When my younger daughter was around 6 months old, we gave her mashed up prune. She grimaced and shivered a little, appearing to be absolutely disgusted. But then she grunted and reached for more.

Most babies are ready for solid food around 6 months of age, and feeding them can be fun. One of the more entertaining approaches does not involve a spoon. Called baby-led weaning, it involves allowing babies to feed themselves appropriate foods.

Proponents of the approach say that babies become more skilled eaters when allowed to explore on their own. They’re in charge of getting food into their own mouths, gumming it and swallowing it down — all skills that require muscle coordination. When the right foods are provided (yes to soft steamed broccoli; no to whole grapes), babies who feed themselves are no more likely to choke than their spoon-fed peers.

Some baby-led weaning proponents also suspected that the method might ward off obesity, and a small study suggested as much. The idea is that babies allowed to feed themselves might better learn how to regulate their food intake, letting hunger and fullness guide them to a reasonable calorie count. But a new study that looked at the BMIs of babies who fed themselves and those who didn’t found that babies grew similarly with either eating style.

A clinical trial of about 200 mother-baby pairs in New Zealand tracked two different approaches to eating and their impact on weight. Half of the moms were instructed to feed their babies as they normally would, which for most meant spoon-feeding their babies purees, at least early on. The other half was instructed that only breast milk or formula was best until 6 months of age, and after that, babies could be encouraged to feed themselves. These mothers also received breastfeeding support.

At the 1- and 2-year marks, the babies’ average BMI z-scores were similar, regardless of feeding method, researchers report July 10 in JAMA Pediatrics. (A BMI z-score takes age and sex into account.) And baby-led weaning actually produced slightly more overweight babies than the other approaches, but not enough to be meaningful. At age 2, 10.3 percent of baby-led weaning babies were considered overweight and 6.4 percent of traditionally-fed babies were overweight. The two groups of babies seemed to take in about the same energy from food, analyses of the nutritional value and amount of food eaten revealed.

The trial found a few other differences between the two groups. Babies who did baby-led weaning exclusively breastfed for longer, a median of about 22 weeks. Babies in the other group were exclusively breastfed for a median of about 17 weeks. Babies in the baby-led weaning group were also more likely to have held off on solid food until 6 months of age.

While baby-led weaning may not protect babies against being overweight, the study did uncover a few perks of the approach. Parents reported that babies who fed themselves seemed less fussy about foods. These babies also reportedly enjoyed eating more (though my daughter’s prune fake-out face is evidence that babies’ inner opinions can be hard to read). Even so, these data seem to point toward a more positive experience all around when using the baby-led weaning approach. That’s ideal for both experience-hungry babies and the parents who get to savor watching them eat.

Type 2 diabetes and prion disease seem like an odd couple, but they have something in common: clumps of misfolded, damaging proteins.

Now new research finds that a dose of corrupted pancreas proteins induces normal ones to misfold and clump. This raises the possibility that, like prion disease, type 2 diabetes could be triggered by these deformed proteins spreading between cells or even individuals, the researchers say.

When the deformed pancreas proteins were injected into mice without type 2 diabetes, the animals developed symptoms of the disease, including overly high blood sugar levels, the researchers report online August 1 in the Journal of Experimental Medicine.
“It is interesting, albeit not super-surprising” that the deformed proteins could jump-start the process in other mice, says Bruce Verchere, a diabetes researcher at the University of British Columbia in Vancouver. But “before you could say anything about transmissibility of type 2 diabetes, there’s a lot more that needs to be done.”

Beta cells in the pancreas make the glucose-regulating hormone insulin. The cells also produce a hormone called islet amyloid polypeptide, or IAPP. This protein can clump together and damage cells, although how it first goes bad is not clear. The vast majority of people with type 2 diabetes accumulate deposits of misfolded IAPP in the pancreas, and the clumps are implicated in the death of beta cells.

Deposits of misfolded proteins are a hallmark of such neurodegenerative diseases as Alzheimer’s and Parkinson’s as well as prion disorders like Creutzfeldt-Jakob disease (SN: 10/17/15, p. 12).

Since IAPP misfolds like a prion protein, neurologist Claudio Soto of the University of Texas Health Science Center at Houston and his colleagues wondered if type 2 diabetes could be transmitted between cells, or even between individuals. With this paper, his group “just wanted to put on the table” this possibility.

The mouse version of the IAPP protein cannot clump — and mice don’t develop type 2 diabetes, a sign that the accumulation of IAPP is important in the development of the disease, says Soto. To study the disease in mice, the animals need to be engineered to produce a human version of IAPP. When pancreas cells containing clumps of misfolded IAPP, taken from an engineered diabetic mouse, were mixed in a dish of healthy human pancreas cells, it triggered the clumping of IAPP in the human cells.
The same was true when non-diabetic mice got a shot made with the diabetic mouse pancreas cells. The non-diabetic mice developed deposits of clumped IAPP that grew over time, and the majority of beta cells died. When the mice were alive, more than 70 percent of the animals had blood sugar levels beyond the healthy range.

Soto’s group plans to study if IAPP could be transmitted in a real world scenario, such as through a blood transfusion. They’ve already begun work on transfusing blood from mice with diabetes to healthy mice, to see if they can induce the disease. “More work needs to be done to see if this ever operates in real life,” Soto says.

Even if transmission of the misfolded protein occurs only within an individual, “this opens up a lot of opportunities for intervention,” Soto says, “because now you can target the IAPP.”

Verchere also believes IAPP is “a big player” in the progression of type 2 diabetes, and that therapies that prevent the clumps of proteins from forming are needed. Whether or not future research supports the idea that the disease is transmissible, the study is “good for appreciating the potential role of IAPP in diabetes.”

Cross two flashlight beams and they pass right through one another. That’s because particles of light, or photons, are mostly antisocial — they don’t interact with each other. But now scientists have spotted evidence of photons bouncing off other photons at the Large Hadron Collider at CERN, the European particle physics lab in Geneva.

“This is a very basic process. It’s never been observed before, and here it is finally emerging from the data,” says theoretical physicist John Ellis of King’s College London who was not involved with the study. Researchers with the ATLAS experiment at the LHC report the result August 14 in Nature Physics.
Because photons have no electric charge, they shouldn’t notice one another’s presence. But there’s an exception to that rule. According to quantum mechanics, photons can briefly transform into transient pairs of electrically charged particles and antiparticles — such as an electron and a positron — before reverting back to photons. Predictions made more than 80 years ago suggest that this phenomenon allows photons to interact and ricochet away from one another.

This light-by-light scattering is extremely rare, making it difficult to measure. But photons with more energy interact more often, providing additional chances to spot the scattering. To produce such energetic photons, scientists slammed beams of lead nuclei together in the LHC. Photons flit in and out of existence in the lead nuclei’s strong electromagnetic fields. When two nuclei got close enough that their electromagnetic fields overlapped, two photons could interact with one another and be scattered away.

To measure the interaction, ATLAS scientists sifted through their data to find collisions in which only two photons — the two that scattered away from the collision — appeared in the aftermath. “That’s the trickiest part of the whole thing,” says physicist Peter Steinberg of Brookhaven National Laboratory in Upton, N.Y., a member of the ATLAS collaboration. The scientists had to ensure that, in their enormous, highly sensitive particle detector, only two photons appeared, and convince themselves that no other particles had gone unaccounted for. The researchers found 13 such events over 19 days of data collection. Although other processes can mimic light-by-light scattering, the researchers predict that only a few such events were included in the sample.

The number of scattering events the researchers found agrees with the predictions of the standard model, physicists’ theory of particle physics. But a more precise measurement of the interaction might differ from expectations. If it does, that could hint at the existence of new, undiscovered particles.