People who weigh more have lower circulating levels of Vitamin D according to recent research conducted at the Rikshospitalet-Radiumhospitalet Medical Center in Oslo, Norway and published in the Journal of Nutrition. Lead researcher, Zoya Lagunova, MD and her colleagues measured the serum levels of Vitamin D and 1,25(OH)2D in 1,779 patients at a Medical and Metabolic Lifestyle Management Clinic in Oslo, Norway. The associations among 1,25(OH)(2)D, serum 25-hydroxyvitamin D [25(OH)D], and body composition were analyzed. Lagunova noted that generally people with higher BMI had lower levels of Vitamin D. Age, season, and gender were also found to influence serum 1,25(OH)(2)D.
Vitamin D is not a true vitamin, but rather a vitamin-steroid thought to play a key role in the prevention of cancer, cardiovascular disease, diabetes, multiple sclerosis and other diseases. It is likely not coincidental that obesity is also a risk factor for many of these diseases. Vitamin D is vital to the regulation of calcium. Studies have shown that calcium deficiency increases the production of synthase, an enzyme that converts calories into fat. It has been shown that calcium deficiency can increase synthase production by up to 500 percent. Vitamin D has also been shown to play a role in the regulation of blood sugar levels; proper blood sugar regulation is vital to the maintenance of a healthy weight. Vitamin D is produced from sunlight and converted into various metabolites. It is stored in fat tissue. According to Lagunova, obese people may take in as much Vitamin D as other people; however, because it is stored in fat it may be less available. This may result in lower circulating levels of Vitamin D.
A previous study conducted by Shalamar Sibley, MD, MPH, an assistant professor of medicine at the University of Minnesota, showed that subjects who have higher levels of Vitamin D at the start of a weight loss diet lose more weight than those with lower levels. The study measured Vitamin D levels of 38 overweight men and women both before and after following an 11-week calorie-restricted diet. Vitamin D levels at the start of diet was an accurate predictor of weight loss…those with higher levels of Vitamin D lost more weight. It was found that for every nanogram increase in Vitamin D precursor, there was an 1/2 pound increase in weight loss.
Seventy-five percent or more of Americans, teenage and older, are Vitamin D deficient according to a recent study published in the Archives of Internal Medicine. According to the Gallup-Healthways Well-Being Index, 26.5% of American are obese. More research needs to be conducted into the exact role Vitamin D plays in obesity and weight loss and the possibility of increased Vitamin D consumption (through the form of supplementation and/or increased sun exposure) being a key factor to achieving a healthy weight.
Recent studies show that grapefruit and diabetes may share a close link. Researchers concluded that naringenin found in grapefruit may increase the body's sensitivity to insulin. This research was conducted only in the laboratory, and further studies are still needed. Grapefruit and diabetes may share a close link given some recent studies suggesting that eating of the fruit can help in controlling the disease. One recent report suggests that grapefruit may become an effective part of the treatment for type 2 diabetes as it contains the antioxidant Naringenin that can break down fats and increase a person's sensitivity to insulin.
The study also concluded that grapefruit is also capable of treating abnormal levels of cholesterol, warding off metabolic syndrome and improving a person's tolerance to glucose, factors that are all associated with diabetes. The study was conducted by scientists from the Massachusetts General Hospital Center for Engineering in Medicine and Hebrew University of Jerusalem. Although more research needs to be completed, grapefruit is a safe source of vitamins for diabetics. One-half of a grapefruit contains 52 calories and 13g of carbohydrates, and the fruit has a low rating on the glycemic index, indicating a lower propensity to drive up blood sugar levels.
The antioxidant Naringenin is found in grapefruit and has been largely credited for its ability in heping to treat type 2 diabetes. Naringenin is specifically noted for being able to break down fatty acids in the liver, similar to what happens when a person undergoes fasting. Yaakov Nahmias, PhD of the Hebrew University of Jerusalem reports that the results of their study indicate that Naringenin antioxidant was found to be capable of breaking down fatty acids similar to those induced by significant amounts of fasting. It does so by activating nuclear receptors, a family of proteins that can cause the liver to break down fatty acids instead of storing them.
Another study conducted by researchers at the University of Western Ontario showed that Naringenin can correct increases in triglyceride and cholesterol levels, while resisting insulin resistance and normalizing glucose metabolism. The said study showed that Naringenin genetically reprograms the liver to burn up more excess fat, instead of storing it. The said study also showed that Naringenin is able to suppress appetite and decrease food intake, which are common strategies in controlling diabetes.
The study of MGH and Hebrew University scientists also noted that Naringenin can lower bad cholesterol called vLDL while able to cure several symptoms of type 2 diabetes.
Research on grapefruit and diabetes, however, has not yet been conducted on humans, and were only done in the laboratory on the liver cells of humans and rats. Until further studies are done to confirm the effects of grapefruit in the treatment of diabetes type 2 in humans, it is still not safe to conclude that the naringenin in grapefruits can indeed cure diabetes. Further studies are still needed to establish its efficacy as well as its overall effects in the body, including the negative effects it might have.
Thus, many health experts do not encourage patients with diabetes to increase their consumption of grapefruits or increase grape juice intake, especially if they are also taking medications. There are patients prescribed with some type of drugs to lower their cholesterol level who are advised not to drink grapefruit juice as it can increase risk of side effects.
Could the Mediterranean diet actually help prevent diabetes? The Mediterranean Diet, which is rich in vegetables, fruits, whole grains, healthy fats from nuts and olive oil, with moderate amounts of fish, low-fat dairy, and wine, and minimal red meat and processed meats, is considered to be an especially healthy eating plan.
Previous research conducted on newly diagnosed diabetic participants showed the diet did indeed help control the sugar spikes. The previous study found the mediterranean diet eating diabetics had better glycemic control. Furthermore, they had less needs for diabetes medications when adhering to the Mediterranean diet as opposed to a simple low-fat diet.
Recently, a team of researchers in Spain conducted a study using data from a large clinical trial to determine the effects of the Mediterranean Diet on preventing the onset of Type-2 diabetes. Participants were followed for an average of 4 years. Upon completion of the study, 54 participants had developed diabetes–but the split varied significantly among groups. The researchers found that the risk of developing diabetes was reduced by 52% among both groups of people who followed the Mediterranean Diet plans compared to the low-fat control group. In analyzing diet adherence, the researchers further noted that the closer an individual followed the Med-Diet plan, the lower their risk of developing diabetes. Interestingly, the weight of all participants did not change significantly throughout the study, nor did it vary significantly among the three groups.
The participants were divided in one of three groups: adherence to the Med-Diet with 1 liter per week of extra virgin olive oil, adherence to the Med-Diet with 1 oz per day of mixed nuts, or a standard low-fat diet as a control. No calorie restrictions were imposed on any of the groups. The two Med-Diet groups were instructed to increase fruit and vegetable intake, decrease meat intake, stay away from refined sweets and unhealthy fats such as butter, and consume red wine in moderation, if desired. The control group was given general instructions to lower overall fat intake. Baseline measurements and annual follow-up involved an oral glucose tolerance test and interviews to assess diet adherence.
Interestingly, the weight of all participants did not change significantly throughout the study, nor did it vary significantly among the three groups.
This study reinforces prior study results suggesting that the Mediterranean Diet – even without weight loss – may be protective against Type-2 diabetes. The researchers suggest that future studies should focus on the Med-Diet’s effects on younger people, and point out the possible benefits of the Mediterranean Diet as an effective intervention against complications of Type-2 diabetes.
The study was conducted in mice, some of which were fed a normal diet of rodent chow and some a 16-week diet of fructose and sucrose-enriched drinking water and trans-fat solids. Their liver tissue was then analyzed for fat content, scar tissue formation (fibrosis), and the biological mechanism of damage. This was done by measuring reactive oxygen stress, inflammatory cell type and plasma levels of oxidative stress markers, which are known to play important roles in the development of obesity-related liver disease and its progression to end-stage liver disease.
The investigators found that mice fed the normal calorie chow diet remained lean and did not have fatty liver disease. Mice fed high calorie diets (trans-fat alone or a combination of trans-fat and high fructose) became obese and had fatty liver disease.
“Interestingly, it was only the group fed the combination of trans-fat and high fructose which developed the advanced fatty liver disease which had fibrosis,” says Dr. Kohli. “This same group also had increased oxidative stress in the liver, increased inflammatory cells, and increased levels of plasma oxidative stress markers.”
Dr. Kohli hopes to further investigate the mechanism of liver injury caused by high fructose and sucrose enriched drinking water and study a therapeutic intervention of antioxidant supplementation. Antioxidants are natural defenses against oxidative stress and may reverse or protect against advanced liver damage, according to Dr. Kohli.
The investigators also would like to use this model to better understand human fatty liver disease and perform clinical trials using novel therapeutic and monitoring tools.
“Our data suggest that supplementation with pharmaceuticals agents should be tested on our new model to establish whether one is able to reverse or protect against progressive liver scarring and damage,” says Dr. Kohli.
The study was supported by grants from the National Institutes of Health and the Children's Digestive Health and Nutrition Foundation.
The paper directly compared findings from two separate studies: 'The Diets of British Schoolchildren' conducted by the Department of health (DH) in 1983 (Department of Health 1989); and the National Diet and Nutrition Survey (NDNS) from 1997 (Gregory & Lowe, 2000).
Gibson's analysis found that total sugar intake averaged at 115g/day in 1983, compared with 113g/day in 1997. Allowing for exclusions of low and high energy reporters, intake levels were 122g/day (1983) and 127g/day (1997), showing a marginal and insignificant increase over the study period. Contrastingly, mean body weight increased significantly during the period of the DH and NDNS surveys, showing a rise of 1.9kg for 10-11 year olds and 3.4kg among 14-15 year olds. BMI increased from 17.9 to 18.6 units in the younger group, and 20.2 to 21.3 units in the older group. According to these calculations, the prevalence of being overweight (plus obesity), as defined by the International Obesity Taskforce (IOTF) cut-offs (91st percentile) rose from 13% to 21-22% between surveys. Gibson concluded that the slight increase in consumption of total sugars did not account for the significant increase in BMI, equivalent to 2-3 kg over the review period.
During the same period, Gibson found that mean energy intake (EI) was 3% lower in 1997 than in 1983, mainly as a result of lower fat intake. This change in overall energy consumption meant that sugars represented a higher proportion of daily energy intake in 1997 (23.6% versus 22.3%), despite total sugar consumption remaining relatively static in comparison. The review surmises that the most likely cause for the increased BMI is a decline in energy expenditure.
In addition, Gibson's paper found that basal metabolic rate (BMR) increased by approximately 3% between surveys as a result of higher body weights, and it is estimated that EI in relation to basal requirements was even lower at 6%. Gibson found that the paradox of rising BMI, despite a 2-3% rise in BMR and an EI that is static or falling, pointed to declining energy expenditure as an important factor in the change.
The Gibson analysis showed that the key sources of sugars in the diet have changed with a marked shift away from table sugar and smaller falls in consumption of sugars through milk, biscuits and cakes, counterbalanced by a significant increase in sugars consumed in soft drinks and, to a lesser extent, fruit juice and breakfast cereals.
A conclusion of Gibson's reanalysis of data from the DH and NDNS studies, that consumption of total sugars remained relatively static during the period, providing an estimated 22% of energy, is supported by findings from a repeated cross sectional study of children's food and drink intake, conducted in Northumberland in 1989, 1990 and 2000 which looked at trends in children's food and drink intake.
Sigrid Gibson, the paper's author, said: “There are very few studies that have assessed trends in sugar intake over time and particularly over such an extended period. The findings of the reanalysis strongly contradict widespread assumptions that sugar levels in the diet are responsible for rising obesity levels. With dietary sugar intakes relatively static, and overall energy consumption showing decline, increased BMI levels cannot be attributed to sugar consumption.”