What is the perfect treatment that can help type 2 diabetes (!) and lead to effortless weight loss? Listen to the eloquent Dr. Jason Fung describe it in this 12-minute part of a longer interview.
A study by Monash University has uncovered that liver metabolism is disrupted in people with obesity-related type 2 diabetes, which contributes to high blood sugar and muscle loss – also known as skeletal muscle atrophy.
Using human trials as well as mouse models, collaborative research led by Dr Adam Rose at Monash Biomedicine Discovery Institute has found the liver metabolism of the amino acid alanine is altered in people with obesity-related type 2 diabetes. By selectively silencing enzymes that break down alanine in liver cells, high blood sugar and muscle loss can be reversed by the restoration of skeletal muscle protein synthesis, a critical determinant of muscle size and strength.
The research, published today in Nature Metabolism, has shown the altered liver metabolism directly affects muscle size and strength and the mechanism behind this is driven by elevated levels of the hormones cortisol and glucagon which enhance the cycling of amino acids between liver and skeletal muscle, causing muscles to become smaller and weaker.
Along with metabolic dysfunction and related complications, an often overlooked co-morbidity of obesity is skeletal muscle atrophy, which causes frailty, and is related to reduced life-quality and death.
“The ageing-related diseases of skeletal muscle loss and type 2 diabetes are very prevalent and are a huge societal and economic burden. We have known for some time that the ageing-related diseases of skeletal muscle loss and type 2 diabetes were linked but we didn’t know how,” Dr Rose said.
He adds: “Our studies demonstrate that the liver is a critical control point for muscle protein metabolism; a discovery that is quite surprising. We believe that our new findings highlight the need to examine the role of skeletal muscle atrophy in type 2 diabetes more closely in human clinical populations.”
The study solidifies the long-known metabolic biochemistry staple, the glucose-alanine cycle, as a fundamental part of metabolism in health and disease.
A modeling study suggests a majority of adult COVID-19 hospitalizations nationwide are attributable to at least one of four pre-existing conditions: obesity, hypertension, diabetes, and heart failure, in that order.
The study, published today in the Journal of the American Heart Association (JAHA) and led by researchers at the Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University, used a mathematical simulation to estimate the number and proportion of national COVID-19 hospitalizations that could have been prevented if Americans did not suffer from four major cardiometabolic conditions. Each condition has been strongly linked in other studies to increased risk of poor outcomes with COVID-19 infection.
“While newly authorized COVID-19 vaccines will eventually reduce infections, we have a long way to go to get to that point. Our findings call for interventions to determine whether improving cardiometabolic health will reduce hospitalizations, morbidity, and health care strains from COVID-19,” said Dariush Mozaffarian, lead author and dean of the Friedman School. “We know that changes in diet quality alone, even without weight loss, rapidly improve metabolic health within just six to eight weeks. It’s crucial to test such lifestyle approaches for reducing severe COVID-19 infections, both for this pandemic and future pandemics likely to come.”
The researchers estimated that, among the 906,849 total COVID-19 hospitalizations that had occurred in U.S. adults as of November 18, 2020:
In epidemiological terms, the attributable proportion represents the percentage of COVID-19 hospitalizations that could have been prevented in the absence of the four conditions. In other words, the study found the individuals might still have been infected but may not have had a severe enough clinical course to require hospitalization. When numbers for the four conditions were combined, the model suggests 64% (575,419) of COVID-19 hospitalizations might have been prevented. A 10% reduction in national prevalence of each condition, when combined, could prevent about 11% of all COVID-19 hospitalizations, according to the model.
The four conditions were chosen based on other published research from around the world showing each is an independent predictor of severe outcomes, including hospitalization, among people infected with COVID-19. The specific risk estimates for each condition were from a published multivariable model involving more than 5,000 COVID-19 patients diagnosed in New York City earlier in the pandemic. The researchers used other national data to model the number of COVID-19 hospitalizations nationally; the distributions of these hospitalizations by age, sex, and race; and the estimated distribution of the underlying comorbidities among adults infected with COVID-19. They then estimated the proportions and numbers of COVID-19 cases that became severe enough to require hospitalization owing to the presence of one or more of the conditions.
“Medical providers should educate patients who may be at risk for severe COVID-19 and consider promoting preventive lifestyle measures, such as improved dietary quality and physical activity, to improve overall cardiometabolic health. It’s also important for providers to be aware of the health disparities people with these conditions often face,” said first author Meghan O’Hearn, a doctoral candidate at the Friedman School.
The model estimated that age and race/ethnicity resulted in disparities in COVID-19 hospitalizations due to the four conditions. For example, about 8% of COVID-19 hospitalizations among adults under 50 years old were estimated to be due to diabetes, compared to about 29% of COVID-19 hospitalizations among those age 65 and older. In contrast, obesity had an equally detrimental impact on COVID-19 hospitalizations across age groups.
At any age, COVID-19 hospitalizations attributable to all four conditions were higher in Black adults than in white adults and generally higher for diabetes and obesity in Hispanic adults than in white adults. For example, among adults age 65 and older, diabetes was estimated to cause about 25% of COVID-19 hospitalizations among white adults, versus about 32% among Black adults, and about 34% among Hispanic adults.
When the four conditions were considered combined, the proportion of attributable hospitalizations was highest in Black adults of all ages, followed by Hispanics. For example, among young adults 18-49 years old, the four conditions jointly were estimated to cause about 39% of COVID-19 hospitalizations among white adults, versus 50% among Black adults.
“National data show that Black and Hispanic Americans are suffering the worst outcomes from COVID-19. Our findings lend support to the need for prioritizing vaccine distribution, good nutrition, and other preventive measures to people with cardiometabolic conditions, particularly among groups most affected by health disparities,” Mozaffarian said. “Policies aimed at reducing the prevalence of these four cardiometabolic conditions among Black and Hispanic Americans must be part of any state or national policy discussion aimed at reducing health disparities from COVID-19.”
Researchers from the Department of Pharmacology, Paediatrics and Radiology at the University of Seville, in collaboration with Dr. Rodriguez from the International University of Catalonia, have confirmed that Orujo Olive OIL (POCTA), when introduced into the diet, produces a significant reduction in obesity and vascular and inflammatory complications in obese mice. In addition, given that POCTA has been obtained from a by-product of olive oil, orujo, which is considered as industrial waste, this study helps to increase its biological and nutritional value as a functional food, being its main source of bioactive compounds, the triterpenic acids.
To carry out this research, a comparative study was made over the course of 10 weeks in mice with two types of diets; a diet high in saturated fats, called “prejudicial” fat, and another, with the same calorie content, but with orujo olive oil. After this time was over, a significant reduction in weight was observed (around 30%) in the mice fed with POCTA in comparison with the group fed with the high-fat diet.
This study shows for the first time that POCTA, “does not only reduce body weight in obese animals, but also reduces body fat (adipose tissue), hepatic inflammation, while, at the same time, reducing resistance to insulin and vascular dysfunction associated with obesity”, explains the University of Seville researcher Carmen Maris Claro Cala.
These preliminary studies in animals provide very important information about the traditional use of orujo olive oil as a functional food due to its content of triterpenic acids, such as oleanolic acid and maslinic acid as bioactive molecules. However, the researcher indicates that “before being able to establish the therapeutic potential of these molecules, controlled clinical trials should be carried out so as to be able to arrive at conclusions about their action in humans and any repercussions on health”.
Other oils on the market
Unlike other types of oils, like coconut or palm oil, the oil obtained from the orujo of the olive, a product forgotten in recent years, has shown itself to be a source of bioactive molecules with great therapeutic potential against obesity and the metabolic dysfunctions developed with Metabolic Syndrome. The results of this study “open a new line of research in investigating the Mediterranean diet”, the researcher adds.
With obesity now affecting almost a third (29%) of the population in England, and expected to rise to 35% by 2030, should we now recognise it as a disease? Experts debate the issue in The BMJ today.
Obesity, in which excess body fat has accumulated to such an extent that health may be adversely affected, meets the dictionary definition of disease, argue Professor John Wilding at the University of Liverpool and Vicky Mooney, representing the European Coalition for People living with Obesity (ECPO).
They point out that more than 200 genes influence weight, and most of these are expressed in the brain or in adipose tissue. “Thus body weight, fat distribution, and risk of complications are strongly influenced by biology – it is not an individual’s fault if they develop obesity.”
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They argue that the recent rapid increase in obesity is not due to genetics but to an altered environment (food availability and cost, physical environment, and social factors).
Yet the widespread view is that obesity is self inflicted and that it is entirely the individual’s responsibility to do something about it, while healthcare professionals seem ill informed on the complexity of obesity and what patients with obesity want.
Recognising obesity as a chronic disease with severe complications rather than a lifestyle choice “should help reduce the stigma and discrimination experienced by many people with obesity,” they add.
They disagree that labelling a high proportion of the population as having a disease removes personal responsibility or may overwhelm health services, pointing out that other common diseases, such as high blood pressure and diabetes, require people to take action to manage their condition.
They suggest that most people with obesity will eventually develop complications, and those who do not could be considered as not having disease. “But unless we accept that obesity is a disease, we are not going to be able to curb the epidemic,” they conclude.
But Dr Richard Pile, a GP with a special interest in cardiology and Clinical Lead for Prevention for Herts Valleys Clinical Commissioning Group, argues that adopting this approach “could actually result in worse outcomes for individuals and society.”
He believes that the dictionary definition of disease “is so vague that we can classify almost anything as a disease” and says the question is not whether we can, but whether we should, and to what end.
If labelling obesity as a disease was harmless then it wouldn’t really matter, he writes. But labelling obesity as a disease “risks reducing autonomy, disempowering and robbing people of the intrinsic motivation that is such an important enabler of change.”
There is an important difference psychologically between having a risk factor that you have some responsibility for and control over and having a disease that someone else is responsible for treating, he says.
What’s more, making obesity a disease “may not benefit patients, but it will benefit healthcare providers and the pharmaceutical industry when health insurance and clinical guidelines promote treatment with drugs and surgery,” he warns.
While self determination is key in enabling change, “we should acknowledge that the origins of obesity for most people are social, and so too is the solution,” he adds. “If people meet, shop, cook, eat, and engage in activities together the end result will be improved wellbeing and reducing obesity will be a consequential beneficial side effect.”
Classifying obesity as a disease is neither essential nor beneficial. It’s much more complicated than that, he concludes.