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Proton Pump Inhibiters Promote Acid Rebound Effects

Friday, 09 September 2011 by | Comments: 1

Diagram depicting the major determinants of gastric acid secretion, with inclusion of drug targets for peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD).

Many millions of people are currently prescribed proton pump inhibitors (PPI’s) to manage excess acid production in the stomach. There are many disease and adverse health related outcomes linked to people taking PPI’s.

The associations of fractures of hip, wrist, forearm and other sites appear weak and only slightly higher than the risks in control populations matched for age. They may increase with drug exposure, but probably do so only in individuals in whom other risk factors are also operational (smoking, alcohol, poor nutrition, steroids, etc.).

The Role of HCL In Gastric Function And Health

Thursday, 20 January 2011 by | Comments: 5

Many Nutritional Therapists and their patients are interested in the effects and consequences of altered hydrochloric acid (HCL) production by virtue of the high frequency of proton pump inhibitors that are prescribed annually – $13.6 billion world wide sales in 2009.[1] These medications are designed to limit the production of HCL and reduce gastric distress. They have potent anti secretory effects on gastric acid. They block the terminal step in acid production by irreversibly inhibiting the function of the hydrogen-potassium adenosine triphosphatase present on the luminal aspect of parietal cell membranes in the stomach.

Most patients accept the consensus view that their GI symptoms are related to an excess of HCL not a deficiency and take these medications willingly. The consequences can be an increase in gastric infection from B12 deficiency,[2] Clostridium difficile,[3] SIBO,[4] increased risk of death, increased risk of fracture.[5]

Antony Haynes reviews the mechanisms and investigations that can assist you in supporting your patients and help define their need to supplement HCL due to a relative deficiency or to continue to manage their condition through inhibition.

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Calcium deficiency in the elderly is associated with low gastric acid secretion and bone loss. A new study linking defects in gastric acid secretion with bone destruction and impaired mineralization bolsters the view that calcium supplements can prevent these bone defects-but do they all work. This paper suggests that altered acidification of the stomach and specific gene deficiencies will dictate the form of calcium supplementation most suitable for the reduction and resolution of osteoporosis.

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