Does The Immune System Regulate Social Behaviour?

Scientists hail “profound” discovery: Findings support theories pointing to immune response as factor in Autism and other complex conditions.

A new study, published in the journal Nature (Filiano A J et al**) reports the discovery of indicators suggesting that the immune system can affect, and may even control, our social behaviour.

The research, conducted at the University of Virginia School of Medicine, revealed that the blocking of a single immune molecule rendered mouse brains hyperactive, and led to a reduction in social behaviour. These effects were reversed when blocking of the molecule was lifted.

Anthony Filiano & Jonathan Kipnis
Dr Anthony Filiano & Dr Jonathan Kipnis

The new discovery, hailed by scientists as being of “profound” importance to social functioning research, is set to trigger new discoveries on a range of neurological conditions. Amongst conditions set to benefit most are autism, schizophrenia and depression, for which inflammatory or auto-immune factors have been posited as possible contributory factors.

Speaking to science media, Dr John Kipnis, chairman of the University’s Department under whose aegis Filiano et al conducted their research, explained the significance of the finding:

“…some of our behaviour traits might have evolved because of our immune response to pathogens,” added that, “…maybe we are just multicellular battlefields for two ancient forces: pathogens and the immune system. Part of our personality may actually be dictated by the immune system.”

Paradigm-busting

Filiano and colleagues’ findings follow hot on the heels of an earlier, paradigm-busting discovery, that came out of the same Virginian research centre just last year. In that pioneering study, the investigators found a direct link between the brain and the lymphatic system.

This completely up-ended decades of clinical orthodoxy, which held that no such link exists, and helped lay the groundwork for Filiano et al’s discovery of a link between the immune system and social behaviour.

More specifically, what Filiano’s team reported is that the immune factor, interferon-gamma (a cytokine secreted by T lymphocytes) is activated in mice when they engage in social behaviour. Until this discovery, it had been believed that production of interferon-gamma was normally only triggered by an assault on the immune system by pathogens.

Further, Filiano’s team also reported that blocking interferon-gamma led to hyperactivity and an accompanying reduction in social behaviour in their mice subjects; whilst lifting the block served to restore the mice’s sociability.

Evolutionary Significance

primate group
Immune System may play important role in social behaviour

Quoted by online media, Dr Anthony Filiano, observed that social behaviour is key to a species survival, not only in the search for food and drink but also to successful sexual reproduction and, he continued: “…the hypothesis is that when organisms come together, you have a higher propensity to spread infection. So you need to be social, but you [also] have a higher chance of spreading pathogens. The idea is that interferon gamma, in evolution, has been used as a more efficient way to both boost social behaviour while [also] boosting an anti-pathogen response.”

Implications for Autism and other neurological conditions

These findings raise the possibility that dysfunctions in the immune system may account for the social deficits which are present in a range of neurological and psychiatric disorders.

To be clear, there is no suggestion that a particular immune molecule may be responsible for complex presentations like autism, schizophrenia or depression.

However, it does seem entirely reasonable to postulate a role for the immune system and, in turn, perhaps even particular pathogens – as possibly significant factors in the genesis of a range of complex disorders that have a significant social component in their presentation.

Sources:

**Filiano A. J. et al. Unexpected role of interferon-gamma in regulating neuronal connectivity and social behaviour. Nature: 535, 425–429 (Published online 13 July 2016).

This post also includes quotes from study contributors, as carried by the University of Virginia online news portal, UVA Today, and by online science news outlets Neuroscience News and Science Daily.

www.peakhealthonline.com

Lack of sleep alters brain chemicals to bring on cannabis-style ‘munchies’

Sleep deprivation may cause overeating by boosting chemicals for appetite as well as those that increase the pleasure of eating sweet or salty, high-fat foods

Too little sleep may bring on a form of the “munchies” usually brought-on by cannabis users, with sleep-deprived people craving crisps, sweets and biscuits far moreGluttony0 than healthier foods.

The US-based researchers believe that missing-out on sleep alters brain chemicals in much the same way as the hunger-boosting chemicals found in cannabis, which for years has accounted for much of the snack sales in 24-hour convenience stores.

After several nights of limited sleep, healthy volunteers who took part in the study selected foods containing more calories, and almost twice as much fat, than subjects who slept well during the study.

Erin Hanlon, who led the study at the University of Chicago, reported that when sleep deprived, participants had difficulty resisting the snacks, even when they were full.

Research has shown repeatedly that sleep loss raises the risk of obesity, but the reasons are complex and unclear 1

Lack of sleep disrupts hormones that govern appetite and satiety. But those who sleep less have more time to eat, and may also be too tired to exercise. To confound matters further, obesity can lead to breathing problems which, in themselves, disrupt sleep patterns.

In a small-scale study published in the journal Sleep2 Hanlon invited 14 men and women in their twenties to spend two, four-day sessions, at Chicago University’s clinical research centre. The volunteers’ time in bed was controlled, so that on one visit they averaged 7.5 hours of sleep a night, but on the other only 4 hours 11 minutes. During all visits to the lab, the participants ate identical meals, served at 9am, 2pm and 7pm.

After the fourth night of each leg of the study, subjects were offered a range of snacks. The sleep-deprived participants felt a strong urge to binge on fatty foods, and this was most intense in the late afternoon and early evening, when snacking is most linked to weight gain. They consumed high-fat snacks even when they had eaten a solid meal containing tired_eyes_800px90% of their recommended daily calories only two hours earlier. Typically, the sleep deprived participants ate 300 calories in snacks, which is noteably in excess of energy requirements for their extra waking hours.

To explore just why sleep loss might trigger such changes in eating patterns, the researchers looked at various substances in the participants’ blood, including the hormones ghrelin, which boosts appetite, and leptin, which tells the brain when the stomach is full. Previous studies3 have shown that sleep loss tends to be reflected in high ghrelin and low leptin levels.

Hanlon also looked at levels of endocannabinoids and found that the sleep-deprived volunteers had raised and more persistent levels of endocannabinoid 2-AG, a chemical that increases the pleasure felt when eating (particularly sweet or salty high-fat foods). “We know that marijuana activates the endocannabinoid system and causes people to overeat when they are not hungry, and they normally eat yummy sweet and fatty foods,” Hanlon said. “Sleep restriction may cause overeating by acting in the same manner.”

In well-rested volunteers, levels of 2-AG rose in the morning, peaked around midday, and declined again. But in the sleep-deprived, levels rose 33% higher, peaked at 2pm, and remained high until 9pm. Writing in the journal, Hanlon posits that this may boost and prolong the pleasure people get from snacking, so putting them at greater risk of weight gain: “The early afternoon drive for hedonic eating may be stronger and last longer in a state of sleep debt.”

In a commentary published alongside Hanlon’s paper, Frank Scheer, director of medical chronobiology at Brigham and Women’s Hospital in Boston, says that the new findings make for “compelling evidence” that endocannabinoids and food reward mechanisms underpin the excessive eating and weight gain that comes with sleep loss.

References:

1. Cappuccio FP, Taggart FM, Kandala NB, Currie A, Peile E, Stranges S, Miller MA.: Meta-analysis of short sleep duration and obesity in children and adults. SLEEP 2008; 31(5):619-26.

2. Bodez D, Guellich A, Kharoubi M, Covali-Noroc A, Tissot CM, Guendouz S, Hittinger L, Dubois-Randé JL, Lefaucheur JP, Planté-Bordeneuve V, Adnot S, Boyer L, Damy T.: Prevalence, severity, and prognostic value of sleep apnea syndromes in cardiac amyloidosis. SLEEP 2016; 39(7):1333–1341.

3. Klok MD, Jakobsdottir S, Drent ML.: The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007; 8(1):21-34.

Source: Amended from an original article by Ian Sample, Science editor, The Guardian, published Monday 29th February 2016

www.peakhealthonline.com

Mindfulness Meditation – developing skills using biofeedback technology

Quote -Dean Ornish

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