Fat
Episodes
Dr. Rhonda Patrick discusses silicone safety, grounding, pentadecanoic acid, and the potential benefits of olive leaf extract and peptides.
In this clip, Dr. Layne Norton discusses seed oils, health risks, and the benefits of olive oil for heart health.
In this clip, Dr. Martin Gibala outlines the relationship between exercise types, mitochondrial growth, and their combined effect on fat metabolism.
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Dr. Rhonda Patrick discusses silicone safety, grounding, pentadecanoic acid, and the potential benefits of olive leaf extract and peptides.
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In this clip, Dr. Layne Norton discusses seed oils, health risks, and the benefits of olive oil for heart health.
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In this clip, Dr. Martin Gibala outlines the relationship between exercise types, mitochondrial growth, and their combined effect on fat metabolism.
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In this clip, Dr. Martin Gibala explains VO2 max's role in health and how non-athletes can optimize workouts to boost their cardiorespiratory fitness.
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Dr. Martin Gibala discusses HIIT's health benefits and describes common HIIT protocols.
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In this clip, Dr. Dominic D'Agostino outlines strategies to initiate a ketogenic diet and mitigate its side effects.
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In this clip, Dr. Dominic D'Agostino discusses the metabolic flexibility of the brain to use various substrates, including ketones, for energy.
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In this clip, Dr. Dominic D'Agostino discusses how the body adapts to a ketogenic diet and the possible impacts on age-related chronic diseases.
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In this clip, Dr. Dominic D'Agostino describes different approaches that allow the ketogenic diet to be more accessible.
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Several associative studies that have found a link between saturated fat and heart disease... should we be concerned?
Topic Pages
News & Publications
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The brain's vagus nerve controls fat absorption in the intestine—a possible pathway for managing obesity. pubmed.ncbi.nlm.nih.gov
Fat is a vital energy source, but when consumed in excess, it can promote obesity. However, the amount of fat the body absorbs may be more related to the brain than the gut. A recent study in mice found that signals from the brain’s vagus nerve regulate fat uptake in the intestine, offering a potential means to moderate obesity.
Researchers manipulated the dorsal motor nucleus of the vagus (DMV), which plays a crucial role in digestion. They inactivated DMV neurons that connect to the jejunum (the middle portion of the intestine), shortening the length of the microvilli in the gut and reducing fat absorption. However, stimulating DMV neurons increased fat absorption and promoted weight gain. Finally, they injected mice with puerarin, a bioactive compound derived from the kudzu plant, and found that the compound mimicked the effect of DMV suppression, further reducing fat absorption.
These findings suggest that controlling the DMV-vagus-jejunum pathway could provide a novel approach to managing fat absorption and weight. They also highlight yet another way the brain-gut axis influences human health.
Puerarin is an isothiocyanate, a class of sulfur-containing compounds known for their potent anti-inflammatory, anti-cancer, and anti-obesity effects. Sulforaphane, another well-known isothiocyanate, shares many of these beneficial properties. To learn more about the health effects of sulforaphane, check out our overview article.
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Many cancers are influenced by excess body fat, with overall accumulation playing a larger role than fat distribution, despite sex-specific difference www.eurekalert.org
Excess body fat increases a person’s risk for many types of cancer. However, body fat distribution patterns tend to be sex-specific, with males carrying more fat in the upper abdomen and females carrying more in the hips, thighs, buttocks, and lower abdomen. A new study has identified differences in obesity-driven cancer rates between males and females.
Researchers drew on data from more than 440,000 adults enrolled in the UK Biobank study. They used statistical analysis to determine how various measures of body fat, such as body mass index (BMI) and waist circumference, influenced the risk of developing 19 types of cancer over a follow-up period of about 13 years.
They found that nearly all 19 cancers were associated with excess body fat, except brain, cervical, and testicular cancers. They also found that overall body fat had a greater influence on cancer risk than fat distribution. However, they noted sex-specific effects of body fat on colorectal, esophageal, and liver cancer rates between males and females. For example, excess abdominal fat increased the rates of esophageal cancer in females but not males. Similarly, excess overall fat increased the rates of liver cancer in males but not females.
These findings suggest body fat plays important but differential roles in cancer risk between males and females. Evidence suggests a ketogenic diet promotes weight loss and reduces cancer risk. Learn more about ketogenic diets and cancer in this episode featuring Dr. Dominic D'Agostino.
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Heart disease is the number one cause of death in the United States, owing 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 of a new 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 is incorporated into bile acids needed for the digestion of fats; however, some gut microbes convert choline into trimethylamine (TMA), 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, but 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 colon are mostly anaerobic (meaning they do not use oxygen for metabolism). This low oxygen environment is needed to promote the growth of more beneficial bacteria such as Clostridia and suppress the growth of more 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 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 signatures of cancer 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 lard and soybean oil, 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.
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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 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.
Time-restricted eating, along with regular training, improved exercise performance in 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.
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One 60-minute bout of aerobic exercise increases mitochondrial metabolism in sedentary adults. www.sciencedaily.com
Exercise puts a demand on skeletal muscle cells to produce energy at a faster rate than at rest. To do this, the body increases the delivery of fats to the muscle mitochondria while increasing the mitochondrial capacity to metabolize fats, a process called beta-oxidation. Researchers of a new study aimed to illuminate the cellular mechanisms of mitochondrial fat metabolism following moderate intensity aerobic exercise.
Mitochondria are cellular structures responsible for the production of energy in the form of adenosine triphosphate (ATP). The inner membrane of mitochondria possess a series of enzymes called the electron transport chain. These enzymes transfer electrons from carbohydrates and fats (as well as proteins and nucleic acids to a lesser extent) to the final enzyme in the chain that produces ATP. Electron transfer flavoprotein is an enzyme in this chain that transfers electrons from fats, specifically. The authors of this report have previously presented data demonstrating an increase in electron transfer flavoprotein activity in mice after aerobic exercise training.
The investigators recruited fifteen healthy sedentary adults (average age, 28 years) with a normal body mass index. Participants completed one hour of cycling at 65 percent of their maximum aerobic capacity on one day and rested the next day. The researchers collected biopsies from the participants' thigh muscle after they had rested and 15 minutes after they exercised. They analyzed the muscle mitochondria for the abundance of electron transfer flavoprotein activity and for the metabolism of fats and nonfat fuel sources.
Following exercise training, mitochondrial metabolism of fats and non-fat sources increased, although this relationship was not statistically significant. Also noted was a six percent increase in hydrogen peroxide, which is a byproduct of fat metabolism that damages cells. Although fat metabolism increased, the authors reported no increase in electron transfer flavoprotein activity abundance.
They authors concluded that just one session of moderate intensity aerobic exercise in sedentary adults increases energy metabolism of both fats and non-fat sources. They suggested future research would include a larger sample of participants.
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From the article:
“Up to now the only known approach to inducing brown fat has been through exposure to chronic cold. Our research reveals a novel way of doing this without cold exposure. We show that animals living in an enriched environment become lean and resistant to diet-induced obesity, even in the presence of unlimited food.”
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The current study used a similarly designed environment, with 15-20 mice housed in large containers equipped with running wheels, tunnels, huts, wood toys, a maze, and nesting material, in addition to unlimited food and water.
Key findings include the following:
• Enriched animals showed a significant reduction in abdominal white fat mass (49 percent less than controls).
• Exercise (running in a wheel) alone did not account for the changes in body composition and metabolism of enriched animals.
• Fed a high fat diet (45 percent fat), enriched animals gained 29 percent less weight than control mice and remained lean, with no change in food intake. Enriched animals also had a higher body temperature, suggesting that greater energy output, not suppressed appetite, led to the resistance to obesity.
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Increased visceral fat impairs cognition through chronic microglial activation mediated by IL-1 beta release [animal research] www.sciencedaily.com
Scientists find that visceral fat, a type of adipose tissue that produces high levels of inflammatory signals known as adipokines, impair learning and memory in mice by setting off an inflammatory cascade mediated by the release of IL-1 beta, which crosses the blood-brain barrier leading to chronic activation of microglia.
From the article:
“We have identified a specific signal that is generated in visceral fat, released into the blood that gets through the blood brain barrier and into the brain where it activates microglia and impairs cognition.”
Visceral fat as the ring leader:
They looked further and found that just transplanting the visceral fat caused essentially the same impact as obesity resulting from a high-fat diet, including significantly increasing brain levels of interleukin-1 beta and activating microglia. Mice missing interleukin-1 beta’s receptor on the microglia also were protected from these brain ravages.
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To measure cognitive ability, the scientists looked at mice’s ability to navigate a water maze after 12 weeks on a high- or low-fat diet. They found it took the normal, or wild type, mice consuming the higher fat diet as well as the visceral transplant recipients with NLRP3 intact longer to negotiate the water maze. In fact, while they could reach a platform they could see, they had trouble finding one beneath the water’s surface that they had been taught to find. Mice with the interleukin-1 receptor knocked out, could find it just fine, Stranahan says.
The high-fat diet, transplant mice also had weaker connections, or synapses, between neurons involved in learning and memory. Mice on a high-fat diet but missing NLRP3 were spared these changes, like mice on a low-fat diet.