Let medicine be thy food and food be thy medicine.
Hippocrates
THAT PHRASE, WIDELY attributed to Hippocrates, has conjured up a host of novel nutrition fads, from the low-carbohydrate Atkins diet to the ‘caveman’ Palaeolithic diet, spawning an industry worth billions. They’re so popular, in fact, that the evidence for many of these diets has taken a backseat. We all know we should eat more fruit and fewer fats, more vitamins and less salt, but linking fixed diets to particular diseases is rocky terrain. Once again the problem lies in trying to prove causation based on observational studies. Nevertheless, there does appear to be some kind of relationship between Alzheimer’s and diet.
In early 2015 a group of researchers in Chicago, led by a neurologist named Neelum Aggarwal, published a report suggesting that a Mediterranean diet might prevent Alzheimer’s.1 Aggarwal and her team observed the diets of nearly 1,000 people aged between fifty-eight and ninety-eight over four and a half years. They found that those who followed a hybrid diet, i.e. a Mediterranean diet combined with one that lowers blood pressure, were 52 per cent less likely to develop Alzheimer’s. This included plentiful leafy vegetables, whole grains, fish, nuts and berries; minimal red meat, cheese, fried food, sweets and pastries.
Again, this is only an observation, but the link remained after factoring in the usual suspects: age, medical history, body mass index, education, depression and possession of the APOE4 gene. Moreover, a systematic review carried out at the prestigious Mayo Clinic in Minnesota concluded that ‘while the overall number of studies is small, pooled results suggest that a higher adherence to the MeDi [Mediterranean diet] is associated with a reduced risk of developing MCI [mild cognitive impairment] and AD [Alzheimer’s disease], and a reduced risk of progressing from MCI to AD’.2
How does what we eat protect us? It’s all due to a foggy connection between the brain and the gut. Collectively known as the microbiome, the bacteria that reside symbiotically inside us are vital to brain health. This was demonstrated most starkly in November 2014, when Swedish researchers at the Karolinska Institute in Stockholm showed that germ-free mice–gnotobiotic mice, housed and fed inside sterile containers–are born with leaky, defective blood–brain barriers.3 The blood–brain barrier is a wall of cells that decides what can and cannot enter the brain from the blood coursing through its capillaries. In Alzheimer’s, it’s one of the first things to break down, especially around the hippocampus, where memories are made.
But the microbiome can be a dangerous bedfellow too. If excessive amounts of bacteria breach the blood–brain barrier, they will activate the brain’s immune cells–microglia, the cellular protagonists of the Alzheimer’s vaccination story in chapter seven–and cause a form of inflammation that weakens the blood–brain barrier even more, setting in motion a vicious cycle in which more bacteria are let in and more inflammation ensues.
An irresistible case for this very scenario happening in Alzheimer’s was made six years ago by a Swiss-Hungarian neuropathologist named Judith Miklossy. She found that the density of bacteria is eight times higher in Alzheimer’s brains than in healthy people.4 Spirochaetes, the spiral-shaped variety of bacteria, were the main culprit. They have ‘the ability to invade the brain, persist in the brain and cause dementia’, Miklossy wrote. She also pointed out that dementia is a feature of late-stage Lyme disease, an infectious disease caused by the Borrelia bacterium. These micro-organisms can evade host defence mechanisms and ultimately help lead to the formation of plaques and tangles.
It turns out that the Mediterranean diet is filled with anti-bacterial foods–such as garlic, olive oil and honey. Cinnamon also weighs in, with one study demonstrating that cinnamon extracts fed to Alzheimer’s mice shrink plaques and improve cognition.5
Since writing this, a randomised clinical trial–the gold standard for assessing interventions, where participants are randomly assigned to either a treatment or placebo group to reduce bias–has been done on the role of diet in age-related cognitive decline (that’s not Alzheimer’s, of course, but experts agree this may apply nonetheless). Sweden’s Karolinska Institute was again leading the way. In what they dubbed the ‘Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability,’ or FINGER, scientists randomly assigned over 1,200 sixty- to seventy-seven-year-old Fins to a strict, two-year diet, and those who followed the diet did significantly better on cognitive tests than those who did not.6
As someone who obsesses over those colour-coded boxes divvying up food groups on food packaging, I loved the details of the study. The diet was as follows:
10–20% of daily energy from proteins, 25–35% daily energy from fat [less than 10% saturated fat, 10–20% mono-saturated fatty acids, 5–10% polyunsaturated fatty acids, and 2.5–3 grams per day of omega-3 fatty acids], 45–55% daily energy from carbohydrates [less than 10% from refined sugar], 25–35 grams per day of dietary fibre, less than 5 grams per day of salt, and less than 5% daily energy from alcohol.
In plain English: ‘These goals were achieved by recommendation of high consumption of fruit and vegetables, consumption of wholegrain cereal products and low-fat milk and meat products, limiting of sucrose intake to less than 50 grams per day, use of vegetable margarine and rapeseed oil instead of butter, and fish consumption at least two portions per week.’
Reading the study, I was almost disappointed. This advice has been a common narrative among doctors and dieticians for years. Now, however, we may have even more cause to listen.