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Dementia risk and BGLs. 
Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, according to the findings of a recent study published in the New England Journal of Medicine. For example:

  • In people without diabetes, risk for dementia was 18% higher for people with an average glucose level of 115 milligrams per deciliter (6.4 mmol/L) compared to those with an average glucose level of 100 mg/dl (5.6 mmol/L)
  • In people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40% higher for people with an average glucose level of 190 mg/dl (10.6 mmol/L) compared to those with an average glucose level of 160 mg/dl (8.9 mmol/L).

The measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c).

Dr Paul K. Crane
Dr Paul Crane

‘The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes,’ said first author Dr Paul K. Crane. ‘There was no threshold value for lower glucose values where risk leveled off.’ However, he emphasized that these results come from an observational study: ‘What we found was that people with higher levels of glucose had a higher risk of dementia, on average, than did people with lower levels of glucose,’ he said. ‘While that is interesting and important, we have no data to suggest that people who make changes to lower their glucose improve their dementia risk. Those data would have to come from future studies with different study designs.’

GI News’s Dr Alan Barclay stated that it is good to see Dr Crane emphasising the point that the results are from an observational study and as such do not prove causality; just an association. At this point in time, we don’t know if reducing glucose will reduce dementia risk. We need to conduct a randomised controlled trial to test that hypothesis.

Catching up on sleep.  
Dr Peter Liu
Dr Peter Liu

Men who lose sleep during the working week may be able to lower their risk of developing Type 2 diabetes by getting more hours of sleep, according to research findings presented at The Endocrine Society’s 95th Annual Meeting in San Francisco. ‘We all know we need to get adequate sleep, but that is often impossible because of work demands and busy lifestyles,’ said Dr Peter Liu an LA BioMed lead researcher. ‘Our study found extending the hours of sleep can improve the body’s use of insulin, thereby reducing the risk of type 2 diabetes in adult men.’

Liu and researchers from the University of Sydney studied 19 non-diabetic men, with an average age of 28, who for six months or longer (average, 5 years) self-reported inadequate sleep during the work week – around 6 hours a night. But they regularly caught up on their sleep on the weekends, getting at least a third more sleeping time a night. Their reported sleep times were verified by actigraphy, in which each man wore a small device on his wrist that monitored sleep-wake cycles. The men spent three nights in a sleep lab on each of two separate weekends and each individual had the same food intake during the study visits, so that diet would not influence the results. When the men slept 10 hours a night on each of three nights of catch-up sleep, their insulin sensitivity was much better than when they had persistent sleep restriction. Their insulin resistance test score also improved (decreased) with sleep extension.

Being rich or poor in gut bacteria. 
A study in Nature reports that people with fewer bacterial species in their intestines may be more likely to develop cardiovascular disease and diabetes. The researchers examined the intestinal flora of 169 obese Danes and 123 non-obese Danes using an analytical approach called quantitative metagenomics. When comparing the two groups, they discovered that people with a low richness microbiota have more body fat and less healthy; they are more resistant to the action of insulin, have unfavorably altered blood lipids and show increased blood levels of inflammation markers and white blood cells, bringing them at increased risk of type 2 diabetes and cardiovascular disorders. They also observed that obese people from the low richness group gained on average significantly more weight than the high richness one during the past nine years.

The gut is like a rainforest says Oluf Pedersen. It appears that the richer and more diverse the composition of our intestinal bacteria, the stronger our health. The bacteria produce vital vitamins, mature and strengthen our immune system and communicate with the many nerve cells and hormone-producing cells in the intestinal system. And, not least, the bacteria produce a wealth of bioactive substances which penetrate into the bloodstream and affect our biology in countless ways.

Is stomach damage why diets are doomed to fail?  
Associate Professor Amanda Page

Associate Professor Amanda Page

The way the stomach detects and tells the brain how full the body is becomes damaged in obese people, but does not return to normal once they lose weight, according to findings of a mouse study published in the International Journal of Obesity. The nerves in the stomach that signal fullness to the brain appear to be desensitised after long-term consumption of a high-fat diet. Researchers believe this could be a key reason why most people who lose weight on a diet eventually put that weight back on.

‘The stomach’s nerve response does not return to normal upon return to a normal diet,’ said Associate Professor Amanda Page from the University of Adelaide’s Nerve-Gut Research Laboratory and the study’s lead author. ‘This means you would need to eat more food before you felt the same degree of fullness as a healthy individual. In normal conditions, leptin (a hormone) acts to stop food intake. However, in the stomach in high-fat diet induced obesity, leptin further desensitises the nerves that detect fullness. These two mechanisms combined mean that obese people need to eat more to feel full, which in turn continues their cycle of obesity,’ she said. The researchers said there were not yet sure whether the desensitisation of the stomach nerves is a permanent effect, or just a long-lasting one. ‘We know that only about 5 per cent of people on diets are able to maintain their weight loss, and that most people who’ve been on a diet put all of that weight back on within two years.’

What’s new?
Disease-Proof. DNA is not destiny.

Disease-Proof. DNA is not destiny.

Abundant scientific evidence shows that not smoking, eating well, being active, and maintaining a healthy weight play an enormous role in our health. Drawing upon the latest scientific evidence and decades of clinical experience, Dr. Katz arms us with the skills to make lasting changes in each of these areas. Disease-Proof equips readers with the knowledge to manage weight, improve immune function, reprogram our genes, and prevent and reverse life-altering illnesses. DNA is not destiny. To a much greater extent, choices under our control determine our fate. We have scientific evidence to show that if we change our own behavior, we change the behavior of our genes. We can nurture nature. The relevant skills aren’t trivial, but they aren’t really hard, either. You can have them — but you have to go get them. Remember you once had to learn how to ride a bike. But then… you’ve known how ever since. Without the right skill set, health is elusive.