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Alzheimer’s linked to gut health

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The latest evidence about the main cause of Alzheimer’s has nothing to do with the head and everything to do with the gut, says Tony Edwards

The 20 feet of convoluted tubing linking your stomach to the outside world is commonly known as the gut, and until recently its functions were believed to be simple: finish off the messy business of food digestion, extract as many nutrients as possible and expel the remainder as waste. 

The gut is also known to be populated by bacteria, all of which were once thought to be harmful. But no more. Many gut bacteria are now recognized as vital for one’s health—not just locally but, perhaps surprisingly, throughout the whole body. These microscopic inhabitants of our midriffs are increasingly being linked to a whole raft of diseases—even dementia.

Leaky gut

The new buzzword is microbiome, coined to describe the colony of literally trillions of bacteria that are the semipermanent residents of our gut. Why semipermanent? Because we ourselves can at least partly control what types of bacteria live there, simply by deciding what to put in our mouths. 

At one extreme, the bacteria can be exterminated by oral antibiotics, and at the other, encouraged to proliferate in a healthy diversity by consuming fermented foods or probiotics.

There are an estimated 5,000 strains of gut bacteria—some beneficial but many not. In practice it’s impossible to have a microbiome that is completely free of harmful bacteria, and it’s the beneficial bacteria’s job to keep the harmful ones in check by what is called competitive inhibition—in other words, crowding them out. If they fail, pathogenic bacteria can gain the upper hand, causing gut “dysbiosis” or imbalance.

WDDTY was probably the very first periodical to report on this field back in the 1990s. Then, a tiny band of doctors—among them Professor Theron Randolph in the US, and in the UK Professor Jonathan Brostoff and Dr Damien Downing (still on WDDTY’s advisory panel)—developed the science of what they called “clinical ecology.” 

They pioneered the theory that gut health might lie at the root of many intractable diseases. One of their first discoveries was that gut dybiosis creates local inflammation, leading to actual perforations in the walls of the intestines. This so-called “leaky gut syndrome” was found to cause food allergies and intolerance, as well as major diseases of the gut such as irritable bowel syndrome and Crohn’s disease. 

Largely ridiculed 40 years ago, leaky gut has become an accepted medical condition. According to a recent review, it’s now seriously considered as a cause of not just food allergies and bowel disease but obesity, hepatitis, lupus, celiac disease, type 1 diabetes and even some cancers.1 

More astonishingly given the distance between the brain and the gut, currently the most exciting area of gut research is in disorders of the mind. There is growing evidence that the gut and the brain are very closely connected. 

First, there is a major physical connection between the two areas, via the vagus nerve. What’s more, the communication isn’t one-way: the gut sends signals to the brain and vice-versa. This is known as the “gut-brain axis.” Furthermore, some gut bacteria produce metabolites that are identical to brain chemicals. The most important of these are serotonin, a major mood-altering chemical, and dopamine, the “reward” chemical. Surprisingly, both these neurotransmitters are thought to be produced almost entirely within the gut, which helps explain why the gut is increasingly being referred to as “the second brain.”

But can altering gut bacteria actually affect mental states? The answer is yes. Inevitably, the initial evidence has come from laboratory experiments on rodents. Deliberately altering animals’ gut microbiota can seriously affect their behavior—inducing stress and anxiety, for example.2 

But what about us humans? 

There’s been a surge of interest among neurologists keen to explore the gut-brain axis in mental health, with some interesting findings. “Over the past decade, a growing body of evidence has suggested that compositional changes in the gut microbiome are highly correlated with several mental disorders,” said a review of the evidence late last year.3 

One of the most dramatic findings is the link between gut dybiosis and autism—research partly pioneered by Dr Andrew Wakefield in the late 1990s.4 Although he’s best known for his ‘controversial’ research on vaccines, Wakefield’s early gut dysbiosis/autism work has now been replicated by other researchers, with some finding a link between autism spectrum disorders (ASD) and antibiotics. 

Indeed, an alternative theory to vaccines as a cause of the exponential rise in ASD is the exponential prescribing of antimicrobial drugs to the very young. So far, attempts to ameliorate childrens’ existing ASD by treating their gut dysbiosis have been limited but promising.5 

Among the old, too, neurological diseases are being increasingly linked to the microbiome. Parkinson’s disease (PD), for example, is now thought to be at least partly related to gut health. In one  series of experiments,  mice treated with fecal samples from PD patients went on to develop “motor dysfunction,” i.e. Parkinsons-like symptoms.6

The reason appears to be that when the health of the gut bacteria is compromised, body-wide inflammatory reactions occur; these penetrate the blood-brain barrier, promoting “neuroinflammation and ultimately neurodegeneration,” says a recent review of the animal evidence.7  

And recent evidence from Aarhus University in Denmark shows that PD can start in the intestines and travel to the brain. 7 There are more grounds for hope with the other great challenge of old age: Alzheimer’s disease (AD). Again, mice have led the way. For example, in 2019, Hungarian scientists reported finding that probiotics and exercise improved the cognitive functions of mice genetically engineered to develop AD.8 

Similarly, US scientists have found that altering the gut bacteria of mice can prevent the formation of the beta-amyloid plaques in the brain associated with AD.9 But again, how relevant are these animal studies for us?

Promise for prevention

The human research data is fairly thin on the ground, but last November Italian neurologists announced some exciting new findings.10 They had compared 150 Italian seniors between the ages of 65 and 85, roughly 90 of whom were diagnosed with AD, while the rest were mentally fully functioning. 

Brain scans of the dementia group confirmed the classic signs of AD—amyloid plaques in the brain. Once thought to be the root cause of AD, these plaques are now believed to be the result of the disease rather than its cause. 

The researchers went on to discover that, as in the animal experiments, the gut bacteria profile of AD sufferers was also significantly different from the mentally healthy seniors. “Their microbiota has a reduced microbial diversity, with an over-representation of certain bacteria and a strong decrease in other microbes,” reported Professor Giovanni Frisoni. 

“Our results are indisputable: certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain,” said his colleague Dr Moira Marizzoni. 

But how can the gut affect the brain? The clue came from the AD patients’ blood samples, where the research team found specific “inflammation markers” produced by gut bacteria, corresponding to the presence of amyloid plaques; these were not present in the blood of the cognitively healthy participants.

The Italians aren’t the only group to find this astonishing connection between gut bacteria and dementia. A Wisconsin research team has reported “the gut microbiome of AD patients has decreased microbial richness and diversity.”11

This is all very promising. Dementia is a terrifying disease, and its incidence is rising exponentially, now rivaling cancer and heart disease as a major cause of death. Despite billions spent by the pharmaceutical industry, there is currently no cure for it. Could something as simple as manipulating gut bacteria be the answer—perhaps with a cocktail of bacteria tailored to the individual? 

Frisoni thinks this scenario is too optimistic, but he does foresee a major role for gut bacteria in prevention. “We must first identify the bacterial strains of the cocktail,” he says. “Then, a neuroprotective effect might be effective at a very early stage of the disease, with a view to prevention rather than therapy.” 

The good news about prevention gets even better for people who are at much greater risk of AD than average—those with a genetic mutation known as the APOE4 allele, which multiplies their risk of AD up to 12 times. A team at the University of East Anglia has discovered that people with that gene have a unique gut microbiome, specific to their condition. This offers “the prospect of reversing the risk of AD by altering the gut bacteria,” say the researchers encouragingly.12


Feeding your gut bacteria

Everyone’s microbiome is unique, but the key strategy is to create a permanently rich and diverse personal population of gut bacteria. 


  • Antibiotics
  • Sugar
  • Processed foods
  • Sugary and energy drinks
  • Artificial sweeteners



  • Full-fat live yogurt and probiotics
  • Fermented foods (kefir, sauerkraut, etc.)
  • Polyphenol-rich foods (chocolate, red wine, berries, etc.)
  • High-fiber foods (kale, beans, cabbage, etc.)
  • A wide variety of plant foods
  • Quality protein sources, including meat 
  • Quality fats, including animal fats

Article by Tony Edwards



Front Immunol, 2017; 8: 598


J Clin Invest, 2015; 125: 926–38


Exp Neurobiol, 2020 doi: 10.5607/en20047 


J Pediatr Gastroenterol Nutr, 2002; 34 Suppl 1: S14–7 


Minerva Gastroenterol Dietol, 2018; 64: 333–50


Cell, 2016; 167: 1469–80.e12


Mol Neurobiol, 2019; 56: 1841–51; Brain, 2020; 143:3077–88


Exp Gerontol, 2019; 115: 122–31 


Sci Rep, 2016; 6, 30028


J Alzheimers Dis, 2020; 78: 683–97


Sci Rep, 2017; 7: 13737


FASEB J, 2019; 33: 8221–31

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Article Topics: bacteria
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