Hi, Premium Members!
Here’s your Friday dose of happy – a Science Digest chock full of interesting stories about the latest in nutrition, aging, and health. Read on to learn how…
Magnesium reduces pancreatic cancer risk.
Antibodies to the ACE2 receptor drive “long COVID” complications.
Allulose, a low-calorie sweetener, reduces blood sugar and insulin levels.
And much more!
In other news, we released a new video this week, featuring Dr. Roger Seheult and me. He and I tackle vaccine myths, questions, and rumors surrounding COVID-19. You won’t want to miss this one. Watch it here.
And be sure to sign up for our next Crowdcast live Q&A, coming up Saturday, October 2, at 9:30 am PDT. The code for this event is vitaminc. Remember, you can always access the most recent event code and Q&A calendar by visiting your dashboard at foundmyfitness.com/dashboard.
Catch ya later!
Rhonda and team
Science Digest – September 25, 2021
Magnesium reduces pancreatic cancer risk.
Pancreatic cancer is a rare, aggressive cancer, expected to claim the lives of more than 48,000 people this year. The lack of reliable screening tests and the vague, non-specific symptoms associated with pancreatic cancer make diagnosing the disease difficult and often late. Even when diagnosed early, pancreatic cancer has a poor prognosis, with only about 8 percent of people who develop the disease surviving longer than five years. Findings from a 2015 study suggest that magnesium reduces the risk of pancreatic cancer.
Magnesium is an essential mineral and a cofactor for hundreds of enzymes. It is involved in many physiological processes, including energy production, nucleic acid and protein synthesis, ion transport, and cell signaling. Magnesium deficiency is linked with increased risk of cardiovascular disease, osteoporosis, hypertension, and type 2 diabetes. Current magnesium intakes among people living in the United States are below the recommended dietary allowance (RDA) of 400-420 milligrams per day for males and 310-320 milligrams per day for females.
The study involved more than 66,000 adults between the ages of 50 and 76 years of age. The authors drew on data from the VITamins and Lifestyle Study, a cohort investigation of the associations of supplement use with cancer risk over an eight-year period.
Compared to study participants who met the RDA for magnesium, those who obtained 75 to 99 percent of the RDA were 42 percent more likely to develop pancreatic cancer, and those who obtained less than 75 percent of the RDA were 76 percent more likely to develop pancreatic cancer. For every 100-milligram-per-day decrease in magnesium intake, pancreatic cancer occurrence increased 24 percent. This association held true regardless of age, gender, body mass index, or non-steroidal anti-inflammatory drug use.
These findings suggest that magnesium reduces the risk of pancreatic cancer. They also underscore the importance of obtaining sufficient magnesium from supplemental or dietary sources, such as green leafy vegetables, unrefined grains, legumes, beans, and nuts. To bolster your magnesium intake, try this magnesium-rich smoothie.
Link to full publication.
Antibodies to the ACE2 receptor may drive “long COVID” symptoms.
SARS-CoV-2, the virus that causes COVID-19, binds to a receptor on a cellular receptor called angiotensin-converting enzyme 2 (ACE2) to enter the cell and replicate. This process markedly impairs ACE2 receptor function. Findings from a recent study suggest that antibodies for the ACE2 receptor develop after COVID-19 illness, driving long-term complications.
Most people recover from COVID-19 illness within a few weeks of symptom onset. Some, however, experience long-term complications that last several weeks or months, a phenomenon previously referred to as “long COVID” and now known as “Post-Acute Sequelae after SARS-CoV-2 infection,” or PASC.
Many of the acute symptoms of COVID-19 arise from overactivation of the body’s immune system following loss of ACE2 function. A key player in this overactivation is the renin-angiotensin-system, an important regulator of blood pressure, inflammation, and body fluid homeostasis. Disturbances in this system in the setting of SARS-CoV-2 infection can drive poor outcomes, such as acute respiratory distress syndrome and death in COVID-19.
The authors of the study analyzed blood samples for the presence of ACE2 antibodies in 67 people who had a history of previous SARS-CoV-2 infection and 13 people with no history of infection. They also measured ACE2 levels and activity in the participants’ blood.
Whereas 81 percent of the participants with previous infection had antibodies against ACE2, none of the participants who had never been infected had antibodies. Even though ACE2 levels were comparable in both infected and non-infected participants, ACE2 activity was lower among participants with antibodies compared to those without antibodies.
These findings suggest that following SARS-CoV-2 infection, antibodies against the ACE2 receptor can be detected in the blood. These antibodies, which likely form early in the disease process, impair ACE2 function, providing a potential mechanism for PASC. One limitation of this study is that the blood samples were de-identified, meaning that they carried no identifiers or information about whether the samples were from people who experienced long-term complications of COVID-19.
Link to full publication.
Learn more about the role ACE2 plays in COVID-19 in this Q&A featuring Dr. Rhonda Patrick.
Allulose reduces blood sugar and insulin levels.
Foods with a high glycemic index, such as sugar-sweetened soft drinks, desserts, and white bread products, contain sugars that are rapidly absorbed into the bloodstream, causing hyperglycemia (high blood glucose). Regular consumption of high glycemic foods may lead to insulin resistance, type 2 diabetes, and obesity. Low-calorie sweeteners (i.e., artificial sweeteners) such as allulose have a low glycemic index and can be used in place of sugar to reduce the intake of calories and high-glycemic carbohydrates; however, the effects of allulose in addition to sugar require further investigation. Findings published in a new report show that allulose significantly reduces glucose and insulin levels following sugar consumption.
Allulose is a rare sugar that can be found in small amounts in some fruits and grains and is sold as a low-calorie sweetener. Allulose is an epimer of fructose, meaning its chemical structure is very similar to fructose, giving it a nearly identical taste and texture; however, allulose provides only 0.4 calories per gram, compared to 4 calories per gram of fructose. A meta-analysis of previous research found that small doses of allulose improved glucose and insulin regulation; however, additional randomized controlled trials are needed, especially in Western populations and in people without type 2 diabetes.
The researchers recruited 30 participants (average age, 33 years) without type 2 diabetes and asked them to follow an individualized diet plan that provided 50 to 65 percent of calories from carbohydrates for up to eight weeks. Participants completed five study visits with one to two weeks between visits. At each visit, the researchers gave participants a beverage containing 50 grams of fructose (the amount in about 16 ounces of sugar-sweetened soda) with escalating doses of allulose (0, 2.5, 5, 7.5, or 10 grams). They measured glucose and insulin levels in the blood 0, 30, 60, 90, and 120 minutes after beverage consumption.
Allulose consumption reduced plasma glucose levels among participants in a dose-dependent manner, meaning as the dose of allulose increased from 0 to 10 grams, glucose levels at each time point decreased. The relationship between allulose and lower glucose levels was statistically significant at the 30-minute time point when either 7.5 or 10 grams of allulose was added to the fructose beverage. Compared to consuming a fructose beverage with no added allulose, the 10-gram dose of allulose also significantly decreased insulin levels 30 minutes after beverage consumption.
These findings demonstrate that allulose decreased glucose and insulin levels when added to a high-sugar beverage in healthy young people without diabetes. The authors suggested that future studies explore more of the mechanisms underlying these results.
Link to full publication.
Learn more about the effects of refined sugar on death rates, the brain, cancer, hormones, and more in this episode of the FoundMyFitness Podcast.
Delayed administration of Pfizer vaccine provides robust immunity.
Early data indicated that the Pfizer BioNTech mRNA vaccine demonstrated 90 percent efficacy in preventing infection from the alpha variant of SARS-CoV-2, the virus that causes COVID-19. The vaccine is typically administered in two doses, delivered three to four weeks apart. However, in the setting of vaccine shortages in some areas of the United States, some public health agencies have opted to deliver the vaccines on an extended interval. Findings from a recent study suggest that the vaccine elicits robust humoral immunity even when doses are delivered 16 weeks apart.
Humoral immunity, also known as antibody-mediated immunity, is an aspect of the immune response to specific antigens. It occurs when foreign material, such as a pathogen, is detected in the body. Lymphocytes are the primary drivers of humoral immunity.
The authors of the study measured humoral responses to two doses of the Pfizer BioNTech vaccine, delivered 16 weeks apart. The study included 22 people who had never been infected with SARS-CoV-2 and 21 people who had been infected. Among those who had previously been infected, ten participants did not receive a second dose, leaving 11 recipients of two doses. The authors collected blood samples for testing prior to the first dose, three weeks after the first dose, three months after the first dose, and three weeks after the second dose.
They found that providing a second dose to previously infected people did not significantly improve humoral responses. However, humoral responses in people who had never been infected increased markedly after the delayed second dose, achieving levels comparable to those observed in previously infected people.
These findings suggest that delaying the second dose of the Pfizer BioNTech vaccine as much as 16 weeks provides robust humoral immunity against SARS-CoV-2 infection. Learn more about COVID-19 vaccines in this episode featuring Dr. Roger Seheult and Dr. Rhonda Patrick.
Link to full publication.
Redefining the causes of obesity.
Obesity is a complex, multifactorial disease influenced by genetic, molecular, environmental, and behavioral factors. Characterized as having excessive body fat, obesity affects more than 650 million people worldwide and markedly increases a person’s risk for many chronic diseases, including cardiovascular disease, type 2 diabetes, cancer, and depression, among others. The authors of a recent report challenge the prevailing theory regarding the root causes of obesity.
A widely espoused concept in bodyweight management is the “eat less, exercise more” model, based on the principle that the number of calories consumed must be equivalent to (or less than) the number of calories expended. This model is supported by evidence suggesting that consuming high-fat foods drives overconsumption of calories due the foods’ high caloric levels, poor ability to provide satisfaction and fullness, and high “pleasure factor.” However, this concept, which forms the basis for national dietary guidelines, public health messaging, and dietary counseling, is inherently flawed, because it fails to take into consideration the biological mechanisms that promote weight gain. Ultimately it places blame on people with obesity and promotes stigmatization.
In recent decades, scientists have proposed a new model for explaining the root causes of obesity. In this model, body fat accumulation arises from hormonal responses to the consumption of high-glycemic load carbohydrates, ultimately driving a vicious cycle of body fat accumulation, hunger, and food intake. Commonly referred to as the “carbohydrate-insulin” model of obesity, this new paradigm reverses causation and provides a starting point for developing testable hypotheses.
The concepts presented in this report suggest that what a person eats, rather than how much, plays key roles in body weight management. The authors of the report posited that if the carbohydrate-insulin model is accurate, dietary modifications that limit carbohydrate intake, such as a ketogenic diet, may alter hormonal responses and promote fat oxidation and weight loss. Learn more about the health benefits of the ketogenic diet in this clip featuring Dr. Dominic D’Agostino.
Link to full publication.
Age-related changes in glucose homeostasis differ in commonly studied animal models.
Scientists use animal models to answer a variety of scientific questions about humans, from basic science to the pathophysiology of complex diseases. The reliability of these models is based on remarkable similarities in the biology of most mammals and the fact that many human diseases often affect other animal species. Findings from a recent study suggest that glucose homeostasis in aging differs between some commonly studied animals and humans.
As humans age, they experience significant changes in glucose metabolism and body composition. For example, insulin resistance is common among older adults, increasing their risk for type 2 diabetes. In addition, a person’s fat mass typically increases and muscle mass and bone mineral density decrease.
The authors of the study compared the trajectories, change rates, and death rates associated with fasting blood glucose, body weight, and fat mass in mice, nonhuman primates, and humans across their lifespans. They drew on data from the Study of Longitudinal Aging in Mice, the Nonhuman Primate Study, and the Baltimore Longitudinal Study of Aging.
They found that body weight and body fat across the three species followed similar trajectories, typically peaking in mid to late life and decreasing thereafter. However, fasting blood glucose levels decreased as the mice aged but increased as the nonhuman primates and humans aged. Having low glucose in mice and high glucose in nonhuman primates and humans translated to higher death rates.
These findings suggest that aging-related changes in glucose homeostasis differ among species and underscore the need for choosing appropriate animal models in aging research.
Link to study abstract.
Prebiotics may help restore circadian rhythms.
Circadian rhythms play critical roles in human health. Maintaining these rhythms can be challenging, especially for people who work night shifts or travel across multiple time zones. Findings from a new study suggest that prebiotics can help restore the body’s natural rhythms.
Prebiotics are food components that support the maintenance of a healthy microbiota and create an environment that is conducive to its survival. Fructo-oligosaccharides, galacto-oligosaccharides, and trans-galacto-oligosaccharides are the most common prebiotics. Their fermentation by gut microbiota produces short-chain fatty acids, including lactic acid, butyric acid, and propionic acid. Many commonly consumed fruits and vegetables, such as apples, bananas, and legumes, contain prebiotics.
The authors of the study fed rats either a prebiotic-enriched diet or a standard diet. After the rats had been on their respective diets for five weeks, the authors either flipped their light/dark schedules (roughly equivalent to flying across 12 time zones) or left them on a normal schedule once a week for eight weeks. They measured the animals’ sleep, brain activity, core body temperature, and locomotor activity. They also collected fecal samples from the animals and identified the types and number of gut microbes present.
The rats that ate the prebiotic-enriched diet resumed their normal sleep-wake cycles, core body temperature, and activity levels faster than the rats that ate the standard diet. The rats on the prebiotic diet also had greater abundance of several health-promoting microbes, including Ruminiclostridium 5, compared to those on the standard diet. Previous research indicates that Ruminiclostridium 5 is associated with improved sleep.
These findings suggest that eating a diet rich in prebiotics can help restore normal circadian rhythms following disruption, such as would occur after working shifts or traveling. Learn more about the effects of shiftwork on human health in this episode featuring Dr. Satchin Panda.
Link to study abstract.
Maternal diabetes causes birth defects by increasing cellular aging.
Neural tube defects, such as spina bifida and hydranencephaly, are a group of birth defects caused by incomplete development of the outer layers of the brain or spinal cord. Prenatal folate supplementation prevents an estimated 70 percent of neural tube defects, but additional therapies are needed. A recent report describes the relationship between maternal diabetes and abnormal cell aging in the fetal nervous system in mice.
Previous research has demonstrated a relationship between maternal diabetes and the incidence of neural tube defects in mice; however, the mechanisms that drive this relationship are unknown. High blood glucose levels cause oxidative damage and promote cellular senescence, a state in which cells are not metabolically active and do not reproduce. Aging cells accumulate damage over time and become senescent. In adults, an excess of senescent cells can promote inflammation and disease. In the developing fetus, senescence is vital for tissue remodeling and the building of limbs and organs. However, inappropriate senescence may lead to abnormal development.
The investigators used multiple mouse models in their study. In a first experiment, they used a strain of mice that are predisposed to developing diabetes and compared them to wild-type mice that are not predisposed to any disease. They injected pregnant females from both groups with either rapamycin, a compound that slows cellular aging by inhibiting the enzyme mTOR, or a placebo. In a second experiment, they examined embryos from diabetic and non-diabetic strains of knockout mice whose genomes do not contain the gene FoxO3a, a regulator of aging that may slow cellular senescence, to determine determine whether FoxO3a is responsible for maternal diabetes-induced premature senescence.
Maternal diabetes increased the abundance of biomarkers of cellular senescence and DNA damage in the lining of the brain in offspring. Pregnant diabetic mice that were exposed to rapamycin had offspring with lower levels of senescence biomarkers and fewer neural tube defects compared to placebo. Offspring from FoxO3a knockout mice experienced the same decrease in senescence biomarkers and neural tube defect rates as rapamycin-treated mice.
These results elucidate the mechanisms by which maternal diabetes can cause birth defects through metabolic changes that accelerate aging. Learn more about the role of cellular senescence in aging in this episode featuring Dr. Judith Campisi.
Link to full publication.
Maternal body weight influences risk of ADHD and obesity in offspring.
A woman’s body weight before and during pregnancy can have profound health effects on both mother and child. Women with obesity are at greater risk for developing pregnancy complications that can impair infant neurodevelopment, such as gestational diabetes, preeclampsia, preterm birth, and birth trauma. Findings from a new study suggest that maternal obesity contributes to attention deficit hyperactivity disorder (ADHD) and obesity in offspring.
ADHD is a neuro-behavioral condition characterized by inattention and/or hyperactive or impulsive behavior that interferes with functioning, learning, or development. Obesity is characterized as having excessive body fat – typically defined as having greater than 25 percent body fat for males and greater than 33 percent body fat for females.
The study included nearly 3,000 Finnish women and their offspring (~9,400 children). The authors of the study collected information about the children’s behavior and attention span from mothers and teachers. They gathered anthropometric data to determine the mothers’ and children’s body mass index (BMI), a proxy for body fatness. They used Mendelian randomization and polygenic risk scores to assess risk for ADHD and/or obesity. Mendelian randomization is a research method that provides evidence of links between modifiable risk factors and disease based on genetic variants within a population. A polygenic risk score estimates a person’s genetic propensity for developing a trait or disease.
They found that children whose mothers had a high BMI were more likely to develop ADHD, independent of genetic makeup. The Mendelian randomization analysis identified a bidirectional link between developing ADHD and obesity-related traits, suggesting that certain genetic variations may predispose children to both ADHD and obesity concurrently. The polygenic risk score revealed evidence for genetic overlap between having ADHD and greater BMI.
These finding suggest that both genetic and prenatal environmental factors influence the likelihood that a woman’s child will develop ADHD and obesity. They also underscore the importance of maintaining a healthy maternal body weight before and during pregnancy.
Link to full publication.
