Maybe synthetic poop is the solution of the future?

This column is written by Stig Bengmark – Professor Emeritus, scientist, lecturer and writer. Read more of Stig Bengmark’s columns here.

This column is a direct continuation of my column ‘Poop is the best cure?’

In this column, I spoke about the enormously successful treatments with faecal transplantation (FMT) – repeated transfer of poop from a donor to a sick person – which are becoming increasingly topical. However, the authorities in different countries find it difficult to accept the method as it is now designed – namely, even though it happens only rarely, it is possible to transmit disease instead of health. There’s a lot of poop that you want to avoid. Therefore, the authorities require extensive testing of both the donor and the recipient’s poop, before permission for a transfer is given. FMT is also a treatment that healthcare staff are reluctant to engage in – after all, making sludge and transferring poop is perceived as being ‘disgusting’ by most people, both staff as well as recipients. Therefore, there’s a real need to find alternative methods that give equivalent results but which are more pleasant and much easier to manage. A ‘synthetic poop’, produced in a laboratory, made to contain both effective bacteria and plenty of active fibre, seems like a very attractive option. This type of synthetic poop is called SYNBIOTICS – I’ve been busy for the past 20 years searching for a good option like this.

The problem is bigger than you think – at least half of the population are infected with resistant strains – and hundreds of thousands die every year in both North America and Europe.

In particular, it’s people with poor immune systems – the elderly and the chronically ill – that are affected. A recently published report from a study involving about ten nursing homes in the United States gives a picture of the daily reality. On average, patients are given antibiotics just over twice a year and almost half (47%) are infected with severe antibiotic resistance (1). Almost all patients suffer from recurrent episodes of severe diarrhoea or constipation.

Advertisement

Successful trials of probiotics when ‘forced’ to take antibiotics.

The first attempt at treatment with so-called ‘synthetic poop’ i.e. a laboratory-made composition of healthy bacteria (but unfortunately no fibre), was made in the late 1980s. As early as 1989, the Danes, Tvete and Rask-Madsen, reported a very successful treatment using a probiotic composition of gut bacteria – to replace FTM – they had great success trying a mixture of 10 different gut bacteria grown in a laboratory, on five patients with resistant Clostridium difficile infections (CDI) , who were all healthy after the treatment (2). A few years later, attempts were made to give probiotics to all patients who were ‘forced’ to take antibiotics. It then turned out that those who had also received probiotics at the same time as the antibiotic treatment had signs of remaining severe and deadly C diff bacteria in their gastrointestinal tract just less than half as often (3). Similar results were reported the following year with simultaneous treatment of probiotics during antibiotic treatment of children with otitis media (4). In another study, only 7/57 (12%) had antibiotic-induced diarrhoea if treated simultaneously with probiotics, compared with almost three times as often among the 19/56 (34%) who received antibiotics without the addition of probiotic bacteria (P = 0.007). However, giving probiotics to everyone, every time, when they’re being treated with antibiotics – a simple, cheap and effective method – has so far not become standard practice.

What is poop?

80% of poop is water, but more than half of the remainder is made up of intestinal bacteria, and the rest is mostly fibre of various kinds – although mostly such fibre as today’s severely handicapped, western ‘poop organs’ are unable to break down. The composition I’m working with, Synbiotic 2000, is put together in such a way as to mimic poop, i.e. containing plenty of beneficial and effective bacteria and also plenty of highly bioactive fibre, often called prebiotics. It’s not widely known, but only a small proportion – less than 10% – of what’s called ‘probiotics’ on the market actually has any effect. A lot of products actually have the opposite effect, and only those that have undergone extensive preclinical and clinical trials can be expected to have any effect. Before buying such products, these types of studies should always be demanded. It’s actually true that even if the lactobacilli the product contains have been given the exact same name, they could have completely different effects – the name of the bacteria is not always a guarantee of the expected effect.

A very small minority of lactobacilli can break down and metabolise ‘tough’ fibres.

Lactobacillus plantarum, Lactobacillus paracasei subsp. paracasei and Pediococcus pentosaceus are known to be the best at breaking down tough, healthy fibres – I call them TRIPLE-P (all the names start with P) – ‘The Champions League’ of probiotics. After extensive tests, I have chosen exactly these to be included in my synbiotics. One classic study is very interesting – it showed that when 712 different lactobacilli were studied, only four strains of lactobacilli could break down tough fibres including very important oligofructan fibres (phlein and inulin), and these were several strains of Lactobacillus plantarum, Lactobacillus paracasei subsp. paracasei, Pediococcus pentosaceus & Lactobacillus brevis (5) – the first three have been selected for inclusion in Synbiotics 2000. People who don’t normally have access to these strains in their poop organ will develop problems of the gastrointestinal tract when they eat these types of fibres (see my column on fibre for further reading).

Very few lactobacilli can eliminate resistant bacteria such as Clostridium difficile (Cdiff).

It was found in the study that only three strains out of 50 examined can kill off all the Clostridium strains that were tested, namely one Lactobacillus plantarum and two strains of Lactobacillus paracasei subsp. Paracasei. When an internationally renowned group of microbiologists in Estonia examined the ability of 50 different strains of lactobacilli to kill off 23 different strains of Clostridium difficile, they found a large variation in effectiveness.  No less than 27 strains of lactobacilli were found to be totally ineffective, 18 strains had partial effect while, as stated, only a total of three strains, one Lactobacillus plantarum and two strains of Lactobacillus paracasei subsp. Paracasei showed 100% success (6). The strains of Lactobacillus plantarum and lactobacillus paracasei that we’ve chosen from more than 500 Lactobacilli strains that we’ve collected, have shown unique anti-inflammatory and anti-infective properties, and they are included in Synbiotic 2000 after being the subject of extensive clinical studies for more than 15 years.

The majority of westerners and EVERYONE who is obese have completely lost their Lb plantarum and Lb Paracasei.

Previous studies clearly show that our collection of intestinal bacteria is becoming increasingly ‘poorer’ with an increasing transition to industrially produced and heavily processed food. For more than fifty years, we’ve known that most of us have already lost our significant fibre digesters/ decomposers such as. Lb plantarum and Lb paracasei. A study conducted in 2012 shows that the ‘deterioration’ of the intestinal flora is continuing and that the majority of French people examined nowadays have lost several species of lactobacilli strains, and mainly Lactobacillus plantarum and Lactobacillus paracasei. In fact, people whose well-being has led to obesity have completely lost their plantarum and at least 90% of obese people have also lost their Lb paracasei (7).

Synbiotic 2000 consists of large doses of four anti-inflammatory lactobacilli and large amounts of bioactive fibre.

Synbiotic 2000 contains four lactobacilli that have been selected for their properties for maximising inflammation, namely: Lactobacillus plantarum 2362, Lactobacillus paracasei sbsp. Paracasei, Leuconostoc mesenteroides 32-77:1, Pediococcus pentosaceus 5-33:3. In addition, this composition contains 10 grams of the following fibres, one of which is for particularly tough fibres: beta-glucan, inulin (tough), pectin and resistant starch. My hope is that Synbiotic 2000 will have as good results as faecal microbial transplantation (FTM) does, and thus be a comfortable and hygienic replacement for this time-consuming and often unpopular form of treatment.

Faecal transplantation has had great success with extremely severe diseases – now it’s about showing that Synbiotic treatment has the same effects.

There is now great interest in trying Synbiotic on all the chronic diseases where FLT has been successful – such as autism, type 2 diabetes, obesity, Hashimoto’s goiter, idiopathic thrombocytopenic purpura, inflammatory bowel diseases (Crohn’s disease and ulcerative colitis), irritable bowel syndrome (IBS), chronic fatty liver (NAFLD), chronic fatigue syndrome, metabolic syndrome, multiple sclerosis, myoclonal dystonia, Parkinson’s disease, psoriasis, rheumatoid arthritis and Sjögren’s syndrome. I look forward to telling you all about them in my column on the first Monday of December.

Synbiotics can also be given as an enema.

10 patients with severe inflammation of the lower large intestine (distal colitis) were treated with an enema with Synbiotic. They were then followed for 3 weeks during which all manifestations of the disease disappeared – the urge to defecate, the number of episodes of diarrhoea, nocturnal diarrhoea, blood in the stool. The consistency of the stool was also massively improved.

Literature references:

  1. Hood K et al. Health Technol Assess. 2014;18:1-84.
  2. Tvede M, Rask-Madsen J.. 1989;1:1156-1160.
  3. Plummer S. Int Microbiol. 2004;7:59-62.
  4. Kotowska M et al. Aliment Pharmacol Ther. 2005;21:583-590.
  5. Müller M, Lier D. J Appl Bact1994;76:406-411.
  6. Naaber P et al. Med Microbiol 2004;53:551-554.
  7. Million M et al. Int J Obes (Lond). 2012;36:817-825.

More from Prof. Bengmark

s