Age-related brain atrophy refers to the gradual loss of neurons and shrinkage of brain tissue, which is a natural part of the ageing process. This condition can contribute to cognitive decline and various neurological issues. While ageing itself cannot be prevented, recent research from an 18-month dietary intervention provides hope that lifestyle and dietary changes may help slow down brain ageing.
Brain age, determined through MRI measurements of the hippocampus and lateral ventricles, reflects the biological aging of the brain, which may differ from a person’s chronological age. Chronological age is simply the number of years a person has lived, while brain age indicates the actual health of the brain. Generally, as we age, the hippocampus tends to shrink, and the lateral ventricles tend to expand, which serve as indicators of brain ageing. Some individuals may have a brain age that is younger or older than their chronological age. A younger brain age suggests better cognitive health, whereas an older brain age may indicate accelerated ageing and an increased risk of cognitive decline.
The study found that a decline in HbA1c and key markers of long-term blood sugar levels is associated with significant positive changes in specific brain regions commonly affected by age-related atrophy. It suggests that improved blood sugar control could be one of the most important factors in slowing down age-related brain changes.
Previous research has shown the benefits of the Green Mediterranean (Green-Med) diet, particularly its positive effects on blood sugar control. This diet is rich in polyphenols from plant-based sources such as Mankai—a high-protein aquatic plant—and green tea, while being low in red and processed meats. The current study reinforces these findings, suggesting that the Green-Med diet not only supports metabolic health but may also have protective effects on brain structure and function.
Researchers have long believed that the keto diet could help reduce an overactive immune system and benefit individuals with conditions such as multiple sclerosis.
Now, they have reason to believe it could be true.
Scientists at UC San Francisco have discovered that the diet makes the gut and its microbes produce two factors that attenuated symptoms of MS in mice.
If the study translates to humans, it points toward a new way of treating MS and other autoimmune disorders with supplements.
The keto diet severely restricts carbohydrate-rich foods like bread, pasta, fruit and sugar but allows unlimited fat consumption.
Without carbohydrates to use as fuel, the body breaks down fat instead, producing compounds called ketone bodies. Ketone bodies provide energy for cells to burn and can change the immune system.
Working with a mouse model of MS, the researchers found that mice who produced more of a particular ketone body, called β-hydroxybutyrate (βHB), had less severe disease.
The additional βHB also prompted the gut bacterium Lactobacillus murinus to produce an indole lactic acid (ILA) metabolite. This blocked the activation of T helper 17 immune cells involved in MS and other autoimmune disorders.
“What was exciting was discovering that we could protect these mice from inflammatory diseases simply by putting them on a diet supplemented with these compounds,” said Peter Turnbaugh, PhD, of the Benioff Center for Microbiome Medicine.
Earlier, Turnbaugh had shown that when secreted by the gut, βHB counteracts immune activation. This prompted a postdoctoral scholar working in his lab, Margaret Alexander, PhD, to see if the compound could ease the symptoms of MS in mice.
In the new study, which appears Nov. 4 in Cell Reports, the team examined how the ketone body-rich diet affected mice unable to produce βHB in their intestines and found that their inflammation was more severe.
However, when the researchers supplemented their diets with βHB, the mice got better.
To find out how βHB affects the gut microbiome, the team isolated bacteria from the guts of three mice fed either the keto diet, a high-fat diet, or the βHB supplemented high-fat diet.
Then, they screened the metabolic products of each group’s distinct microbes in an immune assay and determined that the diet’s positive effects were coming from a member of the Lactobacillus genus: L. murinus.
Two other techniques, genome sequencing and mass spectrometry, confirmed that the L. murinus they found produced indole lactic acid, which is known to affect the immune system.
Finally, the researchers treated the MS mice with either ILA or L. murinus, improving their symptoms.
Turnbaugh cautioned that the supplement approach still needs to be tested in people with autoimmune disorders.
“The big question now is how much of this will translate into actual patients,” he said. “But I think these results provide hope for the development of a more tolerable alternative to helping those people than asking them to stick to a challenging restrictive diet.”
Recent research published in the journal *Glia* has uncovered important connections between dietary choices and the progression of multiple sclerosis (MS). The study, led by Patrizia Casaccia, the founding director of the Advanced Science Research Center at the CUNY Graduate Center’s Neuroscience Initiative and an Einstein Professor of Biology and Biochemistry at the same institution, investigated the role of enzymes known as ceramide synthase 5 and 6. These enzymes are linked to the harmful effects of a diet high in palm oil on neurons in the central nervous system, which may lead to an increase in the severity of MS symptoms.
Multiple sclerosis (MS) is an inflammatory autoimmune disease characterized by significant damage to the myelin sheath, which protects nerves throughout the body. Current treatments aim to control the immune system’s response, but the exact mechanisms leading to neurodegeneration in MS are still not well understood. Previous research from the Casaccia lab and others has indicated that a high-fat diet can exacerbate the severity of MS symptoms. In their study, researchers investigated potential mechanisms by which a diet high in palm oil may negatively affect neuronal health.
Neuroprotection From Palm Oil-Induced Toxicity
In the experimental autoimmune encephalomyelitis (EAE) model of inflammatory demyelination, researchers discovered that mice with diets high in palm oil had a more severe disease course.
“We hypothesized that within neuronal cells, palm oil is transformed into a toxic substance known as C16 ceramide by specific enzymes called CerS5 and CerS6,” explained principal investigator Casaccia. “This ceramide causes damage to mitochondria, depriving neurons of the energy they require to combat inflammation in the brain. Consequently, we investigated whether inactivating these enzymes could provide neuroprotection.”
The researchers found that genetically deleting the enzymes CerS6 and CerS5 in neurons could prevent neurodegeneration in an experimental model of MS.
“This was true even when mice were given a diet high in palmitic acid,” said Damien Marechal, a research associate with the Casaccia Lab and co-first author of the paper. “This new information highlights a specific metabolic pathway that shows how dietary fats can exacerbate MS symptoms.”
Significance for MS Patients and Clinicians
The paper’s findings have significant implications for individuals diagnosed with MS, clinicians treating patients, and neuroscientists researching the disease. The work reinforces that lifestyle choices, such as diet, can profoundly impact the course of the disease. The study’s results build on previous concepts about careful dietary decisions in managing the symptoms of MS. The findings also identify potential molecules that could help slow diet-induced symptom severity.
“Our research provides a molecular explanation for how to protect neurons from the palm-oil-dependent creation of molecules that harm them,” said Casaccia. “We hope this information can empower patients to make informed dietary decisions that could positively impact the course of the disease while identifying strategies to counteract the effect of cerS5 and cerS6 in a neuron-specific fashion.”
A new study has found that a low-sugar diet in utero and in the first two years of life can meaningfully reduce the risk of chronic diseases in adulthood. This provides compelling new evidence of the lifelong health effects of early-life sugar consumption.
A study published in the journal Science reveals that children who had sugar restrictions during their first 1,000 days after conception faced up to a 35% lower risk of developing Type 2 diabetes and a 20% reduced risk of hypertension in adulthood. The research indicates that low sugar intake by mothers during pregnancy was sufficient to lower these health risks, and maintaining sugar restrictions after birth further enhanced the benefits.
Using an unintended “natural experiment” from World War II, researchers at the USC Dornsife College of Letters, Arts and Sciences, McGill University in Montreal, and the University of California, Berkeley, examined how sugar rationing during the war influenced long-term health outcomes.
The United Kingdom introduced limits on sugar distribution in 1942 as part of its wartime food rationing program. Rationing ended in September 1953.
The researchers used contemporary data from the U.K. Biobank, a database of medical histories and genetic, lifestyle and other disease risk factors, to study the effect of those early-life sugar restrictions on health outcomes of adults conceived in the U.K. just before and after the end of wartime sugar rationing.
“Studying the long-term effects of added sugar on health presents challenges,” explains Tadeja Gracner, a senior economist at the USC Dornsife Center for Economic and Social Research and the study’s corresponding author. “It is difficult to identify situations where individuals are randomly exposed to different nutritional environments early in life and tracked over a span of 50 to 60 years. The end of rationing provided us with a unique natural experiment that helped us overcome these obstacles.”
On average, during rationing, sugar intake was about 8 teaspoons (40 grams) per day. When rationing ended, sugar and sweets consumption skyrocketed to about 16 teaspoons (80 grams) per day.
Notably, rationing did not involve extreme food deprivation overall. Diets generally appeared to have been within today’s guidelines set by the U.S. Department of Agriculture and the World Health Organization, which recommend no added sugars for children under two and no more than 12 teaspoons (50g) of added sugar daily for adults.
The immediate and large increase in sugar consumption but no other foods after rationing ended created an interesting natural experiment: Individuals were exposed to varying levels of sugar intake early in life, depending on whether they were conceived or born before or after September 1953. Those conceived or born just before the end of rationing experienced sugar-scarce conditions compared to those born just after who were born into a more sugar-rich environment.
The researchers then identified those born in the U.K. Biobank data collected over 50 years later. Using a very tight birth window around the end of sugar rationing allowed the authors to compare midlife health outcomes of otherwise similar birth cohorts.
While living through the period of sugar restriction during the first 1,000 days of life substantially lowered the risk of developing diabetes and hypertension, for those later diagnosed with either of those conditions, the onset of disease was delayed by four years and two years, respectively.
Notably, exposure to sugar restrictions in utero alone was enough to lower risks, but disease protection increased postnatally once solids were likely introduced.
The researchers say the magnitude of this effect is meaningful as it can save costs, extend life expectancy, and, perhaps more importantly, improve quality of life.
In the United States, individuals with diabetes face average annual medical expenses of approximately $12,000. Additionally, an earlier diagnosis of diabetes is associated with a significantly reduced life expectancy; specifically, for each decade that diagnosis occurs earlier, life expectancy decreases by three to four years.
The researchers note that these numbers underscore the value of early interventions that could delay or prevent this disease.
Experts continue to raise concerns about children’s long-term health as they consume excessive amounts of added sugars during their early life, a critical period of development. Adjusting child sugar consumption, however, is not easy—added sugar is everywhere, even in baby and toddler foods, and children are bombarded with TV ads for sugary snacks, say the researchers.
“Parents need information about what works, and this study provides some of the first causal evidence that reducing added sugar early in life is a powerful step towards improving children’s health over their lifetimes,” says study co-author Claire Boone of McGill University and University of Chicago.
Co-author Paul Gertler of UC Berkeley and the National Bureau of Economics Research adds: “Sugar early in life is the new tobacco, and we should treat it as such by holding food companies accountable to reformulate baby foods with healthier options and regulate the marketing and tax sugary foods targeted at kids.”
This study is the first of a larger research effort exploring how early-life sugar restrictions affected a broader set of economic and health outcomes in later adulthood, including education, wealth, and chronic inflammation, cognitive function and dementia.
The study finds that a low-carbohydrate diet may improve beta-cell function in people with type 2 diabetes.
Adults with type 2 diabetes on a low-carbohydrate diet may see benefits to their beta-cell function, allowing them to manage their disease better and possibly discontinue medication, according to new research published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
Beta-cells are endocrine cells in the pancreas that produce and release insulin, the hormone that controls blood sugar levels.
More than 38 million Americans have diabetes, and over 90% of them have type 2 diabetes. Type 2 diabetes most often develops in people 45 or older, but more and more children, teens and young adults are also developing the disease.
People with type 2 diabetes have a compromised beta-cell response to blood sugar, possibly due in part to eating too many carbohydrates. Beta-cell failure or insufficiency on top of insulin resistance is responsible for the development and progression of type 2 diabetes.
“This study shows people with type 2 diabetes on a low-carbohydrate diet can recover their beta-cells, an outcome that cannot be achieved with medication,” said lead study author Barbara Gower, PhD, of the University of Alabama at Birmingham in Birmingham, Ala. “People with mild type 2 diabetes who reduce their carbohydrate intake may be able to discontinue medication and enjoy eating meals and snacks that are higher in protein and meet their energy needs.”
The researchers gathered data from 57 white and Black adults with type 2 diabetes, half on a low-carbohydrate diet and the other half on a high-carbohydrate diet. They examined their beta-cell function and insulin secretion at baseline and after 12 weeks.
All of the participants’ meals were provided. People on the carbohydrate-restricted diet ate 9% carbohydrates and 65% fat, and participants on the high-carbohydrate diet ate 55% carbohydrates and 20% fat.
The researchers found that those on a low-carbohydrate versus a high-carbohydrate diet saw improvements in the acute and maximal beta-cell responses, which were 2-fold and 22% greater, respectively. Within each race group, Black adults on a low-carbohydrate diet saw 110% greater improvements in the acute beta-cell response and White adults had improvements in the maximal beta-cell response that was 48% greater than their respective counterparts on the high-carbohydrate diet.
“Further research is needed to determine if a low-carbohydrate diet can restore beta-cell function and lead to remission in people with type 2 diabetes,” Gower said.
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