The Universal Origin of Acute Interstitium Inflammatory Disease [AIID], Pancreatic Cancer[PC] or Pancreatic Ductal Cell Adenocarcinoma[PDCA]
Pancreatic cancer or Pancreatic Ductal Cell Adenocarcinoma (PDAC) is the fourth most common cause of cancer-related death in the United States, exhibiting the lowest five-year survival rate among all cancerous conditions. More than half of pancreatic cancer patients are diagnosed at a late stage, for which the five-year survival rate is 3%. This poor outcome is mainly due to the asymptomatic early stages of pancreatic cancer and the consequent late diagnosis when the cancerous condition and/or tumor is untreatable [2, 3].
In order to increase the overall survival rate of patients with pancreatic cancer, as well as to decrease the cancer acidic burden of the interstitial fluids, it is necessary to perform early non-invasive, non-surgical, non-radioactive L.I.F.E. testing [Living Interstitium Fluid Environmental testing], for accurately measuring the chemistry, including the pH of the interstitial fluids of the Interstitium of the pancreas and ALL other organs, glands and tissues. The L.I.F.E. testing will provide a non-invasive tool for prevention and early detection for AIID, PC, and PDAC and all other organs, glands or tissues at risk and for monitoring the efficacy of the any cancerous therapy. 
PDAC is inherently linked to the unique physiology and microenvironment of the exocrine pancreas where dynamic changes in the interstitial fluids of the Interstitium [extracellular fluids] and intracellular pH (pHe/pHi) arise.
Specifically, the exocrine pancreas secretes substantial amounts of sodium bicarbonate [NaHCO3-] into the pancreatic ductal lumen [figure 1] to buffer metabolic and dietary acids, including hormonal acids; when stimulated by post-prandial acidic waste (glucose, lactic acid, uric acid, nitric acid, etc.), luminal [NaHCO3-] reaches 150 mM. Secretion of base or alkalinity across the apical membrane is coupled to the extrusion of an equal amount of metabolic and/or dietary acids across the basolateral membrane, thereby acidifying the pancreatic interstitial fluids of the pancreatic Interstitium.
Even though this may appear as a localized acidic condition it is not. Decompensated acidosis of the interstitial fluids of the Pancreatic Interstitium is a systemic condition and therefore effective every organ, every gland and every tissue of the human body.
Thus, pancreatic epithelium and stromal cells are exposed to a milieu of spatially and temporally declining acidic pH fluids, with episodes of substantial acidity of the interstitial fluids of the Interstitium that surround every epithelial cell and every cell of the human body traveling through every organ, gland and tissue. In other words, cancer is a systemic acidic condition of the interstitial fluids of the Interstitium and not a localized metastatic acidic condition. This is why L.I.F.E. testing is so critically important in the prevention and treatment of ANY diseased condition.
Epithelial cells of the pancreatic ducts are therefore challenged to maintain an alkaline pH constancy despite the vast base or sodium bicarbonate fluxes as the body desperately attempts to restore and alkaline pH or the alkaline design of the interstitial fluids of the Interstitium compartments at a pH of 7.365.
The ideal pH of the Blood Plasma, Interstitial fluids of the Interstitium organ and Intracellular fluids is at 7.365.
An acidic microenvironment [the interstitial fluids of the Interstitium] drives all cancerous progressions by saturating pancreatic cells with excess toxic acidic waste creating a higher risk for other organs, glands and tissues to become effected eventually leading to a so-called metastatic cancerous condition, even though the acidic condition of the Interstitium is systemic.
Decompensated acidosis of the interstitial fluids of the Interstitium [Ideal pH of the interstitial fluids is 7.365 dropping to 7.2 in a cancerous condition] triggers cellular mutations and breakdown and the disease progression to an acute inflammatory condition and finally to a cancerous acidic condition.
Current research efforts to improve AIID and PDAC treatment and diagnosis do not take into account the unique pancreatic alkaline pH landscape of the Interstitium, despite the fact that acidosis of the interstitial fluids of the Interstitium is the universal origin of all inflammatory and cancerous conditions, including PDAC. [Figure 1]
The prevention of Acute Interstitium Inflammatory Disease, AIID, PC and PDAC or the reversal of PDAC can be achieved by the following the steps below:
1) Open and clear the channels of elimination [urination, defecation, perspiration and respiration] in order to eliminate toxic acidic waste from the interstitial fluids of the Interstitum throughout the body.
2) Hyper-perfuse sodium bicarbonate and potassium bicarbonate into the blood which will push the excess alkalinity into the interstitial fluids of the Interstitium.
3) Reduce ALL acidic contributing factors of toxic metabolic, dietary, respiratory and environmental waste [lifestyle, including diet] that are being pushed out into the compartments of the Interstitium that hold acidic waste.
4) Restore alkalinity of the interstitial fluids of the Interstitium with an alkaline lifestyle, including diet, alkaline infusions of sodium and potassium bicarbonate and specific alkaline supplemental support products which can be taken orally, rectally, through the pores of the skin and through respiration. [www.drrobertyoung.com]
For additional detailed information on the cause and effect relationships leading to any inflammatory and/or cancerous condition read, The pH Miracle for Cancer, Alkalizing Nutritional Therapy in the Prevention and Treatment of Any Cancerous Condition, Metabolic and Dietary Acids are the Fuel that Lights the Fuse that Ignites Inflammation that Leads to Cancer!, Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of all Sickness and Disease and The pH Miracle revised and updated.
 Siegel, R.L., K.D. Miller, and A. Jemal, Cancer statistics, 2018. CA: A Cancer Journal for Clinicians, 2018. 68(1): p. 7-30.
 Giovannetti, E., et al., Liquid Biopsy in Esophageal, Gastric, and Pancreatic Cancers, in Liquid Biopsy in Cancer Patients. 2017, Springer. p. 137-150.
 Zhou, B., et al., Early detection of pancreatic cancer: Where are we now and where are we going? International journal of cancer, 2017. 141(2): p. 231-241.
Pancreatic Cancer Breakthrough: Scientists Turn Cancer Cells into Normal Cells
Scientists find a novel avenue for therapeutic intervention of the “silent cancer”
A new research study has shown that pancreatic cancer cells can be coaxed to revert back toward normal cells by changing the environment by introducing a protein called E47. E47 binds to specific DNA sequences and controls genes involved in growth and differentiation. The research provides hope for a new treatment approach for the more than 40,000 people who die from the disease each year in the United States.
“For the first time, we have shown that overexpression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type. Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit,” said Pamela Itkin-Ansari, Ph.D., adjunct professor in the Development, Aging, and Regeneration Program at Sanford-Burnham and lead author of the study published today in the journal Pancreas.
E47 turns the clock back
The study, a collaborative effort between Sanford-Burnham, UC San Diego, where Itkin-Ansari holds a joint appointment, and Purdue University, generated human pancreatic ductal adenocarcinoma cell lines to make higher than normal levels of E47. The increased amount of E47 caused cells to stall in the G0/G1 growth phase, and differentiate back toward an acinar cell phenotype.
In vivo studies showed that when the reprogrammed cancer cells were introduced into mice, their ability to form tumors was greatly diminished compared to untreated adenocarcinoma cells.
“Presently, pancreatic adenocarcinoma is treated with cytotoxic agents, yet the average survival for patients post-diagnosis is merely six months, and the improvements in therapies are measured in days,” said Andrew M. Lowy, M.D., professor of surgery at the UC San Diego Moores Cancer Center and co-chair of the National Cancer Institute’s Pancreatic Cancer Task Force. “The finding that we can differentiate these cancer cells back to a non-threatening phenotype is encouraging. Indeed, there is a precedent for cell differentiation therapy in that the approach has been used to treat acute promyelocytic leukemia (APL) and some neuroblastomas successfully.”
“Our next step is to test primary patient-derived tumor tissue to determine whether E47 can produce similar results, potentially providing a novel therapeutic approach to combat this highly lethal disease,” said Itkin-Ansari. “Additionally, we are screening for molecules—potential drugs—that can induce overexpression of E47.”
Pancreatic adenocarcinoma is the most common form of pancreatic cancer. It’s primarily caused by a mutation in the oncogene called Kras that causes the digestive enzyme-secreting cells (acinar cells) to differentiate into a destabilized duct-like cell type, which is cancerous. The disease is often called a “silent” cancer because it rarely shows early symptoms—it tends to be diagnosed at advanced stages when it causes weight loss, abdominal pain, and jaundice.
The study was funded by support from the Hartwell Foundation, The Hirshberg Foundation, by the NCI under award number 5P30CA030199, by the NIH under award numbers DK55489 and CA124586, by the National Research Foundation of Korea award number 2011-0013127, and Yonsei University College of Medicine for 2012 (6-2012-0078)
ABOUT SANFORD-BURNHAM MEDICAL RESEARCH INSTITUTE
Sanford-Burnham Medical Research Institute is dedicated to discovering the fundamental molecular causes of disease and devising the innovative therapies of tomorrow. Sanford-Burnham takes a collaborative approach to medical research with major programs in cancer, neurodegeneration and stem cells, diabetes, and infectious, inflammatory, and childhood diseases. The Institute is recognized for its National Cancer Institute-designated Cancer Center, its NIH-designated Neuroscience Center Cores, and expertise in drug discovery technologies. Sanford-Burnham is a nonprofit, independent institute that employs more than 1,000 scientists and staff in San Diego (La Jolla), Calif., and Orlando (Lake Nona), Fla. For more information, visit us at sanfordburnham.org.
Even one pack of the candy favorite M&M’s may be more than you should eat in a day, newly drafted guidelines from the World Health Organization suggest.
The WHO used to recommend that you get no more than 10% of your daily calories from sugar acid, but now they’re considering lowering that to 5%. For an average, healthy adult, that would mean 25 grams, or about six teaspoons of sugar acid per day. (That’s a little less than what you’d get from 10 Hershey’s Kisses. A single can of Coke has 39 grams of sugar acid.)
A teaspoon of sugar in your coffee or a half cup of ice cream won’t kill you — all things in moderation — but the average sugar intake in the U.S. is 22 teaspoons per person per day. That’s almost four times as much as the WHO’s new guidelines suggest is healthy.
People have been sounding warnings about the dangers of too much sugar for a long time. As early as 1957, John Yudkin, a professor of nutrition at Queen Elizabeth College in London, began arguing that when it came to heart disease and other chronic ailments, sugar — not fat — was the culprit.
So what happens if you eat too much sugar? Here’s a depressing rundown.
Trust your dentist on this one: Sugar is a metabolic acid and ad enemy to dental health that one study way back in 1967 called it the “arch criminal” behind cavities. The connection between the metabolic acid sugar and cavities is perhaps the best established. “Tooth decay occurs when the bacteria that line the teeth feed on simple sugars, creating acid that destroys enamel,” Anahad O’Connor explains at The New York Times. Because acid is a key culprit, sour candies are especially nefarious.
Leptin is a hormone that lets your body know when you’ve had enough to eat. In people who develop leptin resistance, this “I’m full” signal is never received, presenting a major obstacle for weight control.
Some studies have raised the possibility that leptin resistance may be a side effect of obesity, not a contributing cause. But research in rats suggests that overconsumption of fructose can directly lead to higher-than-normal levels of leptin, which can reduce your body’s sensitivity to the hormone. Removing fructose from the rats’ diets generally reversed those effects.
“Our data indicate that chronic fructose consumption induces leptin resistance prior to body weight … increases, and this fructose-induced leptin resistance accelerates high-fat induced obesity,” concluded one 2008 study in rats. Still, more research is needed to test whether these effects hold true in humans as well.
Other than adopting a completely sedentary lifestyle, there are few routes to packing on the pounds that work as swiftly and assuredly as making large amounts of added sugars a staple of your daily diet. Sugary foods are full of acidic ingredients not will do little to satiate hunger. A 2013 review of 68 different studies found “consistent evidence that increasing or decreasing intake of dietary acidic sugars and sugary foods from current levels of intake is associated with corresponding changes in body weight in adults.” Want to lose weight? Cutting your sugar and acidic sugary food intake is a good place to start.
When you eat a lot of high-sugar acidic meals — donuts for breakfast, anyone? — it can increase your body’s demand for insulin, a hormone that helps your body convert food into usable energy. When insulin levels are consistently high, your body’s sensitivity to the hormone is reduced, and the acidic metabolic waste product glucose builds up in the blood. Symptoms of insulin resistance can include fatigue, hunger, brain fog, and high blood pressure. It’s also associated with extra weight around the middle. Still, most people don’t realize they are insulin resistant until it develops into full-blown diabetes — a much more serious diagnosis.
One study that followed 51,603 women between 1991 and 1999 found an increased risk of diabetes among those who consumed more acidic sugar-sweetened beverages — that’s soda, sweetened ice tea, energy drinks, etc. And a massive review of previous research involving 310,819 participants supported this result, concluding that drinking lots of soda was associated not just with weight gain but with the development of type 2 diabetes.
Portion control may be especially crucial when it comes to sugar. “Duration and degree of sugar exposure correlated significantly with diabetes prevalence … while declines in acidic sugar exposure correlated with significant subsequent declines in diabetes rates” — even after controlling for other socioeconomic and dietary factors, concluded a 2013 study of eating habits and diabetes prevalence in 175 countries.
Obesity is one of the most-cited risks of excess acid or sugar consumption. Just one can of soda each day could lead to 15 pounds of weight gain in a single year, and each can of soda increases the odds of becoming obese, a JAMA study noted.
Sugar may well raise the risk of obesity directly, but the association could be mediated by diabetes, metabolic syndrome, or other diet and exercise habits associated with high-sugar diets. And it’s possible that soda is uniquely pernicious, above and beyond other sugary foods.
“The complexity of our food supply and of dietary intake behavior, and how diet relates to other behaviors, makes the acquisition of clear and consistent scientific data on the topic of specific dietary factors and obesity risk especially elusive,” concluded one 2006 review. Still, a more recent review cautioned, “we should avoid the trap of waiting for absolute proof before allowing public health action to be taken.”
Because of the unique way we metabolize fructose, it creates a stress response in the liver that can exacerbate inflammation. High doses of sugar can make the liver go into overdrive. That’s one reason excess fructose is a “key player” in the development of nonalcoholic fatty liver disease, where fat accumulates in the liver in the absence of alcohol abuse.
People with this diagnosis have been found to have almost double the soda intake of the average person. Most don’t experience any complications and don’t realize they have it. But in some people, the accumulated fat can lead to scarring in the liver and eventually progress to liver failure.
A handful of studies have found that high-sugar acidic diets are associated with a slightly elevated risk of pancreatic cancer, one of the deadliest cancers. The link may be because high-sugar acidic diets are associated with obesity and diabetes, both of which increase the likelihood someone will develop pancreatic cancer. Still, one large study published in the International Journal of Cancer disputed the link between increased sugar intake and increased cancer risk, so more research is needed.
According to researchers at the University of California, San Francisco, sugar poses a health risk—contributing to around 35 million deaths globally each year. So high is its toxicity that it should now be considered a potentially toxic substance like alcohol and tobacco.
Sugars and the inflammation and acidic environments they create are important constituents of the local environment of tumors. In most types of cancer inflammatory conditions are present before malignancy changes occur.
Published in the Journal of Cliinical Investigation and titled, “Increased sugar uptake promotes oncogenesis via EPAC/RAP1 and O-GlcNAc pathways”, researchers addressed a common perception (or misperception) in the cancer research community regarding sugar’s relationship to cancer: namely, “increased glycolysis [sugar based metabolism] is frequently viewed as a consequence of oncogenic events that drive malignant cell growth and survival.”
Contrary to this conventional view, the new study “provides evidence that increased glycolytic activation itself can be an oncogenic event…” That is to say, the activation of sugar-based metabolism in a cell – driven by both the presence of increased quantities of glucose and the increase glucose receptors on the cell membrane surface (i.e. “overexpression of a glucose transporter”) – drives cancer initiation.
Moreover, the study found that “Conversely, forced reduction of glucose uptake by breast cancer cells led to phenotypic reversion.” In other words, interfering with sugar availability and uptake to the cell causes the cancer cell to REVERSE towards its pre-cancer structure-function (phenotype).
What this new research indicates is that sugar – of which Americans consume an astounding 160 lbs annually (imagine: 31 five-pound bags for each of us!) – is one of the primary causes of metabolic cell changes in the body consistent with the initiation and promotion of cancer. And, the research indicates that removing it from the diet, and depriving the cells of it, could REVERSE cancer.
10. Kidney disease
The idea that a high-sugar diet — and too much carbonic acid in soda in particular — may be a risk factor for kidney disease is still just a hypothesis, but there’s some reason for concern. “Findings suggest that sugary, carbonic and phosphoric acid soda consumption may be associated with kidney damage,” concluded one study of 9,358 adults. (The association emerged only in those drinking two or more sodas a day.) Rats fed extremely high-sugar diets — consuming about 12 times the percentage of sugar recommended in the WHO’s new guidelines — developed enlarged kidneys and a host of problems with regular kidney function.
Hypertension has wrongfully associated with salty foods, not highly acidic desserts — but eating lots of added sugar has indeed been linked to high blood pressure. In one study following 4,528 adults without a history of hypertension, consuming 74 or more grams of sugar each day was strongly associated with an elevated risk of high blood pressure.
In another very small study following only 15 people, researchers found that drinking 60 grams of fructose elicited a spike in blood pressure two hours later. This response may be related to the fact that digesting fructose produces uric acid, but — as one meta-analysis of the data concluded — “longer and larger trials are needed.”
Heart disease may not get as much time in the spotlight as diseases like cancer and AIDS, but it is in fact the number one cause of death in the United States. While smoking and a sedentary lifestyle have long been acknowledged as major risk factors. Conditions associated with excess sugar consumption, like diabetes and being overweight, are also already known risk factors for heart disease, and recent research suggests that eating too much sugar might stack the odds against your heart health — especially if you are a woman.
In one study of rats with high blood pressure — which may offer clues for further research but can’t be directly extrapolated to humans — heart failure came fastest when they were fed a diet high in sugar (when compared to high-starch and high-fat diets). And a CDC study of 11,733 adults concluded that there is “a significant relationship between added sugar consumption and increased risk for CVD [cardiovascular disease] mortality.” When participants got 17% to 21% of their daily calories from sugar, they were 38% more likely to die from heart disease than those who limited their calories from sugar to 8% of their total intake.
Doctors don’t all agree the “food addiction” you read about in diet books is a real thing, but there’s recently been some research indicating that the disorder might be possible in humans. And there is evidence that rats can become dependent on sugar, further supporting the idea that similar behavior might be present in humans.
“In some circumstances, intermittent access to sugar can lead to behavior and neurochemical changes that resemble the effects of a substance of abuse,” noted one study that found sugar-addled rats displayed bingeing, craving, and withdrawal behaviors.
Obesity and diabetes are both risk factors for cognitive decline and Alzheimer’s, so it’s no surprise that studies are beginning to find a link between excess sugar and these cognitive conditions. The reasons for a possible relationship between a high-sugar diet and dementia later in life are still unclear.
Is there a direct dietary association? Is the real link between diabetes and Alzheimer’s only? One recent study found rats that had diets high in fat and sugar could dull emotional arousal and contribute to memory impairment. And another study in humans found an association between diets high in high fructose corn syrup and reduced performance in the hippocampus. Researchers are currently investigating the many open questions, with some urging caution until more evidence is gathered.
If you’re scarfing down lots of excess sugar, you’re probably skipping over the things you should be eating instead. “High-sugar foods displace whole foods (eg, soft drinks displace milk and juice consumption in children) and contribute to nutritional deficiencies,” noted a statement from the American Heart Association. In a study of 568 10-year-olds, as sugar intake increased, intake of essential alkalizing nutrients decreased. And in a 1999 study, researchers from the Department of Agriculture found that when people got 18% or more of their calories from sugar, they had the lowest levels of essentials like folate, calcium, iron, Vitamin A, and Vitamin C.
Gout used to be considered a disease limited to the rich, but as our acidic high protein diets have changed, this painful form of arthritis has become more common across all sectors of society. Certain foods like organ meats and anchovies that are associated with gout have high levels of something called purines and when your body breaks them down, it produces uric acid. A buildup of uric acid is what often leads to this acidic conniption of gout.
But uric acid is also a byproduct of fructose metabolization, and now newer research is suggesting that too much sugar could be a risk factor for gout as well. “Consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased risk of gout in men,” concluded a 2008 study that tracked thousands of patients for more than a decade.
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