Sugar: It’s Killing US!

Sugar: It’s Killing US!

like sugar

Direct from the sugar people. Truth

https://experiencelife.com/article/sugar-breakdown/

When it comes to evaluating sugar’s negative health impacts, the threat of extra pudge is just the beginning. Even great health threats—including inflammation-based diseases—may lurk at the bottom of the sugar bowl.

New research is revealing disturbing links not just between sugar and obesity, but also between sugar and inflammation. Inflammation, of course, has been implicated as a major factor in a number of vitality zapping diseases, from cancer and diabetes to atherosclerosis and digestive disorders.

The Refined-Carb Connection

On the spectrum of dietary dangers, processed sugars are on a par with unhealthy fats. “High-fructose corn syrup is the primary cause of obesity in our culture,” says Elson Haas, MD, author of Staying Healthy with Nutrition (Celestial Arts, 2006, New Edition). “Our bodies simply aren’t built to process all that sugar.”

Still, to date, sugar doesn’t have nearly as bad a reputation as it probably deserves. One of the reasons it slips under the radar is that connecting the dots between sugar and disease requires widening the nutritional net to include all refined carbohydrates (like processed flours, cereals and sugars of all sorts). This may seem like a fine point, but it’s an important distinction.

Most dietary sugars are simple carbohydrates, meaning that they’re made up of one or two sugar molecules stuck together, making them easy to pull apart and digest. Complex carbohydrates, like those found in whole grains, legumes and many vegetables, are long chains of sugar molecules that must be broken apart during digestion, therefore offering a longer-lasting surge of energy. The presence of naturally occurring fiber, protein and fat in many whole foods further slows the sugar-release process.

The more processed and refined the carbohydrate, as a rule, the faster it breaks down in the digestive system, and the bigger the sugar rush it delivers. That’s why refined flours, sugars and sugar syrups pose such a problem for our systems.

The body is exquisitely designed to handle small amounts of sugar. But refined carbs deliver a larger rush than our bodies were designed to accommodate, or even cope with. In ancient times, hunter-gatherers coveted the occasional piece of fruit or slab of honeycomb as a rare treat and source of rapid-fire energy for, well – hunting and gathering.

Today, sugar lurks behind most cellophane wrappers, and the energy it provides is more likely to get socked away on our hips than burned while stalking dinner. Being active goes a long way toward vanquishing excess sugar in the bloodstream, but it doesn’t negate the need to watch your intake. To make matters worse, unlike the fruit sugar (fructose) our ancestors savored, today’s sugary treats are made with refined sugars (usually some derivative of table sugar or high-fructose corn syrup), which can overwhelm the body’s ability to balance blood sugar.

“Refined sugar is a genetically unfamiliar ingredient,” says Jack Challem, a nutrition researcher and author of The Inflammation Syndrome (John Wiley & Sons, 2003). “A lot of health problems today are the result of ancient genes bumping up against modern foods.”

Take it a little further with this report from Haaaaavard.

http://www.health.harvard.edu/family_health_guide/what-you-eat-can-fuel-or-cool-inflammation-a-key-driver-of-heart-disease-diabetes-and-other-chronic-conditions

What is inflammation?

Inflammation’s aim is to defend the body against bacteria, viruses, and other foreign invaders, to remove debris, and to help repair damaged tissue. Inside arteries, inflammation helps kick off atherosclerosis and keeps the process smoldering. It even influences the formation of artery-blocking clots, the ultimate cause of heart attacks and many strokes.

What is an inflammatory cytokine. Back to the mothership.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785020/

Cytokines are small secreted proteins released by cells have a specific effect on the interactions and communications between cells. Cytokine is a general name; other names include lymphokine (cytokines made by lymphocytes), monokine (cytokines made by monocytes), chemokine (cytokines with chemotactic activities), and interleukin (cytokines made by one leukocyte and acting on other leukocytes). Cytokines may act on the cells that secrete them (autocrine action), on nearby cells (paracrine action), or in some instances on distant cells (endocrine action). There are both pro-inflammatory cytokines and anti-inflammatory cytokines. There is significant evidence showing that certain cytokines/chemokines are involved in not only the initiation but also the persistence of pathologic pain by directly activating nociceptive sensory neurons. Certain inflammatory cytokines are also involved in nerve-injury/inflammation-induced central sensitization, and are related to the development of contralateral hyperalgesia/allodynia. The discussion presented in this chapter describes several key pro-inflammatory cytokines/chemokines and anti-inflammatory cytokines, their relation with pathological pain in animals and human patients, and possible underlying mechanisms.

What is the connection between cytokines and the immune system.

http://www.uptodate.com/contents/role-of-cytokines-in-the-immune-system

Cytokines are important mediators of immune responses that allow integration of the behavior of cells in time and geographical location as immune responses are generated.

Cytokine-directed treatments are being developed by the pharmaceutical and biotechnology industry as therapeutic agents for a number of autoimmune diseases.

Here is our friend Dr Jill Smith from Penn State who explained this all to us. It was her presentations that helped me to understand inflammatory cytokines.

http://www.ldnscience.org/ldn-researchers/61-researchers/researcher-profiles/123-dr-jill-p-smith

Dr. Jill Smith is a Professor of Medicine in the Gastroenterology Division of the Department of Medicine, Hershey Medical Center, Penn State University. Dr. Smith has a long track record of conducting pre-clinical scientific research as well as translational clinical trials in patients.

Over the course of her twenty two years at Penn State University she has mentored thirty eight post-doctoral Fellows and students, thereby ensuring continuing excellence in medicine for future generations.

Dr. Smith’s research focus is on disorders of the gastrointestinal tract and pancreas. In her role as a Professor in the College of Medicine’s Internal Medicine Department she treats patients with Inflammatory Bowel Diseases.

Simultaneously, in her role as Professor of Cellular and Molecular Physiology she teaches and conducts basic science research in the graduate school. For over two decades, Dr. Smith has conducted industry-sponsored trials and investigator-initiated research involving inflammatory bowel disease. One of her areas of expertise is in translational medicine.

Another area of expertise for Dr. Smith involves her research on pancreatic cancer. Dr. Smith’s team discovered that growth of pancreatic cancer is controlled by a small protein called gastrin. They further discovered a novel receptor on human pancreas cancer through which gastrin exerts its effects. Dr. Smith’s discovery led to her being the recipient of the Basic Science Research Award, a prestigious award given by the European Pancreas Society for outstanding discoveries in science. Ongoing research using this novel receptor or targeting therapy and early detection of pancreatic cancer is underway. Dr. Smith is also is a co-discoverer of the role of another protein called OGF (Opioid Growth Factor) that inhibits growth of pancreatic cancer. This discovery has been confirmed in both Phase 1 and Phase 2 clinical trials treating patients with advanced pancreatic cancer with OGF.

Dr. Smith was the first ever researcher to carry out a clinical trial of low dose naltrexone. The results of the successful trial in patients suffering from Crohn’s disease has spearheaded ongoing clinical trials by other researchers at several institutions worldwide.

Knowing Dr Smith she will find the cure for pancreatic cancer.

LDN CONFERANCES

http://www.lowdosenaltrexone.org/conf2007.htm

This one was Vanderbilt University

Sincere thanks also to Cyndi Lenz and Adam Lenz who videotaped and photographed the entire conference, providing the multimedia files accessed through this webpage.

This is audio you should listen to -Dr Grossman

http://www.lowdosenaltrexone.org/_conf2007/T_Grossman.mp3

Listen to his talk about sugar and cancer at about 13:27

“Cancer cells can only eat sugar” The first thing that Dr Grossman does in his practice is put people on a low sugar diet.

Dr Mercola on sugar feeding cancer

http://www.mercola.com/article/sugar/sugar_cancer.htm

The 1931 Nobel laureate in medicine, German Otto Warburg, Ph.D., first discovered that cancer cells have a fundamentally different energy metabolism compared to healthy cells. The crux of his Nobel thesis was that malignant tumors frequently exhibit an increase in anaerobic glycolysis — a process whereby glucose is used as a fuel by cancer cells with lactic acid as an anaerobic byproduct — compared to normal tissues.1 The large amount of lactic acid produced by this fermentation of glucose from cancer cells is then transported to the liver. This conversion of glucose to lactate generates a lower, more acidic pH in cancerous tissues as well as overall physical fatigue from lactic acid buildup.2,3 Thus, larger tumors tend to exhibit a more acidic pH.4

This inefficient pathway for energy metabolism yields only 2 moles of adenosine triphosphate (ATP) energy per mole of glucose, compared to 38 moles of ATP in the complete aerobic oxidation of glucose. By extracting only about 5 percent (2 vs. 38 moles of ATP) of the available energy in the food supply and the body’s calorie stores, the cancer is “wasting” energy, and the patient becomes tired and undernourished. This vicious cycle increases body wasting.5 It is one reason why 40 percent of cancer patients die from malnutrition, or cachexia.6

Hence, cancer therapies should encompass regulating blood-glucose levels via diet, supplements, non-oral solutions for cachectic patients who lose their appetite, medication, exercise, gradual weight loss and stress reduction. Professional guidance and patient self-discipline are crucial at this point in the cancer process. The quest is not to eliminate sugars or carbohydrates from the diet but rather to control blood glucose within a narrow range to help starve the cancer and bolster immune function.

From the University of California Television

Irony

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