Dreams – repressed desires or warning signals for disease?

This is an article I wrote for the London Student

Our fascination with dreams dates back centuries. Ancient cultures such as the Egyptians and Greeks even had dedicated gods of dreams. In the early 20th century, the founding father of psychoanalysis, Sigmund Freud, suggested that dreams are a manifestation of our most secret and repressed desires; and instead of living them in real life, we act them out in our dreams. Recent research has shown, however, that there might be more to dreams than just unfulfilled needs. In fact, dreams could be an indicator and predictor of certain diseases.

Nightmares, for example, could be a sign of heart conditions, migraine, sleep deprivation or a side effect of beta-blockers. Many dreams could be an indication for either being too hot or cold during the night, hormones, chronic pain, or coming off antidepressants.

Too much alcohol, an infection, the menopause or anti-malaria pills could cause memorable or bizarre dreams. A fatty meal, too much weight, stress or depression could give you dreams that wake you early; and sexual dreams do not necessarily represent anything about a person’s sex life, but could actually be triggered by creativity. Many pensioners reported having increased sexual dreams, which could be caused by taking up new hobbies during retirement.

Bashing about in your dreams, or dreams of attacks or wild animals, could be an early warning sign for Alzheimer’s or Parkinson disease. These dreams can be one of the first recognisable symptoms and can appear even a decade before the actual onset of the disease.

Alzheimer’s is a neurodegenerative disease, in which insoluble mutated protein (amyloid-β)clumps called plaques accumulate in the spaces between nerve cells. Protein tangles can even build up in nerve cells, thus hindering nerve cells to function properly.

Sleep disturbances, and in particular increased daytime sleepiness, could be an early sign of Alzheimer’s, which could be caused by the protein plaques. Researchers discovered that in mice the plaque concentration peaked during wake times, but fell when mice were asleep. Depriving mice of sleep increased the protein concentration dramatically. Once the plaques were removed, their sleep pattern went back to normal. Daily fluctuations in the concentration of the mutated protein were also found in humans.

It remains unclear whether the sleep disturbances lead to Alzheimer’s, or if they are caused by it, but it is suspected that they might reinforce each other. “Abnormal sleep in mid-life might cause protein aggregation that starts the disease off,” Holtzman tells Nature “, and the damage it causes may further disrupt sleep.” “Once we saw that amyloid-β was going up and down with the sleep–wake cycle, the implications began to unfold,” says Holtzman. These findings suggested that sleep disturbances might actually precipitate plaque formation. And if a sleep deficit could increase the concentration of soluble amyloid-β, says Holtzman, then sleep abnormalities in earlier life may predispose people to Alzheimer’s.”

During an 8-hour sleep period, the brain goes through different stages of electric activity in repeating cycles that change about every 90 minutes. We spend about 20-25% of our sleep in the REM phase (rapid eye movement), which is often associated with dreaming. During sleep, information is downloaded from one brain region to another, so sleep is a crucial time for learning and memory consolidation. It is now known that memory processing and even dreaming are not confined to the REM phase. It might help us, however, to deal with emotional processing of events that happened during the day. Research has shown that the slow wave sleep phase is very important for memory consolidation and learning, but it becomes shorter in the ageing brain. It seems that an ageing or deteriorating brain, bad memory and bad sleep are somehow connected.

Many factors can influence the sleeping and dreaming pattern, we can control some, but others we cannot. Despite a lot progress in research, our understanding of the brain and its functions remain partly unclear. Until we have resolved the mystery of why we dream, what our dreams mean, dreaming will certainly remain an enigma that will not cease to surprise and entertain.

Crossfire of Sensations

Check out my article about synesthesia: Crossfire of sensations

I wish I were a synaesthesist. “A what?” you ask. No, I am not talking about a profession or a new religious cult. Synaesthesia is a “neurological condition”, although this description hardly does it justice. Imagine a world, where every word, letter, number, emotion or music comes with its own signature colour or taste. This is what it is like for a synaesthesist. Their world is colourful and tasteful because of a crossfire of senses. Synaesthesist can have blue Mondays, yellow Tuesdays, sour evenings or green threes, amongst others.

Synaesthesia comes from the ancient Greek words syn (union, together) and aisthēsis (sensation) meaning joined sensation. And that’s what it is—two independent senses experienced together1.

There are over 60 forms of synaesthesia2. In ‘grapheme-colour’ synaesthesia, words, letters and/or numbers are in colour and are often arranged in space. In ‘lexical-gustatory’ synaesthesia, words can elicit different tastes. Music or emotion can also evoke colours, and in the mirror-touch synaesthesia, people experience tactile sensations when they see others being touched. This is also associated with a heightened emphatic ability3. In a rarer form of synaesthesia, people see auras, coloured outlines, around other people and objects1.

Surprisingly, synaesthesia is relatively unknown and unresearched. The first documented case dates back to 18124, and synaesthesia has been more systematically described by Galton (1822-1911)5 later on, but after the early 1900s, research almost ceased.

Probably around 2-4% of the population have synaesthesia6. Many synaesthesists are not even aware that they experience the world differently to others, and sometimes only discover it by chance. Synaesthesia occurs from childhood on and people usually do not tend to lose it (and if they do lose it, usually it will be before the age of seven)1. Some forms of synaesthesia can be induced, either through accident, loss of a sense or drugs. In the early 1960s, it was shown that LSD can lead to synaesthesthetic experiences1,5. But it is unclear if the mechanisms are similar.

New research into synaesthesia has only recently been picked up again; but its mechanisms and causes remain partly unknown. Structural differences in the brain and/or interactions between different brain centres are thought to explain some of the mechanisms7,8. Cross wiring and cross activation between different regions in the brain could lead to different senses being experienced at the same time. But researchers are unsure if the cross wiring between different brain areas is caused by the connectivity between neurons or by chemicals1,5.

Brain imaging studies have also revealed differences in the brain anatomy. Synaesthesists appear to have connectivity clusters and the grey matter in some parts of the brain (parietal cortex and hippocampus) is thicker than in non-synaesthesists7,8. Researchers have also found increased connectivity and activity in centres processing texture, colour and form7,8, 13. Imaging techniques revealed that depending on the type of synaesthesia, centres processing taste, visual information or emotion are more active. Others suggest that the whole brain, and not just some areas, is strongly hyper-connected9.

Cases of synaesthesia are often common among family members, suggesting that a genetic component may be passed on through genes10. Although some similarities or patterns in the sensations can be observed between people, everyone experiences different sensations or combinations, even identical twins1. These combinations usually stay for life1.

Many synaesthesists work in the artistic industry. Some famous synaesthesists include the philosopher Ludwig Wittgenstein, the musician Miles Davis, the Nobel Prize physicist Richard Feynman, the author Vladimir Nabokov, and many more5.

I have to say that I envy synaesthesists a little bit. Although their sensations can lead to an overload of experiences at times, it must be amazing to see the world in technicolours. This “additional sense” shows us how fascinating the brain is and how little we still know about all its functions. Synaesthesia opens a new window of research for neuroscientists, philosophers and linguists, not only to understand this phenomenon, but also to learn more about brain mechanisms and individual differences in perception.

1.       Cytowic, R. E., & Eagleman, D. M. (2009). Wednesday is indigo blue: Discovering the brain of synesthesia. MIT Press.

2.    Spector, F., & Maurer, D. (2009). Synesthesia: a new approach to understanding the development of perception. Developmental psychology, 45(1), 175.

3.     Banissy, M. J., & Ward, J. (2007). Mirror-touch synesthesia is linked with empathy. Nature neuroscience, 10(7), 815-816.

4.     Jewanski, J., Day, S. A., & Ward, J. (2009). A colorful albino: the first documented case of synaesthesia, by Georg Tobias Ludwig Sachs in 1812. Journal of the History of the Neurosciences, 18(3), 293-303.

5.     Ward, J. (2013). Synesthesia. Annual Review of Psychology, 64, 49-75.

6.     Simner, J., Mulvenna, C., Sagiv, N., Tsakanikos, E., Witherby, S. A., Fraser, C. & Ward, J. (2006). Synaesthesia: The prevalence of atypical cross-modal experiences. Perception, 35(8), 1024.

7.     Rouw, R., & Scholte, H. S. (2007). Increased structural connectivity in grapheme-color synesthesia. Nature neuroscience, 10(6), 792-797.

8.     Rouw, R., Scholte, H. S., & Colizoli, O. (2011). Brain areas involved in synaesthesia: a review. Journal of Neuropsychology, 5(2), 214-242.

9.     Hänggi, J., Wotruba, D., & Jäncke, L. (2011). Globally altered structural brain network topology in grapheme-color synesthesia. The Journal of Neuroscience, 31(15), 5816-5828.

10.   Baron-Cohen, S., Burtlf, L., Smith-Laittan, F., Harrison, J., & Bolton, P. (1996). Synaesthesia: prevalence and familiality. Perception, 25, 1073-1079.