Stem cells and cancer cells have enough molecular similarities that the former can be used to trigger immunity against the latter.
Understanding our primate ancestors’ relationship with alcohol can inform its use by modern humans.
June 1, 2014|
UNIVERSITY OF CALIFORNIA PRESS, MAY 2014When we think about the origins of agriculture and crop domestication, alcohol isn’t necessarily the first thing that comes to mind. But our forebears may well have been intentionally fermenting fruits and grains in parallel with the first Neolithic experiments in plant cultivation. Ethyl alcohol, the product of fermentation, is an attractive and psychoactively powerful inebriant, but fermentation is also a useful means of preserving food and of enhancing its digestibility. The presence of alcohol prolongs the edibility window of fruits and gruels, and can thus serve as a means of short-term storage for various starchy products. And if the right kinds of bacteria are also present, fermentation will stabilize certain foodstuffs (think cheese, yogurt, sauerkraut, and kimchi, for example). Whoever first came up with the idea of controlling the natural yeast-based process of fermentation was clearly on to a good thing.
Using spectroscopic analysis of chemical residues found in ceramic vessels unearthed by archaeologists, scientists know that the earliest evidence for intentional fermentation dates to about 7000 BCE. But if we look deeper into our evolutionary past, alcohol was a component of our ancestral primate diet for millions of years. In my new book, The Drunken Monkey, I suggest that alcohol vapors and the flavors produced by fermentation stimulate modern humans because of our ancient tendencies to seek out and consume ripe, sugar-rich, and alcohol-containing fruits. Alcohol is present because of particular strains of yeasts that ferment sugars, and this process is most common in the tropics where fruit-eating primates originated and today remain most diverse.
Unfortunately, the sensory mechanisms that once usefully promoted rapid identification and consumption of scarce nutritional resources are now triggered, sometimes to ruinous effect, by the widespread and copious amounts of alcohol available in modern industrial societies. The virtually unlimited supply of this psychoactive compound means that consumption is only limited by one’s appetite—or one’s craving. What once worked safely in the jungle, where fruits naturally contained only small amounts of alcohol, can be dangerous when we forage for booze in the supermarket.
Modern-day alcohol consumption is a double-edged sword, with both benefits but also major costs depending on dosage and genetic background. Both possibilities can be interpreted as an evolutionary outcome, and one that has profound implications for today’s drinkers. Intriguingly, some genetic polymorphisms in modern humans are protective against alcoholism, most notably in East Asia, where the widespread inability to metabolize alcohol renders many individuals reluctant to drink at all. Similar genetically based variation in the capacity to metabolize ethyl alcohol can also be found in fruit flies and in other animals routinely exposed to the molecule in their diet of fermenting fruit and, in some cases, nectar.
Recognition of sustained but low-level exposure to dietary alcohol over evolutionary time also explains a puzzling epidemiological phenomenon—substantial health benefits at intermediate levels of consumption. According to the toxicological theory termed hormesis, physiological benefits will be maximized for low-level exposure to compounds that naturally occur at low levels in the environment. Either high-level exposure or abstention, by contrast, can have deleterious effects.
Alcohol consumption is common in many human societies, but its evolutionary origins have largely been neglected. The fundamental lack of progress in understanding alcoholism reflects, in part, the failure to place our own addictive behaviors within a broader biological context. We ignore deeply rooted historical effects on human biology at our peril. So the next time you enjoy a drink or two, think about primates enjoying the pleasure of ripe, squishy fruit in tropical rainforests. Realize that you are consuming the products of yeast metabolism. And above all else, drink in moderation.
Robert Dudley is a professor of integrative biology at the University of California, Berkeley, and research associate at the Smithsonian Tropical Research Institute in Panama. Read an excerpt from The Drunken Monkey.
June 14, 2014
Interesting article, however, I think acids produced by microorganisms while fermenting sugars are more significant than alcohol to the health of primates (humans included).
A pH of 5 or less prevents bacteria (Cholera for example) from growing in the water, beer, ale, wine, and so fortth.
June 20, 2014
Very implausible. Drunken monkeys would have been dead ducks in the arboreal habitat.
June 21, 2014
not necessarily. a gene that says "drink alcohol" only causes drunkenness if large amounts of fermented fruit is available. If like in the forest, only small amounts of alcohol are available, the advantage of increased calorie intake outweights the chance of getting drunk
June 21, 2014
Epigenetic changes induced by ethanol in astrocytes link nutrient-dependent histone acetylation, DNA methylation, and non-coding microRNAs in the developing and adult brain from frugivory to the de novo creation of olfactory receptor genes in bats. The link from the epigenetic landscape to the physical landscape of DNA in the organized genome of humans also appears to involve classically conditioned hormone-organized and hormone-activated effects on morphological phenotypes and affects on behavioral phenotypes, which are associated with the epigenetic effects of olfactory/pheromonal input on luteinizing hormone (LH) and testosterone (T) in other mammals. For example, only the smell of ethanol was required to elicit the change in these hormones. Cause and effect was not established in 1990 because individual responses varied.
I am reminded that the clear link from human pheromones to the LH and T response via the conserved molecular mechanisms that result in sex differences in cell type differentiation also has not been established. Thus, although nutrient-dependent alternative splicings of pre-mRNA and amino acid substitutions are typically responsible for all cell type differentiation in all individuals of all species, only recently did others begin to acknowledge the concept of late-emerging epigenetic effects on hormone-organized and hormone-activated behavior in mammals.
With few exceptions social scientists have heretofore proclaimed that human pheromones do not exist because they seemingly expected our response to pheromones to be unvarying and immediate -- like the response to food odors and pheromones in insects. Serious scientists have since provided details that link the conserved molecular mechanisms of cell type differentiation in species from microbes to man to the epigenetic effects of olfactory/pheormonal input on receptor-mediated differences in behaviors that social scientists portray in the context of mutation-initiated natural selection and the evolution of biodiversity.
Thus, the ongoing problem with alcoholism and with some -- if not all other -- addictions can be attributed to the pseudoscientific nonsense of population geneticists who invented neo-Darwinian theories. See for review: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
July 14, 2014
I will have to read the book, but with just this short description, I will have to disagree on several levels. First, kids HATE alcohol. Perhaps this is a built in defense mechanism. Second, when it comes to cancer, "No Amount of Alcohol is Safe". I do understand that studies have shown that there is a small CV benefit to alcohol consumption, but, if I remember correctly, this applies only to wine, not to beer. I would think that something other than alcohol is providing this benefit (perhaps probiotic effects in the digestive tract). Lastly, our ancestors did not live long enough to gain survival or reproductive benefits from diet modifications. You may still be correct with your premise, but because of a different effect. Would an intoxicated animal be an easier target for a hungry predator or . . . would a monkey wearing beer goggles be more likely to take on a revival, pursue a hard to get mate or even target a larger animal as food?