we have discovered is that, beyond these harmful effects on sleep, consuming high amounts of sugar in your breakfast, and having a spike in blood sugar following any type of breakfast meal, markedly blunts your brain’s ability to return to waking consciousness following sleep.”
It wasn’t all about food, however. Sleep mattered significantly. In particular, Vallat and Walker discovered that sleeping longer than you usually do, and/or sleeping later than usual, resulted in individuals ramping up their alertness very quickly after awakening from sleep. According to Walker, between seven and nine hours of sleep is ideal for ridding the body of “sleep inertia” – the inability to reach functional cognitive alertness after waking up. Most people need this amount of sleep to remove adenosine, a chemical that accumulates in the body throughout the day and brings on sleepiness in the evening, something known as sleep pressure.
“Considering that the majority of individuals in society are not getting enough sleep during the week, sleeping longer on a given day can help clear some of the adenosine sleepiness debt they are carrying,” Walker speculated.
“In addition, sleeping later can help with alertness for a second reason,” he said. “When you wake up later, you are rising at a higher point on the upswing of your 24-hour circadian rhythm, which ramps up throughout the morning and boosts alertness.”
It’s unclear, however, what physical activity does to improve alertness the following day.
“It is well known that physical activity, in general, improves your alertness and also your mood level, and we did find a high correlation in this study between participants’ mood and their alertness levels,” Vallat said. “Participants that, on average, are happier also feel more alert.”
But Vallat also noted that exercise is generally associated with better sleep and a happier mood.
“It may be that exercise-induced better sleep is part of the reason exercise the day before, by helping sleep that night, leads to superior alertness throughout the next day,” Vallat said.
Walker noted that the restoration of consciousness from non-consciousness — from sleep to wake — is unlikely to be a simple biological process.
“If you pause to think, it is a non-trivial accomplishment to go from being nonconscious, recumbent and immobile to being a thoughtful, conscious, attentive and productive human being, active, awake, and mobile. It’s unlikely that such a radical, fundamental change is simply going to be explained by tweaking one single thing,” he said. “However, we have discovered that there are still some basic, modifiable yet powerful ingredients to the awakening equation that people can focus on — a relatively simple prescription for how best to wake up each day.”
It’s not in your genes
Comparisons of data between pairs of identical and non-identical twins showed that genetics plays only a minor and insignificant role in next-day alertness, explaining only about 25% of the differences across individuals.
“We know there are people who always seem to be bright-eyed and bushy-tailed when they first wake up,” Walker said. “But if you’re not like that, you tend to think, ‘Well, I guess it’s just my genetic fate that I’m slow to wake up. There’s really nothing I can do about it, short of using the stimulant chemical caffeine, which can harm sleep.
“But our new findings offer a different and more optimistic message. How you wake up each day is very much under your own control, based on how you structure your life and your sleep. You don’t need to feel resigned to any fate, throwing your hands up in disappointment because, ‘… it’s my genes, and I can’t change my genes.’ There are some very basic and achievable things you can start doing today, and tonight, to change how you awake each morning, feeling alert and free of that grogginess.”
Walker, Vallat and their colleagues continue their collaboration with the Zoe team, examining novel scientific questions about how sleep, diet and physical exercise change people’s brain and body health, steering them away from disease and sickness.
Tea has long been known to have many health benefits, but now a study of 881 elderly women found they were far less likely to have extensive build-up of abdominal aortic calcification (AAC) if they consumed a high level of flavonoids in their diet – found in black and green tea, apples, nuts, citrus fruit, berries.
AAC is the calcification of the abdominal aorta and is a predictor of cardiovascular risk such as heart attack and stroke. It has also been found to be a reliable predictor for late-life dementia.
Edith Cowan University researcher and study lead Ben Parmenter said while there were many dietary sources of flavonoids, some had particularly high amounts.
“In most populations, a small group of foods and beverages – uniquely high in flavonoids – contribute the bulk of total dietary flavonoid intake,” he said.
“The main contributors are usually black or green tea, blueberries, strawberries, oranges, red wine, apples, raisins/grapes and dark chocolate.”
The flavonoid family
There are many different types of flavonoids, such as flavan-3-ols and flavonols, which the study indicated appear to also have a relationship with AAC.
Study participants who had a higher intake of total flavonoids, flavan-3-ols and flavonols were 36–39% less likely to have extensive AAC.
Black tea was the study cohort’s main source of total flavonoids and was also associated with significantly lower odds of extensive AAC.
Compared with respondents who didn’t drink tea, participants who had two-to-six cups per day had 16–42% less chance of having extensive AAC.
However, some other dietary sources of flavonoids such as fruit juice, red wine and chocolate, did not show a significant beneficial association with AAC.
Not just tea
Though black tea was the main source of flavonoids in the study – likely due to the age of the participants – Mr Parmenter said people could still benefit from flavonoids without putting the kettle on.
“Out of the women who don’t drink black tea, higher total non-tea flavonoid intake also appears to protect against extensive calcification of the arteries,” he said.
“This implies flavonoids from sources other than black tea may be protective against AAC when tea is not consumed.”
Mr Parmenter said this was important as it allows non-tea drinkers to still benefit from flavonoids in their diet.
“In other populations or groups of people, such as young men or people from other countries, black tea might not be the main source of flavonoids,” he said.
“AAC is a major predictor of vascular disease events, and this study shows intake of flavonoids, that could protect against AAC, are easily achievable in most people’s diets.”
A brief switch to a low-protein diet could be a key to enhancing colon cancer treatment, say researchers investigating cancer metabolism. They reported their findings in the journal Gastroenterology.
Like all cells, cancer cells need nutrients to survive and grow. One of the most important nutrient sensing molecules in a cell is called mTORC1. Often called a master regulator of cell growth, it lets cells sense different nutrients, thereby growing and proliferating. When nutrients are limited, cells dial down nutrient sensing cascade and turn off mTORC1.
While mTORC1 is known to be hyperactive in colon cancer, the key question is whether colon tumours hijack nutrient sensing pathways to fire up the master regulator.
“In colon cancer, when you decrease the nutrients available in the tumours, the cells don’t know what to do. Without the nutrients to grow, they undergo a kind of crisis, which leads to massive cell death,” said senior author Yatrik M. Shah, PhD, professor at Michigan Medicine.
Researchers found in cells and in mice that a low-protein diet blocked the nutrient signalling pathway that fires up a master regulator of cancer growth.
The regulator, mTORC1, controls how cells use nutritional signals to grow and multiply. It’s highly active in cancers with certain mutations and is known to cause cancer to become resistant to standard treatments. A low-protein diet, and specifically a reduction in two key amino acids, changed the nutritional signals through a complex called GATOR.
GATOR1 and GATOR2 work together to keep mTORC1 in business. When a cell has plenty of nutrients, GATOR2 activates mTORC1. When nutrients are low, GATOR1 deactivates mTORC1. Limiting certain amino acids blocks this nutrient signalling.
Previous efforts to block mTORC have focused on inhibiting its cancer-causing signals. But these inhibitors cause significant side effects — and when patients stop taking it, the cancer comes back. The study suggests that blocking the nutrient pathway by limiting amino acids through a low-protein diet offers an alternative way to shut down mTORC.
“We knew that nutrients were important in mTORC regulation but we didn’t know how they directly signal to mTORC. We discovered the nutrient signalling pathway is just as important to regulate mTORC as the oncogenic signalling pathway,” said study first author Sumeet Solanki, Ph.D., a research investigator at the Rogel Cancer Center.
Researchers confirmed their findings in cells and mice, where they saw that limiting amino acids stopped the cancer from growing and led to increased cell death. They also looked at tissue biopsies from patients with colon cancer, which confirmed high markers of mTORC correlated with more resistance to chemotherapy and worse outcomes. Solanki said this could provide an opportunity to direct treatment for patients with this marker.
“A low-protein diet won’t be standalone treatment. It has to be combined with something else, such as chemotherapy,” Solanki said.
The risk with a low-protein diet is that people with cancer often experience muscle weakness and weight loss, which limiting protein could exacerbate.
“Putting cancer patients on a protein-deficient diet long-term is not ideal. But if you can find key windows – like at the start of chemotherapy or radiation – when patients could go on a low protein diet for a week or two, we could potentially increase the efficacy of those treatments,” Shah said.
Further research will refine this concept of a therapeutic window to limit amino acids. Researchers will also seek to understand how these pathways are creating resistance to treatment and whether an inhibitor could block the GATOR complexes.
A systematic review has revealed that plant-based or plant-heavy diets may offer a level of protection against prostate cancer and other male sexual health issues according.
The analysis included 23 studies, 12 of which included prostate cancer, and suggested a link between a plant-based diet and reduced prostate cancer risk. Some evidence also suggested benefits for erectile dysfunction and benign prostate hyperplasia. The findings were reported at the Sexual Medicine Society of North America (SMSNA) annual meeting.
“Medicine has moved to a more holistic approach overall, and with that, more researchers have started to look into [the question of] ‘Can we use these plant-based diets to help manage and prevent conditions like prostate cancer, erectile dysfunction [ED], and benign prostate hyperplasia [BPH]?’ Nathan Feiertag, MD, a medical student at Albert Einstein College of Medicine in New York City, told MedPage Today. “There were relatively few studies that we were able to find for this literature review, but that’s the current state.”
With the growing popularity of plant-based diets, studies have shown their benefits for patients with hypertension or diabetes. Dr Feirtag said that less is known about their effect on prostate cancer, ED and BPH.
Dr Feiertag told MedPage Today that “Urologists can maybe consider our review as an opportunity to incorporate or modify existing diet counselling for their patients, especially the ones who are eager to implement lifestyle changes, particularly as it pertains to prostate hyperplasia, ED, and prostate cancer.”
The review mostly consisted of cohort studies, along with cross-sectional studies, and a handful of randomised controlled trials. Studies included those on vegan diets, vegetarian diets, and plant-heavy diets, such as the Mediterranean diet. In a number small cohort studies, there was a significant decrease in prostate cancer velocity, though not sustained at six months, Dr Feiertag said.
Two of the five ED studies found a link between plant-based diets and improved International Index of Erectile Function scores, though one reported worsening scores. The two studies included on ED reported a reduced relative risk of ED for patients on plant-based diets. For BPH, five of six studies reported an inverse relationship between plant-based diets and developing BPH.
Limitations including not being generalisable due to the number of observational and cohort studies that relied on patient-reported evaluations of diet. Additional high-quality studies are needed to confirm the link between diet and urological conditions.
Fortunately, the studies all reported no non-association or no harmful effects of following a plant-based or plant-forward diet. “For the patients who want to change their diet, this is useful for them. It definitely won’t hurt,” Dr Feiertag told MedPage Today.
