Study one of few to examine health benefits of Mediterranean diet in a non-Mediterranean context and to assess the health benefits of an overall Mediterranean lifestyle
In a study of adults in the United Kingdom, those who adhered closely to a Mediterranean lifestyle—including eating a healthy, plant-based diet with limited added salts and sugars and getting adequate rest, exercise, and socialization—were found to have a 29% lower risk of all-cause mortality and a 28% lower risk of cancer mortality compared to those who were nonadherent to the lifestyle.
Adherence to Mediterranean lifestyle habits around adequate rest, exercise, and socialization was most strongly associated with lower risk of all-cause and cancer mortality, and was independently associated with a lower risk of cardiovascular disease mortality.
Embargoed for release: Wednesday, August 16, 2023, 4:00 PM ET
Boston, MA—People who adhere to a Mediterranean lifestyle—which includes a diet rich in fruits, vegetables, and whole grains; healthy eating habits like limiting added salts and sugars; and habits promoting adequate rest, physical activity, and socialization—have a lower risk of all-cause and cancer mortality, according to a new study led by La Universidad Autónoma de Madrid and Harvard T.H. Chan School of Public Health. People who adhered to the lifestyle’s emphasis on rest, exercise, and socializing with friends had a lower risk of cardiovascular disease mortality.
The study will be published on Wednesday, August 16, in Mayo Clinic Proceedings.
While many studies have established the health benefits of a Mediterranean diet and lifestyle, little research has been conducted on the diet outside of its region of origin. “This study suggests that it’s possible for non-Mediterranean populations to adopt the Mediterranean diet using locally available products and to adopt the overall Mediterranean lifestyle within their own cultural contexts,” said lead author Mercedes Sotos Prieto, Ramon y Cajal research fellow at La Universidad Autónoma de Madrid and adjunct assistant professor of environmental health at Harvard Chan School. “We’re seeing the transferability of the lifestyle and its positive effects on health.”
The researchers analyzed the habits of 110,799 members of the UK Biobank cohort, a population-based study across England, Wales, and Scotland using the Mediterranean Lifestyle (MEDLIFE) index, which is derived from a lifestyle questionnaire and diet assessments. Participants, who were between the ages of 40 and 75, provided information about their lifestyle according to the three categories the index measures: “Mediterranean food consumption” (intake of foods part of the Mediterranean diet such as fruits and whole grains); “Mediterranean dietary habits” (adherence to habits and practices around meals, including limiting salt and drinking healthy beverages); and “physical activity, rest, and social habits and conviviality” (adherence to lifestyle habits including taking regular naps, exercising, and spending time with friends). Each item within the three categories was then scored, with higher total scores indicating higher adherence to the Mediterranean lifestyle.
a) Patterns of whorl direction. (b) Manhattan plot and quantile-quantile plot from the discovery and replication cohorts. CREDIT Journal of Investigative Dermatology
The first gene mapping study on human scalp hair whorls not only shows that hair whorl direction has a genetic basis, but also that it is affected by multiple genes. Four associated genetic variants that are likely to influence hair whorl direction are identified, as reported in the Journal of Investigative Dermatology, published by Elsevier.
A hair whorl is a patch of hair growing in a circular pattern around a point specified by hair follicle orientations. As an easily observed human trait, scalp hair whorl pattern is typically defined by the whorl number (single or double whorl) and whorl direction (e.g., clockwise, counterclockwise, or diffuse).
Because atypical whorl patterns have been observed in patients with abnormal neurological development, understanding the genetic basis of whorl patterns may help unravel important biological processes.
The first genome-wide association study (GWAS) on human scalp hair whorls was performed among 2,149 Chinese individuals from the National Survey of Physical Traits cohort, followed by a replication study in 1,950 Chinese individuals from the Taizhou Longitudinal Study cohort.
Lead investigator Sijia Wang, PhD, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, explained, “We know very little about why we look like we do. Our group has been looking for the genes underlying various interesting traits of physical appearance, including fingerprint patterns, eyebrow thickness, earlobe shape and hair curliness. Hair whorl is one of the traits that we were curious about. The prevailing opinion was that hair whorl direction is controlled by a single gene, exhibiting Mendelian inheritance. However, our results demonstrate that hair whorl direction is influenced by the cumulative effects of multiple genes, suggesting a polygenic inheritance.”
The study identifies four associated genetic variants (at 7p21.3, 5q33.2, 7q33, and 14q32.13). These genetic variants are likely to influence hair whorl direction by regulating the cell polarity of hair follicles, with cranial neural tube closure and growth also potentially playing a role.
Professor Wang continued, “While previous work proposed the hypothesis of associations between hair whorl patterns and abnormal neurological development, no significant genetic associations were observed between hair whorl direction and behavioral, cognitive, or neurological phenotypes. Although we still know very little about why we look like we do, we are confident that curiosity will eventually drive us to the answers.”
Researchers analyzed 120 previous clinical trials, finding no evidence that treatment efficacies depend on number of comorbidities. Peter Hanlon (CC-BY 4.0, https://creativecommons.org/licenses/by/4.0/)
Treatment efficacy for a broad range of chronic diseases does not differ depending on patients’ comorbidities, according to a new study publishing June 6thin the open access journal PLOS Medicine by David McAllister of the University of Glasgow, UK, and colleagues.
There is often uncertainty about how treatments for single conditions should be applied to people who have multiple chronic conditions (multimorbidity). This confusion stems, in part, from the fact that people with multimorbidity are under-represented in randomized controlled trials, and trials rarely report whether the efficacy of treatment differs by the number of comorbidities or the presence of specific comorbidities.
In the new study, the researchers used existing data from 120 industry-sponsored randomized controlled phase 3 and 4 clinical trials carried out between 1990 and 2017. The dataset included a total of 128,331 participants and spanned 23 common long-term conditions, including asthma, diabetes, hypertension, osteoporosis, and migraine. For each trial as well as each treatment type spanning multiple trials, the team modeled whether there were any interactions between treatment efficacy and comorbidities.
Across trials, the percentage of participants with three or more comorbidities ranged from 2.3% (in allergic rhinitis trials) to 57% (in trials for systemic lupus erythematosus). Overall, the new study found no evidence of comorbidities modifying treatment efficacy across any of the 23 conditions studied. However, the authors noted that the trials were not designed to assess variation in treatment efficacy by comorbidity.
“The standard assumption used in evidence syntheses is that efficacy is constant across subgroups, although this is often criticized,” the authors say. “Our findings suggest that for modest levels of comorbidities, this assumption is reasonable.”
Coauthor Peter Hanlon adds, “Many people live with multiple long-term conditions, however deciding on the most appropriate treatment for these people is often challenging because clinical trials rarely report whether treatments work as well in people with multiple conditions and clinical guidelines rarely address the specific needs of these people. We found that treatments had similar effects in people with multiple conditions, which is important as this information can be used to help experts decide which treatments they should recommend in clinical guidelines.”
A new study from Keck Medicine of USC shows that metabolic syndrome, a cluster of conditions that raise the risk of heart disease, diabetes, stroke and other health problems, more than doubles the risk of advanced liver disease among heavy drinkers
Two people regularly have a few alcoholic drinks daily. One develops liver disease. The other doesn’t.
What explains the different outcomes?
The answer may lie in a condition known as metabolic syndrome, a cluster of conditions that together raise the risk of coronary heart disease, diabetes, stroke and other serious health problems. This syndrome, characterized by symptoms such as abdominal fat, high blood pressure, high cholesterol and high blood sugar, affects more than one in three Americans.
A new study from Keck Medicine of USC published in the Annals of Internal Medicine shows that heavy alcohol use may be dramatically more damaging to the liver for people with metabolic syndrome.
“Our research suggests that metabolic syndrome and alcohol interact in such a way that they multiply the effect of alcohol on the liver, more than doubling the risk of advanced liver disease among heavy drinkers,” said Brian P. Lee, MD, MAS, a hepatologist and liver transplant specialist with Keck Medicine who is the lead author on the study. “Drinking is harmful to the liver, but especially so for this segment of the population.”
In the study, heavy alcohol use was defined as two drinks (a total of 12 fluid ounces) a day for women and three drinks (a total of 18 fluid ounces) per day for men.
Lee and his colleagues were motivated to research a connection between advanced liver disease, alcohol use and metabolic syndrome after noticing that between 2009-2018, deaths from alcohol-associated liver disease surged in the United States by more than 30% while alcohol use, including heavy drinking, remained stable or declined.
During the last 20 years, the number of Americans with metabolic syndrome increased significantly. Previous research has shown that metabolic syndrome can cause liver abnormalities.
“We therefore hypothesized that metabolic syndrome could be an important contributor to this unexplained surge in advanced liver disease,” said Lee.
For the study, Lee and his fellow researchers used data from the National Health and Nutrition Examination Survey, which assesses the health and nutritional status of adults and children in the United States, pulling together samples representing the U.S. population 20 years or older between 1999 and 2018.
While the data revealed a slight increase in advanced liver disease with heavy alcohol use without metabolic syndrome, the greatest increase in advanced liver disease was found in those with combined heavy alcohol use and metabolic syndrome.
Lee believes that the increased risk of liver damage from drinking is a result of an increase in the amount of fat in the liver. A healthy liver contains less than five percent fat; any more than that can lead to inflammation and cirrhosis (scarring) of the liver, liver cancer and liver failure.
“Both metabolic syndrome and drinking increase liver fat, and we think that the combination of the two accelerates the accumulation of fat in the liver and fuels inflammation, resulting in a greater chance of liver disease,” said Lee.
He hopes the study will encourage physicians who screen and diagnose patients with metabolic syndrome to also ask about alcohol use and look for liver disease.
“Our study indicates that these conditions may often coexist, and it is in patients’ best interest to address both issues,” he said. “It’s also important for people with metabolic syndrome to realize they may be at an increased likelihood of advanced liver disease, and to monitor their drinking accordingly,” he added.
Mitochondria (green) within a cell are depicted in this colorized transmission electron micrograph. The folds are called cristae, and are where chemical reactions occur that produce energy for cellular and metabolic functions. CREDIT Thomas Deerinck, National center for Microscopy and Imaging Research, UC San DIego
In a wide-ranging paper, a UC San Diego physician-scientist explains why all chronic diseases, from diabetes to autism, are linked by the underlying failure of cells and the body to heal completely
In medicine and science, the term “pathogenesis” describes the origin and development of disease. There is not, however, a broadly accepted term to describe the other half of the equation: the process of healing and recovery.
In a new and far-reaching paper, published May 10, 2023 in the journal Mitochondrion, Robert K. Naviaux, MD, PhD, professor of Medicine, Pediatrics and Pathology at UC San Diego School of Medicine, proposes both a term and, more importantly, outlines the array of processes and players, beginning with cellular mitochondria, that drive the healing process – and whose dysfunction underlies chronic illnesses from diabetes and autoimmune disorders to long COVID and autism spectrum disorder.
“Great strides in medicine since World War II have focused on and addressed the triggers and risk factors of disease,” said Naviaux. “This pathogenesis-based approach has been very effective in developing treatments for acute illnesses, such as those caused by physical trauma, infection, vitamin deficiencies and poisoning.”
The greater health threat now, he said, lies with chronic disease. Six in 10 adults in the United States have a chronic disease; 4 in 10 have two or more. These conditions, such as heart disease, cancer, diabetes, Alzheimer’s and chronic kidney failure, account for 7 out of 10 deaths in the U.S. each year, according to the Centers for Disease Control and Prevention.
“In the last 70 years, not a single chronic illness is curable using current medical paradigms unless it has a cause that can be bypassed, killed, burned out or cut out,” said Naviaux.
“When cures are achieved, they rely on recovery by spontaneous healing — an essential process that operates silently in the background and is still poorly understood. Antibiotics can cure a pneumococcal pneumonia and a stent can reopen an occluded (blocked) coronary artery, but active healing is required after the intervention to repair the damaged lung and heart.
“Without healing,” said Naviaux, “multicellular life on Earth would not exist. Without healing, one injury predisposes to another, leading to disability, chronic disease, accelerated aging and death.”
“In most cases, pathogenesis-based drugs like insulin for diabetes and statins for dyslipidemia (an imbalance of blood lipids, such as cholesterol, that leads to cardiovascular disease) must be taken for life because the root cause of the chronic symptoms is not changed by treatment.”
In his new paper, Naviaux posits that the root cause of many chronic diseases lies with disruption in the normal sequence of mitochondrial transformations needed to initiate and complete the healing cycle. He has called this universal response to infection, stress, or injury, the cell danger response or CDR. The CDR is an evolutionarily conserved metabolic response that protects cells and hosts from harm. CDR is triggered by exposure to chemical, physical or biological threats. It is a normal part of the immune response that prompts cells to take protective measures.
But sometimes, as Naviaux has shown in past published work, including a ground-breaking preclinical study in 2014, and a seminal Phase 1b/2a Clinical Trial involving young boys with autism published in 2017, CDR continues to sound the alarm even after the originating threat is gone. Inflammation and cell dysfunction persist, resulting in chronic symptoms.
“Abnormal persistence of any phase of the CDR inhibits the healing cycle, creates dysfunctional cellular mosaics, causes the symptoms of chronic disease and accelerates the process of aging,” said Naviaux.
“New research reframes the rising tide of chronic disease around the world as a systems problem caused by the combined action of pathogenic triggers and anthropogenic factors (from human activity, such as pollution) that interfere with the mitochondrial functions needed for healing. Once chronic pain, disability or disease is established, salugenesis-based therapies will start where pathogenesis-based therapies end.”
What is Salugenesis?
Salugenesis derives from the Latin word for the Roman goddess of health, safety and prosperity, Salus. It is related to “salutogenesis,” a word coined in 1976 by the medical sociologist Aaron Antonovsky to describe lifestyle choices and coping skills people use to produce, restore and preserve good health despite all manner of hardship.
Salutogenesis is a sort to big picture concept. Salugenesis is more narrowly focused on the sequential, hard-wired molecular, metabolic and cellular stages of the healing cycle. Both words involve redirecting energy to oppose and reverse the arrow of entropy or decay. They are the opposite of pathogenesis, which is about disorganization and disintegration driven by disease.
Naviaux’s paper makes several key points, among them:
Chronic diseases are currently and mistakenly studied in isolation. Diabetes, for example, looks a lot different from post-traumatic stress disorder. But both, and many other conditions, share an underlying failure of the body to fully heal. “Once the pathogenic trigger has been treated or removed, chronic disease persists because healing is incomplete,” said Naviaux.
Disease is governed by biological logic, which is intrinsic and the result of millions of years of evolution to address internal problems. Modern medicine has advanced through engineering logic, which looks at external issues generally involving non-living systems.
Health and healing are dynamic circles with a beginning, middle and end. The phases are the same whether the injury is a scrape or a stroke. They proceed sequentially by information exchanged between cells and with the environment, directing and informing what happens next. “Mitochondria generate most of the chemical energy needed to power a cell’s biochemical reactions,” said Naviaux. “But they are also cellular canaries in the coal mine, the early warning system that determines the nature and location of a problem or threat, and when to sound the alarm.”
Mitochondria naturally prioritize safety and respond to threats of all kinds—from microbial infections, to physical injury, to chemical pollutants in the air, water, and food chain—by stopping their normal anti-inflammatory functions, and shifting to pro-inflammatory functions needed to contain the damage, replace the cells lost, and finally, to restore normal metabolic communication between cells needed for optimum organ function.
CDR is both alarm and the proportional response to threat, he said. If mitochondria do not function properly — or CDR gets stuck in a phase — healing stops and disease prevails.
Curing chronic disease, according to Naviaux, must account for the fact that all such conditions are systems-wide failures, likely caused by multiple factors. “The same disease can be caused by different things in different people,” said Naviaux. Most diseases involve factors such as multiple genes, infection, environmental or microbial exposures, lifestyle choices and more.
With his work and latest publication, Naviaux argues for development of salugenesis-based research, which would explore the unified biological response to injury, harm and disease. Acute illness, he said, is a temporary state; chronic illness results from the long-term inability to heal completely after an acute injury has passed. They are two sides of the same coin.
Naviaux said he hopes that new research will lead to a “second book of medicine” that will collect new knowledge about the cause and treatment of complex chronic disease viewed through the lens of the healing cycle and salugenesis.
“If healing can be rebooted or unblocked after it has been derailed, cures of disorders once thought incurable may one day be possible,” he said.
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