Monty Lyman

“There is plenty of evidence to suggest a correlation between dementias such as Alzheimer’s disease and excessive, long-term inflammation in the body, known as chronic inflammation. A 2010 meta-analysis (an analysis of multiple papers, combining their findings) of 1,500 individuals found that those with Alzheimer’s disease tended to have raised levels of inflammatory cytokines in their blood.5 Curiously, further studies found that levels of systemic inflammation tend to be high in the early stages of the disease but not in advanced dementia.6 We also know that suffering from multiple infections increases the risk of developing dementia.7 There is also a dose-response relationship: the more infections (regardless of type), the higher the risk of dementia.8 An intriguing study, published by researchers at Stanford University in 2023, points the finger at one specific infectious agent: the varicella-zoster virus.9 This is the form of herpes virus we met in the last chapter, which has the dishonourable role of causing both chickenpox and shingles. The team analysed data from the National Health Service in Wales, because in late 2013 the Welsh Government enacted a health intervention that doubles up as a large natural experiment: they rolled out the shingles vaccine to people born on or after 2 September 1933. Over a seven-year follow-up comparing the vaccinated to the unvaccinated, they found that the shingles vaccine reduced the chance of developing dementia by around 20 per cent. While these are early days – and this study raises as many questions as it answers – it is looking likely that infectious agents are responsible for some proportion of dementia cases. Non-infectious inflammatory stimuli also increase the risk of developing dementia, from surgical operations to chronic autoimmune diseases.10 A remarkable link between systemic inflammation and dementia was uncovered in 2016, when researchers at the University of Southampton found that those with gum inflammation (periodontitis) had a six-fold increased risk of developing Alzheimer’s disease over a six-month period.11 In summary: it appears that inflammation in the body can drive the development of Alzheimer’s disease.”
― Monty Lyman, The Immune Mind: The Hidden Dialogue Between Your Brain and Immune System

“Almost a century later, in the 1970s, the American psychologist Robert Ader decided to do something conceptually daring and to see whether classical conditioning worked on the immune system.7 His experiment was audaciously, heretically interdisciplinary. Ader took three groups of rats. He injected the rats in Group 1 with cyclophosphamide, an immunosuppressant that also makes one feel very sick, and at the same time fed them with sugar-flavoured water. Rats in Group 2 were also injected with cyclophosphamide but drank plain water. Group 3 were injected with a placebo and had plain water. Afterwards, all of the rats were injected with red blood cells from sheep: something that should trigger a strong immune response. After a few days, the rats were given the sugar-flavoured water to drink. Those rats that had earlier been given the horrible immunosuppressant when they last drank the sugar-water became very averse to drinking it again. This finding is not hugely surprising; it’s not uncommon to develop taste aversion to a food that once carried a bacterium that gave you gastroenteritis or to an alcoholic drink you once over-imbibed to the point of bringing it all back up again. But the curious thing that Ader found was that when these rats drank the sugar-flavoured water again – this time in the absence of cyclophosphamide – they still became immunosuppressed. Some even died. It seemed that the brain and the immune system were predicting together.”
― Monty Lyman, The Immune Mind: The Hidden Dialogue Between Your Brain and Immune System