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Lifelong exposure to dietary isoflavones reduces risk of obesity
Max Rubner Institute (Germany), January 29 2023
Investigators from Max Rubner Institute zero in on obesity reduction due to a lifelong exposure to dietary isoflavones
According to news originating from Karlsruhe, Germany, research stated, “Traditional Asian diet rich in soy isoflavones (ISOs) is linked to a lower obesity prevalence. In lifelong and short-term exposure scenarios we investigated effects of an ISO-rich diet on the body composition and development of obesity in female rats.”
The Max Rubner Institute reported, “Female Wistar rats grew up on ISO-free or ISO-rich control diet (CON ISO: 467 mg/kg diet). Starting postnatal day 83, ovariectomized and intact animals received high calorie Western diet (WD) in the absence or presence of ISO (WD ISO: 431 mg/kg diet) for 12 weeks to induce obesity or maintained on respective control diet (CON). One group starting ISO exposure after ovariectomy mimics short-term ISO exposure in postmenopausal Western women. Lifelong but not short-term ISO exposure resulted in reduced body weight, visceral fat mass, serum leptin, and smaller adipocytes. ISO decreased hepatic SREBP-1c, ACC, FAS, and PPAR gamma mRNA expression in nonobese animals. Moreover, ovariectomy reduced skeletal muscle weight, which was antagonized by both short-term and lifelong ISO exposure. Our results indicate that in female rats lifelong but not short-term ISO intake reduces the risk to develop obesity.”
The research concluded: “Furthermore, lifelong and short-term ISO exposure may antagonize loss of skeletal muscle mass induced by ovariectomy.”
L-carnitine combination may promote muscle growth, strength in older adults
Tufts and Georgetown universities, February 1, 2023
Supplementation with a novel L-carnitine formulation may increase lean muscle mass and leg strength in healthy older adults compared to placebo, says a new study.
Eight weeks of supplementation with a combination of L-Carnitine (Lonza’s Carnipure), L-leucine, creatine, and vitamin D3 was also associated with an increase in the expression of the expression of mTOR (mammalian target of rapamycin), which is known to cause muscle cells to increase protein synthesis, according to results published in Nutrition & Metabolism .
“In our study, the increase in total mTOR correlated with the increase in muscle mass and strength observed after supplementation with the L-Carnitine-combination,” wrote scientists from KGK Synergize, Georgetown University Medical Center, Parexel, Tufts University, and Lonza.
“Targeting and increasing mTOR expression/activity has been proposed to attenuate age-associated sarcopenia. Our data suggest a chronic effect of the L-Carnitine-combination on protein anabolism by increasing mTOR, as evidenced by increased muscle mass and functional strength.”
Muscle loss is a natural part of aging, and researchers have estimated that, after the age of 50, we lose 1-2% of our muscles each year. Strength declines as well, at a rate of 1.5% per year beginning at 50 years and accelerating to 3% after the age of 60.
The researchers recruited 42 healthy older adults aged between 55 and 70 to participate in their randomized, double-blind placebo-controlled study. Participants were randomly assigned to one of three groups: The L-carnitine combination supplement (1,500 mg of L-carnitine, 2,000 mg of L-leucine, 3,000 mg of creatine, and 10 micrograms of vitamin D3), L-carnitine only, or placebo for eight weeks.
Results showed that, compared to placebo, the combination supplement resulted in a 63.5% improvement in the composite outcome, which measured muscle mass loss, muscle strength loss, and physical activity. However, this score did not change significantly in the L-Carnitine only group.
In addition, the L-carnitine-combination supplement was associated with a 1.0 kg increase in total lean muscle mass, a 0.35 kg increase in leg lean muscle mass, and a 1.0 kg increase in lower leg strength, and these were statistically significant compared with placebo.
Statistically significant increases in mTOR expression were observed in the L-Carnitine-combination group, compared to placebo and baseline values.
Chronic fatigue syndrome is associated with distinct changes in the microbiome
Columbia University & Jackson Laboratory, February 8, 2023
Over the past three years, the emergence of long-term effects associated with COVID-19 has led to increased focus on a disease with similar hallmarks and symptoms—myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Two studies published in the journal Cell Host & Microbe are taking a closer look at ME/CFS as it relates to the microbiome and the metabolites that microbial species produce.
Both studies found that ME/CFS is associated with reduced levels in the gastrointestinal microbiome of microbes known to produce the fatty acid butyrate. These microbiome disruptions could explain in part how the immune system becomes disrupted in people with ME/CFS.
“It’s important to note that this research shows correlation, not causation, between these microbiome changes and ME/CFS,” says Julia Oh, an associate professor at the Jackson Laboratory and senior author of one of the two papers. “But these findings are the prelude to many other mechanistic experiments that we hope to do to understand more about ME/CFS and its underlying causes.”
“This research demonstrates that there are robust bacterial signatures of gut dysbiosis in individuals with ME/CFS,” says Brent L. Williams, an assistant professor at Columbia University and senior author of the other paper. “It helps to expand on this growing field of research by pinpointing the structural and functional disturbances in the microbiome in a chronic disease that affects the quality of life of millions of people.”
ME/CFS is a chronic, complex, and systemic disease associated with neurological, immunological, autonomic, and energy metabolism dysfunctions. It has been recognized for decades, but its causes remain poorly understood. Like long COVID, it is believed in most cases to be triggered by exposure to viruses or other infectious agents.
Oh’s study used shotgun metagenomics to compare microbiome samples from people with both short-term ME/CFS (defined as those diagnosed in the previous four years; 74 patients) and long-term ME/CFS (defined as those who have had symptoms for more than 10 years; 75 patients) as well as 79 age- and sex-matched healthy controls.
The analysis showed that patients with short-term disease had a number of changes to their microbiomes with regard to diversity. Most notably, they had a depletion of microbes known to be butyrate producers. Butyrate is important for protecting the integrity of the gut barrier and is also known to play an important role in modulating the immune system.
In contrast, those with long-term disease had gut microbiomes that had reestablished and were more similar to the healthy controls. However, those participants had accumulated a number of changes in the metabolites in their blood plasma, including many of those related to the immune system. They also had differences in levels of certain types of immune cells compared with the healthy controls.
The study from the Columbia team found significant relationships between the severity of fatigue symptoms and levels of specific species of gut bacteria—in particular the butyrate-producing bacterium Faecalibacterium prausnitzii. It also revealed a higher overall load of bacteria in the stool and disturbances in the interactions among bacterial species in patients with ME/CFS.
150 minutes of aerobic exercise per week reduces liver fat, study finds
Pennsylvania State University, February 8, 2023
The 150 minutes of moderate to intense aerobic activity per week that is recommended by the U.S. Department of Health and Human Services can significantly reduce liver fat, according to new research by Penn State College of Medicine researchers. The team’s meta-analysis of 14 previous studies confirms that exercise leads to clinically meaningful reductions in liver fat for patients with nonalcoholic fatty liver disease.
While prior research suggested that physical activity was beneficial, it had not determined the specific amount of exercise needed to make clinically meaningful improvement.
“Our findings can give physicians the confidence to prescribe exercise as a treatment for nonalcoholic fatty liver disease,” said Jonathan Stine, associate professor of medicine and public health sciences, and hepatologist at Penn State Health Milton S. Hershey Medical Center. “Having a target amount of physical activity to aim for will be useful for health care and exercise professionals to develop personalized approaches as they help patients modify their lifestyles and become more physically active.”
Stine reviewed 14 studies with a total of 551 subjects who had NAFLD and participated in randomized, controlled trials involving exercise interventions. His team evaluated data pooled from all the studies including age, sex, body mass index, change in body weight, adherence to the exercise regimen and MRI-measured liver fat.
The researchers primary goal in the study was to examine the association between exercise training and a clinically relevant improvement in liver fat. Independent of weight loss, the team found exercise training was 3 1/2 times more likely to achieve clinically meaningful treatment response (greater than or equal to 30% relative reduction in MRI-measured liver fat) compared to standard clinical care.
In its secondary analysis, the team determined what the optimal “dose” of exercise was to achieve clinically meaningful improvements in liver fat. They found that 39% of patients prescribed greater than or equal to 750 metabolic equivalents of task (for example, 150 minutes per week of brisk walking) achieved significant treatment response compared to only 26% of those prescribed lesser doses of exercise.
This is the same amount of physical activity recommended by the American Gastroenterological Association and the European Association for the Study of the Liver. The results were published in the American Journal of Gastroenterology.
Red Rice Bran Extract Alleviates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease and Dyslipidemia
University of Phayao School of Medicine (Thailand), January 30, 2023
Red rice bran extract (RRBE) is rich in phytonutrients and has been shown to have anti-diabetic, anti-inflammatory, and antioxidant properties. However, its anti-hepatic steatosis and anti-dyslipidemic properties have not been thoroughly investigated.
This study examined the aforementioned properties of Red rice bran extract, the underlying mechanism by which it alleviated non-alcoholic fatty liver disease in high-fat diet (HFD)-fed mice, and its major bioactive constituents.
The mice were divided into four groups based on their diet: (1) low-fat diet (LFD), (2) LFD with high-dose RRBE, (3) HFD, and (4) HFD with three different doses of Red rice bran extract (0.25, 0.5, and 1 g/kg/day).
The administration of RRBE, especially at medium and high doses, significantly mitigated HFD-induced hepatosteatosis and concomitantly improved the serum lipid profile.
Further, RRBE modified the level of expression of lipid metabolism-related genes (adipose triglyceride lipase (ATGL), cluster of differentiation 36 (CD36), lipoprotein lipase (LPL), liver X receptor alpha (LXRα), sterol regulatory element-binding protein-1c (SREBP-1c), SREBP-2, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), and carnitine palmitoyltransferase 1A (CPT1A) in hepatic or adipose tissues and improved the expression of hepatic high-density lipoprotein cholesterol (HDL-C) cmetabolism-related genes (hepatic lipase (HL) and apolipoprotein A-ǀ (ApoA-ǀ)).
Red rice bran extract also attenuated markers of liver injury, inflammation, and oxidative stress, accompanied by a modulated expression of inflammatory (nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase (iNOS)), pro-oxidant (p47phox), and apoptotic (B-cell lymphoma protein 2 (Bcl-2)-associated X and Bcl-2) genes in the liver.
High-performance liquid chromatography analyses indicated the presence of protocatechuic acid, γ-oryzanol, vitamin E, and coenzyme Q10 in RRBE. Our data indicate that RRBE alleviates HFD-induced hepatosteatosis, dyslipidemia, and their pathologic complications in part by regulating the expression of key genes involved in lipid metabolism, inflammation, oxidative stress, and apoptosis.
Alzheimer’s: Healthy lifestyle linked to slower memory decline, regardless of genetic risk
Capital Medical University (China), February 2, 2023
- Researchers followed 29,072 older adults (60 years old and over) over 10 years to investigate the link between lifestyle choices and memory loss.
- They found a link between a healthy lifestyle and slower memory decline, even in the presence of the APOE Ɛ4 gene, which is associated with Alzheimer’s disease.
- The researchers hope their findings will inform public health initiatives seeking to prevent memory loss in older adults.
The gradual loss of thinking abilities such as memory, reasoning, and psychomotor speed is a natural part of aging. However, studies such as the FINGER clinical trial have shown that it is possible to prevent cognitive decline through lifestyle improvements.
Dr. Jianping Jia, Ph.D., neurologist and professor at Capital Medical University, Beijing, China, and his colleagues investigated the combined effects of six lifestyle factors on memory decline in a large study population over a 10-year period.
The researchers recruited 29,072 study participants from North, South, and West China aged 60 or older with typical cognitive functions. Their mean age was 72.2 years, and 51.5% were men.
Genetic testing at baseline showed that 20.43% of the study participants were carriers of the APOE ε4 gene, the strongest known risk factor for Alzheimer’s disease and related dementias.
The researchers followed up with the participants at intervals over the next 10 years, in 2012, 2014, 2016, and 2019.
At baseline and each follow-up, the researchers assessed the participants’ memory using the Auditory Verbal Learning Test (AVLT), which includes measurement of immediate recall, short delay-free recall (3 min later), long delay-free recall (30 min later), and long delay recognition.
For this study, Dr. Jia and colleagues used American guidelines and the findings of previous studies to define a healthy lifestyle. They identified six factors:
- a healthy diet – adherence to the recommended intake of at least 7 of 12 eligible food items (fruits, vegetables, fish, meat, dairy products, salt, oil, eggs, cereals, legumes, nuts, and tea)
- regular physical exercise – at least 150 minutes of moderate-intensity activity or at least 75 minutes of vigorous-intensity activity per week
- Active social contact (participation in meetings or attending parties, visiting friends or relatives, traveling, and chatting online) – at least twice per week
- active cognitive activity (writing, reading, playing cards, mahjong, and other games) – at least twice per week
- never smokes (participants who had smoked less than 100 cigarettes in their lifetime) or used to smoke (participants who had quit smoking at least 3 years before the study)
- never drank alcohol or drank occasionally
All participants’ mean memory test scores declined continuously over the decade, consistent with how memory declines with age. However, the highest memory test scores were observed in the favorable lifestyle group and the lowest in the unfavorable lifestyle group, indicating that participants with favorable lifestyles had slower memory decline than those with unfavorable lifestyles (by 0.028 points/year).
The results showed that a healthy diet had the strongest effect on memory, followed by an active cognitive activity, regular physical exercise, active social contact, never or former smoking, and never drinking.