We’ve lined up another great collection of stories about the latest research on health, nutrition, and fitness, delivered right to your inbox. Read on to learn how…
Graying of hair is related to mental stress – but may be reversible.
COVID-19 causes gray matter losses in the brain.
Omega-3 fatty acids reduce symptoms of depression.
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Rhonda and team
Science Digest – July 2, 2021
Graying of hair is related to psychological stress but may be reversible.
The loss of hair pigmentation (graying) is a hallmark of aging. Although it typically begins during a person’s twenties, the timing and extent of graying vary according to genetics and interactions between biological and psychological factors. Graying is generally considered irreversible, but findings from a recent study demonstrate that graying is not necessarily a linear process and may be reversible.
One of the primary drivers of graying is oxidative stress, which damages the pigment-producing region of the hair shaft. Oxidative stress occurs during the process of oxidative phosphorylation (the generation of energy) in mitochondria and can be reflective of exposures to both physical and psychological stressors. Evidence suggests that depigmented hairs may exhibit altered mitochondrial energy metabolism. Interestingly, case and anecdotal reports suggest that hair re-pigmentation can occur, causing bicolor hairs.
The authors of the study collected dark, depigmented, and bicolor hairs from 14 healthy young adults (average age, 35 years) who did not color, bleach, or chemically treat their hair. The authors digitally mapped pigmentation patterns in the hairs over time and assessed protein content in the hair shafts. Some of the participants completed a retrospective stress assessment questionnaire using a life event calendar, in which they recorded major events over a given time. Then the authors overlaid the hair pigmentation patterns on the participants’ life events.
The authors found that depigmentation and re-pigmentation events corresponded with specific moments in the participants’ lives, with depigmentation linked to stressful events (such as marital discord) and re-pigmentation linked with non-stressful events (such as a vacation). The authors also found that depigmented hairs contained more proteins linked to mitochondrial function and energy use, suggesting that mitochondria and metabolism are involved in the graying process.
These findings suggest that graying of hair is a more malleable process than once thought and indicate that studying changes in hair color may provide insights into how psychological stressors influence health.
Link to full study.
Listen to this episode in which Dr. Rhonda Patrick discusses how meditation can buffer the harmful effects of stress.
COVID-19 causes gray matter losses in areas of the brain involved in taste, smell, and memory.
At the time of this publication, more than 182,000,000 cases of COVID-19 have been diagnosed worldwide. Although most cases are mild to moderate in severity, lasting only a few weeks, the long-term effects of the disease are unknown. Findings from a recent study suggest that COVID-19 causes long-term gray matter losses in areas of the brain involved in taste, smell, and memory.
COVID-19 affects multiple organ systems and elicits a wide range of flu-like symptoms, including cough and fatigue. Many infected persons experience loss of taste or smell, with one study finding that 96 percent of people with active COVID-19 had some loss of smell. Approximately one-third of these had altered smell six to eight weeks after initial diagnosis. Some researchers have hypothesized that SARS-CoV-2, the virus that causes COVID-19, crosses the olfactory mucosa and progresses to the olfactory bulb in the brain, thus gaining access to the nervous system.
The current study involved 782 adults who had undergone initial brain imaging as part of the UK Biobank study. Approximately half of the participants developed COVID-19 after their initial scan (15 of whom were hospitalized), while the remainder (matched for age, sex, and ethnicity) did not. All participants underwent a second scan, and the two scans were compared.
The comparison revealed substantive COVID-19-related damage and gray matter losses in the areas of the brain responsible for taste and smell, especially in the left parahippocampal gyrus, the left superior insula, the left lateral orbitofrontal cortex, the left anterior cingulate cortex, the left supramarginal gyrus, and the right temporal pole. Those who were hospitalized showed losses in smell- and memory-related brain regions, especially in the areas around the left cingulate cortex, the right hippocampus, and the amygdala.
Although these findings have not been peer-reviewed, they suggest that COVID-19 affects the brain in ways that are not fully understood and underscore the need for continued monitoring of COVID-19 patients. The proximity of these losses to areas of the brain responsible for memory raise concerns that people who have had COVID-19 might be at greater risk for developing Alzheimer’s disease or other forms of dementia. A newly formed international consortium is investigating this possibility.
Link to full study (under review).
Learn more about COVID-19 in this episode featuring Dr. Roger Seheult.
Omega-3 fatty acids reduce symptoms of depression.
Depression – a mood disorder that affects 322 million people worldwide – is characterized by profound sadness, anxiety, and physical complaints. People who have depression often have higher levels of systemic inflammation (which can affect brain health) compared to those without depression. Findings from a new study suggest that omega-3 fatty acids reduce symptoms of depression through their anti-inflammatory effects on the brain.
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega-3 fatty acids derived primarily from fish. They exert a wide range of beneficial effects on the human body. Evidence from a clinical trial indicates that omega-3 fatty acids reduce symptoms of depression associated with inflammation.
Chronic inflammation plays key roles in the development of many diseases, including cancer, cardiovascular disease, and diabetes. Inflammation in the brain impairs neurogenesis, the process of forming new neurons. Impaired neurogenesis negatively influences mood and cognitive function.
The authors of the study conducted two experiments. In the first experiment, they pre-treated human hippocampal cells with either EPA or DHA and then exposed the cells to interleukin (IL)-1 beta, IL-6, and interferon-alpha – proteins that drive chronic inflammation. They found that EPA and DHA maintained neurogenesis and prevented programmed cell death via the effects of lipid mediators – a class of omega-3 fatty acid byproducts that influence immune health and inflammation.
In the second experiment, the authors gave 22 people who had been diagnosed with depression either 3 grams of EPA or 1.4 grams of DHA for 12 weeks. They measured lipid mediators in the participants’ blood and assessed their depression symptoms. The authors found that the anti-inflammatory lipid mediators increased in the participants’ blood. They also noted that the participants’ depressive symptoms decreased approximately 64 percent with EPA and 71 percent with DHA.
These findings suggest that omega-3 fatty acids reduce the inflammation associated with depression and improve depressive symptoms. This was a very small study, however, and did not include a control group. Further research is needed to confirm these findings. Learn more about the role of inflammation in depression in this clip featuring Dr. Charles Raison.
Link to full study.
For a quick and tasty way to get more omega-3 fatty acids into your diet, check out this recipe video featuring Dr. Rhonda Patrick.
Previous infection with the common cold protects against SARS-CoV-2 infection and COVID-19 illness.
The SARS-CoV-2 virus and the associated COVID-19 disease remain significant global health threats. Since the emergence of SARS-CoV-2 at the end of 2019, much has been learned about its infection course, including transmission, replication, and immune reactivity. Findings of a new report demonstrate the effects of previous infection with the common cold virus on the course of SARS-CoV-2 infection.
The SARS-CoV-2 virus first enters the upper respiratory tract (i.e., the nasopharynx) via the angiotensin-converting enzyme (ACE) 2 receptor and replicates in epithelial tissue, peaking in concentration within one week of infection. The amount of viral replication in the early stages of infection determines transmissibility and predicts the severity of COVID-19 illness. As the number of viral particles increases, the immune system enhances the expression of interferon-stimulated genes, which are necessary for the antiviral response. People who have had a recent viral infection, such as the common cold, may have greater interferon-stimulated gene expression at the time of SARS-CoV-2 infection, limiting viral replication.
The researchers used nasopharyngeal swabs from 170 patients with a confirmed SARS-CoV-2 infection and eight healthcare workers who did not have an infection. The researchers used swabs from multiple time points to monitor infection progression, including viral replication and immune response. They obtained information regarding previous viral infections, health history, and COVID-19 status from medical records. In a second experiment, the researchers exposed in vitro human bronchial epithelial cells to rhinovirus, which causes the common cold, before exposure to the SARS-CoV-2 virus to determine the effects of previous infection on immunity.
The authors found that the SARS-CoV-2 virus elicits increased expression of interferon-stimulated genes after four days of replication similar to other viral infections. Participants with the highest concentration of the protein CXCL10 (a proxy for interferon-stimulated gene expression) were less likely to require hospitalization but had a higher concentration of viral particles in their nasopharynx. The authors posited that patients in the hospital had likely been sick for a longer period of time and had passed the point of infection when viral replication and interferon-stimulated gene expression are highest.
In vitro cells that had been previously infected with rhinovirus increased their expression of interferon-stimulated genes, including the short version of the ACE2 receptor. Unlike the long version, SARS-CoV-2 cannot enter through the short ACE2 receptor, meaning that previous rhinovirus infection prevents SARS-CoV-2 entry and dampens viral replication.
These findings demonstrate that previous infection with rhinovirus decreases the risk of contracting the SARS-CoV-2 virus and may decrease the severity of COVID-19 disease.
Link to full report.
Vitamin D improves outcomes among breast cancer survivors.
Breast cancer is the most common cancer in women worldwide, with nearly 2.6 million new cases diagnosed in 2020. Robust evidence demonstrates that nutritional factors may mediate the risk of many types of cancer. Findings presented at the annual conference of the American Society of Clinical Oncology suggest that vitamin D status influences outcomes among breast cancer survivors.
Vitamin D is a fat-soluble vitamin stored in the liver and fatty tissues. It plays key roles in several physiological processes. Research suggests that vitamin D exerts anti-cancer properties through its effects on the regulation of cell growth.
The current study involved nearly 4,000 women with breast cancer who were enrolled in the Pathways Study, an ongoing investigation of breast cancer survivorship. The study presenters measured vitamin D concentrations (measured in nanograms per milliliter, ng/ml) in blood samples collected from the women at the time of diagnosis. They categorized the women’s status as deficient (< 20 ng/ml), insufficient (20 to < 30 ng/ml), or sufficient (≥30 ng/ml) and then conducted a statistical analysis to determine if vitamin D status was related to the women’s survival. They also looked at factors that could influence vitamin D status, such as genetic variants, body mass index, race/ethnicity, and supplemental vitamin D intake. They found that women categorized as having sufficient vitamin D concentrations had better survival outcomes than women categorized as deficient. Supplemental vitamin D intake, body mass index, and race/ethnicity had the greatest influence on vitamin D concentrations, and genetic variants had only a minor influence. Black women had the lowest vitamin D concentrations among the cohort, possibly contributing to their poorer outcomes following breast cancer diagnosis. Although these findings have not been peer-reviewed, they suggest that vitamin D status influences outcomes among breast cancer survivors and underscore the need for further research to assess the roles that vitamin D plays in cancer. Link to presentation abstract. Coffee reduces liver disease risk. Chronic liver disease, which may be caused by hepatitis infection, alcohol misuse, or non-alcoholic fatty liver disease, is a major public health concern worldwide. Previous epidemiological research has reported a link between coffee consumption and decreased risk of liver cancer and fatty liver disease. A new report describes the relationship between different types of coffee and liver disease risk. Coffee contains a number of bioactive plant compounds including chlorogenic acid, cafestol, and kahweol, which have anti-inflammatory and anti-cancer effects. Coffees vary widely in their preparation including decaffeination, roasting duration, brewing temperature, and filtering. Decaffeinated and filtered coffees may have fewer bioactive compounds, but how these and other processing characteristics impact chronic liver disease risk reductions is unclear. The authors collected data regarding coffee consumption from almost 500,000 participants in the United Kingdom Biobank, a long-term registry study of United Kingdom citizens. Participants completed surveys asking about the amount and type of coffee (decaffeinated, instant, ground, or other) they consumed. The researchers used medical and death records to assess disease presence. The average length of time that participants were followed for the study was 10 years. Most participants (about 78 percent) consumed coffee, and the average amount of coffee consumed daily was two cups. Compared to non-coffee drinkers, coffee drinkers had a 21 percent lower risk of developing chronic liver disease and a 49 percent lower risk of dying from chronic liver disease. Coffee type did not have an effect on disease risk, with instant and decaffeinated coffee producing similar risk reductions compared with normal ground coffee. The authors concluded that the consumption of coffee, regardless of preparation, is protective against chronic liver diseases. They suggested that future research should investigate the effects of a coffee intervention in treating liver disease. Link to full report. mRNA vaccines elicit long-term immunity against COVID-19. Evidence indicates that immunity following infection with SARS-CoV-2, the virus that causes COVID-19, lasts as long as 11 months. Questions remain, however, regarding the duration of immunity elicited by mRNA vaccines against the virus. Findings from a recent study indicate that mRNA vaccines elicit long-term immunity due to the presence of germinal centers in the lymph tissue. Germinal centers are small, transient structures that form in the lymph nodes, gut, and spleen in response to an acute infection or vaccination. They produce plasma cells and memory B cells – long-lasting immune cells that secrete antibodies that provide protection against future reinfection. Germinal centers are important components of the body’s adaptive immune response. The authors of the study conducted a two-part experiment. The first experiment involved 14 healthy adults who had received the Pfizer BioNTech COVID-19 vaccine and had never been infected with SARS-CoV-2. The authors of the study sampled cells taken from the lymph nodes of the participants three, four, five, and seven weeks after they received the first dose of the two-dose vaccine. They sampled lymph tissue from 10 of the participants 15 weeks after their first dose. Analysis of the lymph tissue indicated that germinal centers were generating antibody-producing B cells three weeks after the initial dose. Germinal center activity remained high through successive weeks, and at 15 weeks after the first dose 80 percent of participants still demonstrated germinal center activity. The second experiment involved 41 healthy adults who received the Pfizer BioNTech vaccine, including eight who had previously been infected with SARS-CoV-2. The authors collected blood samples from each of the participants before the first dose and again at four, five, seven, and 15 weeks afterward. The blood samples revealed that antibody levels increased slowly among participants who had never been exposed to the virus, peaking about one week after the second dose. In contrast, antibody levels among those who had previously been infected with SARS-CoV-2 were high before the first dose. These levels increased rapidly upon vaccination and peaked higher than those who had never been infected. These findings suggest that the immune response to mRNA vaccines is robust and long-lasting. They also underscore the value of vaccination even after having been infected with SARS-CoV-2. Link to full study. Learn more about mRNA vaccines in this clip featuring Dr. Roger Seheult. A very-low-calorie diet increases harmful gut bacteria. The gut microbiota is composed of the community of bacteria, archaea, fungi, and viruses that live in the human intestine and is unique to each individual. Diet can modulate the structure and function of the gut microbiota in ways that either increase or decrease disease risk. Findings of a new report detail the effects of a very-low-calorie diet on the gut microbiota, weight loss, and infection risk. Following the absorption of most macronutrients (carbohydrates, fats, and proteins) and micronutrients (vitamins and minerals) present in food in the small intestine, undigested food travels to the large intestine where microbes metabolize any remaining nutrients. The amount and type of food consumed in the diet directly affect the amount and type of microbes that can flourish in the large intestine. Consuming a wide variety of foods in the diet supports a wide variety of microbes, while restricting certain foods or restricting caloric intake may reduce the abundance and diversity of the microbiota, a risk factor for disease. The authors of the report recruited 80 females who had completed menopause and who had overweight or obesity. They randomized participants to complete a medically supervised weight-loss program or to maintain a stable weight for 16 weeks. Participants in the weight-loss program consumed a very-low-calorie diet (800 calories per day) for eight weeks, followed by four weeks of a conventional low-calorie diet and four weeks of a weight maintenance diet. The researchers sequenced DNA from the participants' gut microbiota to determine the number and type of microbes present. Finally, they collected gut microbiota samples from the baseline and 12-week timepoints from the participants who lost the most weight during the weight loss program. They transplanted these samples into germ-free mice, which lack a microbiota. Participants in the weight-loss program lost an average of 14 percent of their body weight (about 27 pounds) after 12 weeks. A very-low-calorie diet reduced the abundance and diversity of microbes in the gut, but these changes were reversed when participants returned to a normal diet. Microbiota samples from the participants in the very-low-calorie diet intervention were enriched in Clostridioides difficile (commonly referred to as “C. diff”), a gastrointestinal pathogen. This increase was associated with a reduction in the production of bile acids, which aid in dietary fat digestion and are protective against gastrointestinal pathogens. Mice that received a microbiota transplant from the very-low-calorie diet timepoint lost significantly more body weight due to changes in microbiota structure and reduced nutrient absorption, compared to mice that received a microbiota transplant from baseline. This research highlights the importance of diet in the interplay between pathogenic and beneficial microbes in the gut microbiota. Link to full report. Learn more about how the microbiota and immune system interact in this video featuring Dr. Rhonda Patrick.) A ketogenic diet improves immunity and reduces excessive inflammation. A Western dietary pattern, characterized by a low intake of fruits and vegetables and a high intake of red and processed meats and added sugars, promotes chronic diseases, including obesity. It also increases low-grade inflammation by directly reprogramming immune cells to become pro-inflammatory. Authors of a recent report investigated the impact of a ketogenic diet on immunity. Glucose is the primary energy source for most cells in the body. However, when a person fasts or restricts carbohydrate intake, the body produces ketones from dietary and body fat for energy. One such ketone is beta-hydroxybutyrate, which has been shown to ameliorate low-grade inflammation and related diseases in mice. Whether consuming a very low carbohydrate diet alters immunity in humans is unclear. The investigators recruited 44 healthy adults to complete a three-week ketogenic diet that provided less than 30 grams of carbohydrates per day (the amount in about two slices of sandwich bread). Participants gave blood samples before and after the diet period for measurement of immune cells, including antibody-producing T cells. The researchers exposed white blood cells from the pre-diet and post-diet timepoints to varying concentrations of beta-hydroxybutyrate for 48 hours, stimulated them to produce an immune response, and measured the effect. When exposed to beta-hydroxybutyrate, pre-diet white blood cells associated with the innate immune system (the driver of chronic low-grade inflammation) did not alter their behavior; however, antibody-producing white blood cells associated with the adaptive immune system became more active. CD4+ and CD8+ T cells exposed to the highest concentration of beta-hydroxybutyrate (10 millimolar), comparable to the maximum circulating level in humans, produced more cytokines used to fight infection. Regulatory T cells, which prevent autoimmunity and excessive inflammation, also increased their activity, including the mitochondrial metabolism of ketones. Participants lost a significant amount of weight over the three-week ketogenic diet period, and their post-diet T cells showed the same metabolic and immunological responses as those in the in vitro experiment. The authors concluded that a very low carbohydrate diet or ketogenic diet is a clinical tool for improving T cell-mediated immunity. They suggested that nutrition and dietary interventions should be used more in modern medicine. Link to full report. Learn more about the metabolic benefits of a ketogenic diet in this episode featuring expert Dr. Dominic D'Agostino. A ketogenic diet may reduce COVID-19 severity. Aging impairs the body’s ability to fight infection due to chronic low-grade inflammation and a decrease in antibody-producing T cells. Consequently, 80 percent of deaths due to COVID-19 in the United States have been among adults 65 years of age and older. Researchers investigated the use of a ketogenic diet in mice as a strategy for treating COVID-19. A ketogenic diet is a high fat, low carbohydrate diet. Adherence to a ketogenic diet reduces blood glucose levels, which are associated with increased inflammation. Adopting a ketogenic diet may be an effective strategy for limiting excessive inflammation, especially in older adults, who are more likely to have poor blood glucose control. The SARS-CoV-2 virus, the cause of COVID-19 illness, induces lung inflammation. In severe cases, patients may need mechanical ventilation to breathe and may have long-lasting respiratory problems after recovery. Previous COVID-19 research has shown that white blood cells such as neutrophils and monocytes accumulate in the lungs. There they become more reliant on glucose, accelerate their mitochondrial metabolism, and produce more damaging oxidative compounds, contributing to unchecked inflammation and disease severity. The researchers used mice that express the human angiotensin-converting enzyme (ACE) 2 receptor, which is the point of entry for the SARS-CoV-2 virus in the lungs and other organs. They fed young adult mice and older adult mice either a standard diet or a ketogenic diet for five days before exposing them to a hepatitis virus that closely mimics the SARS-CoV-2 infection in humans. The mice continued their assigned diet for an additional seven days following infection. The investigators measured markers of inflammation and metabolic function. Older mice had significantly higher levels of inflammation and metabolic dysfunction at the beginning of the study. Upon infection, they had greater inflammation in the heart, adipose tissue, and hypothalamus; worse pneumonia symptoms and increased blood clot formation; and were more likely to die due to infection, compared to younger mice. The increased inflammation was due to an increase in neutrophil accumulation and a decrease in tissue-protective T cells in the lungs. A ketogenic diet reprogrammed metabolism and the immune system to a greater extent in older mice by increasing the number of beneficial T cells and reducing the number of harmful monocytes in the lungs, leading to less inflammation overall and reduced disease severity. Although this study was conducted in mice, the authors concluded that a ketogenic diet may be a potential treatment for SARS-CoV-2 infection in older adults due to its ability to modulate immune function and dampen excessive inflammation. Link to full report. Learn more about COVID-19 and how vitamin D may reduce inflammation and disease severity from Dr. Roger Seheult.