Poisoning The Pancreas With PUFAs

Ouch The idea that sugar causes the pancreatic diseases – although popular – is unscientific and unsubstantiated. Experiments have consistently shown that the unsaturated fats damage the pancreas and promote the development of pancreatic cancer.

“…diets high in unsaturated fat appear to promote pancreatic carcinogenesis…while a diet high in saturated fat failed to show a similar degree of enhancement…”

Cholecystokinin (CCK) is a gastrointestinal hormone that has been demonstrated to have a direct role in this process.

“Research…suggests that CCK has a role in the formation of the desmoplastic microenvironment surrounding pancreatic cancer…”

“In human pancreatic cancers, CCK receptors are ubiquitous and over-expressed and activation of these receptors with CCK or its related peptide gastrin, stimulate tumor growth…it may be possible to use CCK receptor antagonists as a chemopreventive treatment for those patients who are at high risk for pancreatic cancer…”

Studies have exhibited the fact that the unsaturated fats more strongly stimulate CCK release than the saturated fats and this may in part explain their carcinogenic effect.

“The finding that unsaturated fats are stronger stimulants of CCK release than saturated fats may explain the promotion of pancreatic carcinogenesis in rats by unsaturated but not saturated fats and may support the role of CCK in this effect.”

Although oleic acid – the main fatty acid in olive oil – promotes CCK release at a rate slightly slower than the more highly unsaturated fats like sunflower or safflower oil, it is still a far more powerful stimulant of the release of this hormone than is saturated fat.

“The…monounsaturated fatty acid oleic acid…produced a significantly greater integrated CCK response than that of the saturated fatty acid stearic acid.”

Cancer in general is an inflammatory disease driven largely by chronic stress. Pancreatic cancer is associated with increased levels of cortisol and adrenalin as well as numerous other stress substances. Aside from the inflammatory, carcinogenic and diabetogenic effects of the polyunsaturated fats, prolonged release of the stress related hormones are known to interfere with the ability of the pancreas to secrete insulin, and to encourage pancreatic disease in general.

“Our data show…that neurotransmitter responses to psychological stress significantly induced multiple signaling pathways that regulate the proliferation, migration, angiogenesis and apoptosis of pancreatic cancer, resulting in a significant promotion of tumor growth…”

Inflammation promotes chronic pancreatitis, a condition which very often precedes pancreatic cancer. Increased levels of bacterial endotoxin (LPS) passing into circulation into the main system interact with the polyunsaturated fats – and the stress related hormones – and are an important factor causing the systemic rise of inflammation, and the eventual onset and metastasis of cancer of the pancreas.

“Chronic pancreatitis…is considered to be the single most important cause for development of pancreatic cancer…evidence suggests that inflammation and oxidative stress play pivotal roles in the development of…conditions like pancreatitis.”

“Inflammation plays a multifaceted role in cancer progression…We have shown that lipopolysaccharide (LPS)…increased the invasive ability of pancreatic cancer cells.”

Chronic stress and anything else that interferes with metabolism and digestive function increases the likelihood that bacteria will grow in number, moving further up into the small intestine where they create additional inflammatory issues, and directly promote an increased release of serotonin. Serotonin has been shown to play a role in the development of pancreatitis, as well as many kinds of cancer.

“These results suggest that endogenously released 5-HT [serotonin] aggravate[s]…pancreatitis. We propose that selective 5-HT2A antagonists may provide a new therapy for acute pancreatitis.”

Removing sugar from your diet can very quickly promote an increase in the release of the polyunsaturated free fatty acids out of storage and begin a process of rising secretion of a cascade of cancer promoting substances starting with cortisol and adrenalin, and including endotoxin, serotonin, estrogen, prolactin and other inflammation promoting things.

“An intriguing finding was the inverse association of added sucrose and added fructose with pancreatic cancer risk in women…”

The combination of rising levels of stress and the restriction of sugar can gradually suppress mitochondrial energy and thyroid metabolism. Proper thyroid function is a central factor in stress management and has been demonstrated to protect against the progression of pancreatic cancer.

“T3 groups showed significantly reduced tumor volume and weight…suggesting the potential value of thyroid hormone in pancreatic cancer therapy.”

Avoiding the polyunsaturated fats and the digestion interfering grains, beans, nuts and fibrous foods and including sufficient amounts of easy to assimilate protein and sugar – from sweet ripe fruits, fruit juice, milk, honey and white sugar – is one approach to protection against the onset and growth of pancreatic cancer as well as pancreatic disease in general.

Some other things which can be protective against pancreatic cancer include aspirin, niacinamide, a few kinds of antibiotics, emodin, sodium bicarb and a variety of thyroid supporting and stress reducing anti-inflammatory tools.

See more here

Regulation of pancreatic cancer by neuropsychological stress responses: a novel target for intervention.

Saturation of fat and cholecystokinin release: implications for pancreatic carcinogenesis.

Cholecystokinin and pancreatic cancer: the chicken or the egg?

Cholecystokinin receptor antagonist halts progression of pancreatic cancer precursor lesions and fibrosis in mice.

Promotion by unsaturated fat of azaserine-induced pancreatic carcinogenesis in the rat.

Aspirin therapy reduces the ability of platelets to promote colon and pancreatic cancer cell proliferation: implications for the oncoprotein c-MYC.

Thyroid hormone inhibits the growth of pancreatic cancer xenograft in nude mice

Possible involvement of endogenous 5-HT in aggravation of cerulein-induced acute pancreatitis in mice.

Sugars in diet and risk of cancer in the NIH-AARP Diet and Health Study

Aspirin Use and Reduced Risk of Pancreatic Cancer

Inhibition of De Novo NAD+ Synthesis by Oncogenic URI Causes Liver Tumorigenesis through DNA Damage

Neutralization of Tumor Acidity Improves Antitumor Responses to Immunotherapy

Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: treating cancer like an infectious disease.

Hypothyroidism in utero stimulates pancreatic beta cell proliferation and hyperinsulinaemia in the ovine fetus during late gestation

Effect of emodin in attenuating endoplasmic reticulum stress of pancreatic acinar AR42J cells.

Emodin has a protective effect in cases of severe acute pancreatitis via inhibition of nuclear factor‑κB activation resulting in antioxidation.

In vitro effects of emodin on peritoneal macrophage intercellular adhesion molecule-3 in a rat model of severe acute pancreatitis/systemic inflammatory response syndrome

Chronic stress in mice remodels lymph vasculature to promote tumour cell dissemination

Lipopolysaccharide directly affects pancreatic acinar cells: implications on acute pancreatitis pathophysiology.

Lipopolysaccharide (LPS) increases the invasive ability of pancreatic cancer cells through the TLR4/MyD88 signaling pathway.

Inflammatory stimuli promote growth and invasion of pancreatic cancer cells through NF-κB pathway dependent repression of PP2Ac

Inflammation-induced ROS generation causes pancreatic cell death through modulation of Nrf2/NF-κB and SAPK/JNK pathway.

Necro-inflammatory response of pancreatic acinar cells in the pathogenesis of acute alcoholic pancreatitis

LPS Induced miR-181a Promotes Pancreatic Cancer Cell Migration via Targeting PTEN and MAP2K4

Chronic alcohol exposure exacerbates inflammation and triggers pancreatic acinar-to-ductal metaplasia through PI3K/Akt/IKK

Alcohol Exacerbates LPS-Induced Fibrosis in Subclinical Acute Pancreatitis

Role of bacterial infections in pancreatic cancer

Free Fatty Acids Block Glucose-Induced β-Cell Proliferation in Mice by Inducing Cell Cycle Inhibitors p16 and p18

β-Cell Lipotoxicity After an Overnight Intravenous Lipid Challenge and Free Fatty Acid Elevation in African American Versus American White Overweight/Obese Adolescents

Long-term exposure of INS-1 rat insulinoma cells to linoleic acid and glucose in vitro affects cell viability and function through mitochondrial-mediated pathways.

Revisiting the ALA/N ( a -Lipoic Acid/Low- Dose Naltrexone) Protocol for People With Metastatic and Nonmetastatic Pancreatic Cancer: A Report of 3 New Cases

Cyclooxygenase-derived proangiogenic metabolites of epoxyeicosatrienoic acids.


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