Why Did Our Brains Stop Expanding?

Tony Wright will be joining host Dennis McKenna for the live, interactive video course, “What Plants Can Teach You: Consciousness and Intelligence in Nature.” A new paradigm is emerging that recasts how we relate to and understand nature, supported by new scientific evidence. Plants instruct us through their behavior, through their interdependence with the environment, and through direct transmissions conveyed by spirit.  Along with Tony and Dennis, the course gathers  some of the leading experts in the emerging field of plant intelligence, including: Chris Kilham, Stephen Harrod Buhner, Dayna Baumeister, and Simon G. Powell. This 5-part Evolver webinar starts on June 17. Click here to learn more.

The following is excerpted from Return to the Brain of Eden: Restoring the Connection between Neurochemistry and Consciousness by Tony Wright and Graham Gynn, recently published by Inner Traditions. 

In the forest the human brain was expanding and expanding at a phenomenal rate. Sometime at around 200,000 to 150,000 years ago, this process came to an end. The brain stopped expanding and started to shrink. This key point in our evolutionary journey has been noted but rarely addressed, and its significance comprehensively ignored.

Christopher Ruff, of John Hopkins University, and his colleagues thoroughly analyzed the fossil record to determine the evolving body mass and brain size of the various Homo species leading up to us. The results show that the assumption of a straight progression from a pea-brained ancestor to the ultrabrainy modern Homo sapiens is decidedly shaky. Hominid brains appear to have remained fairly constant in size for a long period from some 1.8 million years ago until about 600,000 years ago. But then, from 600,000 to 150,000 years before the present, fossils show that the cranial capacity of our ancestors skyrocketed. Brain mass peaked at about 1,440 grams (3.17 pounds). Since then brain mass has declined to the 1,300 grams (2.87 pounds) that is typical today (Ruff 1997).

Of course, brain size alone does not tell the whole story. Brain size also correlates with body size, and the peak of brain size roughly corresponds to the peak in archaicHomo sapiens’ body size (the Neanderthals). The decline in size of the body in Homo sapiens sapiens (modern humans get two “wises” in our name, but do we really deserve it?) over the past fifty thousand years has raised our ratio of brain-to-body size to just above Neanderthal levels. Yet we have done this by shrinking our bodies to a greater extent than our brains have shrunk. There is some evidence that our brains are still shrinking and that they may have done so over the last ten thousand years by as much as 5 percent.

This very recent period of brain shrinkage coincides with a major dietary change, for it was around this period that cereals and grain (grass seed) came to the fore. Cereals and grains may be the foundation of our diet today and responsible for the huge explosion in our numbers, but they may not be the best foods for optimal function. Indeed, studies of skeletons from early agricultural societies show that ill health accompanies the initial transition to eating more grains and cereals. Skeletons dug up from the East Coast of the United States, dating from around 1000 CE, the era when Native Americans switched to corn-based agriculture, are smaller than earlier skeletons. Studies of skeletons from other societies undergoing this transition show signs of deficiencies such as anemia. Clark Larsen, the physical anthropologist who studied the East Coast skeletons, has stated, “Just about anywhere that this transition to cereals occurs, health declines”(Larsen 2002).

It is thought that humans from such agrarian societies were lucky to live beyond thirty years. In contrast forest apes, such as chimpanzees, can live for some sixty years. We can reasonably assume that humans in the forest lived easily as long if not longer. Furthermore, if man in the forest was as long-lived or even longer-lived than chimps, it would provide a strong argument for the notion that this was both the most natural and most suitable place, particularly in terms of diet, for a human to live.

Ancestral Diets 

If the evolution of the unique human system was somehow linked with our ancestral diet, we would expect the human system still to be best adapted to something approaching this. While there is continued debate on this subject, few dissent from the view that there is an increasing problem with the food we are eating in our sophisticated, time-stressed modern world. In just one six-week period, newspaper headlines in the United Kingdom announced: “World Alert over Cancer Chemical in Cooked Food” (Daily Telegraph, May 18, 2002); “Children at Risk from the Junk Food Time Bomb” (Daily Mail, May 31, 2002); and “Anti-social Conduct May Be Linked to Diet, Says Study” (Guardian, June 26, 2002). This is a small sample of worries arising from recent research. Today, we are told we risk diabetes, heart disease, and cancers from eating the “wrong sort of food.” Weight problems caused by an addiction to high-fat and high-sugar convenience foods, or simply an ignorance of the alternatives, carry the risk of these and other diseases manifesting in later life. One in ten children under age four is now classified as obese, and health problems resulting from being overweight cost Britain some two billion pounds a year. It has been estimated that if we continue eating a “junk food” diet, in forty years time half the population will be obese. Furthermore, specialists also fear that ­anemia due to poor nutrition in early life can have long-lasting effects on a child’s mental development and learning ability.

Although longevity has increased over the last few centuries, many folk live the last years of their lives with the fear of disease, if not the actuality of it, but old age and disease do not necessarily go together. In the remote Andean highlands of Ecuador, there are communities of people who it is claimed live for 140 years or more and who remain agile and lucid right to the end. Death from heart disease and cancer is unknown in these high mountain valleys but rife in nearby towns. David Davies, an English zoologist and member of the gerontology clinic, University College, London, who has made a study of these “centenarians of the Andes,” found that the people who have the best chance of a healthy old age are those who actively use their minds and bodies, even toward the end of their life span. He looked at many elements of their life and environment, from genetic factors to the tranquility and lack of stress in their way of life. The folk who lived longest were found among those who lived on a subsistence diet, which was low in calories and animal fat. Typically, the main meal of the day was eaten in the early evening and was made up of very small wild potatoes, yukka, cottage cheese, and maize or bean gruel. Melons were eaten for dessert. Sometimes green vegetables, cabbage, or pumpkins were added to the menu, and sweet corn cobs were often taken to work for lunch. The people working in the fields ate fruit throughout the day. The climate is ideal for citrus fruits, and many other “hedgerow” fruits such as mora (like a blackberry), guava, and naranjilla are abundant, too. Meat was only eaten rarely, a type of cottage cheese was made from goat or cow milk, and eggs were eaten raw or almost raw (Davies 1975).

Though these people are very healthy and extremely long-lived, we mustn’t necessarily jump to the conclusion that this diet is perfect for the human system; their diet is restricted by the environment they live in. However, if we look at other communities of long-lived folk, the parallels are striking. The Hunzas of northeast Kashmir also live in mountainous regions and have a diet that includes wheat, barley, buckwheat, beans, chickpeas, lentils, sprouted pulses, pumpkins, cottage cheese, and fruit—the famous Hunza apricots and wild mulberries. Meat is again only eaten rarely, and because fuel is in short supply, when food is cooked it is usually steamed—a method of cooking that is the least damaging to the chemical nutrients in the food. Hunzukut males, like the people in the Andean highlands, are also reported to live to 140 years of age. So, we must conclude that these diets are, at the very least, much more suitable than the ones we depend on in the affluent industrialized countries.

There seems to be no definitive study that has so far convinced society as a whole that nutritionally we are barking up the wrong tree (or at least not picking from the right one). But there are many scraps of information that support the thesis that a more natural diet is the most beneficial option. Lymphocyte production and hence resistance to illness is boosted by consuming the nutrients that occur in optimal proportions and quantities in uncooked vegetables. There are also a huge number of cases in which raw food, particularly fruit and vegetable juices, has seemingly cured a wide range of illnesses. Migraines, skin complaints, tuberculosis, mental disorders, heart disease, cancers, and a host of other diseases have responded favorably to a diet rich in raw food. There are clinics, foundations, and institutions throughout the world that offer therapies based on “living nutrition.” Such diets are much closer to our ancestral diets than the chips, pies, and cookies that adorn most of our supermarket shelves.

As with all organisms, hominids in the course of evolution were locked into the biological matrix of their environment. Whether our diet consisted of insects, fruit, or meat, it was all biologically active material. Some primates today eat a bit more of this or that; much coverage has been given recently to meat-eating chimps, but this comprises a relatively small percentage of their diet. Despite their skill in capturing live prey, chimpanzees actually obtain about 94 percent of their annual diet from plants, primarily ripe fruits. Primate biochemistry is largely based on plants, and a plant-based diet is what hominids were eating during their evolutionary development. A pictorial representation of an early human living in the forest, lounging around eating fruit, may be more accurate than one in which he is dressed in animal skins, spear in hand, on the hostile open plains.

The lack of plant material in the fossil record has led, according to Richard Leakey, the paleoanthropologist famed for his work in Kenya, to an overemphasis on meat eating as a component of the early hominids’ life. He also finds some of the work on tooth analysis “very surprising” (Leakey, 1981, 74). The teeth of Australopithecus robustus fall into the fruit-eating category. The patterns of wear and the small scratches left on the enamel appear very similar to those of the forest-dwelling chimpanzees, yet here was a hominid that was supposed to live on the plains in an era when the climate was dry and the vegetation mainly grass. The examples ofRamapithecus teeth that have been similarly analyzed show exactly the same patterns, and the teeth of Homo habilis, the first creature to be awarded Homo status, also have smooth enamel typical of a chimpanzee. This evidence is extremely relevant. All the early hominids and their great ape cousins were mainly fruit-eaters. The teeth of Homo erectus suggest a more omnivorous diet. The enamel from their teeth shows scratches and scars that are compatible with grit damage, possibly from consuming bulbs and tubers. As a response to a cooling climate and a contraction of the forest, did this species widen its diet to adapt to a new environment? Some forest would have remained intact along the wetter river systems. Chimpanzees and gorillas survived there along with, we suspect, another hominid whose teeth were very well adapted to fruit eating—Homo sapiens.

Primates, given a choice, will select fruit in preference to any other food. Fruit is a rich, nutritious, and easily digestible food. If it is available, this is what all the great apes prefer to eat. However, other foods are eaten regularly. Our nearest relative, the bonobo, eats between 60 percent and 95 percent fruit, depending on the fruit productivity of its specific habitat. The rest of its diet comprises mostly shoots and herbs and a small amount of insects, eggs, and the occasional small mammal. Fallback foods like bark may also be eaten in times of fruit scarcity.

What humans in the forest ate is, of course, unknown, but it is likely that they would have eaten a similar balance of foodstuffs. They would not have been purely vegetarians. Even figs (perhaps the most preferred food) contain a small amount of insect matter as their pollination mechanism results in eggs and larvae of small wasp species remaining in the fruit. These insects may have served as an important source of essential micronutrients such as vitamin B12 and provided a little extra protein.

As they were the most highly intelligent animals in the forest and fruit was the best food, it is likely that humans developed strategies to maintain a high percentage of fruit all year round. Being efficient bipeds would have given them the potential to travel easily between widely separated fruit sources. The quest for distant fruit trees may have even honed their bipedal adaptation. The larger arboreal primates are known to travel on the ground between distant fruit trees, as it is more efficient than traveling in the trees. Archaic humans, being better-adapted bipeds than apes, would have found this way of life much easier.

Humans Are by Nature Frugivorous

There has been much study and even more speculation about what sort of diet our teeth and guts are best designed for. From the type of ­dentition, gut length, and toxicity of foods like meat, a very strong case can be built for Homo sapiens being designed to eat and process a largely fruit-based diet. The brain’s requirements for food and the gut’s requirements for energy, the optimal acid/alkali balance, and the structure of the intestines all point to a frugivorous diet. A shift to fruit specialization answers all the problems and anomalies that have spawned countless conflicting theories.

Katherine Milton, professor of anthropology at the University of California, Berkeley, has carried out important work on diet and primate evolution. Her research has led her to believe that “the strategies early primates adopted to cope with the dietary challenges of the arboreal environment profoundly influenced their evolutionary trajectory” (Milton 1993). This has a great significance for us today for the foods eaten by humans now bear little resemblance to the plant-based diets anthropoids have favored since their emergence. She believes these findings shed light on many of the health problems that are common, especially in our industrially advanced nations. Could they be, at least in part, due to a mismatch between the diets we now eat and those to which our bodies became adapted over millions of years?

The plant-based food available in the forest canopy comprises fruit and leaves, but subsisting on this diet poses some challenges for any animal living there. For a start it is high in fiber that is not only difficult to break down and hence digest but also takes up space in the gut that may otherwise be filled with more nutritious foods. Many plant foods also lack one or more essential nutrients such as amino acids, so animals that depend on plants for meeting their daily nutritional requirements must seek out a variety of complementary food sources. Fruit is usually the food of preference, for it is rich in easily digested forms of carbohydrate and relatively low in fiber, but its protein content is low (the seeds may be protein rich, however). Leaves offer higher protein content, but they are lower in nutrients and contain much more fiber. Balancing these constraints has led to different strategies that are reflected in behavior and physiology. Colobine monkeys have compartmentalized stomachs (a system analogous to that of ruminants) that allow fiber to be fermented and hence processed very efficiently, but humans and most other primates pass fiber largely unchanged through their digestive systems. Some fiber can be broken down in the hind gut of these latter species, but the process is not as efficient as that in theColobus genus.

Milton’s research focused on two contrasting species of South American primates: howler and spider monkeys. These two species are about the same size and weight as each other and live in the same environment, eating plant-based foods, yet they are very different. Howler monkeys have a large colon, and food passes through their digestive system slowly, whereas spider monkeys have a small colon through which food passes more quickly. These physiological differences relate to dietary specialization. The foundation of the howlers’ diet is young leaves: 48 percent of their diet is leaves, with 42 percent fruit and 10 percent flowers. The spider monkeys’ diet comprises 72 percent fruit, 22 percent leaves, and 6 percent flowers. Another fundamental difference is that although these animals are the same size, the brains of spider monkeys are twice the size of howler brains. Very significantly, Milton comments, “The spider monkeys in Panama seemed ‘smarter’ than the howlers—almost human” (Milton 1993).

This is something we have commented on before: big brains and a diet high in fruit appear to go together. Why should this be so? Could this brain enlargement result from the need to memorize the location of productive fruit trees, as some have suggested, or did elements within the fruit itself fuel this change more directly, as we propose? Animals such as squirrels, and even birds like jays, memorize the locations of stored food most efficiently without an overlarge brain, thus it seems that something else must be responsible.

Although Milton has concluded that it is quite difficult for primates to obtain adequate nutrition in the canopy, she observed that spider monkeys consume ripe fruits for most of the year, eating only a small amount of leaves. Bonobos also appear to find enough food to eat easily, for much of their time is spent in other “social” activities. Thus being a fruit-eating forest primate appears a very viable option, but one question remains: If fruit is so low in protein, how do these fruit specialists obtain an adequate supply of these essential nutrients? Milton found that spider monkeys pass food through their colons more quickly than leaf-eaters such as howler monkeys. This speed of transit means that spider monkeys have a less efficient extraction process, but as much more food can be processed, it more than makes up. By choosing fruits that are highly digestible and rich in energy, they attain all the calories they need and some of the protein. They then supplement their basic fruit-pulp diet with a very few select young leaves that supply the rest of the protein they require, without an excess of fiber. Of course, by processing so much fruit, a large quantity of chemicals that naturally occur in fruit will also be absorbed. It should also be noted that wild fruit contains a higher percentage of protein than the cultivated fruit that is available to us humans today. It is clear that many wild primates are able to satisfy their daily protein and energy requirements on a diet largely or entirely derived from plants. It is likely that our ancestors in the forest did, too.

As stated, the wild fruit that we propose was the mainstay of our ancestral diet for the longest and most significant part of our evolutionary history contains more fiber than the fruit we buy today in our shops. Chimpanzees take in about 100 grams (3.52 ounces) of fiber a day compared with about 10 grams (0.35 ounces) that the average Western human consumes. At one time it was believed that humans did not possess microbes capable of breaking down fiber. Studies on the digestion of fiber by twenty-four male college students at Cornell University, however, found that bacteria in their colons proved quite efficient at fermenting the fiber of fruit and vegetables. The microbial populations fermented some three-quarters of the cell wall material, and about 90 percent of the volatile fatty acids that resulted were delivered to the bloodstream (Wrick et al 1983). It has been estimated that some present-day human populations with a high intake of dietary fiber may derive 10 percent or more of their required daily energy from volatile fatty acids produced in fermentation.

Furthermore, experimental work on human fiber digestion has shown that our gut microfloras are very sensitive to different types of dietary fiber. We are very efficient at processing vegetable fiber from dicotyledonous sources (flowering plants like fig trees, carrots, and lettuces) but are less so from monocotyledons (grasses and cereals). This provides yet another pointer to the archaic diet of humans as being largely fruit based and indicates that the grass seed that we eat so much of today in cereals, cookies, and much else is a poor substitute.

The chimpanzee gut is strikingly similar to the human gut in the way it processes fiber. As the percentage of fiber in the diet increases, both humans and chimpanzees increase the rate at which they pass food through the gut. These similarities indicate that when food quality declines both these primates are evolutionarily programmed to respond to this decrease by increasing the rate at which food passes through the digestive tract. And this compensates for the reduced quality of the food available.

It appears that the human system then, like those of the chimps and bonobos, is designed for a plant-rich fibrous diet. We are not designed for a diet high in refined carbohydrates and low in fiber or one that includes significant quantities of animal protein. Meat eating in man has been, on an evolutionary timescale, a very recent development. It certainly couldn’t have influenced the development of our physiology. Though the passage of food through the guts of spider monkeys, chimps, and humans is faster than in leaf specialists like howlers, it is much slower than in carnivores. Meat hanging around in the digestive system is bad news because of its inherent toxicity. The transit time for the passage of food through a carnivore’s gut is between seven and twenty-six hours, while for humans it is between forty and sixty hours.

Though we do have a shorter colon and a longer small intestine than the great apes (and this has led one camp of researchers to speculate that our intestines are more similar to those of carnivores), these differences are more appropriately explained by a specialist fruit diet, not a carnivorous or grain-based one. Fruit is easier to digest than leaves, tubers, and stems, and has a lower fiber content. Thus a specialist fruit-eater would not need such a long colon as other apes that have more fibrous bulk to deal with.

Another feature of humans that is strongly indicative of our vegetarian origins is our inability to synthesize our own internal vitamin C. This trait is very rare, but where it occurs, the animals concerned (such as guinea pigs) eat a plant-based diet. In these cases ample supplies of the vitamin are available within the food. Vitamin C plays many extremely important roles within the human body. Research seems to be always finding more functions for this “miracle chemical.” These have been summarized by Ross Pelton, clinical nutritionist and cancer researcher at the University of California, in his book Mind Foods and Smart Pills: Vitamin C stimulates the immune system, enabling one to better resist diseases. Terminal cancer patients taking megadoses of vitamin C have been found to live longer. It promotes faster wound healing and reduces the amount of cholesterol in the blood. It is a powerful detoxifier and protects against the destructive power of many pollutants. In addition, it protects the body against heart disease, reduces anxiety, and is a natural antihistamine. A severe deficiency causes scurvy and eventually death. Increasing its intake has been found to increase mental alertness and brain functioning in a variety of ways. Vitamin C is the main antioxidant that circulates in the blood. When available in sufficient quantity, blood carries it around the body, washing over the cells to create a bath of protection. Whenever a free radical turns up, a molecule of vitamin C gives up one of its own electrons to render the free radical ineffective. According to Pelton this process may take place somewhere between one hundred thousand and one million times a second, depending on the body’s level of metabolism and the amount of vitamin C available. Unfortunately, with each free radical decimated, a molecule of vitamin C is lost, so the body rapidly loses its supply of vitamin C (Pelton 1989).

Vitamin C is a key player in keeping our neural system healthy. The body has a system that operates like a kind of a pump to concentrate vitamin C around our nerve and brain tissues. These tissues have more unsaturated fats than any other organs in the body, making them more vulnerable to attack by free radicals and oxidation. The vitamin C pump removes vitamin C from the blood as it circulates to increase the amount of vitamin C in the cerebrospinal fluid by a factor of ten. The pump then takes the concentrated vitamin C from the ­cerebrospinal fluid and concentrates it tenfold again in the nerve cells around the brain and spinal cord. Thus our brain and spinal cord cells are protected against free radical damage by more than a hundred times as much vitamin C as our other body cells.

For such an important chemical, it is extremely odd that we are dependent on vitamin C from outside sources. But how much of it does the body need? Research carried out by the Committee on Animal Nutrition demonstrated that monkeys needed around 55 milligrams of vitamin C per kilogram (2.2 pounds) of body weight. When this measure is extrapolated to humans, a 150-pound person would need a daily intake of 3,850 milligrams. Nutritional science recommends that a human needs 45 milligrams each day. This is just enough to prevent scurvy but not enough to keep the body functioning at an optimal level. We would not, and indeed do not, obtain the sort of levels our bodies really need from a diet high in meat and low in vegetables and fruit, but we would from one high in fruit, shoots, and leaves. Analysis of wild plant foods eaten by primates shows that many of these foods contain notable amounts of vitamin C. The young leaves and unripe fruit of one species of wild fig were found to contain some of the highest levels ever reported. Our closest living relatives, the great apes, eat a diet that contains between 2 and 6 grams (0.07 to 0.21 ounces) of vitamin C every day. When our ancestors were living in the forest they would have consumed similar amounts.

In contrast, we can and do produce our own vitamin D. This vitamin cannot be obtained from a leaf- and fruit-based diet, but it can from a carnivorous one, thus if we were designed to eat meat we would have less need to synthesize our own. Being able to synthesize vitamin D and not vitamin C is then a strong indication of our true ancestral diet and the one we are really adapted to. Accumulating evidence for meat being an unhealthy food option further strengthens this case. One study at the Cancer Epidemiology Unit in Oxford showed that vegetarians were 24 percent less likely than nonvegetarians to die of ischemic heart disease (Key 1999).

Carbohydrates also appear to be problematical when eaten in large amounts. A diet high in carbohydrates, especially refined carbohydrates (cakes, cookies, pasta, etc.), dumps large amounts of glucose rapidly into our bloodstream. This can cause insulin resistance in which the absorption of glucose from the bloodstream is disrupted. This in turn can lead to obesity, adult onset diabetes, hypertension, heart attacks, and strokes. It can also lead to an excess of male hormones, which, among other effects (e.g., aggression), encourages pores in the skin to ooze large amounts of sebum. Acne-promoting bacteria thrive on sebum. Up to 60 percent of twelve-year-olds and 95 percent of eighteen-year-olds in modern society suffer from acne, yet it is almost unknown in subsistence societies such as the Kitava Islanders in Papua, New Guinea, and the Ache of the Amazon. The Inuit people of Alaska also used to be free of acne, but they began to be affected by these skin complaints after they started to eat processed foods.

The problem with eating highly processed carbohydrates may be further reaching still. If refined cereal consumption results in an excess of male hormones it could have a ripple effect on the immune system for we know that the thymus gland starts to shrink in response to these hormones at the time of puberty. (More carbohydrates lead to more testosterone, which shrinks the thymus gland, which is seat of much of our immune response.) Grain products have also been associated with celiac disease, an autoimmune condition of the gut, and some researchers suspect they trigger rheumatoid arthritis, too.

It is highly significant that these foods have the ability to alter the quantity or at least the activity of our hormones. It is another example of the way our diet can affect the way our bodies work. It is possible, probable even, that they also affect the way we act, and thus how we moderate our sense of self. If we compare refined carbohydrates with fruit, we can see that fruit has a much lower glycemic index, which means it is digested more slowly, thus avoiding the problems of the “glucose rush.” The chemicals within fruit also reduce the activity of sex hormones. They thus have the diametrically opposite effect to that of refined cereals.

There is a view held by some that meat, and particularly the high protein content of meat, was somehow responsible for the enlargement of our brains. The assumed “higher-quality” meat diet theoretically allowed more energy to fuel the brain with a shorter small intestine. This reasoning is flawed on several fronts. First, meat is supposed to be easy to digest and to be a high-energy food, but fruit is much more easily digested and provides more readily available energy, too. Second, if there were sufficient external pressure to bring about such a change as a shortening of the gut, we would expect other adaptations and changes toward a carnivorous diet as well. Certainly we would not expect adaptations to be heading in the opposite direction. Our teeth, for instance, are nothing like the teeth of a carnivore. The teeth of our nearest relative, the bonobo, are much better adapted to eating meat than human teeth are, and bonobos hardly eat any meat. In fact, it is known that bonobos are, if anything, more intelligent than chimpanzees, and it is chimps that eat at least some meat. So, if bringing meat into the diet of an ancestral human was enough to shorten the gut and expand the brain (both major changes), where are the parallel changes in areas that would be needed to cope with a meat diet?

If we look at areas such as dentition, the physiology to digest meat, and the ability to catch it, we find nothing that looks even vaguely carnivorous. If we lined up the three most evolved species of primates—chimps, bonobos, and humans—we would have to conclude that humans are, in fact, the least adapted to eat meat. Humans have much smaller teeth, and they cannot chase the meat nearly so well. Also there is a structural distinction between carnivore guts and those of frugivores or vegetarians. Our guts are like those of the noncarnivores; they are folded, smooth, and still significantly longer than a carnivore gut. There is a difference in saliva as well. Carnivore saliva is acidic, but the saliva of humans is alkaline, which provides the right functional environment for digestive enzymes, such as amylase, to break down starch.

Now, if we ask what sort of food really fits these human adaptations, we have to conclude it is fruit. Fruit fits the brain-gut energy equation: the shorter gut, the more ease of digestion, the lower the toxicity, and the smaller the teeth. Fruit is easy to assimilate, and the nutrition it provides is in a form that needs very little conversion to the real requirement of the brain—glucose. (The sugar in wild fruit tends to be rich in glucose and fructose compared with cultivated fruit that has been bred for its sweeter-tasting sucrose content.) Humans thus have a proportionately shorter small intestine than chimps and bonobos, not because of increased levels of meat in our diet but because of an increased specialization on sugar-rich fruit. High-quality fruit is low in toxicity and provides all the fuel the brain needs. Meat, conversely, is more difficult to digest, particularly without cooking, and then to turn protein into sugar requires yet more energy. So meat as an energy food doesn’t make as much sense as fruit that is full of fruit sugars that are easily assimilated and take little conversion.

The anatomy and physiology of our digestive system support the case for the biochemical role of tropical fruit in human development. However, the case could be stronger still if we could show that the human brain in archaic times actually worked the digestive system in a way that extracted the nutritive elements within the plant-based diets more efficiently. More research needs to be done in this area, but preliminary indications (from T. W.’s private research) hint that a digestive system run without interference from the left hemisphere may do just that.

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Andlauer, W., C. Stumpf, M. Hubert, et al. “Influence of Cooking Process on Phenolic Marker Compounds of Vegetables.” International Journal for Vitamin and Nutrition Research 73 (March 2003): 152–59.

Batmanghelidj, F. Your Body’s Many Cries for Water. Norwich, U.K.: Tagman Press, 2000.

Best, Simon. “A Nutritional Approach to Treating ADHD.” Nexus 8, no. 6 (October 2001): 17–22.

Blaut, M., L. Schoefer, and A. Braune. “Transformation of Flavonoids by Intestinal Microorganisms.” International Journal for Vitamin and Nutrition Research 73 (2003): 79–87.

Brookes, Martin. “Apocalypse Then.” New Scientist, no. 2199 (August 14, 1999).

Colgan, Michael. Your Personal Vitamin Profile. New York: Quill, 1982.

Courtillot, Vincent. Evolutionary Catastrophes. Cambridge University Press, 1999.

Darwin, Charles. The Descent of Man and Selection in Relation to Sex. London: John Murray, 1871.

Davies, David. Centenarians of the Andes. Norwell, Mass.: Anchor Press, 1975.

Fontana, L., J. L. Shew, J. O. Holloszy, et al. “Low Bone Mass in Subjects on a Long-Term Raw Vegetarian Diet.” Archives of Internal Medicine 165 (March 28, 2005): 1–6.

Fox, Douglas. “Cut the Carbs.” New Scientist, no 2230 (March 18, 2000).

Groves, C. A Theory of Human and Primate Evolution. Oxford, U.K.: Oxford Science Publications, 1989.

Herraiz, Tomas. “Analysis of the Bioactive Alkaloids Tetrahydro-B-carboline and B-carboline in Food.” Journal of Chromatography A 881, no. 1 (2000): 483–99.

Kaplan, Matt. “Why Bonobos Make Love, Not War.” New Scientist, no 2580 (December 2006).

Kapleau, Phillip. To Cherish All Life. Rochester, New York: The Zen Center, 1981.

Keeley, Jennifer. “Case Study: Appleton Central Alternative Charter High School’s Nutrition and Wellness Program.” Better Food, Better Behavior. Battle Creek, Mich.: W. K. Kellogg Foundation, 2004.

Kenton, Leslie, and Susannah Kenton. Raw Energy. Salt Lake City: Century, 1984.

Key, T. J., G. E. Fraser, M. Thorogood, et al. “Mortality in Vegetarians and Nonvegetarians: Detailed Findings from a Collaborative Analysis of 5 Prospective Studies. Am J Clin Nutr 70, no. 3, (1999): 516–24.

Khamsi, Roxanne. “You Are What Your Grandmother Ate.” New Scientist News Service. http://www.newscientist.com/article/dn10518-you-are-what-your-grandmother-ate.html#.UmqBjCTB0t4. Accessed October 25, 2013.

Koestler, Arthur. The Ghost in the Machine. New York: Macmillan, 1968.

Kouchakoff, Paul. “The Influence of Food Cooking on the Blood Formula of Man.” InProceedings of First International Congress of Microbiology. Paris, 1930.

Kuratsune, Mananore. “Experiments of Low Nutrition with Raw Vegetables.” Kyushu Memoirs of Medical Science 2, no. 1–2 (June 1951).

Larsen, Spencer. Skeletons in Our Closet: Revealing Our Past through Bioarchaeology. Princeton: Princeton University Press, 2002.

Leakey, Richard. The Making of Mankind. London: Michael Joseph Limited, 1981.

Lewin, R., “Rise and Fall of Big People.” New Scientist 146 no 1874 (April 22, 1995).

Mayell, Hilary. “Oldest Human Fossils Identified.” National Geographic News(February 2005), http://news.nationalgeographic.com/news/2005/
02/0216_050216_omo.html. Accessed February 3, 2014.

Milton, Katherine. “Diet and Primate Evolution.” Scientific American 269 (August 1993): 86–93.

———. “Micronutrient Intake of Wild Primates: Are Humans Different?” Comparative Biochemistry and Physiology Part A 136 (2003): 47–59.

———. “Nutritional Characteristics of Wild Primate Foods: Do the Diets of Our Closest Living Relatives Have Lessons for Us?” Nutrition 15, no. 6 (1999): 488–98.

Morgan, Elaine. Scars of Evolution. New York: Penguin Books, 1991.

Odent, Michael. Primal Health. London: Century Hutchingson Ltd., 1986.

Pelton Ross. Mind Food and Smart Pills. New York: Doubleday, 1989.

Phillips, Roger, and Martyn Rix. Vegetables. London: Pan Books, 1993.

Pottenger, F. M., Jr. Pottengers’s Cats. La Mesa, Calif.: Price-Pottenger Nutritional Foundation, 1983.

Pottenger, F. M., Jr., and D. G. Simonsen. “Heat Labile Factors Necessary for the Proper Growth and Development of Cats.” Journal of Laboratory and Clinical Medicine 25, no. 3 (1939): 238–40.

Powell, C. S., and W. W. Gibbs. “Rambling Road to Humanity.” Scientific American(June 16, 1997).

Price, Weston A. Nutrition and Physical Degeneration. La Mesa, Calif.: Price-Pottenger Nutritional Foundation, 1970.

Raichle, Marcus E., and Debra A. Gusnard. “Appraising the Brain’s Energy Budget.”PNAS 99, no. 16 (2002): 10237–39.

Ruff, C. B., E. Trinkaus, and T. W. Holliday. “Body Mass and Encephalization in Pleistocene Homo.” Nature 387 (1997): 173–76.

Senut, B., M. Pickford, D. Gommery, et al. “First Hominid from the Miocene (Lukeino Formation, Kenya).” Comptes Rendus de l’Académie des Sciences-Series IIA-Earth and Planetary Science 332 (2001): 137–44.

Spinney, Laura. “Slicing through Fat.” New Scientist no. 1974 (April 1995).

Tattersall, Ian. “Out of Africa Again . . . and Again?” Scientific American (April 1997).

———. “Once We Were Not Alone.” Scientific American (January 2000).

Thorpe, S. K. S., R. L. Holder, and R. H. Crompton. “Origin of Human Bipedalism as an Adaptation for Locomotion on Flexible Branches.” Science 316, no. 5829 (2007): 1328–31.

Williams, Roger. Nutrition against Disease. New York: Pitman Publishing Co., 1971.

Wrick, K. L., J. B. Robertson, P. J. Van Soest, et al. “The Influence of Dietary Fiber Source on Human Intestinal Transit and Stool Output.” J Nutr 113, no. 8 (1983): 1464–79.81P6RrQ365L

Scientists Spot New Clues to a Deadly Lung Disease.

Scientists believe they’ve found a key biological player inidiopathic pulmonary fibrosis (IPF), a uniformly fatal lung disease that kills thousands of Americans each year.

The finding may be another step forward for patients who have typically had a bleak prognosis. Last month, studies revealed that two new medications might offer some hope for the first effective treatment of IPF.

Without a lung transplant, IPF remains an incurable, progressive disease that causes tissue deep in the lungs to stiffen and scar. Seventy percent of patients die within five years.

According to the Coalition for Pulmonary Fibrosis, more than 128,000 Americans suffer from IPF, with 40,000 dying from the disease each year.

The disease starts with shortness of breath or a dry, hacking cough, but soon robs the person’s body of the oxygen needed to move about or properly function, according to the U.S National Institutes of Health. Doctors don’t know what causes IPF, although they suspect that smoking, genetics, certain viral infections or acid reflux could play a role in damaging the lungs, the NIH said.

In the new study, researchers found that chronically high levels of an injury-repair protein called chitinase 3-like-1 (CHI3L1) seems linked to an accumulation of scar tissue in the lungs of people with IPF.

“The CHI3L1 is doing exactly what it is supposed to do — it is designed to shut off cell death and decrease injury,” study co-senior author Dr. Jack Elias, dean of medicine and biological sciences at Brown University, explained in a university news release.

According to Elias’ team, CHI3L1 is produced in response to injuries to lung tissue. The protein helps shield injured cells from dying, and at the same time it helps spur tissue repair — fibrosis — to “patch up” the damage. But this mechanism appears to get out of control, so stiff, fibrotic tissue keeps piling up.

“At the same time [the protein] is decreasing cell death it is driving the fibrosis,” Elias said. ” You’ve got this ongoing injury so you’ve got these ongoing attempts to shut off injury, which stimulate scarring.”

The findings came about after the multi-center team of researchers compared tissues and blood from patients with IPF against those of healthy patients. Those biopsies showed consistently elevated rates of CHI3L1 in the IPF group, but not in others.

“This demonstrates that the CHI3L1 plays a key role in controlling lung injury in this setting,” Elias said.

The findings were further corroborated in studies in mice. The rodents were first manipulated to develop an IPF-like condition. When CHI3LI protein levels were high, the mice showed evidence of accelerated scarring of lung tissue, the team said.

But questions remain about widespread screening.

While not all studies conducted in the lab or in mice translate to success in humans, the new research “lays the foundation” for efforts to develop new treatments for IPF, Elias said.

“To my knowledge this is the first comprehensive paper that’s been able to explain the many facets and presentations of IPF,” he added. “It explains and links the injury and the repair responses that are critical in the disease. It also provides an explanation for the slowly progressing patients and the patients that experience acute exacerbations.”

The study was published June 11 in the journal Science Translational Medicine.

The news comes on the heels of two papers published in May in the New England Journal of Medicine. Those studies found that two drugs, pirfenidone and nintedanib, appear to slow the advance of IPF.

“It is an optimistic time for patients with fibrosis,” Dr. Gregory Cosgrove, chief medical officer for the Pulmonary Fibrosis Foundation, said at the time of the studies’ release.

“It’s been frustrating when we have not identified an effective therapy over the past 10 to 15 years,” he said. “But that degree of frustration has prompted the IPF community to really come together to support participation in clinical trials, and those trials have provided a foundation for these new advances.”

Electromagnetic Safety: How Cell Phone Radiation is Causing Harm – disinformation

Photo from "Mobilize: A Film About Cell Phone Radiation"

Most people own a cell phone, and in today’s society it would be difficult to function without one. But what if I told you that some studies (often ignored by mainstream media and politicians, surprise!) have found dangers associated with cell phone use?

Cell phone use has been linked to changes in DNAcancer, and low sperm count. The radiation is especially dangerous to the developing brains in children and adolescents.


According to CNET:

“For a phone to pass FCC certification and be sold in the United States, its maximum Specific Absorption Rate, or SAR level must be less than 1.6 watts per kilogram.”

CNET ranked the top 20 phones with the highest SAR levels and those with the lowest SAR levels. The highest SAR is tied between the Motorola Droid Maxx and the Motorola Droid Ultra, both emitting 1.54 SAR. The VeryKool RS90 has the lowest SAR level at 0.18 SAR.

Photo from "Mobilize: A Film About Cell Phone Radiation"


There are many options available to protect yourself, while still retaining the use of your phone.

  • The most obvious method is to use a pair of earbuds with a microphone. They’re cheap and allow you to keep the radiation away from your brain.
  • The Pong Case: The Pong Case “strengthens your signal, increases your range, and greatly reduces your exposure to potentially harmful wireless energy.”
  • Keep phones away from body parts when not in use.
  • Text whenever possible – keeping the phone about a hand’s length away from the body.


1. “Cellular Telephone Russian Roulette” by Robert C. Kane

You can download a free copy of the eBook here.

“Robert C. Kane has been actively employed in the tele-communications industry for more than thirty years. He holds a BSEE from the Midwest College of Engineering, an MSEE with an emphasis in electromagnetics from the Illinois Institute of Technology where he has also completed the full course of study and research leading to a Ph.D. in electrical engineering with emphasis in the fields of electromagnetics and solid-state physics. As a research scientist and product design engineer, he has been directly involved with programs and projects for the design and development of portable cell phones, radio frequency, mobile radios, microwave telecommunications systems, video display systems, and biological effects research.”

2. International Commission for Electromagnetic Safety (ICEMS)

ICEMS has a lot of educational and prevention resources.

3. Mobilize: A Film About Cell Phone Radiation

Mobilize is one of Disinfo’s newest documentaries that details the effects of cell phone radiation. Its official release is September 9th, but we’re mailing a limited quantity to those who preorder.

“’Mobilize’” is an explosive investigative documentary that explores the potential long-term health effects from cell phone radiation, including brain cancer and infertility. This thought-provoking film examines the most recent scientific research and the harsh challenges politicians face trying to pass precautionary legislation. Featuring interviews with expert researchers, mobile phone industry representatives, and prominent politicians, ‘Mobilize’ illuminates how industry’s economic and political influence can corrupt public health.’”


Comparative Effectiveness Research and Outcomes of Diabetes Treatment.

Randomized clinical trials (RCTs) are the gold standard for advancing the science of medicine. However, many important clinical questions probably will never be answered by RCTs simply because many trials are extraordinarily expensive and RCTs might not always be appropriate for addressing some research questions. In fact, most clinical trials do not enroll typical patients; trial participants are volunteers who agree to be studied with limited compensation and often do so primarily to benefit other patients. Clinical trials are designed to answer questions about whether something works (efficacy), but usually are poorly suited to answer questions about how well something works on usual patients seen in clinical practice (effectiveness). Numerous studies have shown that the effect sizes reported in clinical trials are rarely achieved in practice, raising concerns that more generalizable results are needed to better inform real-world clinical decisions.




From the desk of Zedie.

Scientists find trigger to decode the genome

Scientists from The University of Manchester have identified an important trigger that dictates how cells change their identity and gain specialised functions.

And the research, published today in Cell Reports, has brought them a step closer to being able to decode the genome.

The scientists have found out how embryonic stem cell fate is controlled which will lead to future research into how cells can be artificially manipulated.

Lead author Andrew Sharrocks, Professor in Molecular Biology at The University of Manchester, said: “Understanding how to manipulate cells is crucial in the field of regenerative medicine which aims to repair or replace damaged or diseased  or tissues to restore normal function.”

During the research the team focussed on the part of the cellular genome that gives a gene its expression known as the ‘enhancer’. This controls the conversion of DNA from genes into useful information that provides the building blocks that determine the structure and function of our cells.

Different enhancers are active in different cell types, allowing the production of distinct gene products and hence a range of alternative cell types. In the current study, the team have determined how these enhancers become active.

Professor Sharrocks said: “All of us develop into complex human beings containing millions of cells from a single cell created by fertilization of an egg. To transit from this single cell state, cells must divide and eventually change their identity and gain specialised functions. For example we need specific types of cells to populate our brains, and our recent work has uncovered the early steps in the creation of these types of cells.

“One of the most exciting areas of regenerative medicine is the newly acquired ability to be able to manipulate cell fate and derive new cells to replace those which might be damaged or lost, either through old age or injury. To do this, we need to use molecular techniques to manipulate  which have the potential to turn into any cell in our bodies.”

But one of the current drawbacks in the field of regenerative medicine is that the approaches are relatively inefficient, partly because scientists do not fully understand the basic principles which control  determination.

“We believe that our research will help to make  more effective and reliable because we’ll be able to gain control and manipulate  – thus our understanding of the regulatory events within a cell shed light on how to decode the genome,” concluded Professor Sharrocks.

GMO studies reveal that 18 million Americans suffer from gluten and GMO toxicity.

What is it about gluten and GMO that have the masses asking questions? What’s the latest debate that is constantly engaged on the best health websites in the world? How could it be that 18 million folks just can’t figure out their internal rotting-food problem? Who can’t figure out their inflammation, headaches and IBS, that leads to ulcers, prostate cancer, bladder cancer and pancreatic cancer, when 90% of the food on the shelves of America sticks in your gut, for days, and weeks and even years, in your digestive tract, and it contains pesticides.


Are you a weed or a bug, because if you eat conventional food regularly, you may be dying like one in the fields of Monsanto, Cargill and Bayer.

How would you like to get a glimpse into several GMO studies that you won’t hear about on TV, or read about in the newspapers, that explain how most conventional food gets processed and “fortified” with genetically modified ingredients that cause cancer? Take a look at the countries around the world that are screaming “NO!” to GMO. Countries all over the world ban GMO because of studies like the following:

Three precedent-setting studies on GMO toxicity

1. Research from Canada has successfully identified toxic GMO pesticides in maternal and fetal blood, including Monsanto’s Bt toxin used in corn. The study is published in the journal Reproductive Toxicology. This study uses blood samples from 38 pregnant women and 30 non-pregnant women and points out how susceptible the fetus really is to the adverse affects of foreign chemicals that are not naturally produced (GMO/insecticide/pesticide).

The results provide baseline data for future studies exploring new areas of research relating to nutrition, toxicology and reproduction in women. This study is a “cornerstone in the advancement of research in this area.”

Learn more from Collective-Evolution, a great resource:

2. Pesticide inside gluten infects 18 million Americans — it’s not just an “intolerance.” A new study links GMOs to gluten disorders and comes to you via the US Department of Agriculture and the EPA, released by the one and only Institute for Responsible Technology (IRT), who really looks out for human health on this planet. You will be wise to review this one.

The authors relate GM foods to five conditions that trigger or exacerbate gluten-related disorders, including autoimmune disorder, America’s favorite sick care “catapult.” In fact, imbalanced gut bacteria is where it all begins, and the study delves into intestinal permeability, allergic responses and impaired digestion.

IRT is a world leader in educating policy makers and the public about GMO food and crop concerns. Keep reading.

3. GM corn and rat tumors linked! Rats and fruit flies and bees, oh my! They’re all dying from pesticides and insecticides when given to them as food, or sprayed on their food, or grown into their food using biotechnology gene mutation manipulation. How strange that animals should die when they eat chemicals. Just a couple of years ago, the journal of Food and Chemical Toxicology published a research paper called “Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize.” [emphases added]

If you’re not a frequent “flyer” of Natural News, then you probably don’t know a thing about it. That’s okay; you can learn about the study right now. Under controlled conditions, while examining the possible effects of a diet of GMO maize treated with Monsanto’s Roundup herbicide (only the most popular herbicide on the planet), rats died young with horrific tumors the size of golf balls. The conclusion? GM crop, despite the propaganda spread by the Biotech industry, is LOWERING the United States’ yields and INCREASING pesticide use.

GMO corn causes cancer in animals, and last time anyone looked, human beings are also animals. By the way, this was a LONG-TERM study, for all those biotech “enthusiasts” living in denial.

For more precedent-setting studies, delve into the recent report from Collective-Evolution below. Also read about the Seralini study that should have never been retracted! Hundreds of top scientists know about reality, as do millions of health enthusiasts across the globe!

Are you still eating genetically modified gluten?

For more information and breaking news about GMOs, visit GMOs.NaturalNews.com.

Sources for this article include:








Obesity is not a disability.

Overeating is an addiction – if the EU court labels it otherwise, it will be a monumental act of denial
Ice cream cone on the beach

‘We eat three times more sugar than we did 50 years ago. It is obviously addictive, and marketed at children.’ Photograph: Peter Macdiarmid/Getty Images

Is obesity a disability or a choice gone awry? Danish child-minderKarsten Kaltoft was fired from his job because he was too overweight – at 25 stone – to tie a child’s shoe laces. He is suing for discrimination. His case will he heard by the European court of justice in Luxembourg today. If Kaltoft is successful, the ruling will be binding throughout the EU. Employers will be required to treat overweight employees as disabled and therefore requiring special treatment – priority parking, for instance, and sturdy furniture – and they will be unable to fire them for being overweight. (I will not say “fat”. Eating disorder professionals do not say fat because they know that compulsive eating and anorexia are twins, and dependent on self-hatred to thrive.) The right will scream that this is special treatment for “fat” people – they probably will say “fat”, not being eating disorder professionals, or even particularly kindly – who choose to be “fat” even if now they regret it, and have to be cut from their homes by emergency workers. On your bike, and so forth. Eat some kale.

This is a story about addiction. Sugar is more dangerous than the drugs we are taught to fear. Of course it is harder to wrestle with sugar – who can live without food? We eat three times more sugar than we did 50 years ago. It is obviously addictive, and marketed at children by cartoon characters and other grotesques. These overweight children, of which a too-large proportion are poor, because bad food is cheap and swift and delicious, will grow to be overweight adults, and these overweight adults will die too young.

Why is there no government ban on sugar advertising, you may ask? Don’t be stupid. Dave Lewis, an executive at Unilever – which sells, among other things, Solero, Cornetto, Pot Noodle, Magnum and Viennetta, as well as Carte D’Or, Ben & Jerry’s, Wall’s, Peperami and Marmite – chaired the Conservatives’ public health commission. McDonald’s and Coca-Cola sponsored the London Olympics, an act so cynical and destructive it seemed deliberately designed to kill satire, among other things. McDonald’s, particularly, is gifted in marketing duplicity. Its “restaurant” in the Olympic park was decorated with words like “succulent” blown up to obesity to mislead. Now it is giving fruit away with Happy Meals: children, embrace the pious maker of the McFlurry! Embrace your saviour!

What to do? The problem, as always when discussing addiction, is denial: the government’s denial, which is ideological; the people’s denial, which is comprehensive; and the addict’s denial, which is lethal. (The food industry’s denial is mere professional profiteering, and to be expected.) Since I do not expect the government to emerge from denial any time soon, or the food industry ever, let us move to the addict’s denial. Denial, at least partially – and here I address the hateful puddle of “libertarian” pundits and lobbyists directly, even as they sharpen their pencils to denounce Kaltoft as his own destroyer – is the reason overweight people sometimes need the walls of their homes broken down, and the reason why they continue to overeat when they can no longer bend down to tie a shoelace, or rise to face a mirror. Denial fuels some elements of the fat acceptance movement, which is right when it says that overweight people suffer discrimination, and wrong when it says there is no physical threat from overeating. Denial is both the essential element of addiction and the reason that non-addicts often misunderstand and despise the condition. If the addict says it is a choice to overeat, who are you, or I, to disagree?

The solution is dull, slow and not in the law. Mental health provision is scandalously small; misunderstanding of addiction is endemic; responsible advertising is a fantasy; food is over-processed; society is unequal; cruelty is rife. I have much sympathy for Kaltoft, but I do not think that calling him disabled will lengthen his life or help him to not eat himself to death. I think it is more likely that a friendly ruling will compound his denial and enrage the rest. (The disability advocacy charity Scope asked its Facebook and Twitter followers if obesity is a disability. The response was negative). It would be state-sponsored, continent-wide denial; it would be madness.


An Aspirin a Day? Only If You Have Had a Heart Attack .

FDA issues recommendation against preventative low doses

If you never have had any cardiovascular problems, the Food and Drug Administration (FDA) says you should not take aspirin to avoid a heart attack or stroke.

In a recommendation issued this week, the FDA says scientists have not proven aspirin therapy has any benefit for people without cardiovascular problems. This group includes those with risk factors such as a family history of heart disease.

At the same time, people taking aspirin every day face serious risks. These risks include developing dangerous bleeding into the stomach or brain.

What if I have an existing heart condition?

If you have heart disease, such as a prior heart attack, bypass surgery or stents, everyone agrees that you should be taking a daily baby aspirin (81 mg) unless your doctor determines that you have a very high bleeding risk. For people without previous heart disease, aspirin is generally not recommended because bleeding in the brain or stomach can occur with daily aspirin use—even if you are taking coated aspirin.

For individual patients, your doctor will be able to calculate your risks and benefits from taking aspirin. Every heart condition is different and every patient’s situation is unique. Your doctor will need to know your medical history and weigh the risks.

Only for a select few

When you have a heart attack, it’s because one of the coronary arteries, which provide blood to the heart, has developed a clot. The clot obstructs the flow of blood and oxygen to the heart.

Aspirin thins the blood, which makes it less likely to clot. The logic is that taking an aspirin a day helps prevent heart attacks.

Clinical data since the 1990s does show that a daily low dose of aspirin can help prevent a re-occurrence for people who have had a heart attackstroke or disease of the heart’s blood vessels, the FDA says.

But only a select few patients benefit from aspirin therapy – even among those who have had cardiovascular problems.

The patient who would benefit from aspirin therapy is someone who has every risk factor: high blood pressure, high cholesterol, strong family history, diabetes, smoking. Among patients with all of these risk factors, some of them we will treat with aspirin. But it’s not very many.

Bleeding common

Internal bleeding, especially in the stomach, is quite common with daily aspirin use.

So if you have a low risk of a heart attack, the bleeding risk may overwhelm any potential benefit of aspirin.

The recommendation came on the heels of the FDA denying a request from Bayer. The drug manufacturer asked to change its aspirin packaging to say consumers could use aspirin as a prevention measure, even if they have not had a heart attack, stroke or cardiovascular problems.

You should stop taking aspirin if you’re taking it without a doctor’s guidance to prevent cardiovascular problems and have no history of heart disease or heart attack.

Don’t self-medicate

Above all, talk with your doctor.

Frankly, self-medication is almost never a good idea, whether it’s aspirin or anything else.

The FDA recommendation applies to doses ranging from 81 milligrams in a low-dose tablet to the 325 milligrams in a regular-strength tablet.

For patients with a history of cardiovascular problems, the FDA says your doctor should tell you the aspirin dose and frequency that will provide the greatest benefit with the least side effects.

Levodopa better than any drug.

Whether to begin Parkinson’s treatment with the gold-standard levodopa or other therapy (e.g., dopamine agonist, MAO-B inhibitor) is a question debated among neurologists and patients.

A paper published today in The Lancet reports that early treatment of levodopa provides better mobility and quality of life after seven years over early treatment with dopamine agonists or MAO-B inhibitors. In the largest-ever Parkinson’s disease trial — called PD MED — a group of researchers from 80 sites throughout the United Kingdom and led by Dr. Richard Gray of the University of Oxford compared the three therapies in a total of 1,620 newly diagnosed patients, including those with young onset PD.

In a comment also published by The Lancet, Drs. Anthony Lang and Connie Marras (both from the University of Toronto) wrote, “The results of this study will help to persuade physicians and reassure patients that the fears that have served as the groundwork in establishing levodopa phobia — that often results in patients experiencing unnecessary and easily managed disability and reduction in quality of life in the early years of their disease — are unfounded.”

Some physicians are reluctant to begin patients on levodopa due to the earlier onset of levodopa-induced dyskinesia — a side effect of the medication that presents with jerky, fractured movements — and motor fluctuations or “off” episodes.

The PD MED study asked patients to complete a questionnaire on their quality of life relative to their mobility. After three years, patients on levodopa averaged 1.8 points better than patients on dopamine agonists or MAO-B inhibitors, and that beneficial difference remained seven years into the trial.

Dr. Gray was quoted saying, “Although the differences in favor of levodopa are small, when you consider the short- and long-term benefits, side-effects, quality of life for patients, and costs, the old drug levodopa is still the best initial treatment strategy for most patients.”

Dr Strobe: the man who stopped time and electrified photography .


If you could stop time, here is what you might see: a bullet being shot through an apple, an egg being cracked into a fan, or a play-by-play of Pancho Gonzales’s famous serve. MIT professor Harold Edgerton invented the strobe flash in the 1930s – and his stroboscopic photography captured amazing moments that would otherwise be missed in the blink of an eye

• Dr Harold Edgerton: Abstractions is at Michael Hoppen Gallery in London until 2 August

Bullet through the Apple, 1964
Bullet through the Apple, 1964
Pancho Gonzales Serves, 1949.
Pancho Gonzales Serves, 1949
Dropping an egg into a Fan!, 1940.  Best & HEE, MGM Academy Award Quicker 'n a Wink.
Dropping an Egg Into a Fan!, 1940, before …
Best & HEE, MGM Academy Award Quicker 'n a Wink, 1940.
… and after. This image is from the Oscar-winning short film about stroboscopic photography, Quicker’n a Wink
Cows and Flare at Stonehenge Ruins, 1944.
Cows and Flare at Stonehenge Ruins, 1944
Bubble Through a Helium Bubble ,1971.
Bubble Through a Helium Bubble, 1971
Child's Catapult, 1975.
Child’s Catapult, 1975
Bubble Chamber, 1967.
Bubble Chamber, 1967
Rex Taylor cracking the whip, 1965.
Rex Taylor Cracking the Whip, 1965
Pete Desjardin Diving, 1940.
Pete Desjardin Diving, 1940
Bullet Through Plexiglass, 1962.
Bullet Through Plexiglass, 1962
Foil Salute, 1938.
Foil Salute, 1938
Aerial views of the Stonehenge Ruins, 1944.
Aerial Views of the Stonehenge Ruins, 1944
Fire Cracker, 1975.
Fire Cracker, 1975. Photographs: Harold Edgerton Archive at MIT/Michael Hoppen Gallery