To kick off the new year, our first recap will discuss new and interesting science related to body fat regulation, with a focus on the brain, the gut, and the food industry.
You may remember from previous posts – and from dialog regarding our Ideal Weight Program (first, second) – that the “fat thermostat” in the brain is of key importance for anyone interested in reducing body fat in a sustainable way. So, I was eager to see new research looking at how brain inflammation impairs the control of body fatness and blood sugar, as well as other new research highlighting the brain chemical neuropeptide Y (NPY) as a key regulator to the body weight set-point.
Next, from NPR’s food-oriented blog called ‘The Salt,’ we highlight some of the interview with Michael Moss, who discusses how the food industry has exploited our natural preferences for sweetness and saltiness – and how that has impacted what and how we eat.
Lastly, find out if brain stimulation helps us to eat less, and whether a selective mixture of probiotics could help us shed body fat.
New science of body fat regulation: evidence linking hypothalamic injury, obesity, and insulin resistance
(Via Dr. Stephan Guyenet at Whole Health Source)
“Obesity involves changes in the function of brain regions that regulate body fatness and blood glucose, particularly a region called the hypothalamus. My colleagues and I previously showed that obesity is associated with inflammation and injury of the hypothalamus in rodent models, and we also presented preliminary evidence that the same might be true in humans. In our latest paper, we confirm this association, and show that hypothalamic injury is also associated with a marker of insulin resistance, independently of BMI.”
A key reason why it’s so hard to lose fat is that the brain defends against fat loss by ramping up hunger and the seductiveness of
food, and shutting down calorie expenditure. Early work in rodents showed that diet-induced obesity causes inflammation and injury (gliosis) in the cells of the hypothalamus that act like a fat thermostat for the body. Follow up work in humans using MRI brain scans showed that the higher a person’s BMI, the more evidence of damage in their hypothalamus. That study had a few limitations, so the most recent study published in the journal Obesity, and outlined by Guyenet in his article, aimed to look for a possible role of gliosis in insulin resistance. Why? Because the neurons in the hypothalamus that regulate body fatness intertwine with neurons that regulate blood glucose.
The researchers recruited 70 male and female volunteers, 18-50 years old, of all body weights. They divided the group into thirds based on the degree of suspected gliosis. They then compared the top third to the bottom third to see if they differed in other respects, like body weight and insulin levels. People in the top third of gliosis were much more likely to be obese (64% vs. 39%), and their insulin levels and insulin resistance were about twice as high as people in the bottom third of gliosis. So gliosis could be directly relevant to diabetes as well– even among people who aren’t obese. Interestingly, the association between gliosis and insulin resistance couldn’t be fully explained by the fact that they carried more fat.
Guyenet ends saying, “Previously, I co-led a study showing that hypothalamic gliosis and obesity are reversible in mice when we put them back on a strict whole-food, low-fat diet. Could the same be true in humans? Or could we achieve the same outcome with a different diet?”
New science of body fat regulation: does NPY help maintain bodyweight setpoint?
The setpoint hypothesis states that the amount of fat carried by the body is regulated homeostatically by th
e brain. Unfortunately, it appears that setpoint can raise progressively higher with weight gain – possibly due to the aforementioned inflammation to the hypothalamus. This makes long-term weight reduction very challenging, as the brain “fights back” against weight loss in a variety of ways.
A recent study in the American Journal of Physiology suggests that neuropeptide Y may play a critical role in the establishment of this setpoint. In the experiment, rats were fed a high-fat diet, which rendered them obese and insulin resistant. The investigators then injected a virus that reduces the expression of neuropeptide Y in an important fat-regulating center in the brain (the dorsomedial hypothalamus).
After suppressing NPY, the rats reverted to a normal food intake pattern and lost the excess weight. Additionally, their insulin sensitivity was restored to that of lean controls. Is this link sounding familiar by now?
This suggests that inhibiting NPY in this part of the brain could be useful to help people not only lose weight but maintain it after the weight is lost. It could also help people maintain or restore insulin sensitivity.
New science of body fat regulation: how the food industry helps engineer our cravings
NPR interviewed Michael Moss, investigative reporter and author of Salt Sugar Fat, about the role that the food industry has historically played in our interactions with food.
He describes how accomplished scientists were enlisted to generate the most perfectly delicious foods, imbued with just the right amount of sweetness to reinforce repeat purchases. The problem is that the same properties that ensure people will
repeatedly buy the product also encourage those same people to overeat. Furthermore, food companies injected sugar in products like yogurt and spaghetti sauce. Now, sweet tomato sauce may not sound appealing, but again, it is the added sugar – added in just the right amount to taste great to most people – that is so reinforcing. The ubiquity of added sugar builds expectations that everything should be equally stimulating– making wholesome foods like cabbage and broccoli a bit less inspiring. This is one key reason why you should give up processed foods entirely for several weeks when starting a diet: it takes time for real food to taste as good as it can once again after withdrawal of the hyperstimulation.
New science of body fat regulation: can stimulation of the prefrontal cortex reduce energy intake?
The left dorsolateral prefrontal cortex of the brain is the portion of the brain associated with executive functions and goal oriented behavior. It has been shown to influence food choice in particular.
Marci Gluck et al published a study showing that a technique called cathodal transcranial direct current stimulation (tDCS) may cause people to be less motivated to eat.
In the study, obese participants first followed five days of a diet that maintained their weight. Then, for three consecutive mornings the participants received either cathodal tDCS or a sham version of the procedure (to control for potential placebo effects associated with the treatment). In a second version of the study, the participants in the active group received anodal rather than cathodal tDCS. During these mornings, they ate as much as they wanted from a computerized vending machine. The participants who received the active treatment via anodal stimulation consumed about 700 fewer calories! The sham stimulation had no effect on eating behavior.
The study was too short in duration to actually demonstrate changes in body mass. However, the reduction in caloric intake would be expected to induce weight loss, assuming that this reduction is sustained. Longer term studies using this technique could confirm this supposition. I find this study very exciting because consumer products are impending. For example, Halo Neurosciences intends to launch a tDCS device in the near future. To learn more about tDCS, listen to Dr. Felipe Fregni discuss it with my friend Jesse Lawler at SmartDrugSmarts.com.
New science of body fat regulation: can a combination of probiotics affect body fat and insulin resistance?
(Alard et al, published in Environmental Microbiology)
Although we typically think about bacteria and other microbes in the context of infections, we actually depend upon many of these organisms in order to survive. Probiotics are live microorganisms that have been associated with good gut health.
In this study, Jeanne Alard and colleagues administered two different probiotic treatments to obese mice. The first was a monostrain of Lactobacillus salivarius. This strain had previously been shown to exhibit anti-inflammatory effects in animals with colitis. However, in this application, it did not have an appreciable impact on body mass or other measured metabolic parameters.
The investigators also gave the rodents a mixture of two different strains – Lactobacillus rhamnosus and Bifidobacterium
animalis. This treatment, in contrast, had significant effects on numerous health-related parameters. Not only was weight gain limited, but fasting glucose and insulin levels dropped as well. The obese mice also experienced a marked decrease in fat tissue inflammation.
It appears that the mixture exerted its impact through changes in the uptake of fatty acids in the gut, which changed the composition of the overall microbiota – increasing “good” bacteria and reducing populations of “bad” bacteria. The team also employed an in vitro gut model to demonstrate that the multistrain probiotic mixture enhanced production of butyrate and propionate.
This study not only points to specific strains of bacteria that appear to benefit metabolism in obese animals, but it also provides useful insight into how these probiotics actually work. Undoubtedly, future studies involving human participants will continue to determine the composition of gut bacteria populations most beneficial to our health. This will better enable us to develop therapeutic strategies -like, for example, a daily pre-and-probiotic regime tailored to you – to keep us, lean, healthy, and happy.
