DM and obesity treatments will soon enough completely break the bank on the health care system. Why all the spending on reseach to treat when the emphasis should be on prevention and cure?
There is a horrible cycle of poisoning and treatment for profit that has to be broken ASAP.
================
Mexico pays price for obesity trend
Josefina Fausto, a health expert at the University of Guadalajara, says that behind the explosion in obesity in Mexico is a radical change in diet that stems from the country’s increasing insertion into the global economy.
In other words, they are eating a lot of US-inspired junk food. “A century ago, our biggest challenge was malnutrition,” she says. “Today, it is an excess of foods that are rich in cholesterol and heavy in saturated oils, sugar and salt.”
The worsening diet – the health ministry claims that consumption of vegetables has dropped 30 per cent in a decade – is compounded by a seemingly insatiable appetite for soft drinks, in particular Coca-Cola.
According to the US-based soft-drinks manufacturer, Mexicans drank 573 eight US fluid ounce bottles of Coca-Cola products per capita (roughly 136 litres per person) in 2007 – by far the highest consumption in the world. In the US, the second biggest per-capita consumer, people drank a relatively modest 423 bottles in 2007.
http://www.ft.com/cms/s/0/81779544-f6ca-11dd-8a1f-0000779fd2ac.html?nclick_check=1----------------
Epigenetics and Diabesity
Speaker: Robert Waterland, PhD
Baylor College of Medicine
USDA Children's Nutrition Research Center
Highlights
* Epigenetic processes are emerging as major factors in obesity, diabetes, and heart disease; these effects are not caused by genetic mutations, but are still maintained as our cells divide.
* Even genetically identical animals and humans can show differences in character, appearance, and physiology.
* Early nutrition might play a critical role in disease susceptibility; nutrients influence DNA methylation, thereby influencing gene activation and silencing.
~snip~
Obesity has been increasing steadily in most parts of the world over the past 30 years, and this rise is associated with a concomitant increase in prevalence of type 2 diabetes, dyslipidemia, and hypertension. What's behind this surge in adiposity? Why are we now in the midst of an obesity "epidemic?" It's logical to blame increasingly sedentary lifestyles and the wide availability of palatable foods. But why do some people succumb to these environmental factors by becoming fat whereas others remain lean? Does the answer lie in our genes?
In his keynote address, Robert Waterland of Baylor College of Medicine suggested that epigenetics, specifically the range of environmental influences on genetic expression during early development, may account for these differences.
"The best example of epigenetics at work is tissue-specific gene expression," Waterland explained. "Most cells in our body contain the same complement of DNA—the entire human genome. But our hepatocytes express a very different subset of genes from the cells in, for example, our colonic mucosa. And although those two cell types turn over throughout life, hepatocytes remember to express liver-specific genes; the pattern is established during early development and maintained throughout life through epigenetic mechanisms."
Waterland and others hypothesize that during critical periods of development, nutrition and other environmental stimuli can perturb developmental pathways, thereby leading to permanent changes in gene expression, metabolism, and chronic disease susceptibility. He and a colleague coined the term "metabolic imprinting" to denote a subset of adaptive responses to early nutrition characterized by a persistent effect lasting into adulthood, and with susceptibility limited to a critical period of development.
~snip
Waterland's team is now working to identify specific epigenetic modifications associated with obesity. To do this, they developed a methylation-specific amplification microarray that amplifies hypermethylated regions of the genome. They validated the microarray in a mouse model, showing that it is indeed capable of identifying relatively subtle changes in locus-specific CpG methylation in normal tissues, and that therefore it is a useful tool to study epigenetic alterations associated with obesity as well as environmental influences on these processes.
Investigations detected "an epigenetic storm" in the hypothalamus during the newborn and weaning period.
Using the microarray, they examined the hypothalamus of newborn and weanling non-agouti mice. Genetic mutations in leptin, melanocortin 4 receptor, neuropeptide Y, and other genes involved in hypothalamic regulation of energy balance all lead to obesity; however, "We know almost nothing about epigenetic regulation at these loci," Waterland stated.
Their investigations yielded a surprise, he said: unlike in the liver, where the team found very few epigenetic changes during the newborn and weaning period, they found "huge changes—an epigenetic storm" in the hypothalamus. Four-fold increases or decreases in methylation were seen during the 21-day period.
"It's not clear what it all means at this point, but this is where we're going," he concluded.
http://www.nyas.org/ebriefreps/main.asp?intSubSectionID=6321
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