Worm Menu, War Menu or Worm in You?

You have heard it said, “You are what you eat.” Well I believe it better said, “You eat what you are fed by those you are feeding, and then you eat them.”

Feces, also spelled faeces, also called excrement, solid bodily waste discharged from the large intestine through the anus during defecation. Feces are normally removed from the body one or two times a day. About 100 to 250 grams (3 to 8 ounces) of feces are excreted by a human adult daily.

Normally, feces are made up of 75 percent water and 25 percent solid matter. About 30 percent of the solid matter consists of dead bacteria; about 30 percent consists of indigestible food matter such as cellulose; 10 to 20 percent is cholesterol and other fats; 10 to 20 percent is inorganic substances such as calcium phosphate and iron phosphate; and 2 to 3 percent is protein.

Cell debris shed from the mucous membrane of the intestinal tract also passes in the waste material, as do bile pigments (bilirubin) and dead leukocytes (white blood cells). The brown colour of feces is due to the action of bacteria on bilirubin, which is the end product of the breakdown of hemoglobin (red blood cells). The odour of feces is caused by the chemicals indole, skatole, hydrogen sulfide, and mercaptans, which are produced by bacterial action.

Many diseases and disorders can affect bowel function and produce abnormalities in the feces. Constipation is characterized by infrequent evacuations and the production of excessively hard and dry feces, while diarrhea results in frequent defecation and excessively soft, watery feces. Bleeding in the stomach or intestines may result in the passage of blood with the stool, which appears dark red, tarry, or black. Fatty or greasy stools usually indicate pancreatic or small-intestine afflictionsTyphoidcholera, and amoebic dysentery are among diseases spread by the contamination of food with the feces of infected persons.

Biofilm: What is it and how to get rid of it.

~Content Source

Most bacteria are present in biofilms, not as single-acting cells

The popular image of bacteria depicts single cells floating around, releasing toxins and damaging the host. However, most bacteria do not exist in this planktonic form in the human body, but rather in sessile communities called biofilms. To form a biofilm, bacteria first adhere to a surface and then generate a polysaccharide matrix that also sequesters calcium, magnesium, iron, or whatever minerals are available.

Within a biofilm, one or more types of bacteria and/or fungi share nutrients and DNA and undergo changes to evade the immune system. Since it requires less oxygen and fewer nutrients and alters the pH at the core, the biofilm is a hostile community for most antibiotics. In addition, the biofilm forms a physical barrier that keeps most immune cells from detecting the pathogenic bacteria (12).

The current model of care misses the mark

The current model of care usually assumes acute infections caused by planktonic bacteria. However, since the vast majority of bacteria are hidden in biofilms, healthcare providers are treating most illnesses ineffectively. According to the NIH, more than 80 percent of human bacterial infections are associated with bacterial biofilm (3). While planktonic bacteria can become antibiotic resistant through gene mutations, a biofilm is often antibiotic resistant for many reasons—physical, chemical, and genetic. Treating illnesses associated with biofilms using antibiotics is an uphill battle. For example, in patients suffering from IBD, antibiotics appear initially to work, only to be followed by a “rebound,” where the symptoms again flare up, presumably due to bacteria evading the antibiotic within a biofilm (4).

According to the NIH, more than 80% of human bacterial infections are associated with biofilms.

Biofilms are hidden in the nasal passageways and GI tract

Biofilms are well-known problems associated with endoscopic procedures, vascular grafts, medical implants, dental prosthetics, and severe dermal wounds. Biofilms found along the epithelial lining of the nasal passageways and GI tract are less understood.

The GI tract is an ideal environment for bacteria, fungi, and associated biofilms because of its huge surface area and constant influx of nutrients (4). For protection, the GI epithelium is lined with viscoelastic mucus, but it can be damaged in patients with excessive inflammation, IBD, and other conditions. This creates an opportunity for bacteria to attach to the surface and begin their biofilm construction. The epithelium to which it is attached is altered and often damaged (56).

Biofilms are difficult to diagnose

A number of problems make biofilms difficult to detect.

  • First, bacteria within the biofilm are tucked away in the matrix. Therefore, swabs and cultures often show up negative. Stool samples usually do not contain the biofilm bacteria, either.
  • Second, biofilm samples within the GI tract are difficult to obtain. The procedure would require an invasive endoscope and foreknowledge of where the biofilm is located. What’s more, no current procedure to remove biofilm from the lining of the GI tract exists.
  • Third, biofilm bacteria are not easily cultured. Therefore, even if you are able to obtain a sample, it may again test negative because of the microbes’ adapted lower nutrient requirements, rendering normal culture techniques null (7).
  • Fourth, biofilms might also play a role in the healthy gut,making it difficult to distinguish between pathogenic and healthy communities (47).

Although a culture might come back negative, the microbes in a biofilm could still be pumping out toxins that cause illness. Some clinicians look for mycotoxins in the urine to identify biofilms (8), but I am not impressed by the research behind it yet. Because the bacteria sequester minerals from the host, mineral deficiency is probably associated with the presence of biofilms, although mineral deficiencies are all too common in the general population to use this alone as a diagnostic criterion.

Biofilms in the background of many diseases

The medical community is increasingly dealing with antibacterial-resistant infections, with evidence of a biofilm at work behind the scenes:

  • Up to one-third of patients with strep throat, often caused by pyogenes, do not respond to antibiotics (9). In one study, all 99 strep throat-causing bacterial isolates formed biofilms (9).
  • Ten to 20 percent of people infected with Lyme disease, caused by burgdorferi, have prolonged symptoms, possibly due to antibiotic resistance and/or biofilm presence (1011).
  • Lupus flare-ups are induced by infection, inflammation, or trauma. In this autoimmune disease, cell death by NETosis instead of apoptosis turns the immune system against itself (12). Biofilms are suspected to be involved (13).
  • For chronic rhinosinusitis (CRS), “topical antibacterial or antifungal agents have shown no benefit over placebo in random controlled trials” (14). Bacterial and fungal biofilms are consistently found in these patients’ nasal passageways (1415).
  • Antibiotic treatment of irritable bowel disease (IBD) can work for a time, but flare-ups generally continue throughout a person’s life. Biofilms have been linked to both Crohn’s disease and ulcerative colitis (161718).

Biofilms have also been implicated in chronic ear infections, chronic fatigue syndrome, multiple sclerosis, and acid reflux (41920).

Peta Cohen, a pioneer in treating autism with a biomedical and nutritional approach, has found evidence of biofilms in autistic patients. When she disrupts the biofilm in these patients, she sees a huge “offload” of heavy metals in the urine and stool. Autistic individuals often have elevated mercury and lead levels (21). Bacteria aren’t choosy about which minerals they sequester during biofilm construction, and so Dr. Cohen’s explanation is that these patients also suffer from GI biofilms loaded with mercury and other heavy metals. Her experiences are as of yet only anecdotal; a PubMed search for “autism and biofilm” yields zero results. Check out my podcast here for what I believe are underlying causes of autism.

How to treat biofilms

Antibiotic after antibiotic for IBD. Corticosteroids for CRS. If a biofilm is at work, these standard “treatments” aren’t curing anything. Clinicians instead need to break down the biofilm, attack the pathogenic bacteria within, and mop up the leftover matrix, DNA, and minerals.

Biofilm disruptors are the first course of action. Enzymes such as nattokinase and lumbrokinase have been used extensively as coatings on implants to fight biofilms (2223). Cohen’s protocol recommends half a 50mg capsule of nattokinase and half of a 20mg capsule of lumbrokinase for small children with chronic strep throat and autism. Other promising enzymes include proteases, plasmin, and streptokinase (24).

Mucolytic enzyme N-acetylcysteine (NAC) is a precursor of glutathione and an antioxidant. Effective against biofilms on prosthetic devices, in vitro biofilms, and chronic respiratory infections (25262728), NAC is recognized as a “powerful molecule” against biofilms (29).

Lauricidin (other forms: monolaurin, lauric acid, and glycerol monolaurate) is a natural surfactant found in coconut oil that helps inhibit the development of biofilms (30). In my practice, I also use it as an option for a gentler antimicrobial agent.

Colloidal silver is effective at treating topical biofilms, such as in wound dressings (31,  32). Applications in vivo are still under research. Although used successfully to treat a sheep model of bacterial sinusitis (33), colloidal silver did not show the same effectiveness in a small human trial (3435).

I recommend Klaire Labs InterFase Plus and Kirkman Biofilm Defense, two commercial products formulated to effectively disrupt biofilm.

Antimicrobial treatments follow biofilm disruptors. When necessary, I do use pharmaceutical antibiotics, but mixtures of herbal antimicrobials can be effective:

  • berberine
  • artemisinin
  • citrus seed extract
  • black walnut hulls
  • Artemisia herb
  • echinacea
  • goldenseal
  • gentian
  • fumitory
  • galbanum oil
  • oregano oil

Once the biofilm is destabilized and microbes are treated, binders help clean up the mess. EDTA disrupts biofilms and also chelates minerals in the matrix (3637). Chitosan and citrus pectin are two other options.

I can’t stress enough how important probiotics and prebiotics are in healing the gut and maintaining a healthy GI tract. Probiotics reduce pathogenic bacteria and have even been shown to disrupt the growth, adhesion, and activity of biofilms (3839). I recommend Primal Probiotics and Prebiogen or potato starch for prebiotics.

Hopefully the medical community will soon recognize biofilms as factors in many diseases and properly treat recalcitrant infections and illnesses.

Do gut bacteria inhibit weight loss?

Content Source ~ Harvard Health Publishing-Harvard Medical School

Q. I just can’t lose weight. A friend says that my problem might be due to the types of bacteria that live in my gut. That sounds crazy to me, but is it true, and can I do something about it?

A. Ten years ago, I also would have thought your friend was crazy. Today, I’d say she could well be right. Here’s why. We’ve known for a century that bacteria live in our intestines, but we’ve assumed that they did little to affect our health. We thought that they were just mooching off of us — taking advantage of the warmth and nutrients in our gut.

In the past decade, however, remarkable breakthroughs have allowed scientists to count and characterize the genes in our gut bacteria. The results have been astonishing. Our gut bacteria have 250 to 800 times more genes than we have human genes. Even more remarkable, these bacterial genes make substances that get into the human bloodstream, affecting our body chemistry. That means it is entirely plausible that the bacteria in our gut could be affecting our health.

How could they affect our weight? When we eat food, our gut breaks it down into small pieces. Only the smallest pieces get absorbed into our blood. The rest is eliminated as waste material. In other words, not all of the calories in the food we eat get into our body and increase our weight. The gut bacteria help break down food. Some bacteria are better able to chop food into those smallest pieces that get digested, add calories to our body and thereby tend to increase our weight. Theoretically, if our guts have more of those kinds of bacteria, it should be harder to lose weight.

But is there evidence that it really is true? Several studies in animals, and some in humans, say that it is. For example, scientists transferred bacteria from the guts of two strains of mice — one that naturally becomes obese and one that naturally stays lean — into a third lean strain raised from birth to have no gut bacteria. Gut bacteria transferred from the naturally obese mice made the germ-free mice become fat, but gut bacteria transferred from the naturally lean mice kept them lean.

Then scientists took bacteria from the guts of human identical twins, one of whom was obese and one of whom was lean, and transferred those bacteria into the guts of lean, germ-free mice. Bacteria from the obese twin made the mice become fat, but bacteria from the lean twin did not.

We are just beginning to understand the role of gut bacteria in obesity, and the science hasn’t led yet to treatments that will make it easier to lose weight. However, I believe that day is coming.

— by Anthony L. Komaroff, M.D.
Editor in Chief, Harvard Health Letter