This may change your mind about yogurt and what you eat for breakfast…
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Strange new benefit from yogurt -- or is it?
Everyone hates the dreaded “brain fog” – but the causes of it are often difficult to trace.
Elevated blood ammonia and low thiamine status are a few classic causes, especially in long‑term alcoholics.
Yet recently another metabolite been found responsible.
Lactic acid exists in the body as two stereoisomers – ᴅ‑lactate and ʟ‑lactate.
And, although one is generally considered safe, the other is a veritable brain poison.
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Humans mostly produce the safer ʟ‑lactate, yet many species of bacteria produce both isomers in roughly equal amounts…
And some of these are currently marketed as probiotics.
Recently the intake of probiotics has been linked to ᴅ‑lactic acidosis in normal people, a condition previously thought exclusive to people with short‑bowel syndrome.
People with a shortened small intestine are especially prone to ᴅ‑lactic acidosis…
That’s because more undigested food reaches their colon, the location where most bacteria reside.
So when it comes to pinpointing the exact cause of brain fog, the type of bacteria normally consumed should be considered.
This is because some of the same strains shown to cause ᴅ‑lactic acidosis are found in yogurt, kefir, sauerkraut, kimchi, pickles, red wine, fermented sausage, and many varieties of cheese.
Foods containing Lactobacilli (the bacteria linked with ᴅ‑lactic acidosis) are about as common as brain fog itself.
From a 2018 report:
“Brain fog was so severe that 4/30 (13.3%) had quit their jobs.”
Yet we don’t necessarily need to avoid these foods because we can take some precautions against ᴅ‑lactic acidosis…
And one of these might surprise you.
Of course, cooking food before eating it will destroy any ᴅ‑lactate bacteria present, as will most antibiotics…
They also can be virtually eradicated by other probiotics through competition.
The curative strains are the ones that only synthesize the ʟ‑lactate, the safer isomer also produced by normal metabolism.
Lactobacillus acidophilus has been shown to cause brain fog through ᴅ‑lactate…
So it may sound counterintuitive that its cousin Lactobacillus rhamnosus has been shown to reverse it.
Lactobacillus rhamnosus produces negligible amounts of ᴅ‑lactate, the "GG" strain in particular.
It also occupies the same niche as many high ᴅ‑lactate producers and thus outcompetes them.
Because so many common foods contain ᴅ‑lactate‑producing bacteria (and also ᴅ‑lactate itself), below are some articles that help put this issue into perspective:
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This study gathered 30 patients with brain fog and tested their urinary ᴅ‑lactate concentrations.
The presence of brain fog was defined by mental confusion, cloudiness, impaired judgment, poor short-term memory, and difficulty with concentration for three months or longer.
They found that 76.7% of the brain fog group had clinical ᴅ‑lactic acidosis, as defined by a specific urinary level or greater following glucose ingestion.
And 100% of the brain fog group reported taking probiotics in the recent past, often multiple types.
By contrast, only one of the controls reported taking a probiotic, which just so happened to be Lactobacillus rhamnosus.
As mentioned above, this particular species produces only negligible amounts of ᴅ‑lactate.
“One patient (12%) in the non-brain fog group took probiotics (Lactobacillus rhamnosus)...”
The more common probiotic strains produce high amounts of ᴅ‑lactate.
These include Lactobacillus acidophilus, L. brevis, L. plantarum, and L. delbrueckii (shown in red below).
The only species of Lactobacilli that produce negligible amounts are L. rhamnosus, L. casei, one strain of L. saki, and a subspecies of L. paracasei (shown in blue below).
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In addition, Bifidobacteria and Enterococcus are generally safe as a genus, often producing under 5% of total lactate in the ᴅ‑isomer.
Streptococcus species are sometimes marketed as probiotics, yet they are high ᴅ‑isomer producers.
Although Lactobacilli are generally considered a "good bacteria" already present in the digestive tract, that could actually be the result of routinely ingesting fermented foods.
In other words, the high prevalence of sauerkraut and yogurt ingestion may have led to the impression of colonic Lactobacilli being “natural” and not merely “normal” – re-enforcing this idea through their marketing as probiotics.
Lactobacillus was the predominant anaerobic genera cultured from the brain fog group in this study, yet it was apparently absent from the controls.
Lactobacilli are also present in only 46% of Swedish and 70% of Estonian children, and this also varies by species.
Whatever the case may be, certain Lactobacilli have now been shown to cause brain fog in normal people routinely taking probiotics.
This must have been an unrealized occurrence for quite some time, even though the very first case of ᴅ‑lactic acidosis ever reported was a result of probiotic ingestion:
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This article was published in 1979 and marked the discovery of ᴅ‑lactic acidosis in humans.
The first human case of ᴅ‑lactic acidosis presented with episodes of cognitive impairment marked by delirium, slurred speech, and abusive behavior.
An electroencephalogram during an attack revealed bilateral slow‑wave activity, perhaps indicating that ᴅ‑lactate was affecting the brain directly.
“...when the patient exhibited blunted judgement, abusive behavior, slurred speech, staggering gait, nystagmus, dysdiadochokinesia, confusion, disorientation and delirium.”
His serum ᴅ‑lactate concentration was off the charts at 20.2 mmol per liter, approximately 70 times greater than clinical cut‑off values of ᴅ‑lactate acidosis.
Colonic bacteria were suspected as the origin for the excessive ᴅ‑lactate, and henceforth the patient was given neomycin and treated successfully.
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Although most Lactobacilli produce both isomers, only ᴅ‑lactate accumulates because ʟ‑lactate is more quickly metabolized.
This is because lactate dehydrogenase is specific towards the ʟ‑isomer, having absolutely no effect whatsoever on ᴅ‑lactate.
“About three months before the first attack, the patient began taking Lactobacillus adidophilus tablets…”
The only way for humans to dispose of ᴅ‑lactate is through urinary excretion and ᴅ‑2‑hydroxyacid dehydrogenase.
(ᴅ‑2‑hydroxyacid dehydrogenase is a low‑activity and nonspecific mitochondrial enzyme with many competing substrates).
This enzyme is present in the liver and kidney in useful concentrations…
But it is conspicuously absent from the large intestine where most ᴅ‑lactate enters the body.
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This enzyme is also absent from the brain, the very organ where ᴅ‑lactate exerts the most pronounced effects.
If you take enzymatic expression into account along with findings of plasma ᴅ‑lactate entering the brain readily, you then have a convincing explanation for the following:
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This study examined the metabolism of both ʟ‑ and ᴅ‑lactate in mitochondria isolated from the liver, heart, and brain.
They measured state 3 respiration, i.e. the ability of each substrate to metabolically convert ADP (adenosine diphosphate) into ATP (adenosine triphosphate).
State 3 respiration is determined by measuring oxygen uptake, initial concentrations of ADP, and the final concentration of ATP.
ᴅ‑lactate was found only slightly more inhibitory than ʟ‑lactate in the liver as compared to pyruvate.
Yet in the brain and muscle, ᴅ‑lactate behaved like a mitochondrial poison.
This is consistent with the distribution of ᴅ‑2‑hydroxyacid dehydrogenase, the enzyme needed to convert ᴅ‑lactate into pyruvate.
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Even ʟ‑lactate is somewhat inhibitory to the brain at the concentrations used here.
But the brain can put it to use after it is converted into pyruvate by ʟ‑lactate dehydrogenase – another mitochondrial enzyme.
The ᴅ‑isomer, however, is not a substrate for this enzyme, so it cannot be converted into pyruvate.
For this reason, ᴅ‑lactate is greater metabolic liability and can even inhibit the oxidation of inhibitory ʟ‑lactate.
“However, mitochondria isolated from brain and heart did not oxidize ᴅ‑lactate efficiently…”
The results of this study go a long way in explaining neurological anomalies resulting from ᴅ‑lactic acidosis.
The effect of pH alone has already been ruled out (Oh, 1979), and ammonia has a similar effect on brain mitochondria (Kosenko, 1996).
“Treatment of acidosis with 300 to 600 mmol of sodium bicarbonate increased blood pH but had no effect on the neurological manifestations.”
And intracerebral injections of ᴅ‑lactate (but not pyruvate or acetate) have also been shown to inhibit learning in chickens.
So certain probiotics can be responsible for brain fog caused by ᴅ‑lactate in some people.
But how about Lactobacilli‑fermented foods? Do they do the same?
Well there isn't a lot of data to go on here, but yogurt consumption can raise plasma ᴅ‑lactate nearly threefold:
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In this study, they gave seven healthy Germans either yogurt or an equivalent amount of ᴅʟ‑lactate in water.
They did not modify the yogurt in any way, but selected a brand from the shelves with a high ᴅ‑lactate concentration.
It turned out that ᴅ‑lactate was absorbed from both the ᴅ‑lactate-spiked water and the yogurt…
But the process was somewhat delayed when consuming the yogurt:
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The ᴅ‑lactate from the spiked water reached plasma concentrations that can be defined as transient ᴅ‑lactic acidosis…
And the plasma concentrations from eating yogurt were half that – but lasted twice as long.
In the graph above, the areas under the concentration curves are virtually identical...
So the same amount of ᴅ‑lactate was ultimately absorbed in both instances.
What does this mean?
Normal yogurt consumption can lead to borderline ᴅ‑lactic acidosis for three hours…
But it doesn’t tell us whether yogurt has enough viable Lactobacilli to colonize the colon.
The subjects also consumed the yogurt "neat" without any additives…
So it also remains to be seen what would happen if it was combined with fermentable carbohydrates such as fruit and/or sucrose (e.g. DannonTM).
Regardless, this could be something to consider should a brief episode or longstanding period of brain fog be preceded by yogurt consumption.
“The brain apparently lacks ᴅ‑2-hydroxyacid dehydrogenase, and ᴅ‑lactate may accumulate excessively there.”
As mentioned earlier, ᴅ‑lactate‑producing bacteria can be eradicated by ᴅ‑lactate‑free probiotics through competition.
This fact has been convincingly proven in a study using a commercial mixture of Lactobacillus rhamnosus GG, Bifidobacterium lactis BS01, Bifidobacterium breve BR03, and Bifidobacterium longum (Yilmaz, 2018).
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Spectrumceuticals Pro4‑50TM was used in the above case.
But it's a bit overpriced and ships all the way from Australia. It is also available only in powder form, which could make it relatively awkward to take every day.
Yet capsules containing each bacterial species used are available from U.S. suppliers at a fraction of the price.
Antibiotics are of course effective and could perhaps be used if deemed safe...yet you would have to watch out for yeast overgrowth.
Bacteria aren't strictly necessary for survival at all, with germ‑free animals actually living longer than their “normal” littermates under ideal conditions.
It is also worth mentioning that the main bacteria found in unpasteurized vinegar, Acetobacter aceti, can efficiently metabolize both ᴅ‑lactate and ethanol.
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For this reason, unpasteurized vinegar may also be a useful measure against ᴅ‑lactic acidosis – AND it also inhibits yeast.
In conclusion, certain probiotics on the market are highly implicated in causing brain fog and Lactobacilli‑fermented foods are also suspect.
I personally avoid yogurt and recommend you avoid it also.
As this resarcher notes:
“First of all, if the shortened small intestine served as a predisposing factor, why was the onset of acidosis delayed for two years? It is probably relevant that the patient’s use of Lactobacillus acidophilus tablets preceded shortly the onset of acidosis, and that Lactobacillus acidophilus can produce ᴅ‑lactic acid.” –Oh, 1979
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