Archive for the ‘Probiotics Don’t Work’ Category
Dr. Natasha Campbell-McBride, quacktitioner extraordinaire and author of Gut and Psychology Syndrome (GAPS) believes that salicylates and SLAs are ‘high in antioxidants’ and ‘help the body to detox’. Apparently ADHD and other behavioural symptoms are the result of the ‘detox’ which is of course ‘good for you’. She recommends a gluten-free, casein-free, high salicylate/amine/glutamate diet to ‘cure’ autism and ADHD.
I came across a few blog posts from some poor soul who has been duped into doing GAPS by the bloody idiots at the Weston A. Price Foundation for various symptoms of ill health that rightly ought to be treated with a hospital monitored failsafe elimination diet. I’ll run through the sorry tale:
I had no idea that doing the GAPS diet would be so hard for me and on my family. I have lived without gluten for almost two years and dairy for 6 months so I thought…”hey I can live on soup for awhile”….hahaha….yeah right! I totally underestimated the power food has over my life and the power of the bad bacteria in my gut. This has truly been the hardest week of my life (besides giving birth).
I belive the reason this has been so hard for me was because my body had great difficulty expelling the toxic waste from my body (constipation) and going into the diet thinking that I would be able to add new things quickly.
When I began feeling some constipation issues I immediately noticed my skin starting to itch terribly (I think the toxins were trying to get out any way possible), my nursing daughter woke up with bumpy skin rash/eczema, and I experienced severe mood swings and terrible gas. I literally felt like the dead bacteria in my body were producing some sort of gas that was rocketing into my brain. I almost went to the hospital yesterday to get on anti-depressants. I was really starting to freak my self out. Thankfully my husband has been supportive but there has been some very hard times for us all. Oh another thing….my 12month old wakes every two hours at night crying. I’ve tried letting her cry herself to sleep but she literally continues to cry for hours so I finally go in to nurse her and she sleeps for a few hours and wakes again. This type of sleep is NOT good for either of us. In case we were not already feeling crappy, now we are purely exhausted. This is enough reason for me to want to get us better. I know her sleep troubles are diet related. I’m starting over
Despite this appalling and perhaps even dangerous reaction to the diet, this poor woman persists:
It has been a solid two weeks since beginning our probiotic Bio-Kult by Dr. Natasha Campbell McBride. And at least 4 weeks since beginning the GAPS diet of bone broth soups, veggies, meat, beet kvass, ginger tea, fermented veggies, ghee galore, coconut oil, cod liver oil, some nuts, apple/pear sauce and fresh veggie juices.
Could this diet be any higher in food chemicals? I can just imagine what they are going to do to this poor woman.
I’ll list the positive improvements for Ani and I first: I’ve gained 12lbs, Ani only wakes twice a night and my bowel movements are pretty regular, coming once a day.
Because I began with two bio-kults per day and lots of coconut oil (major candida killer), Ani and I have had head cold type symptoms for last two weeks. Yesterday I began only taking 1 capsule per day and really cut down on the coconut oil. Today we both seem better but I really have to stay consistent with detoxing. We drink a small glass of fresh carrot/celery/beet/cilantro/garlic juice after waking (btw….beets are the best liver cleansers in the world, cilantro is known to expel metal toxicity and garlic kills bad bacteria), I’m drinking lots of beet kvass, and bone broth with ginger (another powerful anti-microbial) and of course eating lots of soups!! Despite these measures, I’ll admit that both Ani and I have die-off coming out of every area in our bodies. Ani has eczema on her legs and neck, she has a runny nose, watery eyes, and some emotional issues every so often. I have a runny nose, my ear aches a little, sporadic mood swings, and exhaustion.
You would think that these classic food chemical intolerance symptoms would clue this poor woman in that perhaps she should avoid these unpleasant and reactive foods. Her child has broken out in eczema for heaven’s sake. But no:
But these are all good signs really, because they present that things are taking place internally. They show me that I really need to work on my liver health and encourage the bad bacteria to be flushed out before traveling into my blood stream. I’m amazed that one capsule of bio-kult is doing so much when Dr. McBride encourages working up to 8 capsules per day and then tapering back down to 4 for maintenance. I’m also amazed by the power of coconut oil in killing candida.
With all my discoveries on this diet I really am beginning to think that probiotics should be slowly administered after a few weeks eating an SCD or anti-candida diet otherwise there is too much die-off at one time causing the body to be overloaded with toxins.
Well anyways, I must end by saying that I’m so happy to be getting better even though at times it seems like we are just suffering. Detoxing and Die-off
The alleged ‘power of coconut oil in killing candida’ is actually this poor woman experiencing horrible physical reactions to coconut oil, which are brought on because it is very high in salicylates and SLAs. In the cult of candida-land, this translates as being ‘a herx’ and ‘it means you are getting better’. I am just amazed how people do such horrible things to their bodies and still think they are doing themselves some good.
What happens a week later?
Though, I thoroughly love Dr. Natasha Campbell McBride and her work and her probiotics, I have currently disowned her procedure for healing leaky gut. Why? A few reasons, firstly, doing the diet as well as the probiotics (even in the tiniest amount) was too harsh on my body. Maybe a young child who has not had candida for very long could handle her method very well but for my own damaged gut, my body had difficulty expelling the toxins. Instead, the toxins were hitch-hiking through my blood stream. And somehow into my nursing daughter’s system too.
The author has been recruited by bonkers Bee Wilder and her anti-candida diet and is now eating a high fat, low carbohydrate diet. The diet is lower in food chemicals, but still relatively high compared to a normal diet.
After just a day or so on this new path, I felt so energized, strong and capable, so happy! It took a little while to balance my blood sugar levels until I learned that I wasn’t getting enough fat. I no longer have any blood sugar issues and my impulsive food cravings (usually for a handful of nuts) has disappeared. I can go longer between meals (I had been eating every other hour). I went running yesterday with my babe and daughter. Jason said I’m much more delightful. No more intense die-off, just a little here and there. A shift
I also experience the same energy rush and increased tolerance to food chemicals on a high fat, low carbohydrate diet. And I assure you it has nothing to do with candida and everything to do with the reasons the ketogenic diet is used to treat intractable epilepsy in children. But just like me, this woman is never going to feel truly ‘right’ on this diet.
How are things going lately?
Last week we went out to dinner and I ordered a thai salad. Though everything on it was ok (besides the dressing which I’m sure had sugar in it) the lettuce was raw and my gut is not ready for raw greens. I seem to do ok with a small amounts of fermented veggies like pickled ginger root and pickled garlic and any sauted veggies. But eating raw greens while healing a damaged gut is like eating sand paper, it is very irritating. I felt terrible for about 36 hours after that dumb mistake. My stomach hurts
She’s blaming all of her problems on tiny mistakes like slightly too many carbohydrates or too much fibre, just like I used to. Actually, the problem is the extremely high chemical Thai dressing she has eaten.
Another tragic victim of WAPF’s promotion of quack cures over science.
Intestinal epithelial cells (IEC) are known to actively participate in the mucosal immune response through the production of cytokines and prostaglandins which are intimately involved in many immunoregulatory activities. Probiotic lactic acid bacteria can affect IEC cytokine production profiles and both fermented milk and soy products have been reported to influence IEC growth. In a study reported in the March 2005 issue of the Journal of Food Science (2005, 70 (2): M81 – M86), Fiander et al. have examined the effect of lactic acid bacteria (LAB) and fermented milks on eicosanoid production. Arachidonic acid (20:4ω6, eicosa=20 in Greek) is the premier eicosanoid precursor in mammalian cells. Eicosanoids are a group of lipid mediators which include prostaglandins and leukotrienes and are involved in numerous inflammatory and allergic reactions in the body. Gastrointestinal pathogenic bacteria like Salmonella, Yersinia and E. coli can induce the synthesis of prostaglandins and this is associated with their ability to invade epithelial cells and cause illness. Previous research has suggested that bioactive peptides (eg. beta-casomorphins) released from casein during milk fermentation by LAB can have analgesic effects, increase gastrointestinal transit times and modulate endocrine secretions. Some of these milk-derived peptides are opioid in nature, and it is known that IECs contain opioid receptors.
Two lines of human intestinal epithelial cells were used in the study. Lactobacillus rhamnosus R0011 and L. acidophilus R0052 were both used to produce samples of fermented milks. The effects of the LAB and their milk ferments on the synthesis of prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) by the IEC cell lines were determined using a competitive enzyme immunoassay. LAB alone did not alter interleukin-induced prostaglandin synthesis by IEC, but milk fermented with L. rhamnosus R0011 significantly suppressed interleukin induced levels of PGE2 and PGF2α. Fermented milks produced with L. acidophilus R0052 showed a similar but not identical pattern of suppression, and were marginally less effective in down-regulating prostaglandin (PG) production by IECs. The addition of L. rhamnosus R0011 culture alone counteracted the suppression induced by the L. rhamnosus milk ferment. Naltrexone, an opioid receptor antagonist, blocked the suppressive effects of L. rhamnosus ferments on PG production, indicating that the bioactivity of the milk ferments could be mediated through opioid receptors in the IECs. These results suggest that the immunomodulatory effects of fermented milks are due to bioactive milk components liberated by the lactobacilli rather than the lactobacilli themselves.
I decided last summer that yoghurt wasn’t actually good for me. I find it highly addictive – much more addictive than fresh milk – and it makes me feel drugged. I crave it and feel grumpy if it is withdrawn. I also gain weight with it. I think this is why.
Here we have lactobacillus apparently liberating both opioid-like peptides and messing with prostaglandins. The prostaglandin enzymes blocked here are slightly further down the prostaglandin pathway than the ones blocked by NSAIDs (COX). I wonder if they still affect the pathway in the same way, by increasing leukotriene production?
Kombucha tea is supposed to protect against toxins and detox the body by supplying an ingredient, glucuronic acid, that is required by one of the phase II detoxification pathways in the liver.
Many sources say kombucha tea is high in glucuronic acid. Apparently Wikipedia thinks otherwise:
Early chemical analyses of kombucha brew suggested that glucuronic acid was a key component of the brew, perhaps assisting the liver by supplying more of the substance during detoxification. However, more recent analyses of kombucha offer a different explanation, as outlined in the book in Analysis of Kombucha Ferments by Michael Roussin. The author reports on an extensive chemical analysis of a variety of commercial and homebrew versions of kombucha, and finds no evidence of glucuronic acid at any concentration.
This author offers a more compelling explanation for anti-cancer properties with the discovery of an alternate compound, D- glucaro- 1,4 lactone, otherwise known as glucaric acid. This compound serves as an inhibitor of the beta-glucuronidase enzyme, a bacterial product from the gut microbiota that can cleave the glucuronic acid conjugates. The activity of this bacterial enzyme has the effect of cleaving the glucuronic acid conjugates and sending bodily wastes back into circulation, thus increasing the exposure time before the waste is ultimately excreted. Therefore, the active component of kombucha likely exerts its effect by preventing bacterial disruption of glucuronic acid conjugates and increasing the detoxification efficiency of the liver.
Interestingly, glucaric acid is being explored independently as a cancer preventative agent. Kombucha
Something I learned from this is that common, normal gut bacteria can produce beta-glucuronidase in order to feed on aromatic compounds in the gut, possibly undoing the liver’s detoxification efforts by sending aromatics back into circulation around the body.
Searching the gene database for producers of beta-glucuronidase returns a veritable who’s-who of common bacteria: Bacteroides fragilis (a normal inhabitant), Clostridium perfringens (unfriendly), Streptococcus strains, Streptomyces strains, Staphylococcus strains, Escherichia coli, Propionibacterium acnes (produces both the non-failsafe additive propionic acid, AND causes acne!), and Bifidobacterium longum, that so-called friendly probiotic. Note, that yet again, candida albicans is not involved in this process. Candida does not produce amines in the gut, bacteria do. Candida does not produce beta-glucuronidase in the gut, bacteria do.
Last week I was interested to read an article about the Japanese company Yakult, who have launched “GABA yoghurt” in Japan, “a new type of fermented milk containing GABA by using two kinds of starters—Lactobacillus casei strain Shirota, and Lactococcus lactis YIT 2027. The Lb. casei strain hydrolyzes milk protein into glutamic acid, and the Lc. lactis converts glutamic acid into GABA.”
I’ve been investigating the various different actions of bacteria in the formation of amines and neurotransmitters, including glutamic acid and GABA. So far I have the following:
Produces free glutamic acid (glutamate hydrolysation):
Converts free glutamate into GABA:
Lactococcus lactis subspecies lactis
Some strains that appear to convert free glutamate into GABA:
Lactobacillus plantarum particularly strain WCFS1
Escherichia coli particularly strain UT481
Saccharomyces cerevisiae strain S288C (Baker’s or pudding yeast)
Clostridium perfringens strain 13 (Note: clostridium infection may be involved in autism!)
Candida albicans strain SC5314 (Shock!)
This article contains more information, or search the PubMed gene database.
Does NOT produce GABA:
Lactococcus lactis subspecies cremoris
The GABA producing activity of these bacteria is via the enzyme glutamate decarboxylase, which requires the cofactor PLP (P5P), the active form of vitamin B6.
With this kind of experimentation, we always run the risk of producing many other amines. But where might we find such yeasts and bacteria?
Bread and Beer
Saccharomyces cerevisiae is also known as baker’s or brewer’s yeast. It produces GABA during long leavening of bread. Store bought bread is not leavened in this way but homemade sourdough bread is. Wheat and other grains are disproportionately high in bound glutamic acid, so it seems logical that a sourdough starter that includes L. casei, L. lactis and L. brevis, as well as saccharomyces cerevisiae will result in the production of glutamate and GABA. Saccharomyces cerevisiae lives happily with gut microflora.
“Lactobacillus brevis OPK-3, having 84.292mg/L/h of gamma-aminobutyric acid (GABA) productivity, was isolated from Kimchi.” Am I correct in thinking that is 84 milligrams of GABA per litre per hour? GABA is not very active – you seem to need a lot of it to cause reactions compared to other amines. But after a 24 hour fermentation, that gives us over two grams of GABA to one litre of kimchi, a biologically active dose.
Cheese cultures fall into two main categories, thermophilic and mesophilic. Thermophilic cheeses are made mainly with streptococcus thermophilus and lactobacillus bulgaricus, and mesophilic cheeses are made mainly with a variety of lactococcus lactis subspecies and streptococcus thermophilus. Cheese – as well as containing a variety of other neurotransmitters like serotonin and tyramine – also contains GABA. More about cheese cultures.
A number of people who consume kefir say they ‘feel relaxed’ after eating it. There could be a number of reasons for this, including opioid-like peptide liberation.
A total of 21 strains of Lactobacillus species were isolated from Turkish kefir samples, in order to select the most suitable strains according to their metabolic activities including probiotic properties. As a result of the identification tests, 21 Lactobacillus isolates were identified as L. acidophilus (4%), L. helveticus (9%), L. brevis (9%), L. bulgaricus (14%), L. plantarum (14%), L. casei (19%) and L. lactis (28%). Metabolic activities of Lactobacillus spp. strains isolated from kefir
Lactobacillus brevis appears to be at least partially responsible for kefiran, the polysaccharide that forms around kefir grains.
In an investigation of the changes in the microflora along the pathway: kefir grains (A)–>kefir made from kefir grains (B)–>kefir made from kefir as inoculum (C), the following species of lactic acid bacteria (83-90%) of the microbial count in the grains) were identified: Lactococcus lactis subsp. lactis, Streptococcus thermophilus, Lactobacillus delbrueckii subsp. bulgaricus, Lactobacillus helveticus, Lactobacillus casei subsp. pseudoplantarum and Lactobacillus brevis. Yeasts (10-17%) identified were Kluyveromyces marxianus var. lactis, Saccharomyces cerevisiae, Candida inconspicua and Candida maris. In the microbial population of kefir grains and kefir made from them the homofermentative lactic streptococci (52-65% and 79-86%, respectively) predominated. Within the group of lactobacilli, the homofermentative thermophilic species L. delbrueckii subsp. bulgaricus and L. helveticus (70-87% of the isolated bacilli) predominated. Along the pathway A–>B–>C, the streptococcal proportion in the total kefir microflora increased by 26-30% whereas the lactobacilli decreased by 13-23%. K. marxianus var. lactis was permanently present in kefir grains and kefirs, whereas the dominant lactose-negative yeast in the total yeast flora of the kefir grains dramatically decreased in kefir C. Lactic acid bacteria and yeasts in kefir grains and kefir made from them
Kefir grains vary considerably in their bacterial makeup, but these particular species seem to be present all or most of the time. Unfortunately such cultures are often an unknown quantity.
Lactococcus lactis produces tyramine. I’ve tried kefir before, and it seemed quite pleasant but it kept me awake at night because of the tyramine content. I was unable to eat it regularly for this reason.
Histamine is also present in cheese cultures. It is largely formed by enterococci.
The following friendly strains of bacteria are safe:
- Lactobacillus Acidophilus
- Streptococcus Thermophilus
- Lactobacillus Bulgaricus
These are the three strains of bacteria that are used traditionally in yoghurt making.
Friendly strains of bacteria in yoghurt do not produce amines. In fact they protect against damage to DNA caused by heterocyclic amines. By being present in milk products, they protect against the formation of amines by suffocating less friendly bacteria, and in fact reduce the formation of amines in the gut.
In the UK a yoghurt with these cultures is Total Greek Yoghurt. Other yoghurts are either unknown or contain bifidus strains – that favourite strain they add to most plain yoghurts these days in order to describe them as ‘probiotic’.
Bifidus are generally thought to be friendly but have a tendency to grow out of control and suffocate other bacteria strains in the gut. Probiotic yoghurts make me feel a little ‘off’ so I suspect that some of the species in them are producing amines or glutamates.
Failsafers should avoid Yakult and and Activa probiotics, which are cultured with lactobacillus casei, a strain which liberates glutamic acid.
Different strains of amine producing bacteria grow under different circumstances:
Dimethylamine, methylamine, propylamine, and pyrrolidine were the major amines formed by Bacteroides fragilis NCDO 2217 during the active phase of growth in batch culture. Production of these metabolites was strongly pH dependent and was optimal under acidic conditions (pH 6.0). Low pH also favored the formation of pyrrolidine, cadaverine, and dimethylamine by Clostridium perfringens C523, but the reverse was the case with putrescine, butylamine, and propylamine, where production was maximal at neutral pH. B. fragilis was grown in continuous culture under either starch or casein limitation. Amine formation was influenced by carbohydrate availability and was greatest when the bacteria were grown at high growth rates (dilution rate, 0.20/h) under starch limitation, where they constituted about 18% of the total fermentation products measured. Amine production was optimal and increased concomitantly with growth rate when C. perfringens was grown in glucose-limited continuous culture. Under conditions of high growth rate and glucose limitation, amines accounted for approximately 27% of the fermentation products measured. When glucose in the feed medium was increased from 5 to 15 g/liter, amine production was repressed, and under these nutritional conditions the growth rate had little effect on the process. Influence of pH, nutrient availability, and growth rate on amine production by Bacteroides fragilis and Clostridium perfringens
Acute laminitis has been associated with the overgrowth of gram-positive bacteria within the equine hindgut, causing the release of factor(s) leading to ischemia-reperfusion of the digits. The products of fermentation which trigger acute laminitis are, as yet, unknown; however, vasoactive amines are possible candidates. The objectives of this study were to use an in vitro model of carbohydrate overload to study the change in populations of cecal streptococci and lactobacilli and to establish whether certain species of these bacteria were capable of producing vasoactive amines from amino acids. Cecal contents from 10 horses were divided into aliquots and incubated anaerobically with either corn starch or inulin (fructan; both at 1 g/100 ml). Samples were taken at 6-h intervals over a 24-h period for enumeration of streptococci, lactobacilli, and gram-negative anaerobes by a dilution method onto standard selective growth media. The effects of the antibiotic virginiamycin (1 mg/100 ml) and calcium hydrogen phosphate (CaHPO4; 0.3 g/100 ml) were also examined. Fermentation of excess carbohydrate was associated with increases in numbers of streptococci and lactobacilli (2- to 3.5-log unit increases; inhibited by virginiamycin) but numbers of gram-negative anaerobes were not significantly affected. A screening agar technique followed by 16S rRNA gene sequence analysis enabled the identification of 26 different bacterial strains capable of producing one or more vasoactive amines. These included members of the species Streptococcus bovis and five different Lactobacillus spp. These data suggest that certain bacteria, whose overgrowth is associated with carbohydrate fermentation, are capable of producing vasoactive amines which may play a role in the pathogenesis of acute laminitis. Identification of Equine Cecal Bacteria Producing Amines in an In Vitro Model of Carbohydrate Overload
Bacteroides fragilis and many species of lactobacillus are normal inhabitants of the gut. They produce amines when they are allowed to feed on poorly digested protein, particularly in the presence of carbohydrate fermentation. Bacteria can even liberate phenols from phenol containing amino acids like tyrosine and phenylalanine. It seems that undigested starch and protein can both play a role in the production of amines. I have yet to find any information that implicates fat, since bacteria don’t really digest fat.