It’s been a busy week…
New genetic variants that influence fat mass
Half the UK population has the fat “gene” – ie “sequence of genes”
…which I affectionately call the “I can’t eat this crap” gene
The sequence they discovered is not a gene, but it sits close to a gene called MC4R, which regulates energy levels in the body by influencing how much we eat and how much energy we expend or conserve. It is thought the sequence might play a role in controlling activity levels of the MC4R gene.
Dairy claims false: neither dairy nor calcium intake promotes weight loss
“Our findings demonstrate that increasing dairy product intake does not consistently result in weight or fat loss and may actually have the opposite effect,” the authors conclude.
Human metabolic phenotype diversity and its association with diet and blood pressure: Causes Of Disease Can Be Revealed By Metabolic Fingerprinting
Metabolic fingerprinting looks at the relative levels of many different metabolites, which are the products of metabolism, in a person’s blood or urine. Metabolites act as markers which can reveal a lot about how diet and lifestyle contribute to risks for certain diseases.
Aspirin-like compounds increase insulin secretion in otherwise healthy obese people
Aspirin-like compounds (salicylates) can claim another health benefit: increasing the amount of insulin produced by otherwise healthy obese people. Obesity is associated with insulin resistance, the first step toward type 2 diabetes.
How is that a benefit? Useful info but bad analysis. Good deconstruction here.
I missed this one earlier… Ha! I didn’t see it until it hit the BBC….
Vitamin A, E & Beta-carotene “seem to increase mortality”
I’d love to hear what the stats were on Vitamin D but it wasn’t covered
After various factors were taken into account and a further 20 studies excluded, the researchers linked vitamin A supplements to a 16% increased risk of dying, beta-carotene to a 7% increased risk and vitamin E to a 4% increased risk.
The Washington Post reports on the correlation between “pre-diabetes” (high blood sugar levels not yet in the diabetic range) and alzheimer’s:
People with elevated blood sugar levels may have an increased risk of developing Alzheimer’s disease, researchers reported yesterday at an international conference. Scientists already have linked Type 2 diabetes with Alzheimer’s, which afflicts 4.5 million Americans.
So what can you do to protect yourself? Go low carb of course… well at least according to Dr. Larry McCleary, the author of The Brain Trust who describes ketones as “the brain’s preferred fuel.”
Via Living La Vida Low Carb
The Journal of Lipid Research, reports on research which indicates that in obese individuals, fat cells are bloated and inflamed because they receive too many nutrients, including lipids. In these cells, various components cannot work properly anymore and, instead, they activate new proteins to cope with the situation.
Researchers show that when a fat cell receives too many nutrients, the ER is overwhelmed and triggers a process called the unfolded protein response (UPR). This process is one of many cellular responses that activate proteins that increase inflammation and can even result in the death of the cell. UPR also causes insulin resistance, a condition in which the production and function of insulin – a hormone produced by the pancreas – is impaired and blood sugar is too high.
In English: too many calories heading to your fat cells leads to inflammation and insulin resistance.
By giving ordinary adult mice a drug – a synthetic designed to mimic fat – Salk Institute scientist Dr. Ronald M. Evans is now able to chemically switch on PPAR-d, the master regulator that controls the ability of cells to burn fat. Even when the mice are not active, turning on the chemical switch activates the same fat-burning process that occurs during exercise. The resulting shift in energy balance (calories in, calories burned) makes the mice resistant to weight gain on a high fat diet.
The Salk Institute scientist who earlier discovered that enhancing the function of a single protein produced a mouse with an innate resistance to weight gain and the ability to run a mile without stopping, has found new evidence that this protein and a related protein play central roles in the body’s complex journey to obesity and offer a new and specific metabolic approach to the treatment of obesity related disease such as Syndrome X (insulin resistance, hyperlipidemia and atherosclerosis).
Via | Marathon Mouse Keeps on Running