Every meal triggers inflammation that activates the immune system

In diabetes patients, this messenger substance triggers chronic inflammation and causes insulin-producing beta cells to die off.

 Every time we eat a meal, an inflammatory response is triggered in the body that activates the immune system, according to a new study which suggests that overweight people may lack this response causing them to develop diabetes. The study also explains why infectious diseases occur more frequently in times of famine.

 It is well known that type 2 diabetes (or adult-onset diabetes) leads to chronic inflammation with a range of negative impacts. A number of clinical studies have therefore treated diabetes by impeding the over-production of a substance involved in this process, Interleukin-1beta (IL-1beta).

In diabetes patients, this messenger substance triggers chronic inflammation and causes insulin-producing beta cells to die off, found researchers from the University Hospital Basel in Switzerland.
In healthy individuals, short-term inflammatory responses play an important role in sugar uptake and the activation of the immune system.

Researchers showed that the number of macrophages (a type of immune cell) around the intestines increases during meal times.
These so-called “scavenger cells” produce the messenger substance IL-1beta in varying amounts, depending on the concentration of glucose in the blood.

This, in turn, stimulates insulin production in pancreatic beta cells. The insulin then causes the macrophages to increase IL-1beta production.

Insulin and IL-1beta work together to regulate blood sugar levels, while the messenger substance IL-1beta ensures that the immune system is supplied with glucose and thus remains active.

According to the researchers, this mechanism of the metabolism and immune system is dependent on the bacteria and nutrients that are ingested during meals.

With sufficient nutrients, the immune system is able to adequately combat foreign bacteria.

Conversely, when there is a lack of nutrients, the few remaining calories must be conserved for important life functions at the expense of an immune response.

This may go some way towards explaining why infectious diseases occur more frequently in times of famine.

The study appears in the journal Nature Immunology.

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Exercise can help lower excessive sleepiness

Exercise is perhaps the single best activity you can do for your health. Not only will you feel better in the short-term, but if you find it too hard to stay awake at work despite a good night's sleep, daily aerobic exercise can help you focus, say researchers.

Exercise reduces the levels of the two proteins, resulting in reduced excessive sleepiness, the findings showed.

The study involved people with hypersomnia, which is characterised by sleeping too much at night as well as excessive daytime sleepiness.

"Identifying these biomarkers, combined with new understanding of the important role of exercise in reducing hypersomnia, have potential implications in the treatment of major depressive disorder," said study senior author Madhukar Trivedi from University of Texas Southwestern Medical Center in the US.

People with hypersomnia are compelled to nap repeatedly during the day, often at inappropriate times such as at work, during a meal, or in conversation.

They often have difficulty waking from a long sleep, and may feel disoriented upon waking, according to the study.

Other symptoms may include anxiety, increased irritation, decreased energy, restlessness, slow thinking, slow speech, loss of appetite, hallucinations, and memory difficulty.

The researchers looked at blood sample provided by study participants who were randomly assigned to two types of aerobic exercise to determine the effects of exercise on their depression.

More than 100 adults ages 18 to 70 who had major depression disorder participated.

Researchers found that reductions in two biomarkers - brain-derived neurotrophic factor (BDNF) and Interleukin-1 beta - are related to reductions in hypersomnia.

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.






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Obesity Affects the Brain

A recent study by researchers  gathered evidence that excess fat alters brain function, at least in mice. The study, published in February in The Journal of Neuroscience, not only supports previously gained knowledge that obesity negatively affects both memory and learning skills, but goes on to determine how excess fat can influence the brain. Until now, researchers did not understand how weight could modify cognitive abilities.

While fat cells create substances that flow through the bloodstream into numerous body parts, the brain lies behind a protective barrier that generally blocks undesirable molecules from entering. When the substance, namely interleukin 1, is released through the bloodstream, it begins biochemical processes that generally lead to inflammation and poor health. According to medical professionals, the passage of interleukin 1 into the brain, specifically the hippocampus, should not be possible. The hippocampus is the area of the brain which is in control of both learning and memory.

What researchers found upon examination of the mice was that the interleukin 1 had entered the brain and was subsequently causing cognitive impairment. The mice were found to have low levels of those biochemicals associated with healthy synapse function as well as high levels of inflammation. Synapses connect neurons and aid message communication in the brain. Traffic patterns of neural activity become negatively affected when synapse health fails. Additionally, if inflammation continues for a long period of time, it eventually hurts the cells.

What research found was that the obese mice performed poorly on memory and reasoning tests, even those in which they previously did well. Original researchers wished to determine if it was the obesity itself affecting the brain or some other physiological factors. To that end, the study’s overseers simply removed the majority of the fat. When the mice recovered, their interleukin 1 levels were almost non-existent. When the surgically reduced mice were run through the same tests they failed pre-surgery, they began to perform very well. To test this further, the scientists took the fat preserved from the obese mice and implanted it into lean mice. These mice began to perform poorly almost immediately after surgery.

The findings, though convincing, were of little practical value to any human patients. The amount of fat removed from the mice was of a percentage that would be impossible to excise in a person. Scientists were of the belief that fat was impairing cognitive function but felt the need to find alternative solutions.

They came up with an experiment that was far less invasive than surgery. The scientists used mice prone to obesity and allowed them to gain weight. When the mice became heavy enough, they began half on a daily 45 minute exercise program and allowed the remaining mice to remain sedentary. Although the mice required to exercise did not lose much weight, they did lose significant fat. These mice not only had biochemical levels that indicated healthy synaptic functioning, they also exhibited low levels of inflammation, and performed much better in testing procedures than the obese mice.

The results indicated that, regardless of actual weight, the difference in overall fat amounts determined if cognitive functioning levels would be higher or lower. These studies were performed on mice, not humans, and therefore may not be indicative of how a human brain may respond to body fat. While the studies may not reveal how the human body reacts to fat, there is no current evidence to the contrary. The possibility remains that humans, as with mice, may experience cognitive impairment due to nothing other than body fat. It is possible, therefore, that obesity in humans may negatively affect the brain and how it functions.

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Brushing your teeth can lower heart disease risk

A new study has revealed that taking care of your gums by brushing, flossing, and regular dental visits could keep heart disease at bay.

Researchers  have shown for the first time that as gum health improves, progression of atherosclerosis slows to a clinically significant degree.

Atherosclerosis or the narrowing of arteries through the build-up of plaque is a major risk factor for heart disease, stroke, and death.

"These results are important because atherosclerosis progressed in parallel with both clinical periodontal disease and the bacterial profiles in the gums. This is the most direct evidence yet that modifying the periodontal bacterial profile could play a role in preventing or slowing both diseases,"  lead author of the paper  said.

The researchers followed 420 adults and randomly sampled prospective cohort of residents. Participants were examined for periodontal infection.

Overall, 5,008 plaque samples were taken from several teeth, beneath the gum, and analyzed for 11 bacterial strains linked to periodontal disease and seven control bacteria.

Fluid around the gums was sampled to assess levels of Interleukin-1a, a marker of inflammation. Atherosclerosis in both carotid arteries was measured using high-resolution ultrasound.

Over a median follow-up period of three years, the researchers found that improvement in periodontal health—health of the gums—and a reduction in the proportion of specific bacteria linked to periodontal disease correlated to a slower intima-medial thickness (IMT) progression, and worsening periodontal infections paralleled the progression of IMT.

Results were adjusted for potential confounders such as body mass index, cholesterol levels,diabetes, and smoking status.

There was a 0.1 mm difference in IMT change over three years among study participants whose periodontal health was deteriorating compared with those whose periodontal health was improving.

Previous research has shown that a .033 mm/year increase in carotid IMT (equivalent to approximately 0.1 mm over three years) is associated with a 2.3-fold increased risk for coronary events.

"When it comes to atherosclerosis, a tenth of a millimetre in the thickness of the carotid artery is a big deal. Based on prior research, it appears to meet the threshold of clinical significance," a co-author of the study said.

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