The majority of global COVID-19 deaths have been in countries where many people are obese, with coronavirus fatality rates 10 times higher in nations where at least 50% of adults are overweight, a global study found.
From Phys.org/Univ. of Michigan (June 9, 2020):
“On a high-sugar diet, we find that the fruit flies’ dopaminergic neurons are less active, because the high sugar intake decreases the intensity of the sweetness signal that comes from the mouth,” Dus said. “Animals use this feedback from dopamine to make predictions about how rewarding or filling a food will be. In the high-sugar diet flies, this process is broken—they get less dopamine neuron activation and so end up eating more than they need, which over time makes them gain weight.”
It is well known that consuming food and drink high in sugar is not great for us, but scientists are continuing to unravel the intricacies of how the sweet stuff drives negative health outcomes. The latest finding comes from researchers at the University of Michigan, who through studies in fruit flies have found that excess amounts of sugar can shut down crucial neural circuits linked to regulating satiety, possibly leading to overeating in humans.
From a Diabetologia online study release (April 15, 2020):
“Having normal body weight is crucial in the prevention of type 2 diabetes, regardless of genetic predisposition.”
“The results suggest that type 2 diabetes prevention by weight management and healthy lifestyle is critical across all genetic risk groups.”
“Overall, the results indicate that a favorable lifestyle should be universally recommended in the prevention of type 2 diabetes, regardless of genetic predisposition, thus supporting current public health guidelines,”
We examined the joint association of genetic predisposition, obesity and unfavourable lifestyle with incident type 2 diabetes using a case-cohort study nested within the Diet, Cancer and Health cohort in Denmark. The study sample included 4729 individuals who developed type 2 diabetes during a median 14.7 years of follow-up, and a randomly selected cohort sample of 5402 individuals.
Obesity (BMI ≥ 30 kg/m2) and unfavourable lifestyle were associated with higher risk for incident type 2 diabetes regardless of genetic predisposition (p > 0.05 for GRS–obesity and GRS–lifestyle interaction). The effect of obesity on type 2 diabetes risk (HR 5.81 [95% CI 5.16, 6.55]) was high, whereas the effects of high genetic risk (HR 2.00 [95% CI 1.76, 2.27]) and unfavourable lifestyle (HR 1.18 [95% CI 1.06, 1.30]) were relatively modest.
From a PLOS Biology Journal study (Feb 20, 2020):
The major finding of this study is that the timing of feeding over the day leads to significant differences in the metabolism of an equivalent 24-h nutritional intake. Daily timing of nutrient availability coupled with daily/circadian control of metabolism drives a switch in substrate preference such that the late-evening Snack Session resulted in significantly lower LO compared to the Breakfast Session.
Developed countries are experiencing an epidemic of obesity that leads to many serious health problems, foremost among which are increasing rates of type 2 diabetes, metabolic syndrome, cardiovascular disease, and cancer. While weight gain and obesity are primarily determined by diet and exercise, there is tremendous interest in the possibility that the daily timing of eating might have a significant impact upon weight management [1–3]. Many physiological processes display day/night rhythms, including feeding behavior, lipid and carbohydrate metabolism, body temperature, and sleep.
These daily oscillations are controlled by the circadian clock, which is composed of an autoregulatory biochemical mechanism that is expressed in tissues throughout the body and is coordinated by a master pacemaker located in the suprachiasmatic nuclei of the brain (aka the SCN [1,4]). The circadian system globally controls gene expression patterns so that metabolic pathways are differentially regulated over the day, including switching between carbohydrate and lipid catabolism [1,3,5–9]. Therefore, ingestion of the same food at different times of day could lead to differential metabolic outcomes, e.g., lipid oxidation (LO) versus accumulation; however, whether this is true or not is unclear.
From a New York Times online article (March 16, 2020):
“Maintaining weight loss can get easier over time. Over time, less intentional effort, though not no effort, is needed to be successful. After about two years, healthy eating habits become part of the routine. Healthy choices become more automatic the longer people continue to make them. They feel weird when they don’t.”
Among the useful strategies identified in the new study is to keep lower calorie foods like fruits and vegetables more accessible. “We eat what we see,” Dr. Phelan noted. The corollary is equally important: keep high-calorie, less nourishing foods relatively inaccessible and out of sight if not out of the house entirely.
The new study led by Dr. Phelan, professor of kinesiology and public health at California Polytechnic State University, identified habits and strategies that can be keys to success for millions. Yes, like most sensible weight-loss plans, they involve healthful eating and regular physical activity. But they also include important self-monitoring practices and nonpunitive coping measures that can be the crucial to long-term weight management.
From The Lancet Diabetes & Endocrinology:
This joint position statement from the International Atherosclerosis Society and the International Chair on Cardiometabolic Risk Working Group on Visceral Obesity summarises the evidence for visceral adiposity and ectopic fat as emerging risk factors for type 2 diabetes, atherosclerosis, and cardiovascular disease, with a focus on practical recommendations for health professionals and future directions for research and clinical practice.
Findings from epidemiological studies over the past 30 years have shown that visceral adipose tissue, accurately measured by CT or MRI, is an independent risk marker of cardiovascular and metabolic morbidity and mortality. Emerging evidence also suggests that ectopic fat deposition, including hepatic and epicardial fat, might contribute to increased atherosclerosis and cardiometabolic risk. We discuss the measurement of visceral and ectopic fat, pathophysiology and contribution to adverse health outcomes, response to treatment, and lessons from a public health programme targeting visceral and ectopic fat. We identify knowledge gaps and note the need to develop simple, clinically applicable tools to be able to monitor changes in visceral and ectopic fat over time. Finally, we recognise the need for public health messaging to focus on visceral and ectopic fat in addition to excess bodyweight to better combat the growing epidemic of obesity worldwide.
To read more click on the following link: https://www.thelancet.com/journals/landia/article/PIIS2213-8587(19)30084-1/fulltext?dgcid=raven_jbs_etoc_email