Some say the quickest route to a man’s heart is through his stomach, others prefer the fifth left intercostal space. Meanwhile, persuasive new evidence indicates that the high road to his testicles may run through the colon and highlights, once again, the importance of the gut-brain connection.
Men’s sperm counts are falling (ie 1-5), as are testosterone (T) levels. (6-9). Both of these trends are driven in part by our expanding waist lines. Obesity drives down T synthesis via insulin resistance and changes in the hypothalamic-pituitary-testicular (HPT) axis, and simultaneously increases the conversion of testosterone to estrogen. This is why fat blokes are prone to moods and moobs (10).
Chronic inflammation, which generally co-presents with obesity, makes things worse by disrupting testosterone synthesis in the all-important Leydig cells in the testes (11), thereby reducing testosterone levels in men of reproductive age (12). By a cruel twist of fate, chronic inflammation has the opposite effect in women; it enhances androgen synthesis in theca cells (13), the main androgen-producing cells of the ovary, and is closely linked to PCOS (14, 15).
It is obvious that it is healthier for men to have higher levels of testosterone, for women to have lower levels, and that the modern diet and lifestyle disrupts endocrine balance and damages both sexes.
It would be reductionist to suggest that these hormonal shifts explain the current vogue for sexual dysphoria, but it would equally be ridiculous to deny that they must be a contributory factor. This in turn suggests that targeted nutritional interventions might help some youngsters find their true genetic path and reduce the numbers who, aided and abetted by ideologues (16-18), become suicidal.
Given our thoroughly obesogenic environment, the inter-connected targets of calorie and weight control are difficult to achieve, let alone maintain. But there may be a hack. A recent paper from a collaborative group based in Adelaide and Essen provides a tantalizing clue.
In men challenged with a dose of the bacterial toxin lipopolysaccharide (LPS) the scientists documented an acute inflammatory response followed by a sustained decline in testosterone levels (12). As there were no changes in the HPT axis, the scientists reasoned that LPS-induced inflammation had directly impaired testosterone synthesis; a finding very much in line with in vitro work done in South Efrica (11). And LPS is, today, very prevalent.
Lipopolysaccharide is a major component of the cell walls of gram-negative bacteria. The modern microbiome is excessively gram negative, an artefact due to our historically low intakes of prebiotic fibers. The resulting excess of LPS and relative absence of butyrate creates chronic inflammation in the large bowel, disrupting the gut epithelial barrier. Macromolecules including LPS then enter the blood stream and the resulting endotoxaemia drives chronic inflammation in multiple tissues, including the testes.
In women, a similar chain of events is implicated in causing ovarian dysfunction and PCOS (19-23).
In both sexes, therefore, it looks as if boosting prebiotic fiber intakes to pre-transitional levels and restoring a pre-transitional microbiota will help restore normal patterns of sex hormones and might reduce the ever-expanding alphabet. Using an omega 3 HUFA / amphiphile polyphenol combination would be expected to work in parallel with the fiber. Even old-fashioned anti-inflammatory aspirin may be helpful (24).
This is not a value judgement. As far as I am concerned, you can self-identify as whatever you want. On waking I generally self-identify as an A10 Warthog, until self-medication with caffeine clears the red mist. A table-spoon of blended prebiotics with your cornflakes might clarify things for you in a totally different way. But this is not the end of the story.
A new paper on the gut microbiome of autistic children with Autistic Spectrum Disorder (ASD) raises further questions about the nature of the relationship between microbes and personality, and the diminishing line between free will and determinism.
Researchers from the University of Hong Kong found that microbiomes in ASD and normally developing children are markedly different (25). Species such as Faecalibacteria, known to modify the synthesis of neurotransmitters including serotonin (26), were significantly depleted in autistic subjects and replaced by Dialister, Caprobacillus and a group of Clostridial species known to produce neurotoxins (ie 27).
Here are putative mechanisms linking dysbiosis with CNS malfunction, and a set of bacterial markers which showed an 80% sensitivity for predicting ASD. A test with sensitivity and specificity of around 90% is considered to be a good diagnostic tool, so 80% is not bad for a first try – and the HK group may be able to improve this.
But which comes first? Do gut bacteria bemuse the brain or do autists, who typically display food aversions and sensitivities, affect the microbiome through their dietary choices? Here is where it starts to get interesting. The scientists observed that while the presence or absence of ASD correlated well with the bacterial markers, diet had no effect; suggesting (but not yet proving) that microbiotal matter was influencing mind.
If you have cultivated the art of believing six impossible things before breakfast, this is not much of a stretch.
We already know, for example, that probiotics (28) and prebiotics (29, 30) impact positively on mood in obese subjects and in patients with IBS. These two groups both experience chronic inflammatory stress, and it is possible that the pro/prebiotics are acting non-specifically, by providing anti-inflammatory cover. Prebiotics appear to enhance specific aspects of cognition (31, 32) too – so there is precedent.
More evidence linking bugs to brain by way of the diet derives from studies of multiple sclerosis.
MS patients have gut dysbiosis (33, 34). Adlercreutzia and Parabacreroides distasonis, two microbial species which metabolise isoflavones, are particularly depleted in these patients (34). Adding isoflavones to a murine model of MS increased numbers of these two species, caused immuno-modulation in the brain and significantly protected against disease progression (35); as do specific prebiotic fibers (35).
The human epidemiology of MS is striking, and consistent with the above findings. In Western nations where dietary consumption of isoflavones is less than 1 mg/day (36), MS affects up to 250 per 100,000 (37, 38). In China and Japan, where isoflavone consumption ranges from 10 to 30 mg/day, MS affects only 1 to 2 per 100,000 (37, 39); although this is increasing as Western junk foods invades those countries (39). Conversely, in MS patients eating the ultra-processed Standard American Diet, switching to the anti-inflammatory Mediterranean diet appears to be helpful (40).
This is relevant to the spectrum disorders too.
Autists are similar in some ways to MS patients.
Their brains are abnormally wired (41), due to exposure to inflammation in utero (ie 42-44), and they are probably more subject to neuro-inflammatory stress themselves (45). They have a dysbiosis (24) which may make them are more vulnerable to microbiomal metabolites, and microbiomal manipulation through diet.
ASD symptoms do not generally appear until 12 or 18 months, and it is possible that the autist microbiome recorded by the Hong Kong scientists pre-dated the emergence of autistic behaviour. We cannot tell, as they specifically examined the microbiome in autistic children aged 3 to 6 (24). Other studies which found an abnormal microbiome in ASD looked at similar age or older children (46-48); so we cannot confirm that dysbiosis is part of the causative chain.
However, a ‘normal’ mirobiome is critical to the normal development of the brain (49, 50).
There is evidence that it influences multiple CNS-mediated parameters ranging from infant temperament (51) to fine motor control (52) and communication, personal and social skills (53).
Logically, therefore, dysbiosis could be a contributory factor for ASD. Given that the genetic factors only account for 10-20% of ASD cases (54), and that the incidence of ASD is rising sharply, public health should concentrate on maternal and infant diet.
The fact that the Mediterranean diet reduces the risk of autism spectrum disorders (55) points the way forward. It indicates that women of child-bearing age should cut down on ultra-processed, pro-inflammatory foods, and cultivate a generally less inflammatory lifestyle. (See earlier post, ‘Inflamed in the Membrane’).
What can we do for those already on the spectrum?
Returning to the dysbiosis / ASD connection. If dysbiosis front-runs ASD, might the ‘wrong’ portfolio of gut microbes during early neurodevelopmental windows affect brain wiring, signalling and behaviour (ie 51-53, 56) in a way that contributes to later food aversions, which subsequently support the dysbiotic species? That might sound crazy, but …
Evolutionary biology teaches us that bacterial components in the microbiome which survive and prosper have either adapted to long-term aspects of the host environment, or have developed the ability to induce host responses that specifically benefit them. There is evidence that microbiomal configurations affect appetite in humans (ie 57, 58); and plenty of examples of parasites that modify host behavior for their own purposes.
Best known is Toxoplasma gondii, the ‘fatal attraction’ bug which spends most of its life cycle inside cats and other felids. It likes to jump into other mammalian hosts and once there it influences their behavior, making them more likely to complete the cycle. Infected mice become attracted to cat pheromones, and more frequently eaten by cats (59). Infected monkeys develop a fetish for leopard urine, and are more likely to become breakfast (60).
It doesn’t stop there. Infected male mice become more sexually attractive to females (61, 64, 65), so the Tox bug spreads; it ‘wants’ to infect as many hosts as possible.
These behavioral changes in infected mammals are mediated by Toxoplasma-induced changes in dopamine and other neuronal chemistry (62, 63); and more specifically, epigenetic changes to genes linked to fear-related and sexual arousal neural circuits (64). Humans are not immune.
T gondii lives in the gut of infected people, and in other tissues too. It boosts testosterone levels (61) and in the brain it raises levels of dopamine (65) while reducing serotonin metabolism (66). These hormonal and neurochemical shifts explain why infected humans, like infected mice and monkeys, tend to be less risk-averse, more aggressive and more sexually adventurous (67-69). You probably won’t, however, become a crazy cat person (70).
These changes are not entirely negative. Individuals with latent toxoplasmosis ‘show superior performance in challenging cognitive control situations … and greatly reduced sensitivity to motivational rewards such as money’ (71). Considering that a third of us are infected (72, 73), this single cell parasite may have done more to affect world history than any human. But I digress, as usual.
Working with Zinzino, I have seen numerous accounts of ASD cases which showed remarkable improvement after their chronic neuroinflammation had been resolved using omega 3 HUFA’s combined with amphiphilic polyphenols. In most cases, adding a blended prebiotic produced further benefits.
These results are obviously preliminary, and could be tested in a prospective RCT. If any pediatric or other specialist working in this area is interested, please contact me.
Next week. The Swarm from the Swamp; viruses, vaccines, quasi-species and central bankers.
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