Addiction researchers at Washington University School of Medicine in St. Louis have found that a risk for alcoholism also may put individuals at risk for obesity. The researchers noted that the association between a family history of alcoholism and obesity risk has become more pronounced in recent years. Both men and women with such a family history were more likely to be obese in 2002 than members of that same high-risk group had been in 1992. “In addiction research, we often look at what we call cross-heritability, which addresses the question of whether the predisposition to one condition also might contribute to other conditions,” says first author Richard A. Grucza, PhD. “For example, alcoholism and drug abuse are cross-heritable. This new study demonstrates a cross-heritability between alcoholism and obesity, but it also says — and this is very important — that some of the risks must be a function of the environment. The environment is what changed between the 1990s and the 2000s. It wasn’t people’s genes.”
Obesity in the United States has doubled in recent decades from 15 percent of the population in the late 1970s to 33 percent in 2004. Obese people – those with a body mass index (BMI) of 30 or more – have an elevated risk for high blood pressure, diabetes, heart disease, stroke and certain cancers.
Reporting in the Archives of General Psychiatry, Grucza and his team say individuals with a family history of alcoholism, particularly women, have an elevated obesity risk. In addition, that risk seems to be growing. He speculates that may result from changes in the food we eat and the availability of more foods that interact with the same brain areas as addictive drugs. “Much of what we eat nowadays contains more calories than the food we ate in the 1970s and 1980s, but it also contains the sorts of calories — particularly a combination of sugar, salt and fat — that appeal to what are commonly called the reward centers in the brain,” says Grucza, an assistant professor of psychiatry. “Alcohol and drugs affect those same parts of the brain, and our thinking was that because the same brain structures are being stimulated, overconsumption of those foods might be greater in people with a predisposition to addiction.”
Grucza hypothesized that as Americans consumed more high-calorie, hyper-palatable foods, those with a genetic risk for addiction would face an elevated risk from because of the effects of those foods on the reward centers in the brain. His team analyzed data from two large alcoholism surveys from the last two decades. The National Longitudinal Alcohol Epidemiologic Survey was conducted in 1991 and 1992. The National Epidemiologic Survey on Alcohol and Related Conditions was conducted in 2001 and 2002. Almost 80,000 people took part in the two surveys.
“We looked particularly at family history of alcoholism as a marker of risk,” Grucza explains. “And we found that in 2001 and 2002, women with that history were 49 percent more likely to be obese than those without a family history of alcoholism. We also noticed a relationship in men, but it was not as striking in men as in women.” Grucza says a possible explanation for obesity in those with a family history of alcoholism is that some individuals may substitute one addiction for another. After seeing a close relative deal with alcohol problems, a person may shy away from drinking, but high-calorie, hyper-palatable foods also can stimulate the reward centers in their brains and give them effects similar to what they might experience from alcohol.
“Ironically, people with alcoholism tend not to be obese,” Grucza says. “They tend to be malnourished, or at least under-nourished because many replace their food intake with alcohol. One might think that the excess calories associated with alcohol consumption could, in theory, contribute to obesity, but that’s not what we saw in these individuals.” Grucza says other variables, from smoking, to alcohol intake, to demographic factors like age and education levels don’t seem to explain the association between alcoholism risk and obesity. “It really does appear to be a change in the environment,” he says. “I would speculate, although I can’t really prove this, that a change in the food environment brought this association about. There is a whole slew of literature out there suggesting these hyper-palatable foods appeal to people with addictive tendencies, and I would guess that’s what we’re seeing in our study.” The results, he says, suggest there should be more cross-talk between alcohol and addiction researchers and those who study obesity. He says there may be some people for whom treating one of those disorders also might aid the other.
Fish oil, when combined with epigallocatechin‑3‑gallate (EGCG—a polyphenol and antioxidant found in green tea), may affect chemical processes in the brain associated with Alzheimer's disease, according to a study published in Neuroscience Letters. This study, which used an animal (mouse) model of Alzheimer's disease, builds on previous research linking the disease to peptides (amino acid chains) called beta‑amyloids and laboratory studies suggesting that EGCG decreases memory problems and beta‑amyloid deposits in mice.
Researchers from the University of South Florida divided Alzheimer's disease‑model mice into five feeding groups. During a period of 6 months, each group was fed one of five diets: fish oil only; high‑dose EGCG; low‑dose EGCG; low‑dose EGCG and fish oil; or a regular diet (control). The researchers observed that low‑dose EGCG alone did not reduce the Alzheimer's disease-related chemical processes in the brain. However, the mice fed the combination of fish oil and EGCG had a significant reduction in amyloid deposits that have been linked with Alzheimer's disease.
Upon examination of blood and brain tissues of the mice, the researchers found high levels of EGCG in the mice that were fed the combination of fish oil and low‑dose EGCG compared with those fed low‑dose EGCG alone. A possible explanation, according to the researchers, is that fish oil enhances the bioavailability of EGCG—that is, the degree to which EGCG was absorbed into the body and made available to the brain. This effect, in turn, may contribute to the increased effectiveness of this combination. Further research is necessary, however, to determine if the combination of fish oil and EGCG affects memory or cognition, and whether it might have potential as an option for people at risk of developing Alzheimer's disease.
Giunta B, Hou H, Zhu Y, et al. Fish oil enhances anti‑amyloidogenic properties of green tea EGCG in Tg2576 mice. Neuroscience Letters. 2010;471(3):134–138.
Researchers employed imaging techniques to examine and analyze brain anatomical differences between 55 female IBS patients and 48 female control subjects. Patients had moderate IBS severity, with disease duration from one to 34 years (average 11 years). The average age of the participants was 31.
Investigators found both increases and decreases of brain grey matter in specific cortical brain regions.
Even after accounting for additional factors such as anxiety and depression, researchers still discovered differences between IBS patients and control subjects in areas of the brain involved in cognitive and evaluative functions, including the prefrontal and posterior parietal cortices, and in the posterior insula, which represents the primary viscerosensory cortex receiving sensory information from the gastrointestinal tract.
“The grey-matter changes in the posterior insula are particularly interesting since they may play a role in central pain amplification for IBS patients,” said study author David A. Seminowicz, Ph.D., of the Alan Edwards Centre for Research on Pain at McGill University. “This particular finding may point to a specific brain difference or abnormality that plays a role in heightening pain signals that reach the brain from the gut.”
Decreases in grey matter in IBS patients occurred in several regions involved in attentional brain processes, which decide what the body should pay attention to. The thalamus and midbrain also showed reductions, including a region – the periaqueductal grey – that plays a major role in suppressing pain.
“Reductions of grey matter in these key areas may demonstrate an inability of the brain to effectively inhibit pain responses,” Seminowicz said.
The observed decreases in brain grey matter were consistent across IBS patient sub-groups, such as those experiencing more diarrhea-like symptoms than constipation.
“We noticed that the structural brain changes varied between patients who characterized their symptoms primarily as pain, rather than non-painful discomfort,” said Mayer, director of the UCLA Center for Neurobiology of Stress. “In contrast, the length of time a patient has had IBS was not related to these structural brain changes.”
Mayer added that the next steps in the research will include exploring whether genes can be identified that are related to these structural brain changes. In addition, there is a need to increase the study sample size to address male-female differences and to determine if these brain changes are a cause or consequence of having IBS.
The study was funded by the National Institutes of Health.
Additional authors include M. Catherine Bushnell, Ph.D., of McGill University, and Jennifer B. Labus, Joshua A. Bueller, Kirsten Tillisch and Bruce D. Naliboff, Ph.D., all of UCLA.
Asymmetries of brain activity
Nonetheless, “by focusing on the asymmetric brain activity of the frontal lobe that occurs when we experience emotions, there are two models that contradict the case of anger”, the researcher highlights.
The first model, 'of emotional valence', suggests that the left frontal region of the brain is involved in experiencing positive emotions, whilst the right is more related to negative emotions.
The second model, 'of motivational direction', shows that the left frontal region is involved in experiencing emotions related to closeness, whilst the right is associated with the emotions that provoke withdrawal.
The positive emotions, like happiness, are usually associated to a motivation of closeness, and the negative ones, like fear and sadness, are characterised by a motivation of withdrawal.
However, not all emotions behave in accordance with this connection. “The case of anger is unique because it is experienced as negative but, often, it evokes a motivation of closeness”, the expert explains.
“When experiencing anger, we have observed in our study an increase in right ear advantage, that indicates a greater activation of the left hemisphere, which supports the model of motivational direction”, Herrero points out.. In other words, when we get angry, our asymmetric cerebral response is measured by the motivation of closeness to the stimulus that causes us to be angry and not so much by the fact we consider this stimulus as negative: “Normally when we get angry we show a natural tendency to get closer to what made us angry to try to eliminate it”, he concludes.
Every emotion is unique
This is the first general study on emotions and more specifically on anger that examines all these different psychobiological parameters (cardiovascular, hormonal response and asymmetric activation response of the brain) in a single investigation to study the changes caused by the inducement of anger. In addition the results of the study are along the same lines as previous investigations and defend what has been noted by Darwin: that the emotions, in this case anger, are accompanied by unique and specific (psychobiological) patterns for each emotion.
The study, to be published in the journal Pain, found that particular areas of the brain were less active as meditators anticipated pain, as induced by a laser device. Those with longer meditation experience (up to 35 years) showed the least anticipation of the laser pain.
Dr Brown, who is based in the University's School of Translational Medicine, found that people who meditate also showed unusual activity during anticipation of pain in part of the prefrontal cortex, a brain region known to be involved in controlling attention and thought processes when potential threats are perceived.
He said: “The results of the study confirm how we suspected meditation might affect the brain. Meditation trains the brain to be more present-focused and therefore to spend less time anticipating future negative events. This may be why meditation is effective at reducing the recurrence of depression, which makes chronic pain considerably worse.”
Dr Brown said the findings should encourage further research into how the brain is changed by meditation practice. He said: “Although we found that meditators anticipate pain less and find pain less unpleasant, it's not clear precisely how meditation changes brain function over time to produce these effects.
“However, the importance of developing new treatments for chronic pain is clear: 40% of people who suffer from chronic pain report inadequate management of their pain problem.”
In the UK, more than 10 million adults consult their GP each year with arthritis and related conditions. The estimated annual direct cost of these conditions to health and social services is £5.7 billion.
Study co-author Professor Anthony Jones said: “One might argue that if a therapy works, then why should we care how it works? But it may be surprising to learn that the mechanisms of action of many current therapies are largely unknown, a fact that hinders the development of new treatments. Understanding how meditation works would help improve this method of treatment and help in the development of new therapies.
“There may also be some types of patient with chronic pain who benefit more from meditation-based therapies than others. If we can find out the mechanism of action of meditation for reducing pain, we may be able to screen patients in the future for deficiencies in that mechanism, allowing us to target the treatment to those people.
“This protein is present in the part of the brain in which memories are stored. We have found that in order for any memory to be laid down this protein, called the M3-muscarinic receptor, has to be activated.
“We have also determined that this protein undergoes a very specific change during the formation of a memory – and that this change is an essential part of memory formation. In this regard our study reveals at least one of the molecular mechanisms that are operating in the brain when we form a memory and as such this represents a major break through in our understanding of how we lay down memories.
“This finding is not only interesting in its own right but has important clinical implications. One of the major symptoms of Alzheimer's disease is memory loss. Our study identifies one of the key processes involved in memory and learning and we state in the paper that drugs designed to target the protein identified in our study would be of benefit in treating Alzheimer's disease.”
Professor Tobin said there was tremendous excitement about the breakthrough the team has made and its potential application: “It has been fascinating to look at the molecular processes involved in memory formation. We were delighted not only with the scientific importance of our finding but also by the prospect that our work could have an impact on the design of drugs for the treatment of Alzheimer's disease.”
People with mild cognitive impairment can be affected by a reduction in their ability to think, such as reduced memory and a short attention span.
“We wanted to find out whether highly educated patients with mild cognitive impairment differed in terms of tolerance of the disease from patients with intermediate and low levels of education,” says Rolstad.
By analysing the patients' spinal fluid, the researchers were able to examine whether there were signs of dementia in the brain.
“Highly educated patients with mild cognitive impairment who went on to develop dementia over the next two years had more signs of disease in their spinal fluid than those with intermediate and low levels of education,” says Rolstad.
Despite having more disease in the brain, the highly educated patients showed the same symptoms of the disease as their less well educated counterparts. This means that patients with higher levels of education tolerate more disease in the brain.
The researchers also studied patients with mild cognitive impairment who did not go on to develop dementia over the next two years.
“We found that the highly educated patients who did not develop dementia during the course of the study showed signs of better nerve function than those with lower levels of education,” says Rolstad. “This finding means that the highly educated not only tolerate more disease in the brain but also sustain less nerve damage during the early stages of the disease.”
The results indicate that a higher reserve capacity delays the symptoms of dementia and the progress of the disease. This can help the care sector to be more aware of dementia in highly educated patients, and thus increase the chances of the correct treatment being given.
The study will be published in the December issue of the Journal of Alzheimer's Disease and was directed by Mercedes Unzeta, professor of the UAB Department of Biochemistry and Molecular Biology. Participating in the study were researchers from this department and from the departments of Cell Biology, Physiology and Immunology, and of Psychiatry and Legal Medicine, all of which are affiliated centres of the Institute of Neuroscience of Universitat Autònoma de Barcelona. The company La Morella Nuts from Reus and the ACE Foundation of the Catalan Institute of Applied Neurosciences also collaborated in the study.