Showing posts with label Fat. Show all posts
Showing posts with label Fat. Show all posts

Thursday, April 22, 2010

HFCS Making Us Fat and Sick

Tags: Sugar Consumption Increased 50% Since Reagan Made Corn Cheap, Fructose, Prepared Foods, Fat, Sick, high BP, Uric Acid,


USA Sugar 10.6% of All Calories 1977-1978 and 1999-2006 15.8% (21.4 Teaspoons, 359 calories) Reagan's Fault?


This journal article was probably submitted before the Princeton study showing that equal calories of HFCS High Fructose Corn Syrup which is 55% Fructose and 45% glucose and cane sugar 50:50 fructose and glucose. Why did this apparently small change make such a difference in our health?


Reagan wanted to greatly increase the profits of large corporations involved in food production so the farmers got subsidies greater than the cost of producing, but so much corn was produced to keep prices low so the farmers had to produce lots of corn to get enough to feed their families! So the large corporations were able to sell corn worldwide and put local farmers out of business.


Cane sugar could not be added to fiberless foods in high amounts because it tended to crystallize out on freezing or standing. Liquid High Fructose Corn Syrup which is sweeter than glucose and sucrose, could be added in any amount to prepared foods without crystallizing. So they did not have to worry about making the taste good from tasteless corn and soybean, but just added HFCS.


Fructose does not convert to glucose in our blood and has to be processed by our liver. There part of it is converted to glucose which is stored as glycogen to be used as needed for energy, but 30 percent are converted to low density lipoproteins or the bad heavy LDL-2 which leads to plaques in our arteries.


Fructose also increases our triglycerides which leads to heart disease. If this was not enough, it also produces uric acid which acidifies our blood and gives us gout and high blood pressure independent of salt. Note salt does increase our blood pressure when used in excess, but salt also works by another mechanism to thicken our heart which leads to congestive heart disease.


We are the only ones that can change this. Complain to our political leaders, to newspapers, and to the food producers themselves. Already Coke and Pepsi have removed their colas from the school vending machines which Oregon did first and greatly improved the health of the students at a young impressionable age. Jaime a chef on ABC on Friday at 9:00 PM is trying to change the food habits of Americans starting with the most obese town in the USA, Huntington, West Virginia. Almost everyone has family members who died from diseases due to obesity.

With our government health department calling french fries vegetables, you can imagine how difficult it is. I will check him out on Friday and record Bill Moyers whose programs have been outstanding on PBS.

Jim Kawakami, April 22, 2010, http://jimboguy.blogspot.com


ScienceDaily (Apr. 22, 2010)Consuming a higher amount of added sugars in processed or prepared foods is associated with lower levels of high-density lipoprotein cholesterol (HDL-C, the "good cholesterol") and higher levels of triglycerides, which are important risk factors for cardiovascular disease, according to a study in the April 21 issue of JAMA.

Jean A. Welsh, M.P.H., R.N., of Emory University, Atlanta, and colleagues assessed the association between consumption of added sugars and blood lipid levels in U.S. adults. The study included 6,113 adults from the National Health and Nutrition Examination Survey (NHANES) 1999-2006. Respondents were grouped by intake of added sugars using limits specified in dietary recommendations (less than 5 percent of total calories [reference group], 5 percent to less than 10 percent, 10 percent to less than 17.5 percent, 17.5 percent to less than 25 percent, and 25 percent or more of total calories).

"In the United States, total consumption of sugar has increased substantially in recent decades, largely owing to an increased intake of 'added sugars,' defined as caloric sweeteners used by the food industry and consumers as ingredients in processed or prepared foods to increase the desirability of these foods," the authors write. No known studies have examined the association between the consumption of added sugars and lipid measures, such as HDL-C, triglycerides and low-density lipoprotein cholesterol (LDL-C).

Various measures calculated in the study included average HDL-C, average triglycerides, and average LDL-C levels and adjusted odds ratios of dyslipidemia (abnormal amounts of lipids and lipoproteins in the blood), including low HDL-C levels (less than 40 mg/dL for men; less than 50 mg/dL for women), high triglyceride levels (150 mg/dL or greater), high LDL-C levels (130 mg/dL or greater), or high ratio of triglycerides to HDL-C (greater than 3.8). Results were weighted to be representative of the U.S. population. ... http://www.sciencedaily.com/releases/2010/04/100420161748.htm

Tuesday, January 19, 2010

Obesity Uncommon in Past, So Our Modern Diet Caused Obesity Due to More Efficient Gut Bacteria

Tags: High Sugar, Salt, Fat, More Efficient Gut Bacteria Based on Our Diet, Diet Books, Never Go Hungry Diet, Eating Every 2 to 3 Hours, Scientific Proof Type of Major Bacteria in Gut Leads to Obesity

It is ironic that many commercial diets seem to lead to obesity. It is no accident that following the model that government is bad as espoused by Reagan and followed through with a vengeance Even though I do not expect you to understand all the words in this excerpted five page article below at www.Medscape.com for doctors, you will understand the concept of what you eat matters a lot. A starvation diet never works because our system produces a hormone which activates your hunger response so if you want to lose weight long-term, never go hungry and change what you eat.

Avoid like a plaque any White Bread, White Flour based foods, and eat whole wheat and brown instead of white rice. There are many kinds of brown rice which maintains its fiber which helps you avoid the immediate high sugar level in your blood which converts to fat and over works the pancreas. Potato, especially with its skin, yams, and the like provide your carbohydrates.

Two new books on diet based on the latest scientific experiments are easy to read with "You on a Diet: Owner's Manual for Waist Management" the http://doctoroz.com team, Michael F. Roizen, MD, and Mehmet C. OZ, MD, the better one than the excellent "The Mayo Clinic Diet: Eat Well, Enjoy life, Lose Weight" Both are about $15 at Costco.

The excerpted article below based on scientific evidence and not error prone anecdotal diet suggestions. The bottom line is that the bacteria in our gut determines whether we are fat and obese rather than normal because of the higher efficiency in converting food in our gut to increased fat and weight (energy) than other major bacteria in our gut.

That is why white bread and flour which are high sources of sugar in our diet favors the bacteria that gets us to eat more so obesity must thrive. Saturated fats also must be controlled so greatly reducing meat, cheese, and other saturated fat sources is necessary. A combination of saturated fat, salt, and sugar is essentially in all Fast Foods because our bacteria craves these high calorie foods and our brain goes into ecstasy!

Jim Kawakami, Jan 19m 2010, http://jimboguy.blogspot.com

Obesity and the Human Microbiome

Ruth E. Ley …

Summary Large-scale alterations of the gut microbiota and its microbiome (gene content) are associated with obesity and are responsive to weight loss. Gut microbes can impact host metabolism via signaling pathways in the gut, with effects on inflammation, insulin resistance, and deposition of energy in fat stores. Restoration of the gut microbiota to a healthy state may ameliorate the conditions associated with obesity and help maintain a healthy weight.

Introduction

Up until the last few decades, obesity has been a rare physiological state. Now however, the number of obese or overweight humans has come to outnumber those suffering from malnutrition.[1] This is an unprecedented state for our species, resulting from a mismatch between our evolutionary biology and our modern environment. The human body is a complex system, made all the more complex through its interactions with the trillions of microorganisms that coat the body surface and densely populate the gut. Recent work has shown that the microbes of the gut may play a role in human metabolism and adiposity. Because they are environmentally acquired, microbes constitute one part of our environment that may contribute to the obese state. This review discusses the most recent findings and insights into the relationship between the human microbiota, obesity, and obesity-associated diseases. …

shotgun sequencing of the microbial community DNA, showed an enrichment in genes involved in energy extraction from food in the obese host's microbiome relative to that of the lean host's microbiome. A microbiota with greater energy extraction efficiency resulted in less energy left over in feces and greater levels of short-chain fatty acids (SCFAs) in the cecum. Furthermore, when the luminal contents from the ceca of obese or lean mice were provided to lean germ-free recipients, the mice receiving the microbes from the obese donors gained more weight over a 2-week period than recipients of the lean microbes, despite equivalent food intake.[3] In a study extending these observations to humans, 12 obese participants were randomly assigned to either carbohydrate-restricted or fat-restricted diets, and on average, the proportion of Bacteroidetes bacteria enumerated via 16S rRNA gene sequencing increased over time, mirroring reductions in host weight but not changes in diet.[4] Together these studies showed that the gut microbiota was generally altered in the obese host and could contribute to host adiposity in humans and mice.

Metagenomics and Obesity

A subsequent and much larger study of the microbiome associated with obesity conducted with humans also showed that obesity was associated with a depletion of Bacteroidetes, together with an enrichment in carbohydrate and lipid-utilizing genes in the microbiome as a whole. Turnbaugh et al.[5••] focused on twins to assess the gut microbiota's relationship to host weight. The fecal microbial communities of young adult female monozygotic (n = 31) and dizygotic (n = 23) twin pairs concordant for either leanness or obesity were compared, along with those of their mothers (n = 46), using a combination of traditional 16S rRNA gene clone libraries and high-throughput metagenomic analyses of the microbiome. Fecal samples were obtained from the majority of participants at an initial time point and then again 2 months later. Comparisons between all 154 participants showed obesity to be associated with reduced bacterial diversity and reduced representation of the Bacteroidetes. Furthermore, the microbiome differed between obese and lean hosts in much the same way it had in the obese mouse model, with obese host microbiomes enriched in gene categories involved in carbohydrate and lipid metabolism. …

Conclusion

An increasing number of studies relate imbalances in the composition of the gut microbiota to obesity and its associated diseases. The approaches used to characterize gut microbiotas vary widely, which might explain in part why the specific alterations in the microbiota associated with excess body fat, or weight loss, can also vary between studies. To compare studies will require some standardization of approaches or use of a variety of approaches within single studies. However, irrespective of the specific changes observed in microbial communities with respect to body fat, evidence suggests that microbes do indeed respond and contribute to host energy balance. They may do this using a number of different and possibly interactive signaling mechanisms involving innate immune responses, endocrine cells, and epithelial cells. An integration of mechanistically based investigations and microbial ecology studies using high-throughput sequencing will provide insights into how best to reshape host-microbial interactions to promote health. http://www.medscape.com/viewarticle/714569