Fwd: Science Digest – August 27, 2021

Hi, Premium Members!

Welcome to another great issue of the Science Digest – a compendium of the latest scientific research about nutrition, health, and lifestyle, delivered straight to your inbox.

Read on to learn how…

COVID-19 may increase a person’s risk for neurodegenerative disease.
Fecal microbiota transplantation from young mice reverses aging effects.
Circadian rhythms influence brown fat activity.
Beige fat protects against dementia.

And more!

ICYMI: We have some awesome new videos to share:

Omega-3 may reduce the risk of premature death
My recent appearance on the Joe Rogan Experience podcast

And stand by for some new releases, coming soon:

#066 Dr. Mark Mattson on the Benefits of Stress, Metabolic Switching, Fasting, and Hormesis (audio only, video coming soon)
Dr. Ashley Mason, on whole-body hyperthermia and depression (audio, coming next week)
Dr. Bill Harris, on omega-3s (audio, week after next)


Rhonda and team

Science Digest – August 27, 2021
COVID-19 increases the risk of neurodegenerative disease.

COVID-19 is an acute illness caused by infection with the SARS-CoV-2 virus. Although most people recover from COVID-19 within a few weeks of presenting with symptoms, some experience chronic complications that affect multiple organs, including the heart, lung, kidney, skin, and brain. Findings from a recent study suggest that SARS-CoV-2 infection may promote chronic neurodegenerative disease.

Neurodegenerative diseases are disorders of the central nervous system that are characterized by chronic progressive loss of neuronal structure and function. They often emerge in mid-to-late adult life and are increasingly common, affecting roughly 37 million people worldwide – a number expected to increase as human lifespan increases. Although scientists don’t fully understand the underlying causes of most neurodegenerative diseases, protein aggregation in the brain is a widely accepted contributing factor. Previous research has shown that the SARS-CoV-2 spike protein binds to heparin (a protein involved in blood clotting) and heparin binding proteins, accelerating the aggregation of proteins involved in neurodegeneration.

Since many of the biological functions of a protein depend upon its affinity to bind with other proteins, the authors of the study used a web-based algorithm called HDOCK to gauge the binding affinity between the receptor binding domain of the SARS-CoV-2 spike protein between heparin and several aggregation-prone heparin-binding proteins implicated in neurodegenerative diseases, including amyloid-beta, alpha-synuclein, tau, and TAR DNA binding protein. They found that SARS-CoV-2 spike protein exhibited differing binding affinities for the various proteins. Heparin showed the highest affinity, with the others exhibiting affinity in decreasing order: prion, amyloid-beta, tau, TAR DNA binding protein, and alpha-synuclein.

These findings suggest that the heparin-binding site on the spike protein facilitates binding to amyloid proteins, potentially leading to neurodegeneration in the brain. Learn more about risk factors that drive Alzheimer’s disease, a type of neurodegenerative disease, in this episode featuring Dr. Dale Bredesen.

Link to full publication.

Fecal microbiota transplantation from young mice reverses aging effects.

Declines in brain function are common with aging due to metabolic and immune alterations that include changes to the gut microbiota, the community of microorganisms that inhabit the intestines. While a diverse microbial community with many species of beneficial bacteria is associated with improved nutritional status and reduced inflammation, older adults (especially residents of long-term care facilities) have perturbations in microbiota composition that increase the risk for cognitive decline and frailty. Findings presented in a recent report demonstrate that fecal microbiota transplantation from young to aged mice reverses age-associated cognitive impairment.

Fecal microbiota transplantation is a therapy in which microbes are isolated from the stool of a donor, processed, filtered, and administered to a recipient by nasogastric tube or enema. Previous research demonstrates the efficacy of fecal microbiota transplantation in treating infection with Clostridium difficile (commonly known as “C. diff”), a hospital-acquired infection that is difficult to treat with antibiotics, and a growing list of other diseases such as inflammatory bowel disease, metabolic syndrome, neurodevelopmental disorders (e.g., autism), and autoimmune diseases. Fecal microbiota transplantation improves health partially by increasing microbiota alpha diversity, meaning the number of species in an individual’s microbiota, often referred to as “richess.” A microbiota with high richness is more likely to contain key beneficial species, such as those that produce neuroprotective short chain fatty acids.

Given the wide range of diseases associated with gastrointestinal microbiota composition, its effects on aging are an area of intense interest. Prior investigations have demonstrated that transfer of the fecal microbiota from aged mice to young mice alters immunity, neurogenesis, and cognition; however, the consequence of fecal transplantation from young mice to aged mice is unknown.

The investigators performed their experiment using young and aged male mice. They assigned aged mice to receive a fecal microbiota transplant from either a young mouse (the experimental group) or an aged mouse (the control group). For further comparison, the researchers also assigned a group of young mice to receive a fecal microbiota transplant from another young mouse. Mice received the fecal microbiota transplant treatments once per day for three days, then twice weekly for four weeks. The mice completed a battery of tests to assess cognitive function. The researchers collected fecal samples in order to sequence the DNA of the microbiota and blood samples in order to measure hormones, cytokines, and other immune markers before and after the four weeks of treatment. Finally, they analyzed changes to gene expression and metabolism in the hippocampus, the brain region most-associated with age-related cognitive decline.

At baseline, young and aged mice had distinctly different microbiota composition. Following four weeks of microbiota transplantation, young mice, aged mice receiving a young transplant, and aged mice receiving an aged transplant all had similar microbiota composition. Aged mice tended to have more over-reactive T cells, dendritic cells, and macrophages, especially in the lymph nodes that line the intestines. Aged mice also showed enlargement of microglia (the predominant immune cells in the brain), a common feature of neurodegenerative diseases. Microbiota transplantation from young mice reversed these age-related effects on brain and peripheral immunity.

Hippocampal amino acid metabolism, which is necessary for neurotransmission and cognition, was impaired in aged mice, but restored following microbiota transplantation from young mice. The improvement in hippocampal metabolism in aged mice that received a young microbiota transplant translated to increased learning and long-term memory and reduced anxiety-related behaviors compared to aged mice receiving an aged microbiota transplant.

These results reveal the potential benefits of fecal microbiota transplantation from young donors as a therapy to promote healthy aging.

Link to full publication.
Learn more about how the gut microbiome regulates immune cell types in this video featuring Dr. Rhonda Patrick.

COVID-19 increases diabetes risk.

SARS-CoV-2, the virus that causes COVID-19, elicits both acute and chronic damage to the lungs and heart. Other parts of the body may be affected, too, including the kidneys, brain, skin, and olfactory tissues. Evidence from a recent study indicates that SARS-CoV-2 infects pancreatic beta cells, increasing the risk of developing diabetes.

Pancreatic beta cells are endocrine cells that produce, store, and release insulin. Beta cell failure and death are hallmarks of type 1 and type 2 diabetes. Multiple factors can promote beta cell death, including viral infection and hyperglycemia (high blood glucose), among others. Cases of new-onset diabetes, hyperglycemia, and diabetic ketoacidosis (a life-threatening condition that can accompany hyperglycemia) in people who have had COVID-19 are on the rise.

The SARS-CoV-2 virus exploits the ACE2 receptor to gain entry into cells and replicate. The ACE2 receptor is widely distributed in the body’s tissues, including pancreatic tissues. Other cellular factors involved in SARS-CoV-2 entry include transmembrane serine protease 2, transferrin receptor, and neuropilin 1. Neuropilin 1 participates in pain sensing and angiogenesis (the development of new blood vessels) and is a receptor for vascular endothelial growth factor-A.

The authors of the study collected pancreatic islet cells from healthy organ donors and from patients who had died from COVID-19 (collected during autopsy). They infected the cells with SARS-CoV-2 and performed various assays to determine the presence of cellular factors that contribute to infection. They measured insulin levels and glucose-stimulated insulin secretion, a measure of beta cell insulin release, in the infected cells.

They determined that SARS-CoV-2 infects beta cells, and this infection promotes beta cell death and decreases insulin release. They also found that beta cells express ACE2, transmembrane serine protease 2, transferrin receptor, and neuropilin 1. They posited that neuropilin 1, and possibly transferrin receptor, provide the stimulus for SARS-CoV-2 entry into beta cells.

These findings demonstrate that SARS-CoV-2 promotes beta cell death and may increase the risk of developing diabetes associated with COVID-19 illness. Learn about some of the other complications associated with COVID-19 in this episode featuring Dr. Roger Seheult.

Link to full publication.

Time-restricted eating improves athletic performance.

Time-restricted eating involves restricting the timing of food intake to certain hours of the day (typically within an 8- to 12-hour time window) without an overt attempt to reduce caloric intake. Increasing the amount of time spent fasting each day has been used to treat metabolic diseases such as type 2 diabetes and high cholesterol, increase muscle mass, decrease fat mass, and improve exercise performance. Findings of a recent report demonstrate the beneficial effects of time-restricted eating on exercise performance in power athletes.

Increasing muscle mass and decreasing fat mass is an important goal for many athletes because increasing their strength-to-mass ratio improves performance. While time-restricted eating is one strategy to improve body composition, previous research has shown that other types of intermittent fasting (e.g., religious fasting during Ramadan) decrease power output and endurance. Another study involving intermittent fasting with caloric restriction found similar deficits in athletic performance. The effects of long-term time-restricted eating without caloric restriction are unknown.

The researchers recruited healthy young males who were currently practicing a power sport at least three times per week and had been practicing for at least three years. Twelve participants (average age, 22 years) completed four weeks of time-restricted eating and four weeks of a standard meal pattern in random order with two weeks of wash-out in between. During the time-restricted eating period, participants consumed all of their food within an eight-hour window. The researchers measured body composition using X-ray and assessed athletic performance using the Wingate test, a cycling challenge that measures power and total work.

Time-restricted eating produced a significant increase in total work (a measure of force over a set distance) and average power output (a measure of work over time). These improvements translated to a one second reduction in sprinting time. The participants achieved this change after four weeks of time-restricted eating, but not after one week.

Time-restricted eating did not improve peak power, endurance, or body composition, but when combined with regular training, it did improve exercise performance in the athletes. Given that the difference between the current and former 400 meter running world records is only 15 hundredths of one second, the one second decrease in sprinting time produced by time-restricted eating is meaningful.

Link to full publication.
Learn more about the relationship between exercise training and time-restricted eating from expert Dr. Satchin Panda.

Circadian rhythms influence brown fat activity.

Circadian rhythms – the body’s daily cycles of biological, hormonal, and behavioral patterns – play critical roles in human health. Disturbances in these rhythms may increase susceptibility to metabolic disorders, such as diabetes and obesity. Findings from a new study indicate that diurnal circadian variations in brown adipose tissue activity may contribute to metabolic disorders.

Brown adipose tissue is a type of fat involved in thermogenesis – the production of body heat. There are two types of thermogenesis: diet-induced and cold-induced. Diet-induced thermogenesis involves an increase in the metabolic rate that occurs after consuming a meal. Cold-induced thermogenesis involves uncoupling electron transport from ATP synthesis and repetitive, non-productive transport of ions across the adipose cell membrane. In the past, scientists believed that brown fat was present only in newborns, where it served to protect against heat loss via cold-induced thermogenesis. However, recent research has identified active brown fat in adults, typically following cold exposure. Brown fat activity contributes to overall energy expenditure and body fat regulation.

The authors of the study conducted a two-part investigation. In the first part, 21 healthy men (20 to 50 years old) underwent positron emission tomography (PET) scans to detect the presence of brown fat. During the PET scans, the men sat in a cool (66°F, 19°C) room for two hours while wearing lightweight clothes (a T-shirt and shorts). They periodically placed a towel-wrapped block of ice against the soles of their feet. The authors of the study categorized the men as having high or low quantities of brown fat based on the findings of the scans. Then the men ate a standardized meal, and the authors of the study measured several parameters of the men’s metabolic function, including energy expenditure, diet-induced thermogenesis, and fat oxidation.

They found that men with high quantities of brown fat tended to have higher diet-induced thermogenesis and fat oxidation than those with low quantities, especially after breakfast, suggesting that brown fat has a greater influence on diet-induced thermogenesis earlier in the day.

In the second part of the study, the authors categorized 23 healthy men (20 to 29 years old) as having high or low quantities of brown fat using the same procedure used in the first study. Then they used a thermal imaging camera to measure the men’s skin temperature at the supraclavicular region (just above the collar bones, an area where brown fat is typically present). They took measurements in the morning and evening in warm (80°F, 27°C) conditions and after the men had been sitting for 90 minutes in cool (66°F, 19°C) conditions. They also measured the men’s energy expenditure, cold-induced thermogenesis, and fat oxidation.

They found that energy expenditure, fat oxidation, and supraclavicular temperature were higher in the men with high quantities of brown fat compared to those with low quantities. The men’s energy expenditure in the morning was nearly equal for both high and low brown fat groups in warm conditions, but it was higher in cool conditions among those with high brown fat quantities. Energy expenditure in the evening was the same among both groups regardless of temperature. Cold-induced thermogenesis among the men with high brown fat quantities was higher in the morning than in the evening.

These findings suggest that brown fat activity exhibits diurnal circadian variations that influence metabolic function. These variations may explain associations between meal timing, obesity, and related metabolic disorders. Time-restricted eating resets the circadian clock to promote metabolic health. Learn more about time-restricted eating in our overview article.

Link to full publication.

Beige fat protects against dementia.

The color of fat tissue – white, brown, or beige – dictates the role the tissue plays in the body. Whereas white fat is involved in lipid storage and the release of free fatty acids for energy, brown fat is involved primarily in thermogenesis – the production of heat. Beige fat, which is typically co-located with white fat, can exhibit either storage or thermogenic properties, depending on environmental conditions. It also exerts anti-inflammatory properties via induction of interleukin 4, an anti-inflammatory molecule. White fat can convert to beige fat, a process known as “beiging.” Findings described in a recent report suggest that beige fat mediates the neuroprotective effects of subcutaneous fat.

Subcutaneous fat, which is composed of both white and beige fat, is stored just beneath the skin. Commonly associated with a “pear” shape, it may protect against dementia. Visceral fat, on the other hand, is composed of white fat only. It is stored in the abdominal cavity close to internal organs such as the liver, pancreas, and intestines. An excess of visceral fat, often referred to as central obesity or abdominal obesity, is commonly associated with an “apple” shape and an increased risk for chronic disease, including dementia.

The authors of the report conducted a two-part study using a type of mouse genetically altered to lack the gene that promotes beiging. Without beiging, subcutaneous fat behaves more like visceral fat.

In the first part of the study, they fed either a low-fat or high-fat diet to the genetically altered mice and normal mice for one month. They tested the animals’ cognitive function and measured markers of inflammation and immune activation. Both groups of mice became obese on the high-fat diet, but cognitive tests revealed that the mice without beige fat showed signs of early cognitive impairment while the normal mice did not. The mice without beige fat also exhibited rapid, robust inflammatory responses to the high-fat diet, including activation of microglial cells (a type of immune cell found in the brain). Microglia activation promotes inflammation, harms brain health, and contributes to dementia.

In the second part of the study, the authors transplanted subcutaneous fat from young, lean healthy mice into the abdominal areas of the obese, cognitively impaired mice. The recipient mice experienced improvements in memory and synaptic plasticity – the ability to form new connections between neurons.

These findings suggest that beige fat drives the neuroprotective and anti-inflammatory effects of subcutaneous fat in mice. A growing body of evidence suggests that cold exposure promotes beiging of white fat. Learn more about the health effects of cold exposure in our overview article.

Link to full publication.

Stimulant medications increase willingness to expend effort, not ability.

Executive function refers to a set of cognitive abilities that facilitate control over voluntary behaviors, including attention control, working memory, and cognitive flexibility. While executive functions are critical for complex tasks such as planning, they are also mentally taxing. Without sufficient motivation, people with poor executive function may struggle to meet goals. Researchers report their findings that dopamine signaling is responsible for the effects of Ritalin and other stimulant medications on motivation and executive function.

Dopamine, one of the most abundant neurotransmitters in the brain, is involved in reward-motivated behavior, learning, and memory. Activities that provide a reward (e.g., eating or earning money) increase dopamine levels, causing a sensation of pleasure that enhances learning by deeply encoding memories related to the rewarding activities. Motivation to complete a task is based, in part, on whether a task is judged to provide sufficient pleasure relative to the cost of its required effort. Capacity to synthesize dopamine varies from person to person; however, lower dopamine levels in key brain areas are associated with attention deficit hyperactivity disorder (ADHD), substance use disorders, and Parkinson’s disease. Drugs such as methylphenidate (i.e., Ritalin), a medication used to treat ADHD, and sulpiride, a medication used to treat schizophrenia and depression, interact with dopamine receptors in the brain and can increase motivation.

The authors recruited 50 healthy adults between the ages of 18 and 43 years. Participants completed a test called a cognitive effort-discounting paradigm. In this test, participants are asked how much money they would want to receive in exchange for completing tasks of varying difficulty. The authors measured the estimated effort cost as the amount of money necessary to make participants willing to perform a cognitively difficult working memory task. Participants completed effort-discounting tasks under the influence of 20 milligrams of methylphenidate, 400 milligrams of sulpiride, or a placebo on three separate testing days. The researchers used a positron emission tomography (PET) scan to measure dopamine synthesis capacity in the caudate nucleus, a brain region responsible for reward-based learning. They used a statistical model based on the effort-discounting task to further explore the effects of methylphenidate and sulpiride on motivation.

While on the placebo treatment, participants’ willingness to expend cognitive effort increased as their baseline dopamine synthesis capacity increased. Notably, while performance on the working memory task decreased with difficulty, there was no relationship between task performance and dopamine levels. Both methylphenidate and sulpiride increased willingness to expend cognitive effort, but only in participants with low baseline dopamine synthesis capacity.

Using their computer model, the investigators found that methylphenidate increased feelings of reward while sulpiride decreased effort cost. Further, they found that the cost-benefit analysis involved in the decision to expend effort occurred early in the decision-making process and was measurable by patterns in gaze (focusing on a reward or cost of a task) during cognitive testing. While higher baseline dopamine synthesis capacity and drug administration did not affect gaze patterns directy, higher dopamine levels strengthened the impact of gaze and attention to the benefits versus the costs of a decision.

These findings indicate that Ritalin and other attention-enhancing drugs work by increasing willingness to attempt cognitively-difficult tasks, not the ability.

Link to full publication.
Learn more about how loss of dopamine-producing neurons affects the brain and behavior with expert Dr. Giselle Petzinger in this clip featuring Dr. Rhonda Patrick.

Time-restricted feeding reduces weight gain and cholesterol in male mice.

A Western dietary pattern, characterized by a low intake of fruits and vegetables and a high intake of sugar and processed foods, promotes the development of obesity and metabolic disease. Time-restricted eating has been shown to decrease weight and improve metabolic health in humans. However, factors such as age and sex modulate both susceptibilty to obesity and likelihood of responding to weight-loss treatments. Authors of a new report found that male mice experienced greater metabolic benefit from time-restricted feeding than females.

Time-restricted eating, the practice of limiting food intake to an 8- or 12-hour window, is an emerging therapy for the treatment and prevention of metabolic diseases. Much of the research about time-restricted eating in humans is based on research of time-restricted feeding in mice, which has elucidated many of the cellular mechanisms related to time-restricted eating’s benefits. These two terms distinguish which population, humans or non-human animals, is practicing time-restricted food intake.

The prevalence of obesity is on the rise in the industrialized world, a problem compounded by an increasing average age in the same populations. The accumulation of extra fat throughout life puts a person at greater risk of metabolic disease as they age. Females are more likely to gain and retain fat mass than males; however, pre-menopausal females tend to have lower rates of type 2 diabetes and cardiovascular disease due to the protective effects of estrogen. Previous research in humans has demonstrated weight loss and improved metabolic health with time-restricted eating; however, additional research is needed to understand the sex- and age-dependent effects of adherence to the dietary pattern.

The researchers used male and female mice of two ages: three months old (equivalent to 20-year-old humans) and 12 months old (equivalent to 42-year-old humans). They fed mice a diet representative of a Western dietary pattern, with 17 percent of calories from sugar (human equivalent of about 25 ounces of soda per day) and 45 percent of calories from fat, including lard and soybean oil. Current dietary guidelines recommend limiting solid fats such as lard. Half of the mice had 24-hour access to food while the other half had restricted access, limited to just nine hours per day. The mice ate their respective diets for a total of 12 to 13 weeks. After 10 weeks, the researchers measured changes in the animals’ body weight, glucose sensitivity, serum cholesterol, fatty liver, muscle performance, and immune response when challenged with bacterial endotoxin.

Although mice in the time-restricted feeding group consumed the same amount of food as mice with constant access to food, time-restricted feeding resulted in 15 percent less weight gain in young male mice and 23 percent less weight gain in older male mice. Time-restricted feeding did not significantly prevent weight gain in female mice. Male mice also experienced a greater reduction in serum cholesterol with time-restricted feeding compared to females.

Both older male and female mice had lower rates of insulin resistance and fatty liver while on time-restricted feeding. This protection was likely due to changes in gene expression that increased glucose uptake by and decreased glucose output from the liver. In young male mice, time-restricted feeding preserved muscle mass, function, and performance, but not in young females. Finally, when challenged with bacterial endotoxin, older mice practicing time-restricted feeding were significantly more likely to survive septic shock than mice with 24-hour access to food, demonstrating better health and resilience.

Time-restricted feeding improved survival from septic shock and provided protection against insulin resistance and fatty liver in both sexes; however, male mice experienced greater reductions in body weight and serum cholesterol and maintained greater muscle mass and performance compared to female mice. The authors noted that their research is of particular interest considering the increased risk of severe COVID-19 illness in people with poor metabolic health.

Link to full publication.
Learn more about the effects of time-restricted feeding and its effects on obesity, muscle mass, and heart health in this episode featuring Dr. Satchin Panda.
Read our overview article on time-restricted feeding to learn even more.

A high saturated fat diet increases heart disease marker, TMAO.

Heart disease is the number one cause of death among people living in the United States, due to a constellation of risk factors including a sedentary lifestyle, disrupted sleep patterns, stress, and poor diet. The average American adult consumes 29 grams of saturated fat per day (the amount in about four tablespoons of butter, four slices of pepperoni pizza, or 1.5 cups of ice cream), possibly contributing to heart disease risk through interactions with the gut microbiota. Findings published in a recent report link high-saturated fat diets to increased heart disease biomarkers among mice with high levels of E. coli bacteria.

The gut microbiota, the community of bacteria, archaea, fungi, and viruses that lives in the human intestine, is highly influenced by changes in diet. Dietary fats that are not absorbed in the small intestine travel to the large intestine where microbes metabolize them. The same is true for other nutrients not absorbed by the gut, including choline, an essential nutrient found in high amounts in organ meats, egg yolks, and legumes. Choline is an important component of cellular membranes, a precursor for the production of neurotransmitters, and an element of bile acids needed for the digestion of fats. However, some gut microbes convert choline into trimethylamine, which is absorbed by the intestine and converted to trimethylamine N-oxide (TMAO) in the liver. High serum levels of TMAO have been shown to increase the risk of major cardiovascular events such as heart attack and stroke by increasing the deposition of cholesterol in arterial walls (i.e., atherosclerosis).

Clostridia and Enterobacteriaceae are the only two bacterial families common to the human gut microbiota that are known to produce TMAO. Of these, only Enterobacteriaceae abundance is substantially increased on a high-fat diet. Oxygen content in the gastrointestinal tract decreases through the small and large intestines so that bacteria in the large intestine (the colon) are mostly anaerobic (meaning they do not use oxygen for metabolism). This low oxygen environment is needed to promote the growth of beneficial bacteria such as Clostridia and suppress the growth of detrimental bacteria such as Enterobacteriaceae. In order to maintain this low oxygen environment, the mitochondria of colon cells must consume high levels of oxygen; however, a diet high in saturated fat may impair mitochondrial function, facilitating the growth of TMAO-producing bacteria and increasing heart disease risk.

The investigators performed their experiments using two mouse strains with altered gut microbiota: mice that do not carry Enterobacteriaceae in their gut microbiota (E. negative) and germ-free mice, which are raised in a sterile environment and do not have a microbiota. They fed both types of mice either a high-fat (60 percent of calories from fat) or low-fat (10 percent of calories from fat) diet for 10 weeks. The main source of fat in the high-fat diet was lard, with casein protein, sugar, and micronutrients added. The researchers added a choline supplement to both the high-fat and low-fat diets one week before administering a single dose of a probiotic containing E. coli, a member of the Enterobacteriaceae family, to both E. negative and germ-free mice. All mice consumed their assigned diet for a total of 14 weeks. The researchers measured changes to epithelial cells in the colon, including mitochondrial metabolism, inflammation, and cancer signatures.

Both E. negative and germ-free mice that gained weight on the high-fat diet had increased inflammation and cancer signatures, suggesting some of the detrimental diet effects were independent of the microbiota. Germ-free mice on a low-fat diet had colon epithelial cells with appropriately low levels of oxygen; however, germ-free mice on a high-fat diet had colon epithelial cells with increased oxygen levels and reduced mitochondrial metabolism. Following E. Coli exposure, E. negative mice fed a high-fat diet supplemented with choline gained more weight and had higher levels of oxygen, inflammation, and cancer signatures in their colons than E. negative mice fed a low-fat diet. These changes were associated with an increased concentration of fecal E. coli. In germ-free mice exposed to E. coli, a high-fat diet supplemented with choline significantly increased serum TMAO levels compared to all other groups.

These results elucidate the mechanisms by which diets high in saturated fat may contribute to heart disease through interactions with choline metabolism by the gut microbiota. However, there are several important factors to consider in translating these results into relevant information for humans. Mouse diets often contain just one or two sources of fat such as soybean oil or lard, as was used in this study. Human diets contain a wider variety of fats, including various saturated and unsaturated fats. These diets also often contain high amounts of simple sugars, such as the sucrose and maltodextrin used in this study. The diet used in this study is also not representative of a standard human diet and limits the ability to distinguish between the effects of saturated fat and sugar. So, while animal studies are a vital foundation for human research, they should not be the basis for individual health recommendations. To hear Dr. Rhonda Patrick review the evidence on saturated fat and heart disease, listen to this episode of the FoundMyFitness podcast.

Link to full publication.
To learn even more about the effects of saturated fat and cholesterol on human health, watch this episode featuring expert Dr. Ronald Krauss, MD.

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