Category: Diabetes 101

Today, almost 26 million Americans — adults and children — have been diagnosed with diabetes. By 2025, that number is projected to rise to 438 million individuals around the world, which would be about 7.8% of the world’s adult population. Combating the rise of diabetes involves multifaceted strategies but promoting a healthy diet is one of the most effective ways of reducing the numbers of the disease. Two recent studies have shown that a common food source can aid in the fight against diabetes, suggesting that including almonds in the diet of a Type 2 diabetic can help to regulate blood sugar and cholesterol levels.

The first study, published in the journal Metabolism, discovered that study participants, who had Type 2 diabetes, had a 30% decrease in their blood glucose levels after consuming a meal high in carbohydrates when they ate an ounce of almonds immediately before the meal. Those who did not have Type 2 diabetes showed a 7% decrease in blood glucose levels when they consumed the same amount of almonds and ate the same meal. The participants also fasted overnight and were then separated into two random groups; one group received a meal without almonds and the other group received a meal that included almonds. Among the Type 2 diabetics in the group that received the meal with almonds, blood sugar levels were shown to be reduced after the meal.

A second, smaller pilot study was conducted with some of the same participants to determine whether regular almond consumption had an effect on blood sugar levels. Participants with Type 2 diabetes were randomly separated into two groups of six to seven subjects; one group ate an ounce of almonds five days a week for 12 weeks. The other group ate two cheese sticks at the same frequency and for the same time period. The almonds and cheese sticks were similar in nutritional properties: the almonds contained 163 calories, 0g carbohydrates, and 14g fat, while the cheese sticks had 160 calories, 0g carbohydrates, and 12g of fat. Other than the almonds and cheese sticks, the two groups ate a very similar diet.

The study found that the group who regularly consumed almonds showed a 4% decrease in levels of hemoglobin A1c (HbA1c), which is a measure of blood sugar levels. They also showed a 4% reduction in body mass index, or BMI, over the group that ate cheese sticks for the period of the study.

Another study published in the journal Diabetes Care discovered that nuts (such as almonds) helped Type 2 diabetics in maintaining healthy cholesterol and blood sugar levels in men and postmenopausal women.

“Both of these studies further deepen our understanding of the benefits of almond consumption for those with Type 2 diabetes,” said Karen Lapsley, Ph.D. “Those with diabetes are faced with many challenges with their disease management, which is why we are always energized when new research is published that supports our understanding of almonds’ role in helping alleviate some of the difficulties.” Lapsley is also the Chief Science Officer for the Almond Board of California.

A one-ounce serving of almonds offers 3.5 grams of fiber, 13 grams of unsaturated fat and only 1 gram of saturated fat. The studies demonstrate that almonds make a healthy food choice for Type 2 diabetics, helping them to maintain blood glucose levels. The studies show that consumption of almonds provides benefits for Type 2 diabetics both in the long and short term, making them an excellent choice for anyone coping with diabetes.

A study that analyzed over 3,400 French adults over a period of 14 years found that those with Type 2 diabetes who received insulin treatment had a significantly increased risk of death.

According to Dr. Emilie Bérard, an epidemiology researcher at the University Hospital Center in Toulouse, France, patients with diabetes who were “treated with insulin at baseline were at increased risk of all-cause mortality.” Dr. Bérard spoke at the yearly meeting of the European Society of Cardiology, adding that the data “provides further information to the debate on the risks and benefits of increasing hypoglycemic treatments.”

The study adjusted for factors that may have affected the outcomes of the data. Even after the adjustments were made, the study found that diabetics who received treatment with insulin were five times more likely to die over the 14 year period of the study than the study participants who did not have diabetes. Those who received insulin were also 1.5 to 2.2 times more likely to die than diabetics who were treated with other hypoglycemic drugs such as metformin or sulfonylurea. The relative risk of death for diabetic patients who were treated with insulin was nearly double that of diabetic patients who did not recieve any treatment at all — the latter group was about 2.8 times more likely to suffer death than patients without diabetes.

Dr. Lars Rydén, a professor of medicine at the Uppsala University in Sweden, cautioned against taking the study’s findings at face value. The study was “on the right track,” according to Dr. Rydén, but its findings must also “be taken with a grain of salt.”

“The results indicate something, but we need further studies,” continued Dr. Rydén. He commented that a major potential flaw in Dr. Bérard’s findings were that it used several adjusting factors in a fairly small sample group of only 171 diabetic patients. “I think [the analysis] is on the edge of controlling for too many things in a small number of people, which led to extremely wide confidence intervals,” said Dr. Rydén.

The findings were also questioned because the participants did not undergo an evaluation of their A1c levels when the study began in 1995 and 1996. According to Dr. Bérard, this means that the adjusted analysis could not account for the varying quality of diabetes control that the patients may have received at baseline. Dr. Bérard speculated that the insulin treatment could have caused a higher rate of hypoglycemia which lead to a higher mortality rate, it could have caused increased weight gain, or it could be indicative of more serious cases of diabetes. It may have also stimulated the sympathetic nervous system, which could have promoted atherosclerosis and triggered vasoconstriction.

The study analyzed data collected from a random sample of 3,403 French adults who were aged between 34 and 64. The study began in 1995 and 1996 and was a part of the MONICA (Multinational Monitoring of Trends and Developments in Cardiovascular Disease) project, a large study sponsored by the World Health Organization. Of the study sample group, 171 participants had diabetes, with 123 on a hypoglycemic regimen and 48 who were not being treated for diabetes at all.

Dr. Bérard’s team analyzed the participants’ data 14 years after their first assessment and found that the mortality rates varied widely, from 7% in the group without diabetes to 33% in the group who were treated with insulin; those who were not receiving hypoglycemic treatment at the beginning of the study had a 23% mortality rate.

For decades, scientists have been trying to identify the molecules that activate beta cell growth in the fight against diabetes. Once these molecules are identified, scientists could develop therapeutics that target them. One research team, funded by the Juvenile Diabetes Research Fund in collaboration with pharmaceutical manufacturer Hoffman-La Roche, recently made significant headway in this area of diabetes research by discovering a protein responsible for beta cell growth as well as a compound that activates it. The team’s findings were published in the journal Cell Metabolism.

The research team was led by Markus Stoffel, M.D., Ph.D., professor at the Swiss Federal Institute of Technology in Zurich, Switzerland a recipient of the Juvenile Diabetes Research Fund’s Gerold & Kayla Grodsky Basic Research Scientist Award. The team is hopeful that its findings will prove to be significant progress in the effort to develop new therapeutics that can be used to regenerate beta cells.

The team’s findings build on research that they conducted five years ago. In that previous research, Dr. Stoffel’s team discovered that a protein known as Tmem27 is found on the surface membranes of beta cells — the insulin-producing cells located in the islets of Langerhans in the pancreas. They found that higher concentrations of Tmem27 on beta cells were linked to increased mass of the islets of Langerhans in mice. Additionally, they discovered that cleaving Tmem27 leaves it totally inactive.

“We hypothesized that if we could prevent Tmem27 from being cleaved and increase the levels of this protein, we could get more beta cell growth,” said Dr. Stoffel. “This observation gave us the rationale to look for what was inactivating Tmem27.”

Once Dr. Stoffel’s team discovered that cleaving Tmem27 de-activated it, they set about searching for molecules that could be responsible for the process. They zeroed in on Bace2, an enzyme protein that can also be found on the surface membrane (or plasma membrane) of beta cells. To confirm their theories, the team analyzed mice and found that those with lower levels of Bace2 had larger islets and a greater number of beta cells in the pancreas through the process of cell regeneration, or proliferation. The mice with lowered levels of Bace2 were also more efficient at removing glucose from the bloodstream than were the mice that had Bace2.

The team’s next goal was to demonstrate the growth of beta cells by inhibiting Bace2. They worked with the scientists of therapeutic company Hoffman-La Roche, who developed an inhibiting compound that prevented Bace2 activity. When the mice were given the compound, their Bace2 was inhibited and their beta cells began to regenerate. Additionally, it was discovered that Bace1, a chemically similar compound to Bace2, does not cleave the Tmem27 protein. Bace1 may be linked to a variety of other diseases, including Alzheimer’s disease and Down syndrome, but since it does not cleave Tmem27, the door is open for anti-diabetes therapeutics that inhibit Bace2 specifically. Research to develop inhibitors for Bace1 is already underway by several companies.

In addition to the identification of a possible target for anti-diabetes therapeutics, the research that Dr. Stoffel’s team conducted may also pave the way for the development of new tests to determine the presence of Tmem27 fragments in the bloodstream, which could be used as a measure of the number of beta cells present in the pancreas.

A joint study conducted by the Scripps Research Institute and the Dana-Farber Cancer Institute at Harvard University has discovered a new type of anti-diabetic therapeutic that works by targeting a particular molecular switch.

The findings set the stage for the development of new anti-diabetic therapeutics that will have drastically reduced adverse side effects compared to current anti-diabetics such as Avandia (rosiglitazone), which will be discontinued from sale this fall amid concerns that it increases the risk of heart attack.

The results of the new study were published in the journal Nature. It describes a newly-discovered compound called SR1664 and was led by Patrick R. Griffin with the Department of Molecular Therapeutics at Scripps Florida, Theodore Kamenecka, the associate scientific director of medicinal chemistry at Scripps Florid, and Bruce Spiegelman, a professor of cell biology at Dana-Farber Cancer Institute.

“In this study, we demonstrate that we have discovered novel compounds that work effectively through a unique mechanism of action on a well-validated clinical target for diabetes,” stated Griffin. “This unique mechanism of action appears to significantly limit side effects associated with marketed drugs. This study is a great example of interdisciplinary, inter-institutional collaboration with chemistry, biochemistry, structural biology, and pharmacology.”

“It appears that we may have an opportunity to develop entire new classes of drugs for diabetes and perhaps other metabolic disorders,” says Spiegelman.

The study is a follow-up on research that the authors published last year in the same journal, Nature. That research suggested that the development of insulin resistance in humans could be caused by a mechanism linked to obesity. The research found that a protein called PPARG affects the normal function of several genes when it undergoes phosphorylation, or the addition of a phosphate group to the protein. The kinase Cdk5, an enzyme involved in multiple sensory pathways, is responsible for causing the phosphorylation of PPARG.

The researchers’ new study confirms what they suspected in their original research: blocking Cdk5 from acting on PPARG could be the basis of effective anti-diabetes therapies. The SR1664 compound discovered in the newer research binds to PPARG but does not activate the transcription of genes.

Griffin’s team is cautious about being overly optimistic in their report on the side effects of anti-diabetes treatment with SR1664. However, the research did clearly demonstrate that this type of treatment causes fewer side effects in mice than medications such as Avandia, which can cause weight gain or increased plasma volume.

In the study, the researchers treated diabetic mice with both Avandia and with SR1664. While both groups showed improved blood glucose levels, the mice treated with Avandia also displayed more fluid retention and weight gain soon after beginning treatment. The mice treated with SR1664, on the other hand, showed neither. The researchers also tested SR1664 in cell cultures for its effect on bone formation and fat generation in bone cells, both side effects of Avandia and other therapies. SR1664 caused no such side effects.

Although SR1664 will likely not be used directly as a drug, its discovery will allow researchers to develop similar compounds that can be used to treat diabetes. “With data in hand showing that our compounds are as efficacious as the currently marketed PPARG modulators, while demonstrating a significant improvement of side effects in limited studies, we are now advancing newer compounds with improved pharmaceutical properties into additional studies,” says Griffin.

Are you one of the millions who finds it hard to get up and exercise regularly? You’re definitely not alone, and new research shows that those who tend to stay active may have been born with different genes. For years, diet and exercise have been prescribed as the best way to stay in shape and maintain one’s health, but a lack of motivation to exercise could be the result of an unlucky drawing in the genetic lottery.

The research was conducted by Professor Gregory Steinberg and his team at McMaster University in Canada. The team was studying health mice that had been specifically bred for the study; some of the mice had two genes removed which are essential in exercise. The two genes are responsible for controlling a protein called AMP-activated protein kinase, or AMPK. The enzyme is “switched on” when an organism such as a mouse or human exercises.

“Mice love to run,” said Professor Steinberg, who is the associate professor of medicine at the Michael G. DeGroote School of Medicine as well as the Canada Research Chair in Metabolism and Obesity. Steinberg described how the removal of the two exercise genes caused an immediate change in the physical capabilities of the mice: “While the normal mice could run for miles, those without the genes in their muscle could only run the same distance as down the hall and back. It was remarkable. The mice looked identical to their brothers or sisters but within seconds we knew which ones had the genes and which one didn’t.”

Those mice lacking the genes that controlled AMPK had decreased mitochondria — the powerhouses that provide energy to cells — and a subsequent dysfunction in the ability of the muscle cells to utilize glucose to generate energy.

“When you exercise you get more mitochondria growing in your muscle. If you don’t exercise, the number of mitochondria goes down,” says Steinberg. “By removing these genes we identified the key regulator of the mitochondria is the enzyme AMPK.”

While there are many research teams around the world studying AMPK and its implications, Professor Steinberg’s team is the first to outline the importance of its role in exercise. Their findings are published in the Proceedings of the National Academy of Sciences.

According to Professor Steinberg, the team’s findings have important implications for individuals who find it difficult to exercise, including disabled people, asthmatics and the obese. When regular physical exercise is neglected over a long-term period, additional complications such as diabetes and heart disease can occur.

“As we remove activity from our lives due to emerging technology, the base level of fitness in the population is going down and that is reducing the mitochondria in people’s muscles. This in turn makes it so much harder for people to start exercising,” says Professor Steinberg. With the lack of exercise required in our modern lives, and the subsequent reduction of mitochondria in our cells, our risk of developing serious complications has risen as industrial technology has taken over and reduced the need for frequent physical exertion.

Steinberg says that he rides his bicycle or runs to work to stay in shape: “It is the only way that I can manage to make sure I stay fit.” Regular exercise has a variety of health benefits, from reducing weight and fighting illnesses and disease to improving mood, increasing energy levels and encouraging healthy sleep patterns.

According to a new study, a variety of lifestyle factors may independently affect an individual’s chance of developing Type 2 diabetes. Such risk factors include diet, exercise, weight, and alcohol and tobacco use.

The researchers found that individuals were less likely to develop Type 2 diabetes if they had healthy lifestyles overall, even if they had family histories of diabetes or were overweight. In addition, each positive lifestyle choice reduced their chances of developing the disease.

“There are implications certainly for individuals to take one step at a time toward a healthy lifestyle,” said Jared Reis with the National Heart, Lung, and Blood Institute, located in Bethesda, Maryland, and an author on the study. “There is certainly benefit for those who may have a tough time with losing weight if they adopt these other healthy lifestyle factors” such as getting more exercise, eating a healthier diet, and eliminating smoking and alcohol.

The study analyzed data from over 200,000 Americans; the data was collected through surveys that the participants filled out themselves and it asked questions about their health in the years 1995 and 1996. At that time, most of the participants were older aged, in their 50s or 60s; however, none had diabetes at the start of the study.

The researchers followed up with those participants ten years later, asking whether they had developed diabetes since the first survey. On average, one in 10 men and one in 13 women had developed Type 2 diabetes since the beginning of the study.

Researchers then looked back at the data collected during the first survey, breaking down the questions according to five categories: body mass index (BMI), exercise, diet, and the use of alcohol and tobacco. According to the results, each healthy behavior that appeared on the survey, such as getting regular exercise or stopping smoking, reduced the participant’s risk of developing diabetes, even when accompanied by other unhealthy lifestyle choices.

As such, a participant who ate a well-rounded diet and avoided unhealthy fats and low-quality refined grains had a lower risk of developing diabetes even if he or she exercised little, smoked cigarettes and drank alcohol regularly.

The results proved consistent even among those who had a family history of diabetes, which put them at a higher risk overall.

The study found that normal weight women who answered positively to adopting healthy lifestyle choices, such as eating healthy, getting regular exercise, and avoiding alcohol and tobacco were 84% less likely to develop diabetes than overweight women who engaged in the opposite unhealthy activities. Similarly, men who made healthy choices were 72% less likely to develop diabetes compared with their less healthy peers.

Although the data pointed to the fact that healthy choices could counteract the risk of developing diabetes, the researchers noted that weight was still the most important determining factor in the development of diabetes.

“While the message is that all these things matter… the number one top-of-the-list take-home is, don’t be overweight in the first place,” said Dr. Lawrence Phillips, an endocrinologist at Emory University in Atlanta. “It’s important not to confuse the baby with the bathwater here,” added Phillips, who was not involved with the study.

While the study is encouraging in its predictions that healthy choices reduce the risk of diabetes, it cannot prove definitively that removing alcohol, tobacco or saturated fats can reduce any one individual’s risk of developing the disease.

Good news for diabetics who love the calming and relaxing influence of yoga — a recent study suggests that yoga classes could help Type 2 diabetics lose some weight and, more importantly, help regulate their blood sugar levels. The study was published in the journal Diabetes Care.

The study was conducted on 123 middle-aged and older adults, and it showed that the patients who participated in yoga classes as a type of supplemental treatment for their existing diabetes care lost a few pounds over the three-month period of the study. In addition, their average blood glucose levels held at a steadier level than the control group of Type 2 diabetics who did not add yoga sessions to their diabetes care.

The study participants who took yoga classes several times a week — 60 of them in all — showed an average decrease in body mass index, or BMI, from 25.9 to 25.4. On the BMI scale, the “overweight” range is from 25 to 30.

While the findings were encouraging in suggesting yoga as a form of supplemental treatment for diabetes, they did not suggest that yoga should replace the typical exercise regimen that is prescribed for Type 2 diabetics.

Shreelaxmi V. Hegde with the Srinivas Institute of Medical Science and Research Center in Mangalore, India was the lead researcher on the study. According to Hedge, although yoga showed some positive benefits, Type 2 diabetics would benefit even more from vigorous exercise such as running.

“In our study the effect of yoga on BMI (body mass index) and blood sugar control was marginal,” said Hegde. “But, it should be noted that yoga controlled the blood sugar levels which otherwise rose in the control group.”

The study also found signs of decreased oxidative stress in the group that participated in yoga. Oxidative stress is the condition where free radicals — dangerous leftovers from cellular energy production — increase to levels that the body cannot handle. Oxidative stress, when present over long periods of time, is known to contribute to the development of several chronic diseases.

The research team studied the participants’ bloodstreams for the presence of chemicals that are indicative of oxidative stress. These results showed that the presence of these chemicals was reduced by an average of 20 percent in the group that took yoga classes.

According to Hedge, if this reduction in oxidative stress could be maintained over a long period of time, the patient could lower his or her risk of developing diabetes complications, including heart disease, kidney disease, and nerve damage. However, more research is needed to determine whether yoga could actually be used to curb oxidative stress in the long term.

In the meantime, Hedge has a theory on why yoga could reduce oxidative stress: yoga stimulates the parasympathetic nervous system, or the part of the nervous system responsible for unconscious activities such as breathing and digestion.

Hedge did state that the type of yoga used in the study was a gentle form that excluded certain poses because they could exacerbate the patients’ complications. However, some yoga classes provide a more intense workout that could be dangerous to those with potential complications while being more beneficial to individuals who can handle the extra stress. Many hospitals and community centers around the U.S. are beginning to offer yoga classes tailored specifically for those with chronic illnesses such as cancer and diabetes, as well as yoga classes for older individuals who want to stay in shape.

Beans and rice are two ingredients that are common to many meals in the typical Western diet. However, a study conducted in Costa Rica has found that lightening up on the rice and eating more beans could be better for overall health.

The study, which was conducted on almost 2,000 men and women, found that those who regularly replaced a serving of white rice with a serving of beans were 35% less likely to display precursor symptoms for diabetes. The researchers reported their results in the American Journal of Clinical Nutrition.

“Rice is very easily converted into sugar by the body. It’s very highly processed, it’s pure starch and starch is a long chain of glucose,” said Frank Hu, one of the researchers with the study. Hu is a professor of nutrition and epidemiology at Harvard School of Public Health in Boston, Massachusetts. “Beans compared with rice contain much more fiber, certainly more protein and they typically have a lower glycemic index — meaning they induce much lower insulin responses,” continued Hu. Though beans do contain significant amounts of carbohydrates, the body must work more to break them down, resulting in slower digestion time and a reduced impact on insulin production and blood sugar.

Hu’s research team analyzed the diets of almost 2,000 men and women from Costa Rica, who were participating in a study lasting from 1994 to 2004 that looked at risk factors for heart disease. At the beginning of the study, none of the participants were diabetic.

As with many industrialized nations, Costa Rica has seen its diabetes rates begin to soar. The urbanization of the country, along with its increased wealth, has caused increases in the consumption of white rice; simultaneously, consumption of beans has decreased, according to Hu. This increase in rice consumption could be part of the reasoning behind the nation’s rising diabetes rates: study participants who ate more white rice over a long-term period had higher blood pressure in addition to lower levels of good cholesterol and increased levels of fat and sugar in their blood.

These are well-known risk factors for metabolic syndrome, a series of conditions that dramatically increase risk of developing Type 2 diabetes and heart disease.

While those who ate more rice were at higher risk for metabolic syndrome, individuals who ate two servings of beans for every serving of white rice were usually at lower risk. Such practices of replacing rice with beans reduced the risk of metabolic syndrome by 35%.

While rice generally makes up a significantly larger portion of the average diet in countries outside the U.S., Americans have been consuming more and more rice every year, according to the U.S. Department of Agriculture. In 1980, Americans consumed 9.5 pounds of rice per person every year; in 2008, that number rose to 21 pounds per person. At the same time, Americans have consumed less dry beans — about 7 pounds per year.

Hu says that such an increase in consumption of white rice is dangerous, especially when compared to brown rice. According to Hu, eating white rice “is like eating a candy bar — the fiber and other nutrients are stripped away.” The increases in consumption of white rice “will have long-term metabolic effects,” added Hu. “It would be useful to introduce more legumes, including beans, into our diet to replace white rice and some of the red meat.”

New research findings relating to low-grade inflammation are sure to cause controversy, as they seem to contradict current mainstream views of diabetes. While increases in low-grade inflammation are commonly believed to be a contributing factor in the development of Type 2 diabetes, a team of researchers at Children’s Hospital in Boston have reported that two proteins activated by inflammation are actually vital in regulating blood sugar levels; not only that, but increasing the activity of these proteins leads to better blood glucose stability in obese and diabetic mice.

The findings were reported in the October issue of Nature Medicine. The research team was headed by Umut Ozcan, M.D., with the Division of Endocrinology at Children’s Hospital.

“This finding is completely contrary to the general dogma in the diabetes field that low-grade inflammation in obesity causes insulin resistance and type 2 diabetes,” said Ozcan. “For 20 years, this inflammation has been seen as detrimental, whereas it is actually beneficial.”

The team headed by Ozcan has shown in the past that obese individuals experience increased stress on the endoplasmic reticulum, or ER. This cellular structure is involved in the assembling, folding, and releasing of proteins to conduct the operations of the cell. “ER stress,” as it’s called, reduces the body’s efficiency in responding to insulin and regulating blood sugar levels; this deficiency is one of the primary links between Type 2 diabetes and obesity.

Ozcan’s team previously found that proteins called XBP1s, which play a role in mitigating ER stress, are unable to function in overweight mice. Then, they showed that inducing XBP1s to activate in the liver resulted in normalization of the blood sugar levels of obese, Type 2 diabetic mice as well as in Type 1 diabetic mice.

The team’s newest study shows that yet another protein which is activated by inflammation, known as p38 MAPK, is responsible for chemically altering XBP1s to increase their activity. Without the increase in activity from p38 MAPK, XBP1s are unable to maintain normal blood sugar levels. In addition, the study showed that activity of the p38 MAPK protein is reduced in obese mice, and re-activating the protein in the liver reduced ER stress while reducing blood glucose levels and increasing glucose tolerance and insulin sensitivity.

When taken together, the findings of the two studies suggest that new therapies for diabetes could be developed by increasing the activity of the p38 MAPK protein and thereby increase XBP1 activity, or by increasing XBP1 activity directly. Since these proteins are associated with low-grade inflammation, any such therapies will likely be controversial and need further study.

The studies also provide new information about Type 2 diabetes that could help with our understanding of the disease. “It may be that inflammatory pathways are not working optimally and there could be a resistance to cytokines which mediates the inflammation,” said Ozcan. “This could be a paradigm shift for the field.” In other words, obesity could be related to diabetes by causing a disruption in the ability of the individual’s cells to respond to inflammatory signals.

Though the research team is hopeful that their findings could lead to new therapeutics, they warn that there could be downsides to using p38 MAPK inhibitors to treat inflammatory diseases, such as asthma, psoriasis and Chrohn’s disease. “These therapeutic approaches should… be evaluated within the context of our results, and in light of the possibility that inhibition of XBP1s activity also decreases the ability of the cell to cope with the inflammatory conditions,” the study states.

A study conducted at the University of Otago in Dunedin, New Zealand, has found that middle-aged women who consume meals at a slower rate are much less likely to become overweight than women of the same age who eat quickly.

The study was the first of its kind to be conducted on a national level. It examined the link between body mass index, or BMI, and the speed of eating as reported by the 1500 women who participated in the study. The women were from New Zealand and ranged in age from 40 to 50 years old; this demographic is at a high risk of weight gain. The study was conducted by the Department of Human Nutrition at the University of Otago.

When the team adjusted its results to take into consideration other factors such as level of physical activity, whether or not the women had reached menopause, smoking status, and ethnicity, they found that the faster the women ate, the higher their BMI numbers grew.

“For every one-step increase in a five-step scale ranging from ‘very slow’ eating to ‘very fast’ ‘the women’s BMI increased by 2.8 percent, which is equivalent to a 1.95 kg weight increase in a woman of average BMI for this group,” said Dr. Caroline Horwath, head of the study and professor at the University of Otago.

Dr. Horwath did note that there is not enough data to prove that the women’s’ increased eating speed was the actual cause of their higher BMI. For this reason, the research team will be following up with the participants to see if those who reported faster eating will continue to gain weight over a longer period of time. However, if a causal link is discovered between speed of eating and weight gain, then advising individuals to slow down their meals could help them lose weight just as much as a typical weight loss management program.

“The size of the association found in this initial research suggests that if there is a causal link, reduction in eating speed is a very promising way to prevent weight gain and may lead to decreases in BMI similar or greater than those sustained in weight management programs,” said Dr. Horwath.

If the team finds that such a causal link exists, Dr. Horwath plans to conduct additional research, including the use of interventions that encourage women to consume their meals more slowly. The interventions would teach participants how to relax when confronted with stressful situations and how to use techniques to recognize and avoid unnecessary eating triggered by stress.

“If such interventions prove effective, they could be used alongside other non-dieting approaches we have previously trialled with overweight or obese women. These approaches successfully prevented weight gain in at-risk women and even produced significant weight loss in some. Our interventions included intensive training in relaxation techniques and how to recognize and avoid stress-related triggers for eating,” said Dr. Horwath.

Non-dieting approaches to weight loss appear to be gaining in popularity, according to Dr. Horwath. Dietitians have begun to seek alternatives for weight loss treatment since traditional treatments such as restriction of food intake have not been wildly successful in helping patients keep off lost weight.

“Studies have found that many dieters regain any weight they lose within five years and often end up heavier than when they began,” says Dr. Horwath.