Prescription drugs – a serious concern

Physicians find gastrointestinal conditions (especially IBS) difficult to treat. Chemical drugs have side effects and may worsen gastrointestinal disease without satisfactory long-term effects. The use of nonsteroidal anti-inflammatory drugs can damage epithelial cell cytoskeletons that regulate tight junctions of the intestinal single-cell-layer gastrointestinal mucosa, causing leaky gut. Alternatively, probiotics have anti-inflammatory effects and reverse intestinal permeability.

Proton pump inhibitors (PPIs) used for ulcers, gastroesophageal reflux (GERD), and indigestion, for example, is not a viable solution and do not address the root cause. Reducing stomach acid, may result in hypochlorydria, increasing susceptibility to nutrient deficiencies, as well as changes in the microbiome. More concerning is the 44% increased risk of dementia.1  and kidney disease2 when using PPIs.

Continuous use of histamine-2 receptor antagonists (H2 blockers), like Pepcid, Zantac and Tagamet, increases the risk of cognitive impairment by 242%.3 And many people are prescribed both PPI’s and H2 blockers.

Using PPIs for 5 years, increase your risk of hip fractures by 62%4. PPIs increase your risk of heart attack by 16% while doubling your risk of dying of a heart attack compared to people not on PPIs5.

References:

  1. JAMA Neurol 2016; doi:10.1001/jamaneurol.2015.4791
  2. AMA Intern Med 2016;176: doi:10.1001/jamainternmed.2015.7193
  3. Journal of the American Geriatrics Society 2007;551248-53
  4. CMAJ 2008;179:319-26
  5. PL0S One 2015;10:e0124653

The gut and brain connection

For many, the symptoms of gut disorders go hand in hand with stress and anxiety – we experience the effects of the brain on the gut every day. Furthermore via signalling, the gut plays a specific role in the regulation of behaviour and mood.1,2 The gastrointestinal tract is sometimes described as our second brain (enteric nervous system) and is controlled by its own complex nervous system, comprising more neurotransmitters than in the entire brain.

It is the connection and bidirectional communication between the gut and brain through the vagus nerve (gut-brain axis)3 that regulate, control and modulate changes in the activity of hypothalamic-pituitary-adrenal axis and changes in the brain, such as memory performance and cognition.

References:

  1. Forsythe P, Sudo N, Dinan T, Taylor VH, Bienenstock J. Mood and gut feelings. Brain Behav Immun2010; 24: 9–16.
  2. Mayer EA. Gut feelings: the emerging biology of gut-brain communication. Nat Rev Neurosci2011; 12: 453–466.
  3. Cryan JF, O’Mahony SM. The microbiome-gut-brain axis: from bowel to behavior. Neurogastroenterol Motil2011; 23: 187–192.

Gut barrier permeability

In addition to its critical role in immune health, the intestinal single-cell-layer gastrointestinal mucosa absorbs nutrients while acting as a barrier to macromolecules and toxins. The gut microflora provide an additional barrier by competing with pathogens and producing a muco-polysaccharide matrix, known as the biofilm. The thickness of the biofilm and its spread, decreases with inflammation, increasing intestinal permeability1 (leaky gut).

Alterations in barrier function through intestinal permeability can have profound effects on anatomic and immunologic barriers to disease2. Intestinal permeability can lead to immune activation, increased inflammatory cytokine production, increased intestinal inflammation3 and tissue damage. Chronic inflammation of the small intestine injures the villi, reducing the available surface area of the small intestine, resulting in a tremendous impact upon vitamin and nutrient absorption.

Stress significantly increases intestinal permeability, and with that the overall toxic burden, and is a leading precursor for many autoimmune diseases. One of the modes of action of the actives used in Progast® appears to interact with your neurological system and counteract the effects of stress and other psychosocial factors via your gut-brain axis.

References:

  1. https://www.ncbi.nlm.nih.gov/pubmed/16908512
  2. https://www.ncbi.nlm.nih.gov/pubmed/12394645
  3. https://www.ncbi.nlm.nih.gov/pubmed/11907349
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