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Behavior

Episodes

Posted on October 4th 2023 (over 1 year)

In the clip, Dr. Gibala discusses high-intensity interval training's future, stressing translating research into public health applications.

Posted on September 7th 2023 (over 1 year)

Dr. Rhonda Patrick discusses concerns about early smartphone and tablet access among kids and its effects on mental health later in life.

Posted on November 2nd 2022 (over 2 years)

When people exercise as part of a treatment for alcohol abuse disorder it reduces their volume of alcohol consumption. But why? One reason may be FGF21.

Topic Pages

  • Depression

    Depression – a neuropsychiatric disorder affecting 322 million people worldwide – is characterized by negative mood and metabolic, hormonal, and immune disturbances.

  • Sulforaphane

    Sulforaphane is a bioactive compound that exerts potent antioxidant and anti-inflammatory properties and may be beneficial against a wide range of chronic and acute diseases.

News & Publications

  • Probiotics attenuate inflammation-associated sickness behaviors.

    The gut-brain axis, a bidirectional signaling pathway between the gastrointestinal tract and the nervous system, plays critical roles in human health. Key elements of this pathway are the tens of trillions of microbes that comprise the intestinal microbiota. Findings from a 2015 study suggest that probiotics attenuate inflammation-associated sickness behaviors.

    Probiotics are typically defined as live microorganisms that, when consumed in sufficient amounts, confer a health benefit on the consumer. They contain a variety of microorganisms, but Lactobacillus and Bifidobacterium bacteria are among the most common. Probiotics can be found in yogurt, kefir, kimchi, and other fermented foods and are widely available as dietary supplements.

    Sickness behaviors are adaptive behavioral changes that occur during infection or chronic inflammatory disorders and may include lethargy, depressed mood, appetite loss, sleepiness, pain, or confusion. Evidence suggests that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine produced by immune cells, activates microglia (the brain’s resident immune cells) and recruits white blood cells to the brain, driving the development of inflammation-associated sickness behaviors.

    The investigators used a model of liver inflammation in mice to study the effects of a probiotic on inflammation-associated sickness behavior. Mice with this form of liver inflammation typically have high levels of pro-inflammatory cytokines and exhibit distinct sickness behaviors. They fed the mice either a probiotic or a placebo and then they studied the animals' behavior. They also measured TNF-alpha levels in the animals' blood and the number of activated immune cells in the animals' brains.

    They found that although the probiotic did not reduce the severity of liver inflammation in the mice, it did reduce sickness behaviors better than the placebo. Mice that received the probiotics also had lower TNF-alpha levels and fewer activated immune cells in their brains compared to mice that received a placebo.

    These findings suggest that probiotics attenuate inflammation-associated sickness behaviors in mice, likely via modulation of the gut-brain axis. Learn about factors to consider when choosing a probiotic supplement in this clip featuring Dr. Jed Fahey.

  • TNF-alpha in the brain drives sickness behaviors associated with liver disease.

    Many liver disorders cause behavioral symptoms, often referred to as sickness behaviors, such as fatigue, loss of appetite, and “brain fog.” Evidence suggests that these symptoms arise from alterations in the central nervous system, but scientists don’t fully understand what drives them. Findings from a 2006 study suggest that sickness behaviors in the setting of cholestasis, a common liver disorder, are caused by the presence of tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine, in the brain.

    Cholestasis is characterized by impaired bile flow and subsequent retention of bile acids, bilirubin, and other substances, including lipopolysaccharide, an endotoxin, in the liver and blood. It is a common disorder of pregnancy but can affect all demographics, including children. Most people with cholestasis report experiencing sickness behaviors, especially fatigue, which occurs in roughly 86 percent of people with the disorder.

    TNF-alpha is produced by many types of immune cells. It exists in soluble and transmembrane forms, both of which mediate a variety of opposing physiological and pathological functions, depending on which of its receptors it binds to. For example, binding to TNF receptor 1 promotes apoptosis (programmed cell death) and inflammation; binding to TNF receptor 2 promotes cell survival, resolution of inflammation, immunity, and cellular repair. Elevated TNF-alpha is associated with chronic pain syndromes and anxious behaviors.

    The investigators tied off the bile ducts of healthy mice to induce cholestasis. Then they isolated endothelial cells from the blood vessels in the animals' brains to see if the cells were activated and if the cells interacted with immune cells. They also measured TNF-alpha production by monocytes (white blood cells).

    They found that endothelial cells were activated in the setting of cholestasis, and these activated cells readily interacted with immune cells that had been recruited to the brain. In turn, the immune cells increased their production of TNF-alpha. In light of the known effects of TNF-alpha on sickness behaviors, these findings suggest that TNF-alpha production in the brain mediates sickness behaviors in mice with liver disease.

  • From linked article:

    The researchers gave the monkeys a two-bottle choice between water and ethanol, and administered one group an analog of FGF21 to see what effect it had. Sure enough, the test monkeys drank 50 percent less alcohol than the control group. Similar tests in mice also saw a 50-percent reduction in alcohol consumption after being given either human FGF21 or an analog. Interestingly though, the mice and monkeys still chose the ethanol just as often as before, but they drank far less each time.

    Fibroblast growth factor 21 happens to be modulated by aerobic exercise:

    In a new study published in the scientific Journal of Clinical Investigation – Insight, the researchers show that cardio training on an exercise bike causes three times as large an increase in the production of the hormone FGF21 than strength training with weights. FGF21 has a lot of positive effects on metabolism.

  • Exposure therapy is a type of cognitive behavioral therapy commonly used to treat people with posttraumatic stress disorder (PTSD). Some evidence suggests that BDNF mediates the response to exposure therapy, which can vary among people. A 2013 study demonstrated that genetic differences in BDNF expression influences how well a person responds to exposure therapy.

    A single-nucleotide polymorphism (SNP) in the region of the DNA that encodes BDNF causes a substitution of the amino acid valine (Val) by methionine (Met) in the BDNF protein. Evidence suggests that carriers of the Met allele (Met/Met or Val/Met genotype) have reduced hippocampal function, poor episodic memory, and decreased exercise-induced secretion of BDNF.

    The study involved 55 people between the ages of 18 and 65 years who had previously participated in an eight-week exposure therapy program. The participants provided DNA (via saliva samples) for BDNF genotyping.

    The genotyping revealed that 30 participants carried the Val/Val BDNF allele, and 25 participants carried the Met-66 allele. Carriers of the Met-66 allele showed a poorer response to exposure therapy than carriers of the Val/Val allele, suggesting that the SNP influenced BDNF expression and subsequent response to cognitive behavioral therapy.

  • From the article:

    Cocaine relapse was significantly reduced in a preclinical model when brain-derived neurotropic factor (BDNF) was applied to the nucleus accumbens deep in the brain immediately before cocaine-seeking behavior, report investigators at the Medical University of South Carolina (MUSC) in an article published online in June 2018 by Addiction Biology.

    […]

    While other research groups have studied how BDNF administration affects drug self-administration and relapse, no one has looked at what happens if BDNF is given immediately before relapse.

    Since low serum BDNF levels are seen in cocaine-dependent patients compared to non-addicts, the MUSC researchers sought to better understand the connection between BDNF and cocaine relapse. The nucleus accumbens was selected as the focal point for BDNF administration since it is a central component of the brain reward circuit.

    “An important aspect of this study is that while others have shown that BDNF is important for establishing the state of addiction, we find that can also be used to reverse addiction,” says Peter Kalivas, Ph.D., professor and chair in the Department of Neuroscience. “This exemplifies that the primary effect of BDNF is to promote changes in the brain, and that this capacity to change the brain contributes to how people get addicted, but also can be harnessed to remove brain pathologies such as drug addiction.”

    The findings reported in Addiction Biology are the first to show that applying BDNF to the nucleus accumbens immediately before the reinstatement phase, when the rats are once again seeking cocaine due to cue exposure, greatly reduces relapse.