New research may help explain why multiple sclerosis rates have risen sharply in the U.S. and some other countries among women, while rates appear stable in men.The study could also broaden understanding of how environmental influences alter genes to cause a wide range of diseases. The causes of multiple sclerosis (MS) are not well understood, but experts have long suspected that environmental factors trigger the disease in people who are genetically susceptible. In the newly published study, researchers found that women with MS were more likely than men with MS to have a specific genetic mutation that has been linked to the disease.
Women were also more likely to pass the mutation to their daughters than their sons and more likely to share the MS-susceptibility gene with more distant female family members. If genes alone were involved, mothers would pass the MS-related gene to their sons as often as their daughters, said researcher George C. Ebers, MD, of the University of Oxford. Ebers’ research suggests that the ability of environmental factors to alter gene expression — a relatively new field of genetic study known as epigenetics — plays a key role in multiple sclerosis and that this role is gender-specific.
The theory is that environmental influences such as diet, smoking, stress, and even exposure to sunlight can change gene expression and this altered gene expression is passed on for a generation or two. “The idea that the environment would change genes was once thought to be ridiculous,” Ebers says. “Now it is looking like this is a much bigger influence on disease than we ever imagined.”
The study by Ebers and colleagues included 1,055 families with more than one person with MS. Close to 7,100 genes were tested, including around 2,100 from patients with the disease. The researchers were looking for MS-specific alterations in the major histocompatibility complex (MHC) gene region. They found that women with MS were 1.4 times more likely than men with the disease to carry the gene variant linked to disease risk. A total of 919 women and 302 men had the variant in the MHC region, compared to 626 women and 280 men who did not have it.
The study appeared in the Jan. 18 issue of Neurology.
Epigenetics is not evolution. Genetic alterations linked to environmental assaults can be passed down for a generation or two, but DNA usually rights itself over time, Ebers says. “This may explain why we hardly ever see MS in families over more than three generations,” he says. Earlier studies by Ebers and colleagues suggest that vitamin D deficiency may be the environmental stressor that triggers the MS-linked gene alterations. Rates of the disease are highest among people living farthest from the equator, and there is widespread speculation that lack of vitamin D due to low sun exposure may explain this. Other than Ebers’ research team, Orhun Kantarci, MD, of the Mayo Clinic in Rochester, Minn., is one of the few researches studying epigenetics as it relates to multiple sclerosis.
Kantarci calls the new research a potentially important piece of the puzzle to explain the gender difference in MS, but he adds that the research must be replicated. “This study provides more questions than answers, but it is very interesting,” he says. “We are learning that inheritance isn’t as simple as [Gregor] Mendel described.”
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.
Food-specific diets rely on the myth that some foods have special properties that can cause weight loss or gain. But no food can. These diets don't teach healthful eating habits; therefore, you won't stick with them. Sooner or later, you'll have a taste for something else – anything that is not among the foods you've been “allowed” on the diet.
The popular high-protein, low-carbohydrate diets are based on the idea that carbohydrates are bad,
that many people are “allergic” to them or are insulin-resistant, and therefore gain weight when they eat them. The truth is that people are eating more total calories and getting less physical activity, and that is the real reason they are gaining weight. These high-protein, low-carbohydrate diets tend to be low in calcium and fiber, as well as healthy phytochemicals (plant chemicals).
Some authors of these fad diets advise taking vitamin-mineral supplements to replace lost nutrients. However, supplements should “bridge the gap” in healthy eating and not be used as a replacement for nutrient-rich foods. Also, the authors of high-protein, low-carbohydrate diets advocate taking advantage of ketosis to accelerate weight loss. Ketosis is an abnormal body process that occurs during starvation due to lack of carbohydrate. Ketosis can cause fatigue, constipation, nausea, and vomiting. Potential long-term side effects of ketosis include heart disease, bone loss, and kidney damage.
Successful weight loss (losing weight and keeping it off for at least five years) is accomplished by making positive changes to both eating habits and physical activity patterns.
How can you spot a fad diet?
Weight-loss advice comes in literally hundreds of disguises. Most often the “new” and “revolutionary” diets are really old fad diets making an encore appearance. Examples of fad diets include those that:
- tout or ban a specific food or food group
- suggest that food can change body chemistry
- blame specific hormones for weight problems
Ten Red Flags That Signal Bad Nutrition Advice:
- Recommendations that promise a quick fix
- Dire warnings of dangers from a single product or regimen
- Claims that sound too good to be true
- Simplistic conclusions drawn from a complex study
- Recommendations based on a single study
- Dramatic statements that are refuted by reputable scientific organizations
- Lists of “good” and “bad” foods
- Recommendations made to help sell a product
- Recommendations based on studies published without peer review
- Recommendations from studies that ignore differences among individuals or groups
Source: American Dietetic Association
The new study comprised 366 people with RA from eight separate trials. Fasting followed by eating a vegetarian diet for 13 months or eating a Mediterranean style diet replete with fruits, vegetables, healthy fats, and legumes for 12 weeks may relieve pain, the study showed. These diets did not improve morning joint stiffness or physical function when compared to regular diets.
There was not enough data to draw any conclusions about how vegan and/or elimination diets affect RA symptoms.
The positive changes seen with vegetarian and Mediterranean diets may be a result of simply adapting a healthier way of eating as opposed to any specific diet, the study researchers conclude.
People with RA who were put on special diets were more likely to drop out of the studies, suggesting that some people may have difficulty adhering to the eating plans.
Some special diets also resulted in weight loss which may not always be a good thing people with RA who are already at risk for nutritional shortfalls.
“There is a need for more and better research on dietary interventions for RA,” conclude researchers led by Geir Smedslund, PhD, a senior researcher at the Centre for Rehabilitation in Rheumatology at the Diakonhjemmet Hospital in Oslo, Norway.