A fat cell has the capacity to expand 1,000 times, but we’re never told what causes the expansion – GAS PRESSURE.

Medical researchers are unable to locate any excess gas in the intestines of patients who complain of “gas pain” and abdominal swelling, so doctors sometimes attribute such pain and swelling to “hysteria.”

When doctors palpate the abdominal region, they must presume that a bloated timpanites is ECTOPLASM since they refuse to admit it could be protoplasm.

Gastroenterologists are looking for gas in all the wrong places.

It’s in the cells of the belly, not in the hollows of the intestines.

The greater omentum of your abdomen is an AIR MATTRESS – and it’s best left uninflated.

Ironically, the only medical books acknowledging “bloat” are veterinary manuals.

For example, The Merck Veterinary Manual, Seventh Edition, edited by Clarence M. Fraser, B.S.A., D.M.V., M.V. Sc., 1991, deals with “bloat” in lambs on pages 160-161, ruminant animals on pages 163-166, and dogs and small animals on pages 234-236.

If an animal’s life-threatening emergency crisis known as gastric dilatation-volvulus syndrome, or GDV, is toned down to a preclinical condition and applied to humans, it has distinct correlations to human “bloat.”

In the words of the aforementioned 1991 edition of The Merck …

“Ingestion of food and water, and aerophagia initiate gastric dilatation. Vigorous exercise or altered body position appears to escalate the process. Gastric volvulus prevents effective vomiting, but still allows air to be swallowed (and an orogastric tube to be passed). The pylorus is also obstructed. Gastric dilatation leads to increased intra-abdominal pressure, which significantly reduces caudal vena caval and portal venous blood flow. Cardiac output diminishes because of decreased venous return. As the dilatation and volvulus progress, gastric arterial blood flow may be compromised. Stasis of blood and tissue hypoxia result in sequestration of fluid and endotoxin accumulation in the splanchnic organs. Arterial hypotension causes decreased coronary blood flow and myocardial hypoxia. Hence, cardiogenic, hypovolemic, and endotoxic forms of shock all contribute to the physiologic derangements seen in GDV. Additional complications include production of myocardial depressant factor from the hypoxic pancreas, hypoxemia due to reduced diaphragmatic excursion (hypoventilation) and altered pulmonary gas exchange, multiple acid-base abnormalities, and disseminated intravascular coagulation (DIC).”

Applied to the CELLS of human beings, a brand-new dimension of etiology and a unifying factor is added to countless mysterious cardiac, pancreatic, gastric, esophageal, pyloric, intestinal, and hepatic ailments.
Michael Tennesen (“Is It Really Heartburn?,” Prevention, Mar. 2002) wrote ….

“‘Excess fat inside the belly puts pressure on the stomach and pushes its contents up into the esophagus,’ explains Eugene Cho, MD, an assistant professor of surgery at the University of Maryland Medical Center in Baltimore. A study in England found that patients who lost an average of 9 lb experienced a 75% reduction in symptoms of GERD.”

For more info on the perils of abdominal distension and intra-abdominal pressure, consult Arthur Agatston, M.D., “Lose Belly Fat and Save Your Life: How to Whittle Your Middle,” Bottom Line/Personal, Jul. 1, 2003; Steve Blechman & Thomas Fahey, Ed.D., “Abdominal Fat Can Kill You,” Muscular Development, Feb. 2004; Atom Bergstrom, Book of Bloat (It’s a Gas!): How to Double Your Calories and STILL Lose Weight, 1989, 2009, etc.