Not all dietary fibers are equal

 

The health benefits of dietary fiber vary across individuals and may depend on the specific type of fiber and the dose consumed, researchers report April 28th in the journal Cell Host & Microbe.

“Our results demonstrate that the physiological, microbial, and molecular effects of individual fibers differ substantially,” says senior study author Michael Snyder (@SnyderShot), a geneticist at Stanford School of Medicine. “Further, our results demonstrate the tantalizing prospect of using targeted fibers, mediated by the microbiome, to drive health and systems biology in a predictable, personalized direction.”

High-fiber diets reduce the risk of heart attack, stroke, and cardiovascular disease. They act by lowering cholesterol and promoting a healthier lipid profile for people eating a Westernized diet. Dietary fibers are carbohydrates that are selectively metabolized by gut microbes but are otherwise indigestible by humans. Understanding how they affect the microbiome and in turn human biochemistry and physiology is critical for effectively using dietary fiber supplementation to improve human health.

Chemically, fibers are diverse in length, branching, solubility, charge, and other properties. “They are usually studied as complex mixtures from their plant source,” Snyder says. “There is a need for determining the unadulterated effects of individual fibers on the microbiome and for establishing associated health biomarkers, ideally by testing different fibers on the same individuals.”

To address this need, Snyder and his colleagues set out to understand how purified individual fiber components affect the same group of participants. Specifically, they investigated the physiological effects of dietary supplementation with two common and structurally distinct soluble fibers: arabinoxylan (AX), which is common in whole grains, and long-chain inulin (LCI), which is found in onions, chicory root, and Jerusalem artichokes.

The researchers used stool metagenomics, plasma proteomics, metabolomics, lipidomics, and analyzed serum cytokines and clinical values in 18 participants. “Fiber is associated with improved metabolic and cardiovascular health, but understanding the effects of individual fibers on microbial and metabolomic response has not been studied using a multiomics dataset,” Snyder says.

The participants consumed 10 grams of fiber per day during the first week, 20 grams per day during the second week, and 30 grams per day during the third week. The results revealed fiber- and often dose-dependent microbial and systemic responses. On average, AX consumption was associated with a significant reduction in low-density lipoprotein (LDL), known as the bad cholesterol, and an increase in bile acids, which may be contributing to the cholesterol reduction. Yet individual responses varied, and some participants saw little to no change in cholesterol levels.

“Several high-fiber foods have cholesterol-reducing effects, and our study suggests that these reductions may be driven by individual constituents of the mix of fibers in unrefined plant foods,” Snyder says.

Meanwhile, LCI was associated with a modest decrease in inflammation markers and an increase in the abundance of Bifidobacterium—a generally beneficial type of gut microbe known to produce healthy short-chain fatty acids. But at the highest dose, there was an increase in inflammation and levels of a liver enzyme called alanine aminotransferase, suggesting that too much of this fiber may be harmful. Again, these potentially negative responses were variable across the participants.

Two limitations of the study were its short duration and the small number of participants. But according to the authors, the study provides insights into mechanisms behind fiber-induced cholesterol reduction, reveals the deleterious effects of high inulin consumption, and highlights the association of individual, purified fibers with the microbiome.

“Overall, our findings show that the benefits of fiber are dependent on fiber type, dose, and participant—a landscape of factors resulting from interactions between fiber, the gut microbiome, and host,” Snyder says. “These 

The longevity diet

 Examining a range of research from studies in laboratory animals to epidemiological research in human populations gives scientists a clearer picture of what kind of nutrition can offer the best chance for a longer, healthier life, said USC Leonard Davis School of Gerontology Professor Valter Longo.

In an article that includes a literature review published April 28 in Cell, Longo and coauthor Rozalyn Anderson of the University of Wisconsin describe the “longevity diet,” a multi-pillar approach based on studies of various aspects of diet, from food composition and calorie intake to the length and frequency of fasting periods.

“We explored the link between nutrients, fasting, genes, and longevity in short-lived species, and connected these links to clinical and epidemiological studies in primates and humans, including centenarians,” Longo said. “By adopting a multi-system and multi-pillar approach based on over a century of research, we can begin to define a longevity diet that represents a solid foundation for nutritional recommendation and for future research.”

What—and when—to eat for longevity

Longo and Anderson reviewed hundreds of studies on nutrition, diseases and longevity in laboratory animals and humans and combined them with their own studies on nutrients and aging. The analysis included popular diets such as the restriction of total calories, the high-fat and low-carbohydrate ketogenic diet, vegetarian and vegan diets, and the Mediterranean diet.

The article also included a review of different forms of fasting, including a short-term diet that mimics the body’s fasting response, intermittent fasting (frequent and short-term) and periodic fasting (two or more days of fasting or fasting-mimicking diets more than twice a month). In addition to examining lifespan data from epidemiological studies, the team linked these studies to specific dietary factors affecting several longevity-regulating genetic pathways shared by animals and humans that also affect markers for disease risk, including levels of insulin, C-reactive protein, insulin-like growth factor 1, and cholesterol.

The authors report that the key characteristics of the optimal diet appear to be moderate to high carbohydrate intake from non-refined sources, low but sufficient protein from largely plant-based sources, and enough plant-based fats to provide about 30 percent of energy needs. Ideally, the day’s meals would all occur within a window of 11-12 hours, allowing for a daily period of fasting, and a 5-day cycle of a fasting or fasting-mimicking diet every 3-4 months may also help reduce insulin resistance, blood pressure and other risk factors for individuals with increased disease risks, Longo added.

He described what eating for longevity could look like in real life: “Lots of legumes, whole grains, and vegetables; some fish; no red meat or processed meat and very low white meat; low sugar and refined grains; good levels of nuts and olive oil, and some dark chocolate.”

What’s next for the longevity diet

The next step in researching the longevity diet will be a 500-person study taking place in southern Italy, Longo said. The longevity diet bears both similarities and differences to the Mediterranean-style diets often seen in super-aging “Blue Zones,” including Sardinia, Italy; Okinawa, Japan; and Loma Linda, California. Common diets in these communities known for a high number of people age 100 or older are often largely plant-based or pescatarian and are relatively low in protein. But the longevity diet represents an evolution of these “centenarian diets,” Longo explained, citing the recommendation for limiting food consumption to 12 hours per day and having several short fasting periods every year.

In addition to the general characteristics, the longevity diet should be adapted to individuals based on sex, age, health status, and genetics, Longo noted. For instance, people over age 65 may need to increase protein in order to counter frailty and loss of lean body mass, as Longo’s own studies illustrated that higher protein amounts were better for people over 65 but not optimal for those under 65, he said.

For people who are looking to optimize their diet for longevity, he said it’s important to work with healthcare provider specialized in nutrition on personalizing a plan focusing on smaller changes that can be adopted for life, rather than big changes that will cause an harmful major loss of body fat and lean mass, followed by a regain of the fat lost, once the person abandons the very restrictive diet.

“The longevity diet is not a dietary restriction intended to only cause weight loss but a lifestyle focused on slowing aging, which can complement standard healthcare and, taken as a preventative measure, will aid in avoiding morbidity and sustaining health into advanced age,” he said.

Seven hours of sleep is optimal in middle and old age

 

Seven hours is the ideal amount of sleep for people in their middle age and upwards, with too little or too much little sleep associated with poorer cognitive performance and mental health, say researchers from the University of Cambridge and Fudan University.

Sleep plays an important role in enabling cognitive function and maintaining good psychological health. It also helps keep the brain healthy by removing waste products. As we get older, we often see alterations in our sleep patterns, including difficulty falling asleep and staying asleep, and decreased quantity and quality of sleep. It is thought that these sleep disturbances may contribute to cognitive decline and psychiatric disorders in the aging population.

In research published today in Nature Aging, scientists from the UK and China examined data from nearly 500,000 adults aged 38-73 years from the UK Biobank. Participants were asked about their sleeping patterns, mental health and wellbeing, and took part in a series of cognitive tests. Brain imaging and genetic data were available for almost 40,000 of the study participants.

By analysing these data, the team found that both insufficient and excessive sleep duration were associated with impaired cognitive performance, such as processing speed, visual attention, memory and problem-solving skills. Seven hours of sleep per night was the optimal amount of sleep for cognitive performance, but also for good mental health, with people experiencing more symptoms of anxiety and depression and worse overall wellbeing if they reported sleeping for longer or shorter durations.

The researchers say one possible reason for the association between insufficient sleep and cognitive decline may be due to the disruption of slow-wave – ‘deep’ – sleep. Disruption to this type of sleep has been shown to have a close link with memory consolidation as well as the build-up of amyloid – a key protein which, when it misfolds, can cause ‘tangles’ in the brain characteristic of some forms of dementia. Additionally, lack of sleep may hamper the brain’s ability to rid itself of toxins.

The team also found a link between the amount of sleep and differences in the structure of brain regions involved in cognitive processing and memory, again with greater changes associated with greater than or less than seven hours of sleep.

Having a consistent seven hours’ sleep each night, without too much fluctuation in duration, was also important to cognitive performance and good mental health and wellbeing. Previous studies have also shown that interrupted sleep patterns are associated with increased inflammation, indicating a susceptibility to age-related diseases in older people.

Professor Jianfeng Feng from Fudan University in China said: “While we can’t say conclusively that too little or too much sleep causes cognitive problems, our analysis looking at individuals over a longer period of time appears to support this idea. But the reasons why older people have poorer sleep appear to be complex, influenced by a combination of our genetic makeup and the structure of our brains.”

The researchers say the findings suggest that insufficient or excessive sleep duration may be a risk factor for cognitive decline in ageing. This is supported by previous studies that have reported a link between sleep duration and the risk of developing Alzheimer’s disease and dementia, in which cognitive decline is a hallmark symptom.

Professor Barbara Sahakian from the Department of Psychiatry at the University of Cambridge, one of the study’s authors, said: “Getting a good night’s sleep is important at all stages of life, but particularly as we age. Finding ways to improve sleep for older people could be crucial to helping them maintain good mental health and wellbeing and avoiding cognitive decline, particularly for patients with psychiatric disorders and dementias.”

Plant-based diet and more physical activity may help reduce the risk of colorectal cancer

 ROCHESTER, Minn. — A review article by Mayo Clinic researchers emphasizes that early onset colorectal cancer, defined as being diagnosed when younger than 50, continues to steadily increase in the U.S. and other higher income countries. This increase, along with a decline in later-onset cases due primarily to screening have shifted the median age at diagnosis from 72 years in the early 2000s to 66 years now.

We are seeing a significant increase in the numbers of younger patients with colorectal cancer at Mayo Clinic, as is occurring around the country. "It is important to recognize that most cases are without a known hereditary basis and have no identifiable cause," says Frank Sinicrope, M.D., an oncologist and gastroenterologist at Mayo Clinic Cancer Center in Minnesota, and an author of the study. The article was published in The New England Journal of Medicine.

"Public health measures are needed to address risk factors for colorectal cancer, beginning in adolescence, including poor dietary habits and physical inactivity, says Dr. Sinicrope." He notes that while the specific causes of early onset colorectal cancer remain elusive, data suggest that diets with high intake of red and processed meat, as well as refined grains and processed sugar can alter gut microbial composition, resulting in chronic inflammation, increased rates of obesity and a higher risk of colorectal cancer.

"Evidence suggests that a plant-based diet and more physical activity may help to promote a more a favorable gut microbiome, which in turn may reduce the risk of colorectal cancer," says Dr. Sinicrope.

He says ongoing research involving large cohorts and international consortia aim to identify early life exposures that are most relevant to the development of early onset colorectal cancer.

Poor diet associated with increased diabetes risk

 Genetic risk factors and diet quality are independently associated with type 2 diabetes; a healthy diet is linked to lower diabetes risk across all levels of genetic risk. That’s the conclusion of a study of more than 35,000 US adults publishing April 26th in PLOS Medicine by Jordi Merino of Massachusetts General Hospital, US, and colleagues.

Both genetic and lifestyle factors are known to contribute to individual susceptibility to type 2 diabetes. Previous studies have shown that adherence to a healthy lifestyle is associated with reduced risk of type 2 diabetes across genetic profiles, but whether genetic profiles, in part, interact with lifestyle factors was unclear. In the new study, researchers analyzed data from three extensive cohort studies, including 35,759 U.S. health professionals followed for 902,386 person-years of follow-up.

The team found that, irrespective of genetic risk, a low diet quality, as compared to high diet quality, was associated with a 30% increased risk of type 2 diabetes (Pinteraction=0.69). The relative risk of type 2 diabetes was 1.29 (95% CI 1.25-1.32, P<0.001) per standard deviation increase in the global polygenic score—one measure of genetic risk—and was 1.13 (1.09-1.17, P<0.001) per 10-unit decrease in Alternate Healthy Eating Index, a measure of diet quality. The joint association of low diet quality and increased genetic risk was similar to the sum of the risk for each factor alone (Pinteraction =0.30), further supporting independent associations. That said, one limitation of the study was that the cohort sampling might not necessarily generalize to other populations.

Merino adds, “This study provided evidence that the risk of type 2 diabetes attributed to increased genetic risk and low diet quality is similar to the sum of the risks associated with each factor alone. Such knowledge could serve to inform and design future strategies to advance the prevention of diabetes.”

T^he freely available paper in PLOS Medicine:

http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1003972 

Varied strength-training programmes increase strength, but not muscle mass

 For years, it has been assumed that variation in strength-training programmes impacts training outcomes. New research at the University of Copenhagen demonstrates that varied strength training has a positive effect on developing strength, but not on muscle growth.

According to the researchers, the answer as to why periodized strength training can promote the development of strength, but not muscle mass, is likely found in our nervous system. Photo: Getty Images

For years, the word around gyms has been that to put on muscle, a person needs to vary their training with regards to weight, repetitions and exercises. But in a new study from the University of Copenhagen’s Department of Nutrition, Exercise and Sports, researchers can see that so-called ‘periodized strength-training’ – where training is varied by increasing and decreasing variables such as the amount of weight lifted, as well as the number of repetitions – benefits strength development.

"The study establishes that periodized strength training is conducive to the development of strength, but not muscle mass. If one wants to get stronger, it is important to vary their training," is the main message from Associate Professor Jesper Lundbye-Jensen, the study’s last author.

Facts:

• Periodized strength training means that both the weight load and number of repetitions are increased and decreased from week to week. For example, a person can do fewer repetitions with more weight one week, before transitioning to more repetitions with fewer kilos the next.
   
• The researchers gathered 35 existing studies in the field with over 1200 participants from around the world, which they reviewed and analyzed anew.
   
• More than 800,000 Danes are active members of a fitness center.

According to the researchers, the answer as to why periodized strength training can promote the development of strength, but not muscle mass, is likely found in our nervous system.

"As people become stronger from periodized workouts compared to non-periodized workouts, it is most likely due to the fact that strength training trains the nervous system as well, and thereby our ability to coordinate and activate muscles to a maximum," explains Jesper Lundbye-Jensen.

According to Lukas Moesgaard, the study’s first author, increasing muscle mass through strength training requires working out until fatigue sets in and putting in a sufficient number of hours at the gym to do so.

"The research suggests that strength training particularly results in muscle growth when training muscles to exhaustion. And, as a rule of thumb, more exercise leads to more muscle growth," he explains.

Trained people get strongest through regular variation

In the study, the researchers could also see that those who already train regularly achieved more progress in strength by varying the intensity of their weekly training and alternating between heavy- and light-lifting exercises.

The untrained, on the other hand, received the same benefit from training, regardless of whether the variation took place on a daily or weekly basis, or whether the training was adjusted linearly – i.e., by increasing loads as an individual gains strength – over an extended period of time.

"All in all, the study demonstrates that variation in weight load and the number of repetitions in strength training can help if one is keen on getting stronger, and that the variation should probably occur more often when one is trained than if one is untrained. However, our results also demonstrate that varying loads and the number of repetitions doesn’t seem to affect the amount of muscle growth," says Lukas Moesgaard.

The article is based on a scientific study known as a systematic review with meta-analysis, where researchers collect and review all relevant scientific literature in a given field.

A calorie-reduced diet can not only delay the development of metabolic diseases, but also has a positive effect on the immune system

 

A calorie-reduced diet can not only delay the development of metabolic diseases, but also has a positive effect on the immune system. Researchers have now shown for the first time that this effect is mediated by an altered gut microbiome*, which slows down the deterioration of the immune system in old age (immune senescence). The study has been published in Microbiome.

Around 2 billion people worldwide are overweight. Obesity increases the risk of developing high blood pressure, heart attack or type 2 diabetes mellitus and can cause inflammation in the body that weakens the immune system through an accumulation of specific memory T and B cells. This process is called immune senescence, an age-related change in the immune system. In obese people, the development of metabolic diseases such as type 2 diabetes can be delayed by a low-calorie diet. In addition, such a diet also has a positive effect on the immune system. But exactly how the positive effects are mediated and what role the gut microbiome plays in this process is not yet known. In a recent study**, researchers have now investigated the interactions between calorie-reduced diets, the microbiome, metabolism and the immune system.

Calorie-reduced diet alters the gut microbiome

For this purpose, they first analyzed how a very low-calorie diet (800 kcal/day for 8 weeks) affected the gut microbiome of an obese woman. In the next step, the researchers transplanted the gut microbiota before and after the diet intervention into germ-free mice  to establish a gnotobiotic mouse model. "In this way, we were able to determine the sole effects of the diet-shaped gut microbiome on metabolism and the immune system," said Reiner Jumpertz von Schwartzenberg, last author of the study and a scientist at the Institute of Diabetes Research and Metabolic Diseases of Helmholtz Munich at the University of Tübingen, a partner of the German Center for Diabetes Research (DZD). He led the study together with Hans-Dieter Volk and Joachim Spranger of Charité.

Diet-altered gut microbiome improves metabolism and delays immune senescence

By transplanting the diet-altered microbiota, glucose metabolism improved and fat deposition decreased. In addition, mass cytometry showed that the level of specific memory T and B cells was also reduced. "This indicates delayed immune senescence," said Julia Sbierski-Kind, first author of the study.

"These findings suggest that the positive effects of a low-calorie diet on metabolism and the immune system are mediated via the gut microbiome," Sbierski-Kind said. However, the authors of the study emphasize that the investigation has so far only been conducted with the microbiome of one person and that the experiments will have to be repeated with additional subjects to confirm the results. The new findings could also be interesting for medical practice in the long term. "An improved understanding of the complex interplay between diet, the microbiome and the immune system may set the stage for the development of new microbiome-based therapeutic avenues to treat metabolic and immune diseases," said Jumpertz von Schwartzenberg.

* Gut microbiome

The gut microbiome is the term used to describe the totality of all microorganisms and intestinal bacteria in our digestive tract. Among other things, it influences the immune system and the metabolism of its host.

Intense exercise while dieting may reduce cravings for fatty food

  In a study that offers hope for human dieters, rats on a 30-day diet who exercised intensely resisted cues for favored, high-fat food pellets.

The experiment was designed to test resistance to the phenomenon known as “incubation of craving,” meaning the longer a desired substance is denied, the harder it is to ignore signals for it. The findings suggest that exercise modulated how hard the rats were willing to work for cues associated with the pellets, reflecting how much they craved them.

While more research needs to be done, the study may indicate that exercise can shore up restraint when it comes to certain foods, said Travis Brown, a Washington State University physiology and neuroscience researcher.

“A really important part of maintaining a diet is to have some brain power—the ability to say ‘no, I may be craving that, but I’m going to abstain,’” said Brown, corresponding author on the study published in the journal Obesity. “Exercise could not only be beneficial physically for weight loss but also mentally to gain control over cravings for unhealthy foods.”

In the experiment, Brown and colleagues from WSU and University of Wyoming put 28 rats through a training with a lever that when pressed, turned on a light and made a tone before dispensing a high-fat pellet. After the training period, they tested to see how many times the rats would press the lever just to get the light and tone cue.

The researchers then split the rats into two groups: one underwent a regime of high-intensity treadmill running; the other had no additional exercise outside of their regular activity. Both sets of rats were denied access to the high-fat pellets for 30 days.  At the end of that period, the researchers gave the rats access to the levers that once dispensed the pellets again, but this time when the levers were pressed, they only gave the light and tone cue. The animals that did not get exercise pressed the levers significantly more than rats that had exercised, indicating that exercise lessened the craving for the pellets.

In future studies, the research team plans to investigate the effect of different levels of exercise on this type of craving as well as how exactly exercise works in the brain to curb the desire for unhealthy foods.

While this study is novel, Brown said it builds on the work of Jeff Grimm at Western Washington University who led the team that first defined the term “incubation of craving” and has studied other ways to subvert it. Brown also credited Marilyn Carroll-Santi’s research at University of Minnesota showing that exercise can blunt cravings for cocaine.

It is still an unsettled research question as to whether food can be addictive in the same way as drugs. Not all foods appear to have an addictive effect; as Brown pointed out, “no one binge eats broccoli.” However, people do seem to respond to cues, such as fast-food ads, encouraging them to eat foods high in fat or sugar, and those cues may be harder to resist the longer they diet.

The ability to disregard these signals may be yet another way exercise improves health, Brown said.

“Exercise is beneficial from a number of perspectives: it helps with cardiac disease, obesity and diabetes; it might also help with the ability to avoid some of these maladaptive foods,” he said. “We’re always looking for this magic pill in some ways, and exercise is right in front of us with all these benefits.”

Brisk walking may slow biological ageing process

A new study of genetic data published today (Wednesday) of more than 400,000 UK adults has revealed a clear link between walking pace and a genetic marker of biological age.

Confirming a causal link between walking pace and leucocyte telomere length (LTL) – an indicator of biological age – the Leicester-based team of researchers estimate that a lifetime of brisk walking could lead to the equivalent of 16 years younger biological age by midlife.

Researchers from the University of Leicester at the National Institute for Health Research (NIHR) Leicester Biomedical Research Centre studied genetic data from 405,981 middle-aged UK Biobank participants and found that a faster walking pace, independent of the amount of physical activity, was associated with longer telomere.

Telomeres are the ‘caps’ at the end of each chromosome, and hold repetitive sequences of non-coding DNA that protect the chromosome from damage, similar to the way the cap at the end of a shoelace stops it from unravelling.

Each time a cell divides, these telomeres become shorter – until a point where they become so short that the cell can no longer divide, known as ‘replicative senescence’. Therefore, scientists consider LTL a strong marker for ‘biological age’, independent from when an individual was born.

Although the relationship between telomere length and disease is not fully understood, the build-up of these senescent cells is believed to contribute to a range of symptoms we associate with aging, such as frailty and age-related diseases.

While the physical, mental, social and health benefits of walking are well-documented, this study is one of the first of its kind to compare genetic data with both self-reported walking speeds, as well as actual measurements of movement intensity from wearable activity tracking devices worn by participants.

Dr Paddy Dempsey is a Lecturer and Research Fellow at the University of Leicester and within the NIHR Leicester Biomedical Research Centre, part of the University Hospitals of Leicester (UHL) NHS Trust, and lead author on the study published in Communications Biology. He said:

“Previous research on associations between walking pace, physical activity and telomere length has been limited by inconsistent findings and a lack of high-quality data.

“This research uses genetic data to provide stronger evidence for a causal link between faster walking pace and longer telomere length. Data from wrist-worn wearable activity tracking devices used to measure habitual physical activity also supported a stronger role of habitual activity intensity (e.g. faster walking) in relation to telomere length.

“This suggests measures such as a habitually slower walking speed are a simple way of identifying people at greater risk of chronic disease or unhealthy ageing, and that activity intensity may play an important role in optimising interventions. For example, in addition to increasing overall walking, those who are able could aim to increase the number of steps completed in a given time (e.g. by walking faster to the bus stop). However, this requires further investigation.”

Researchers from the University of Leicester have previously shown using UK Biobank that as little as 10 minutes of brisk walking a day is associated with longer life expectancy, and that brisk walkers have up to 20 years’ greater life expectancy compared to slow walkers.

This new study demonstrates a causal link between brisk walking and telomere length and, significantly, not the other way round.

Tom Yates, senior author and Professor of Physical Activity, Sedentary Behaviour and Health at the University of Leicester and NIHR Leicester Biomedical Research Centre, added:

“Whilst we have previously shown that walking pace is a very strong predictor of health status, we have not been able to confirm that adopting a brisk walking pace actually causes better health. In this study we used information contained in people’s genetic profile to show that a faster walking pace is indeed likely to lead to a younger biological age as measured by telomeres.”

‘Investigation of a UK Biobank cohort reveals Causal Associations of Self-Reported Walking Pace with Telomere Length’ is published in Communications Biology.

The study was funded by the UK Medical Research Council, Biotechnology and Biological Sciences Research Council, British Heart Foundation, and supported by the NIHR Leicester BRC – a partnership between Leicester’s Hospitals, the University of Leicester and Loughborough University.

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JOURNAL

Communications Biology

DOI

10.1038/s42003-022-03323-x 

Mediterranean-style diet further linked to reduced risk of preeclampsia in pregnant women of all races

 

A new Johns Hopkins Medicine study that surveyed a racially diverse group of more than 8,000 women has added to evidence that following a Mediterranean-style diet could lower the risk of preeclampsia by at least 20%. Preeclampsia is a potentially lethal complication of pregnancy marked by high blood pressure and organ damage that emerges in late pregnancy or shortly after giving birth. Worldwide, it is a significant cause of maternal and fetal death and premature birth. In the United States, preeclampsia occurs in about 2%-6% of women, and twice as often in Black women compared with other racial groups.

A report on the new study, published April 20 in the Journal of the American Heart Association, found that women who self-reported eating a Mediterranean-style diet had a 20% or greater reduced risk of developing preeclampsia overall, even after accounting for a variety of other risk factors.

A Mediterranean diet largely consists of vegetables, fruits, fish, nuts, olive oil, whole grains and significantly limited amounts of red meats and processed foods. It has been linked for decades to reduced risk of cardiovascular disease.

“The United States is the only developed country with a rise in maternal mortality and morbidity, so we are excited about this new finding that strengthens recommendations that following a healthy diet is a safe way to help reduce the risk of pregnancy complications,” said Anum Minhas, M.D., M.H.S., chief cardiology fellow and lead author of the study.

For the study, researchers surveyed 8,507 women enrolled in the Boston Birth Cohort study between 1999 and 2014, a project originally designed to investigate the genetic and environmental factors associated with premature births. Overall, 47% of study participants were Black, 28% were Hispanic and the remaining 25% were white or other races. The average age was 28 years old.

Participants were asked to complete a dietary survey within 24-72 hours after giving birth, with questions focused on how often Mediterranean-style foods were consumed throughout pregnancy. Based on the responses, participants were assigned a diet score and sorted into three groups for analysis and comparison. Higher scores reflected higher frequencies of Mediterranean food consumption.

A total of 10% of surveyed women (848) developed preeclampsia. After adjusting the groupings for age, race, education, marital status, smoking, previous pregnancies and obesity, investigators report that:

• Compared with women who scored in the lowest group, women who scored in the middle and highest groups had 28% and 22% lower risks of preeclampsia.
• Black women who followed the Mediterranean-style diet and scored in the highest group had a 26% reduced risk of preeclampsia compared with those who scored in the lowest group.
• Women entering pregnancy with chronic high blood pressure had nine times the risk of preeclampsia compared with women entering pregnancy without a previous history of hypertension.
• Women with preexisting diabetes and obesity had twice the risk of preeclampsia compared with women without these conditions.

In addition to a healthy diet’s link to overall better pregnancy outcomes, the study, Minhas says, suggests that racial differences in rates of preeclampsia in the U.S. might be more related to socioeconomic factors than genetic or biological ones since all racial groups benefited from the diet.

“While our findings strengthen the case that adherence to a healthy diet reduces pregnancy complications, clinical trials are still needed to precisely evaluate the benefits of the Mediterranean diet in diverse groups of pregnant women,” cautions Noel Mueller, Ph.D., associate professor at the Johns Hopkins Bloomberg School of Public Health and senior author of the study.

“These new findings are exciting in context of other data showing that beyond pregnancy, a greater adherence to a Mediterranean-style diet is associated with reductions in blood pressure, improvement in blood lipids and lower risk of future cardiovascular events like heart attacks and strokes,” adds Erin Michos, M.D., associate director of preventive cardiology at Johns Hopkins Medicine and co-author of this study. “Lifestyle is impactful — one can change the trajectory of their health through following a healthy diet, combined with regular physical activity and not smoking.”

About 1 in 4 adults has an often-missed liver disorder linked to higher heart disease risk

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It is estimated that about one in four adults worldwide has a liver condition that is a risk factor for heart disease, according to a new American Heart Association scientific statement published today in the Association's peer-reviewed journal Arteriosclerosis, Thrombosis, and Vascular Biology. The condition, called nonalcoholic fatty liver disease (NAFLD), occurs when abnormally elevated amounts of fat are deposited in the liver, sometimes resulting in inflammation and scarring. The prevalence of NAFLD is an estimate, given the challenges in diagnosing the condition, which are detailed in the statement.

An American Heart Association scientific statement is an expert analysis of current research and may inform future guidelines. Professional organizations specializing in gastroenterology have previously published statements on the condition, however, they focus on liver toxicity (including scarring, cirrhosis and liver cancer) rather than heart disease risk. This is the Association's first statement about NAFLD.

"Nonalcoholic fatty liver disease (NAFLD) is a common condition that is often hidden or missed in routine medical care. It is important to know about the condition and treat it early because it is a risk factor for chronic liver damage and cardiovascular disease," said P. Barton Duell, M.D., FAHA, chair of the statement writing committee and professor of medicine in the Knight Cardiovascular Institute and Division of Endocrinology, Diabetes and Clinical Nutrition at Oregon Health & Science University in Portland, Oregon.

There are two types of NAFLD: one when only fat is present in the liver (called non-alcoholic fatty liver), and the other when inflammation and scarring are also present (called non-alcoholic steatohepatitis, or NASH). Excess alcohol intake can cause similar fat deposits and liver dysfunction, so the term NAFLD is used to differentiate between disease caused by excess alcohol intake vs. disease without alcohol as the underlying cause.

NAFLD may go undiagnosed for years, thus, the statement emphasizes the need for awareness and monitoring for NAFLD, access to improved screening tools and treatment and highlights the lifestyle changes to help prevent and treat the disorder.

NAFLD raises heart disease risk

Heart disease is the leading cause of death in people with NAFLD. The diseases share many of the same risk factors, including metabolic syndrome (elevated blood sugar and blood triglycerides, increased abdominal fat and high blood pressure); Type 2 diabetes; impaired glucose tolerance (prediabetes); and obesity. However, people with NAFLD are at higher risk of heart disease than people who have the same heart disease risk factors without the liver condition.

NAFLD may sometimes be prevented

NAFLD is often preventable by maintaining a healthy body weight, exercising regularly, eating a heart-healthy foods diet and managing conditions such as Type 2 diabetes and elevated triglycerides (a type of fat) in the blood. Genetic factors also play a role in whether a person develops NAFLD and whether it leads to NASH, cirrhosis or liver cancer.

"Although healthy living can help avert NAFLD in many individuals, some may develop NAFLD despite their best efforts," Duell said. "At the other end of the spectrum, some individuals may have a genetic makeup that protects them from developing NAFLD despite having obesity, Type 2 diabetes, metabolic syndrome, unhealthy dietary habits or being sedentary."

NAFLD can go undiagnosed for years

Most people with NAFLD are undiagnosed, creating a barrier to optimal medical management, according to the statement. The initial stages of NAFLD generally have no symptoms and people feel well, and routine blood tests may not show liver abnormalities. Often, elevated liver enzymes in blood, a possible sign of NAFLD, may be misattributed to a side effect of medication or to recent alcohol consumption. In addition, the absence of elevated liver enzyme levels does not rule out NAFLD or NASH.

According to the statement, a specialized ultrasound that measures liver elasticity, fat and stiffness (a result of scarring) in the liver can detect NAFLD. This type of liver scan is a noninvasive way to help diagnose and monitor treatment in NAFLD and NASH, yet it is underused. Liver biopsy is the definitive test for the diagnosis of more advanced stages of NAFLD, however, it is invasive and expensive.

"The lack of awareness of the high prevalence of NAFLD contributes to underdiagnosis," said Duell. "Individuals with risk factors for NAFLD warrant more careful screening."

If diagnosed in time, liver damage may be reversible

"Part of the good news about managing NAFLD is that healthy eating, regular exercise and weight loss or avoiding weight gain are all valuable interventions to improve health in most of us, regardless of whether we have NAFLD," said Duell.

Lifestyle changes are the cornerstone of treatment for early NAFLD. Dietary recommendations include reducing fat intake, limiting the consumption of simple sugars and choosing more fiber-rich vegetables and whole grains. A Mediterranean-style diet is the only specific dietary pattern recommended by a consortium of professional groups for the treatment of NAFLD and NASH. Avoiding alcohol is encouraged since even light alcohol intake can aggravate NAFLD and interfere with the liver's ability to heal.

Consultation with a dietitian may help people with NAFLD plan and maintain a healthful diet and lose weight, if needed. The statement cites research showing that losing 10% of body weight dramatically reduced liver fat and improved fibrosis, with lower levels of improvement with at least a 5% loss in body weight. Research also supports 20-30 minutes of physical activity per day to decrease liver fat and improve insulin sensitivity even in the absence of weight loss.

Medications may be needed to treat Type 2 diabetes, lower cholesterol or reduce weight. Weight loss surgery may be appropriate for some people because the resulting, marked weight loss can be an effective intervention for NAFLD. Optimal care may also involve consulting with a lipid specialist, endocrinologist or gastroenterologist.

This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association's Council on Atherosclerosis, Thrombosis and Vascular Biology; the Council on Hypertension; the Council on the Kidney in Cardiovascular Disease; the Council on Lifestyle and Cardiometabolic Health; and the Council on Peripheral Vascular Disease. American Heart Association scientific statements promote greater awareness about cardiovascular diseases and stroke issues and help facilitate informed health care decisions. Scientific statements outline what is currently known about a topic and what areas need additional research. While scientific statements may inform the development of guidelines, they do not make treatment recommendations. American Heart Association guidelines provide the Association's official clinical practice recommendations.

Co-authors are Vice Chair Francine Welty, M.D.; Michael Miller, M.D.; Alan Chait, M.D.; Gmerice Hammond, M.D., M.P.H.; Zahid Ahmad, M.D.; David E. Cohen, M.D., Ph.D.; Jay D. Horton, M.D.; Gregg S. Pressman, M.D.; Peter P. Toth, M.D., Ph.D. A

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Story Source:

Materials provided by American Heart Association. Note: Content may be edited for style and length.

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Journal Reference:

1. P. Barton Duell, Francine K. Welty, Michael Miller, Alan Chait, Gmerice Hammond, Zahid Ahmad, David E. Cohen, Jay D. Horton, Gregg S. Pressman, Peter P. Toth. Nonalcoholic Fatty Liver Disease and Cardiovascular Risk: A Scientific Statement From the American Heart Association. Arteriosclerosis, Thrombosis, and Vascular Biology, 2022; DOI: 10.1161/ATV.0000000000000153

Exercise during pregnancy reduces the risk of Type-2 Diabetes in offspring, study finds

A new study has demonstrated that maternal exercise during pregnancy improves the metabolic health of offspring, even when the mother is obese or on a high-fat diet. Physical exercise by the mother induces the placenta to secrete the key protein SOD3, resulting in a lowered risk of diabetes for the offspring. The findings in the paper identified the mechanisms behind this process.

A worrying trend

Maternal obesity and type 2 diabetes are on the rise. Over 30% of women of childbearing age in Western and Asian countries are classified as obese. Meanwhile, 630 million people are expected to be living with type 2 diabetes by 2045. Children born to obese mothers or mothers with type 2 diabetes have an increased risk of diabetes, even after going on to live healthy lives.

"With the growth of maternal obesity, a worrying cycle is forming where the risks of diabetes gets passed down from generation to generation," says assistant professor Joji Kusuyama from Tohoku University's Interdisciplinary Institute for Frontier Sciences (FRIS), and lead author of the study. "Stopping this cycle is a critical and pressing medical problem."

In the research group with Kusuyama was Laurie Goodyear, Nathan Makarewicz, Brent Albertson, Ana Alves-Wagner, Royce Conlin, Noah Prince, Christiano Alves, Krithika Ramachandran, and Michael Hirshman from the Joslin Diabetes Center; Chisayo Kozuka from RIKEN's Center for Integrative Medical Sciences; Toshihisa Hatta from Kanazawa's Medical University; Yang Xiudong and Yang Xia from the University of Texas at Houston; and Ryoichi Nagatomi from Tohoku University's Graduate School of Biomedical Engineering.

Previously, the group showed that exercise during pregnancy has tremendous benefits on an offspring's metabolic health, demonstrating that placenta-derived SOD3, which stands for supuroexide dismutase 3, plays a key role in transmitting the benefits of maternal exercise to the offspring. Building on this, the team set out to understand how SOD3 prevents the negative effects of obesity being passed from mother to child and found that SOD3 inhibited high-fat diet-induced abnormalities in the offspring's glucose metabolism.

The link between maternal and childhood obesity

Histone methylation plays a fundamental role in epigenetic modification - heritable changes to strands of DNA that do not affect the inherited base pairs. Methyl group (-CH3) attaches to an amino acid in the tail of histone proteins that wrap DNA, sometimes activating gene expression, sometimes inhibiting it.

When a mother consumes a diet heavy in fat, the histone H3 trimethylation H3K4me3 gets decreased in the fetal liver and hinders the expression of glucose metabolism genes.

This, the researchers discovered, is caused by two things. Reactive oxygen species (ROS) - oxygen in a reactivated and activated state which aids the body's metabolism and cellular functions - becomes elevated. Meanwhile, WDR82, a key protein that regulates histone methyltransferase, becomes oxidative, impairing protein functions.

The harmful effects of a maternal high-fat diet on an offspring's metabolism are reversed by maternal exercise. Genetic manipulation demonstrated that placental SOD3 is indispensable for the protective effects of maternal exercise on offspring.

The study also highlighted how crucial exercise is for negating this. When the researchers infused N-acetylcysteine (NAC), an antioxidant that boosts performance in the liver, into the fetal liver, it did not reproduce the results of SOD3. This suggests the naturally produced SOD3 from exercise during pregnancy is pivotal for the offspring's metabolic wellbeing.

Implications for the future

Given the simplicity and cost-effectiveness of exercise, encouraging mothers to exercise could help reverse the alarming rates of obesity and type-2 diabetes. The merits of SOD3 may not be limited to the metabolism stresses Kusuyama. "There may be wider benefits of this protein on other organs in the child. We are currently looking into the modifications in placenta tissue brought about by SOD3 that may have positive lifelong impacts on children."

The authors caution the study is only at the preclinical stage and its applicability to humans requires further studies. Additionally, certain aspects of the signaling pathway require further investigation.

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People high in conscientiousness, low in neuroticism, less likely to develop mild cognitive impairment

 

People who are organized, with high levels of self-discipline, may be less likely to develop mild cognitive impairment as they age, while people who are moody or emotionally unstable are more likely to experience cognitive decline late in life, according to research published by the American Psychological Association.

The research, published in the Journal of Personality and Social Psychology, focused on the role three of the so-called “Big Five” personality traits (conscientiousness, neuroticism and extraversion) play in cognitive functioning later in life.

“Personality traits reflect relatively enduring patterns of thinking and behaving, which may cumulatively affect engagement in healthy and unhealthy behaviors and thought patterns across the lifespan,” said lead author Tomiko Yoneda, PhD, of the University of Victoria. “The accumulation of lifelong experiences may then contribute to susceptibility of particular diseases or disorders, such as mild cognitive impairment, or contribute to individual differences in the ability to withstand age-related neurological changes.”

Individuals who score high in conscientiousness tend to be responsible, organized, hard-working and goal-directed. Those who score high on neuroticism have low emotional stability and have a tendency toward mood swings, anxiety, depression, self-doubt and other negative feelings. Extraverts draw energy from being around others and directing their energies toward people and the outside world. They tend to be enthusiastic, gregarious, talkative and assertive, according to Yoneda.

To better understand the relationship between personality traits and cognitive impairment later in life, researchers analyzed data from 1,954 participants in the Rush Memory and Aging Project, a longitudinal study of older adults living in the greater Chicago metropolitan region and northeastern Illinois. Participants without a formal diagnosis of dementia were recruited from retirement communities, church groups, and subsidized senior housing facilities beginning in 1997 and continuing to the present. Participants received a personality assessment and agreed to annual assessments of their cognitive abilities. The study included participants who had received at least two annual cognitive assessments or one assessment prior to death.

Participants who scored either high on conscientiousness or low in neuroticism were significantly less likely to progress from normal cognition to mild cognitive impairment over the course of the study.

“Scoring approximately six more points on a conscientiousness scale ranging 0 to 48 was associated with a 22% decreased risk of transitioning from normal cognitive functioning to mild cognitive impairment,” said Yoneda. “Additionally, scoring approximately seven more points on a neuroticism scale of 0 to 48 was associated with a 12% increased risk of transition.”

Researchers found no association between extraversion and ultimate development of mild cognitive impairment, but they did find that participants who scored high on extraversion – along with those who scored either high on conscientiousness or low in neuroticism – tended to maintain normal cognitive functioning longer than others.

For example, 80-year-old participants who were high in conscientiousness were estimated to live nearly two years longer without cognitive impairment compared with individuals who were low in conscientiousness. Participants high in extraversion were estimated to maintain healthy cognition for approximately a year longer. In contrast, high neuroticism was associated with at least one less year of healthy cognitive functioning, highlighting the harms associated with the long-term experience of perceived stress and emotional instability, according to Yoneda.

Additionally, individuals lower in neuroticism and higher in extraversion were more likely to recover to normal cognitive function after receiving a previous diagnosis of mild cognitive impairment, suggesting that these traits may be protective even after an individual starts to progress to dementia. In the case of extraversion, this finding may be indicative of the benefits of social interaction for improving cognitive outcomes, according to Yoneda.

There was no association between any of the personality traits and total life expectancy.

Yoneda noted that the findings are limited due to the primarily white (87%) and female (74%) makeup of the participants. Participants were also highly educated, with nearly 15 years of education on average. Future research is necessary on more diverse samples of older adults and should include the other two of the big five personality traits (agreeableness and openness) to be more generalizable and provide a broader understanding of the impact of personality traits on cognitive processes and mortality later in life, she said.

Healthy plant-based diets are associated with a lower risk of developing diabetes

 New research published in Diabetologia (the journal of the European Association for the Study of Diabetes [EASD]) finds that the consumption of healthy plant-based foods, including fruits, vegetables, nuts, coffee, and legumes, is associated with a lower risk of developing type 2 diabetes (T2D) in generally healthy people and support their role in diabetes prevention.

The study was conducted by Professor Frank Hu and colleagues at the Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA, and aimed to identify the metabolite profiles related to different plant-based diets and investigate possible associations between those profiles and the risk of developing T2D.

A metabolite is a substance used or produced by the chemical processes in a living organism and includes the vast number of compounds found in different foods as well as the complex variety of molecules created as those compounds are broken down and transformed for use by the body. Differences in the chemical makeup of foods means that an individual's diet should be reflected in their metabolite profile. Recent technological advances in the field of high-throughput metabolomics profiling have ushered in a new era of nutritional research. Metabolomics is defined as the comprehensive analysis and identification of all the different metabolites present within a biological sample.

Over 90% of diabetes cases are the type 2 form, and the condition poses a major threat to health around the world. Global prevalence of the disease in adults has more than tripled in less than two decades, with cases increasing from around 150 million in 2000 to over 450 million in 2019 and projected to rise to around 700 million in 2045.

The global health burden of T2D is further increased by the numerous complications arising from the disease, both macrovascular, such as cardiovascular disease, and microvascular, which damage the kidneys, the eyes, and the nervous system. The diabetes epidemic is primarily caused by unhealthy diets, having overweight or obesity, genetic predisposition, and other lifestyle factors such as a lack of exercise. Plant-based diets, especially healthy ones rich in high quality foods such as whole grains, fruits, and vegetables, have been associated with a lower risk of developing T2D but the underlying mechanisms involved are not fully understood.

The team conducted an analysis of blood plasma samples and dietary intake of 10,684 participants from three prospective cohorts (Nurses' Health Study, Nurses' Health Study II and Health Professionals Follow-up Study). Participants were predominantly white, middle-aged (mean age 54 years), and with a mean body mass index (BMI) of 25.6kg/m2.

Study participants completed food frequency questionnaires (FFQs) which were scored according to their adherence to three plant-based diets: an overall Plant-based Diet Index (PDI), a healthy Plant-based Diet Index (hPDI), and an Unhealthy Plant-Based Diet Index (uPDI). Diet indices were based on that individual's intake of 18 food groups: healthy plant foods (whole grains, fruits, vegetables, nuts, legumes, vegetable oils, and tea/coffee); unhealthy plant foods (refined grains, fruit juices, potatoes, sugar-sweetened beverages, and sweets/desserts); and animal foods (animal fats, dairy, eggs, fish/seafood, meat, and miscellaneous animal-based foods). The team distinguished between healthy and unhealthy plant foods according to their association with T2D, cardiovascular disease, certain cancers, and other conditions, including obesity and high blood pressure.

The researchers tested blood samples taken back in late 1980s and 1990s in the early phase of the three studies mentioned above to create metabolite profile scores for the participants, and any cases of incident T2D during the follow-up period of the study were recorded. Analyses of these data together with the diet index scores enabled the team to find any correlations between metabolite profile, diet index, and T2D risk.

The study found that compared with participants who did not develop T2D, those who were diagnosed with the disease during follow-up had a lower intake of healthy plant-based foods, as well as lower scores for PDI and hPDI. In addition, they had a higher average BMI, and were more likely to have high blood pressure and cholesterol levels, use blood pressure and cholesterol drugs, have a family history of diabetes, and be less physically active.

The metabolomics data revealed that plant-based diets were associated with unique multi-metabolite profiles, and that these patterns differed significantly between the healthy and unhealthy plant-based diets. In addition, metabolite profile scores for both the overall plant-based diet and the healthy plant-based diet were inversely associated with incident T2D in a generally healthy population, independent of BMI, and other diabetes risk factors, while no association was observed for the unhealthy plant-based diet. As a result, higher metabolite profile scores for PDI and hPDI indicated both closer adherence to those diets and having a lower risk of developing T2D.

Further analysis revealed that after adjusting for levels of trigonelline, hippurate, isoleucine, a small set of triacyglycerols (TAGs), and several other intermediate metabolites, the association between plant-based diets and T2D largely disappeared, suggesting that they might play a key role in linking those diets to incident diabetes. Trigonelline, for example, is found in coffee and has demonstrated beneficial effects on insulin resistance in animal studies, while higher levels of hippurate are associated with better glycaemic control, enhanced insulin secretion and lower risk of T2D. The team suggest that these metabolites could be investigated further and may provide mechanistic explanations of how plant-based diets can have a beneficial effect on T2D risk.

Professor Hu explains: "While it is difficult to tease out the contributions of individual foods because they were analysed together as a pattern, individual metabolites from consumption of polyphenol-rich plant foods like fruits, vegetables, coffee, and legumes are all closely linked to healthy plant-based diet and lower risk of diabetes."

The authors conclude: "Our findings support the beneficial role of healthy plant-based diets in diabetes prevention and provide new insights for future investigation…our findings regarding the intermediate metabolites are at the moment intriguing but further studies are needed to confirm their causal role in the associations of plant-based diets and the risk of developing type 2 diabetes."

Since they only collected blood samples at one point in time, the authors also believe that long-term repeated metabolomics data are needed to understand how dietary changes relate to changes in metabolome, thereby influencing T2D risk.