Obesity Shuts off the "I’m Full" Signal in Your Brain.

Success Builds on Success

Scientists have discovered that when a person becomes overweight or obese, the system in your brain designed to regulate appetite doesn’t work anymore. When your body has enough food, it secretes a substance called leptin, which inhibits appetite. However, studies have revealed that when you have too much body fat and too much leptin, the brain becomes insensitive to this feedback mechanism. The result is that hunger is not diminished when it should be and increased food intake results.
The great news about this discovery is you can actually turn the leptin mechanism back on by restricting food intake and exercising. Gradually over time, your body’s brain cells will again become sensitive to leptin if the leptin stimulus (fat cells) is decreased, giving those brain cells an opportunity to switch back on.
Choosing a portion controlled, low glycemic eating pattern, along with an increased activity level, will not only allow the gradual reduction of this block in inhibition, but will decrease high insulin levels, which are also known to be appetite stimulants. These small choices, taken each morning and followed throughout the day, will lead to appetite suppressionand a more healthy and more normal eating patter.
Courtesy Dr. Sennholz

Diabetes is Increasing Dramatically in Asia

by Dr. Ray Strand

In a review article reported in the May 27, 2009 edition of JAMA the incidence of type 2 diabetes throughout Asia is increasing dramatically. In a disease that was once felt to be a disease of the West, over 110 million individuals in Asia were living with type 2 diabetes. This number is projected to grow to over 380 million in just 15 short years. The most concerning thing that the frequency of diabetes is being found in the young and middle aged.

When I was speaking to a group of doctors in Malaysia approximately 2 years ago, they told me that the incidence of type 2 diabetes was nearly 10% already in their adult population. They shared with me that they were not even able to get enough dialysis units to meet the demand for dialysis in this group of patients. It was obvious to me that one of the main problems was their consumption of more and more refined grains, especially Jasmine rice which has a glycemic incidence of 115.

Eating high glycemic foods can lead to metabolic syndrome and to diabetes. Foods with a glycemic index of less than 55 are considered low glycemic and aid in maintaining stable blood sugar levels. An index of 100 is eating straight glucose (sugar) so the refined Jasmine rice was being absorbed and turned into sugar in the blood quicker than if you ate spoonfuls of sugar. In the west we eat so many refined foods what we are on a constant blood sugar roller coaster. Foods like potatoes, french fries, white rice, pasta, most bread & cereals, soda, fruit juices, etc. are all high glycemic foods. Instead eat 100% whole grain bread, cereals, and pasta. Whole fruits and vegetables, whole grain rice, etc.

Greater intake of several nutrients combined with low-glycemic foods linked to reduced risk of macular degeneration

Researchers analyzed data from 4,003 participants in the Age-Related Eye Disease Study (AREDS). Information was collected on the subject’s intake of several nutrients related to eye health, including vitamin C, vitamin E, zinc, lutein/zeaxanthin, and the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Glycemic index was calculated for consumed food items. Photographs of the macula of the eye (taken upon enrollment) were graded for severity and type of macular degeneration.
Participants with a high overall intake of the associated nutrient group, as well as higher intakes of low-glycemic foods, had the lowest risk of early or advanced macular degeneration. When single nutrients were analyzed separately, vitamin E emerged as significantly protective against the disease..
The study is the first to analyze the combination of multiple nutrient groups and a low-glycemic diet on the risk of age-related macular degeneration.
Ophthalmology. May 2009. 116:5(939-946).