Protein Related Quotes

One stretch of the gene is repeated a variable number of times, and the version with seven repeats (the “7R” form) produces a receptor protein that is sparse in the cortex and relatively unresponsive to dopamine. This is the variant associated with a host of related traits—sensation and novelty seeking, extroversion, alcoholism, promiscuity, less sensitive parenting, financial risk taking, impulsivity, and, probably most consistently, ADHD (attention-deficit/hyperactivity disorder).

Stick recording electrodes into numerous species’ amygdalaefn9 and see when neurons there have action potentials; this turns out to be when the animal is being aggressive.fn10 In a related approach, determine which brain regions consume extra oxygen or glucose, or synthesize certain activity-related proteins, during aggression—the amygdala tops the list.

What made this project especially remarkable is that, among the many associations that are relevant to diet and disease, so many pointed to the same finding: people who ate the most animal-based foods got the most chronic disease. Even relatively small intakes of animal-based food were associated with adverse effects. People who ate the most plant-based foods were the healthiest and tended to avoid chronic disease. These results could not be ignored. From the initial experimental animal studies on animal protein effects to this massive human study on dietary patterns, the findings proved to be consistent. The health implications of consuming either animal or plant-based nutrients were remarkably different.

Consider the genesis of a single-celled embryo produced by the fertilization of an egg by a sperm. The genetic material of this embryo comes from two sources: paternal genes (from sperm) and maternal genes (from eggs). But the cellular material of the embryo comes exclusively from the egg; the sperm is no more than a glorified delivery vehicle for male DNA—a genome equipped with a hyperactive tail. Aside from proteins, ribosomes, nutrients, and membranes, the egg also supplies the embryo with specialized structures called mitochondria. These mitochondria are the energy-producing factories of the cell; they are so anatomically discrete and so specialized in their function that cell biologists call them “organelles”—i.e., mini-organs resident within cells. Mitochondria, recall, carry a small, independent genome that resides within the mitochondrion itself—not in the cell’s nucleus, where the twenty-three pairs of chromosomes (and the 21,000-odd human genes) can be found. The exclusively female origin of all the mitochondria in an embryo has an important consequence. All humans—male or female—must have inherited their mitochondria from their mothers, who inherited their mitochondria from their mothers, and so forth, in an unbroken line of female ancestry stretching indefinitely into the past. (A woman also carries the mitochondrial genomes of all her future descendants in her cells; ironically, if there is such a thing as a “homunculus,” then it is exclusively female in origin—technically, a “femunculus”?) Now imagine an ancient tribe of two hundred women, each of whom bears one child. If the child happens to be a daughter, the woman dutifully passes her mitochondria to the next generation, and, through her daughter’s daughter, to a third generation. But if she has only a son and no daughter, the woman’s mitochondrial lineage wanders into a genetic blind alley and becomes extinct (since sperm do not pass their mitochondria to the embryo, sons cannot pass their mitochondrial genomes to their children). Over the course of the tribe’s evolution, tens of thousands of such mitochondrial lineages will land on lineal dead ends by chance, and be snuffed out. And here is the crux: if the founding population of a species is small enough, and if enough time has passed, the number of surviving maternal lineages will keep shrinking, and shrinking further, until only a few are left. If half of the two hundred women in our tribe have sons, and only sons, then one hundred mitochondrial lineages will dash against the glass pane of male-only heredity and vanish in the next generation. Another half will dead-end into male children in the second generation, and so forth. By the end of several generations, all the descendants of the tribe, male or female, might track their mitochondrial ancestry to just a few women. For modern humans, that number has reached one: each of us can trace our mitochondrial lineage to a single human female who existed in Africa about two hundred thousand years ago. She is the common mother of our species. We do not know what she looked like, although her closest modern-day relatives are women of the San tribe from Botswana or Namibia. I find the idea of such a founding mother endlessly mesmerizing. In human genetics, she is known by a beautiful name—Mitochondrial Eve.

Furthermore, because silicon packs on more protons than carbon, it's bulkier, like carbon with fifty extra pounds. Sometimes that's not a big deal. Silicon might substitute adequately for carbon in the Martian equivalent of fats or proteins. But carbon also contorts itself into ringed molecules we call sugars. Rings are states of high-tension- which means they store lots of energy-and silicon just isn't supple enough to bend into the right position to form rings. In a related problem, silicon atoms cannot squeeze their electrons into tight spaces for double bonds, which appear in virtually every complicated biochemical.

Classically, cosmetics companies will take highly theoretical, textbookish information about the way that cells work—the components at a molecular level or the behavior of cells in a glass dish—and then pretend it’s the same as the ultimate issue of whether something makes you look nice. “This molecular component,” they say, with a flourish, “is crucial for collagen formation.” And that will be perfectly true (along with many other amino acids which are used by your body to assemble protein in joints, skin, and everywhere else), but there is no reason to believe that anyone is deficient in it or that smearing it on your face will make any difference to your appearance. In general, you don’t absorb things very well through your skin, because its purpose is to be relatively impermeable. When you sit in a bath of baked beans for charity, you do not get fat, nor do you start farting.

Your waist size is such an important predictor of health because the type of fat that is stored around your waistline—called “visceral fat” or “belly fat”—is related to the release of proteins and hormones that cause inflammation, which can in turn damage your arteries and affect how you metabolize sugars and fats. For this reason, visceral fat is strongly linked to type 2 diabetes, heart disease, stroke, Alzheimer’s, and other chronic diseases. Seeing your waist size come down is a great indicator of improving health.

There is no such thing as protein deficiency in the United States. How many people do you know who were hospitalized last year for protein deficiency? Zero! Now, how many people do you know who were hospitalized for heart disease, cancer, diabetes, or obesity related ailments? Probably lots

Virtually every person who uses the WFPB diet loses weight, reduces their blood sugar and insulin levels, and resolves diabetes and related diseases. A plant protein–based diet (as in the high-carb WFPB diet) also decreases total blood cholesterol and the formation of plaques that lead to heart disease, effects not seen from a low-carb, animal protein–based diet.

Nutrition is relatively simple, actually. It boils down to a few basic rules: don’t eat too many calories, or too few; consume sufficient protein and essential fats; obtain the vitamins and minerals you need; and avoid pathogens like E. coli and toxins like mercury or lead. Beyond that, we know relatively little with complete certainty. Read that sentence again, please.

The biochemist's approach pivots on concentration: find the protein by looking where it's most likely to be concentrated, and distill it out of the mix. The geneticist's approach, in contrast, pivots on information: find the gene by search for differences in "databases" created by two closely related cells and multiply the gene in bacteria via cloning. The biochemist distills forms; the gene cloner amplifies information.

Populations eating a remarkably wide range of traditional diets generally don't suffer from these chronic diseases. These diets run the gamut from ones very high in fat (the Inuit in Greenland subsist largely on seal blubber) to ones high in carbohydrate (Central American Indians subsist largely on maize and beans) to ones very high in protein (Masai tribesmen in Africa subsist chiefly on cattle blood, meat and milk), to cite three rather extreme examples. But much the same holds true for more mixed traditional diets. What this suggests is that there is no single ideal human diet but that the human omnivore is exquisitely adapted to a wide range of different foods and a variety of different diets. Except, that is, for one: the relatively new (in evolutionary terms) Western diet that that most of us now are eating. What an extraordinary achievement for a civilization: to have developed the one diet that reliably makes its people sick!

The other side of this coin is that viruses may be genes who have broken loose from ‘colonies’ such as ourselves. Viruses consist of pure DNA (or a related self-replicating molecule) surrounded by a protein jacket. They are all parasitic. The suggestion is that they have evolved from ‘rebel’ genes who escaped, and now travel from body to body directly through the air, rather than via the more conventional vehicles—sperms and eggs. If this is true, we might just as well regard ourselves as colonies of viruses!

This system can indicate that this mouse is John Smith. How does it also tell that he’s your never-before-encountered brother? The closer the relative, the more similar their cluster of MHC genes and the more similar their olfactory signature. Olfactory neurons in a mouse contain receptors that respond most strongly to the mouse’s own MHC protein. Thus, if the receptor is maximally stimulated, it means the mouse is sniffing its armpit. If near maximally stimulated, it’s a close relative. Moderately, a distant relative. Not at all (though the MHC protein is being detected by other olfactory receptors), it’s a hippo’s

Thermoneutrality”: A hallmark of modern industrial life is spending most of our time indoors at relatively consistent ambient temperatures, a concept we’ll refer to as thermoneutrality. Interestingly, experiencing swings in temperature is great for mitochondrial function, as cold stimulates the body to generate more warmth by increasing mitochondrial activity and stimulates more ATP generation and use. Heat exposure has been shown to activate heat shock proteins (HSPs) within cells, which can protect mitochondria from damage and help to maintain their function. HSPs can also stimulate the production of new mitochondria and improve their efficiency in producing ATP.

Parts of it are surprisingly beautiful. On a vast stretch on chromosome eleven, for instance, there is a causeway dedicated entirely to the sensation of smell. Here, a cluster of 155 closely related genes encodes a series of protein receptors that are professional smell sensors. Each receptor binds to a unique chemical structure, like a key to a lock, and generates a distinctive sensation of smell in the brain—spearmint, lemon, caraway, jasmine, vanilla, ginger, pepper. An elaborate form of gene regulation ensures that only one odor-receptor gene is chosen from this cluster and expressed in a single smell-sensing neuron in the nose, thereby enabling us to discriminate thousands of smells.

There was another inspiring moment: a rough, choppy, moonlit night on the water, and the Dreadnaught's manager looked out the window suddenly to spy thousands of tiny baitfish breaking the surface, rushing frantically toward shore. He knew what that meant, as did everyone else in town with a boat, a gaff and a loaf of Wonder bread to use as bait: the stripers were running! Thousands of the highly prized, relatively expensive striped bass were, in a rare feeding frenzy, suddenly there for the taking. You had literally only to throw bread on the water, bash the tasty fish on the head with a gaff and then haul them in. They were taking them by the hundreds of pounds. Every restaurant in town was loading up on them, their parking lots, like ours, suddenly a Coleman-lit staging area for scaling, gutting and wrapping operations. The Dreadnaught lot, like every other lot in town, was suddenly filled with gore-covered cooks and dishwashers, laboring under flickering gaslamps and naked bulbs to clean, wrap and freeze the valuable white meat. We worked for hours with our knives, our hair sparkling with snowflake-like fish scales, scraping, tearing, filleting. At the end of the night's work, I took home a 35-pound monster, still twisted with rigor. My room-mates were smoking weed when I got back to our little place on the beach and, as often happens on such occasions, were hungry. We had only the bass, some butter and a lemon to work with, but we cooked that sucker up under the tiny home broiler and served it on aluminum foil, tearing at it with our fingers. It was a bright, moonlit sky now, a mean high tide was lapping at the edges of our house, and as the windows began to shake in their frames, a smell of white spindrift and salt saturated the air as we ate. It was the freshest piece of fish I'd ever eaten, and I don't know if it was due to the dramatic quality the weather was beginning to take on, but it hit me right in the brainpan, a meal that made me feel better about things, made me better for eating it, somehow even smarter, somehow . . . It was a protein rush to the cortex, a clean, three-ingredient ingredient high, eaten with the hands. Could anything be better than that?

One of the most studied organisms in this context is the tiny polyp Hydra, which possesses only a hundred thousand cells. Its neural network is concentrated in its head and foot: a first evolutionary step toward developing a brain and spinal cord. Hydra’s nervous system contains a chemical messenger—a minuscule protein—that resembles two of our own: vasopressin and oxytocin. A protein of this kind is called a neuropeptide. In vertebrates, the gene for this particular neuropeptide first doubled and then mutated in two places, creating the two closely related but specialized neuropeptides vasopressin and oxytocin, which have recently become the focus of interest, partly because of their important role as messengers in our social brains (see chapter 9).

Our brains, for instance, are 70 percent fat, mostly in the form of a substance known as myelin that insulates nerve cells and, for that matter, all nerve endings in the body. Fat is the primary component of all cell membranes. Changing the proportion of saturated to unsaturated fats in the diet, as proponents of Keys’s hypothesis recommended, might well change the composition of the fats in the cell membranes. This could alter the permeability of cell membranes, which determines how easily they transport, among other things, blood sugar, proteins, hormones, bacteria, viruses, and tumor-causing agents into and out of the cell. The relative saturation of these membrane fats could affect the aging of cells and the likelihood that blood cells will clot in vessels and cause heart attacks.

The people who actually consumed the roasted flesh were not the dead person’s closest blood relatives, such as wives or children. That honor—and it was indeed an honor—went to chosen people who were like blood to the deceased: in-laws, extended relatives, and community members, known as affines. None of the affines were vengeful, flesh-hungry savages, desperate for the taste of grilled human, and neither were they after the protein the human flesh provided—both common motives ascribed to cannibals. In fact, the corpse, which had been laid out over several days in the warm, humid climate of the Amazon rain forest, was often well into various stages of decomposition. Eating the flesh would have been a smelly, foul experience. The affines often had to excuse themselves to vomit before returning to eat again.

How does the body push the comparatively tiny genome so far? Many researchers want to put the weight on learning and experience, apparently believing that the contribution of the genes is relatively unimportant. But though the ability to learn is clearly one of the genome's most important products, such views overemphasize learning and significantly underestimate the extent to which the genome can in fact guide the construction of enormous complexity. If the tools of biological self-assembly are powerful enough to build the intricacies of the circulatory system or the eye without requiring lessons from the outside world, they are also powerful enough to build the initial complexity of the nervous system without relying on external lessons. The discrepancy melts away as we appreciate the true power of the genome. We could start by considering the fact that the currently accepted figure of 30,000 could well prove to be too low. Thirty thousand (or thereabouts) is, at press time, the best estimate for how many protein-coding genes are in the human genome. But not all genes code for proteins; some, not counted in the 30,000 estimate, code for small pieces of RNA that are not converted into proteins (called microRNA), of "pseudogenes," stretches of DNA, apparently relics of evolution, that do not properly encode proteins. Neither entity is fully understood, but recent reports (from 2002 and 2003) suggest that both may play some role in the all-important process of regulating the IFS that control whether or not genes are expressed. Since the "gene-finding" programs that search the human genome sequence for genes are not attuned to such things-we don't yet know how to identify them reliably-it is quite possible that the genome contains more buried treasure.

With the rise of molecular genetics, it has become possible to search for possible changes (mutations, polymorphisms) in target genes. Much effort has gone into investigating variations in genes that contribute to serotonin transmission, because serotonin-related drugs have antidepressant and anxiolytic properties. This assumes, however, that the treatment mechanism is the same mechanism that gives rise to the disorder.53 Although this is consistent with the old chemical imbalance hypothesis, it is not a conclusion that should simply be accepted without careful assessment. Nevertheless, studies of the genetic control of serotonin have found interesting results. For example, people with a certain variant (polymorphism) of a gene controlling a protein involved in serotonin transmission are more reactive to threatening stimuli, and this hyperreactivity is associated with increased amygdala activity during the threat.54 Further, it has been reported that this variant of the gene can account for 7 percent to 9 percent of the inheritance of anxiety.55

Enzymes have made and unmade every single biomolecule inside every living cell that lives or has ever lived. Enzymes are as close as anything to the vital factors of life. So the discovery that some, and possibly all, enzymes work by promoting the dematerialization of particles from one point in space and their instantaneous materialization in another provides us with a novel insight into the mystery of life. And while there remain many unresolved issues related to enzymes that need to be better understood, such as the role of protein motions, there is no doubt that quantum tunneling plays a role in the way they work. Even so, we should address a criticism made by many scientists who accept the findings of Klinman, Scrutton and others, but nevertheless claim that quantum effects have as relevant a role in biology as they have in the workings of a steam train: they are always there but are largely irrelevant to understanding how either system works. Their argument is often positioned within a debate about whether or not enzymes evolved to take advantage of quantum phenomena such as tunneling. The

Laurie started to really believe that her mind was healing her body by thought alone. And the old fracture that was connected to the old self was healing, because she was literally becoming someone else. She was no longer firing and wiring the circuits in her brain that were connected to the old personality, because she was no longer thinking and acting in the same ways. She stopped conditioning her body to the same mind by reliving her past with the same emotions. She was “unmemorizing” being her old self and remembering being a new self—that is, firing and wiring new thoughts and actions in her brain by changing her mind and emotionally teaching her body what her future self would feel like. Laurie was signaling new genes in new ways during her daily meditation by simply changing her state of being. Those genes were making new proteins that were healing the proteins responsible for the fractures related to her “dis-ease.” From what she learned in the workshops, she reasoned that her bone cells needed to get the right signal from her mind in order to turn off the gene of fibrous dysplasia and turn on the gene for the production of a normal bone matrix.

Despite the advancements of systematic experimental pipelines, literature-curated protein-interaction data continue to be the primary data for investigation of focused biological mechanisms. Notwithstanding the variable quality of curated interactions available in public databases, the impact of inspection bias on the ability of literature maps to provide insightful information remains equivocal. The problems posed by inspection bias extend beyond mapping of protein interactions to the development of pharmacological agents and other aspects of modern biomedicine. Essentially the same 10% of the proteome is being investigated today as was being investigated before the announcement of completion of the reference genome sequence. One way forward, at least with regard to interactome mapping, is to continue the transition toward systematic and relatively unbiased experimental interactome mapping. With continued advancement of systematic protein-interaction mapping efforts, the expectation is that interactome 'deserts', the zones of the interactome space where biomedical knowledge researchers simply do not look for interactions owing to the lack of prior knowledge, might eventually become more populated. Efforts at mapping protein interactions will continue to be instrumental for furthering biomedical research.

Harvard University biologist David Haig has spent the last few years systematically debunking the notion that the relationship between a mother and her unborn child is anything like the rose-tinted idyll that one usually finds on the glossy covers of maternity magazines. In fact, it is anything but. Pre-eclampsia, a condition of dangerously high blood pressure in pregnant women, is brutally kick-started by nothing short of a foetal coup d’état. It begins with the placenta invading the maternal bloodstream and initiating what, in anyone’s book, is a ruthless biological heist – an in utero sting operation to draw out vital nutrients. And I’m not just talking about baby Gordon Gekkos here – I’m talking about all of us. The curtain-raiser is well known to obstetricians. The foetus begins by injecting a crucial protein into the mother’s circulation which forces her to drive more blood, and therefore more nourishment, into the relatively low-pressure placenta. It’s a scam, pure and simple, which poses a significant and immediate risk to the mother’s life. ‘The bastard!’ says Andy. ‘Shall we get some olives?’ ‘And it’s by no means the only one,’ I continue. In another embryonic Ponzi scheme, foetal release of placental lactogen counteracts the effect of maternal insulin thereby increasing the mother’s blood sugar level and providing an excess for the foetus’s own benefit. ‘A bowl of the citrus and chilli and a bowl of the sweet pepper and basil,’ Andy says to the waiter. Then he peers at me over the menu. ‘So basically what you’re saying then is this: forget the Gaddafis and the Husseins. When it comes to chemical warfare it’s the unborn child that’s top dog!’ ‘Well they definitely nick stuff that isn’t theirs,’ I say. ‘And they don’t give a damn about the consequences.’ Andy smiles. ‘So in other words they’re psychopaths!’ he says. BABY

But how did proteins make physiological reactions possible? Hemoglobin, the oxygen carrier in blood, for instance, performs one of the simplest and yet most vital reactions in physiology. When exposed to high levels of oxygen, hemoglobin binds oxygen. Relocated to a site with low oxygen levels, it willingly releases the bound oxygen. This property allows hemoglobin to shuttle oxygen from the lung to the heart and the brain. But what feature of hemoglobin allows it to act as such an effective molecular shuttle? The answer lies in the structure of the molecule. Hemoglobin A, the most intensively studied version of the molecule, is shaped like a four-leaf clover. Two of its “leaves” are formed by a protein called alpha-globin; the other two are created by a related protein, beta-globin.II Each of these leaves clasps, at its center, an iron-containing chemical named heme that can bind oxygen—a reaction distantly akin to a controlled form of rusting. Once all the oxygen molecules have been loaded onto heme, the four leaves of hemoglobin tighten around the oxygen like a saddle clasp. When unloading oxygen, the same saddle-clasp mechanism loosens. The unbinding of one molecule of oxygen coordinately relaxes all the other clasps, like the crucial pin-piece pulled out from a child’s puzzle. The four leaves of the clover now twist open, and hemoglobin yields its cargo of oxygen. The controlled binding and unbinding of iron and oxygen—the cyclical rusting and unrusting of blood—allows effective oxygen delivery into tissues. Hemoglobin allows blood to carry seventyfold more oxygen than what could be dissolved in liquid blood alone. The body plans of vertebrates depend on this property: if hemoglobin’s capacity to deliver oxygen to distant sites was disrupted, our bodies would be forced to be small and cold. We might wake up and find ourselves transformed into insects.

And, even more important for our purposes, these facts are sturdy enough that we can build a sensible diet upon them. Here they are: FACT 1. Populations that eat a so-called Western diet—generally defined as a diet consisting of lots of processed foods and meat, lots of added fat and sugar, lots of refined grains, lots of everything except vegetables, fruits, and whole grains—invariably suffer from high rates of the so-called Western diseases: obesity, type 2 diabetes, cardiovascular disease, and cancer. Virtually all of the obesity and type 2 diabetes, 80 percent of the cardiovascular disease, and more than a third of all cancers can be linked to this diet. Four of the top ten killers in America are chronic diseases linked to this diet. The arguments in nutritional science are not about this well-established link; rather, they are all about identifying the culprit nutrient in the Western diet that might be responsible for chronic diseases. Is it the saturated fat or the refined carbohydrates or the lack of fiber or the transfats or omega-6 fatty acids—or what? The point is that, as eaters (if not as scientists), we know all we need to know to act: This diet, for whatever reason, is the problem. FACT 2. Populations eating a remarkably wide range of traditional diets generally don’t suffer from these chronic diseases. These diets run the gamut from ones very high in fat (the Inuit in Greenland subsist largely on seal blubber) to ones high in carbohydrate (Central American Indians subsist largely on maize and beans) to ones very high in protein (Masai tribesmen in Africa subsist chiefly on cattle blood, meat, and milk), to cite three rather extreme examples. But much the same holds true for more mixed traditional diets. What this suggests is that there is no single ideal human diet but that the human omnivore is exquisitely adapted to a wide range of different foods and a variety of different diets. Except, that is, for one: the relatively new (in evolutionary terms) Western diet that most of us now are eating. What an extraordinary achievement for a civilization: to have developed the one diet that reliably makes its people sick! (While it is true that we generally live longer than people used to, or than people in some traditional cultures do, most of our added years owe to gains in infant mortality and child health, not diet.) There is actually a third, very hopeful fact that flows from these two: People who get off the Western diet see dramatic improvements in their health. We have good research to suggest that the effects of the Western diet can be rolled back, and relatively quickly.

There is no such thing as protein deficiency in the United States. How many people do you know who were hospitalized last year for protein deficiency? Zero! Now, how many people do you know who were hospitalized for heart disease, cancer, diabetes, or obesity-related ailments? Probably lots.

Ultra-Sensitive C-Reactive Protein Blood (HS-CRP) C-reactive protein measures an inflammatory response in the body and has been shown to play a role in atherosclerosis and blood clot formation.  Patients should ask their doctor specifically about HS-CRP, as this test helps determine heart disease risk. Elevated HS-CRP is related to increased risk for heart attack, restenosis of coronary arteries after angioplasty, stroke, and peripheral vascular disease (PVD). While elevated cholesterol, LDL, and triglycerides plus low HDL are independent risk factors for heart disease and cholesterol build-up, HS-CRP provides added information about inflammation in the arteries. This cannot be determined by lipid testing alone. Results Less than 1.0 mg/L = Low Risk for Cardio Vascular Disease (CVD) 1.0 – 2.9 mg/L = Intermediate Risk for CVD Greater than 3.0 mg/L High Risk for CVD

How is regeneration of the spinal cord in the salamander related to its initial development ? There is now evidence that in the salamander, the steps of progenitor cell-patterning and controlled neurogenesis that naturally regenerate a severed tail largely recapitulate the steps followed during early embryonic development to initially build the central nervous system. For example, ependymal cells are descendants of radial glial cells retained from the earliest developmental stages in regenerating vertebrates. The ependymal tube that gives rise to regenerated spinal cord following salamander tail amputation is very similar in appearance to the early structure of the neural tube of developing amniotes. But how does that recapitulation occur ? By using a transgenic axolotl that expresses green fluorescent proteins (GFPs), they further examined the regenerated spinal cord by replacing a segment of the spinal cord from a typical animal with a piece of the spinal cord from a GFP-expressing animal - that is, one with green fluorescent cells. They found that the implanted cells in the experimental animals regenerated a green spinal cord ! Thus, regeneration may be a more neural stem-cell like, or pluripotent, state as a response to injury.

The researchers looked deeper into these observations, in hopes of gaining insight into the mechanisms underlying the high evolutionary rate and extraordinary immunologic plasticity of influenza HA. They probed in more detail the precise codons that are used by the virus to encode the influenza HA1 protein. The discriminated between codons on the basis of volatility. Each three-nucleotide codon is related by a single nucleotide change to nine 'mutational neighbours.' Of those nine mutations, some proportion change the codon to a synonymous codon and some change it to a nonsynonymous one, which directs the incorporation of a different amino acid into the protein. More volatile codons are those for which a larger proportion of those nine mutational neighbours encode an amino acid change. The use of particular codons in a gene at a frequency that is disproportionate to their random selection for encoding a chosen amino acid is termed codon bias. Such bias is common and is influenced by many factors, but here the collaborators found strong evidence for codon bias that was particular for and restricted to the amino acids making up the HA1 epitopes. Remarkably, they observed that influenza employs a disproportionate number of volatile codons in its epitope-coding sequences. There was a bias for the use of codons that had the fewest synonymous mutational neighbours. In other words, influenza HA1 appears to have optimized the speed with which it can change amino acids in its epitopes. Amino acid changes can arise from fewer mutational events. The antibody combining regions are optimized to use codons that have a greater likelihood to undergo nonsynonymous single nucleotide substitutions : they are optimized for rapid evolution.

In 2005, according to the CDC, eleven Americans died of all food allergies—that is, adults as well as children, and from an allergy to any food, not just peanuts. Yet schools across America have banned peanuts and peanut butter, among the few protein-rich foods many children like to eat. Compare this with about ten thousand children who are hospitalized each year for sports-related traumatic brain injuries. The hysteria has been led by school officials, the Asthma and Allergy Foundation of America, and Consumer Reports, a liberal magazine that helped stoke the hysteria about secondhand smoke. It is mind-boggling that schools have banned peanut butter. But in the Age of Hysteria, one child who might die suffices to ban a food for the millions of students who would benefit from it.

Attempts at refining PSA have included PSA velocity (PSAV) (change of PSA over time), PSA kinetics (standardizing levels in relation to the size of the prostate), and PSA isoforms (free vs protein-bound molecular forms of PSA).

So far, we have been considering accounts of cannibalism that involve the eating of enemy prisoners, usually killed or captured in warfare. Cross-culturally this appears to be the basic form of cannibalism; there seems little evidence that shortage of protein had anything to do with it, as materialists like Marvin Harris supposed; and many primitive societies were as strongly opposed to cannibalism as we are. There is, however, a different type of cannibalism, conventionally known as “endo-cannibalism”, in which the relatives of a deceased person eat the corpse, or part of it, as a mortuary

It just so happened that all the psychics were older women. We then found controls who did not have any psychic abilities or family members with those abilities. Because we were looking at genetics, the controls’ demographic characteristics of age, gender, and race had to match our psychics’ demographics so that any differences we saw between the two groups were not a result of those aspects. For example, we had to find controls who were older women to match the older age and gender of the psychics. It took us a much longer time to find the controls. Apparently, it is challenging to find older women with no psychic abilities. We finally collected saliva from all the participants to extract the DNA and decoded all their genes. We compared the gene sequences of the psychics to the controls. Much to our surprise, we found one section of the noncoding DNA that was conserved, or wild-type, in all the psychics but was variable in the controls. Wild-type means that the DNA sequence was the original version and was not mutated. That it was in a noncoding region of the DNA means that it was in a part that does not code for a protein. Instead, it likely acts to regulate the activity levels of its neighboring gene. The gene next to it is highly expressed in the brain. This supports the notion that this conserved region could influence gene activity related to psychic abilities (Wahbeh, Radin, et al. 2021).

Buckwheat: Buckwheat is not related to wheat, so it is a favorable grain for wheat-sensitive people. It is also rich in protein and fiber and has been shown to lower cholesterol. Buckwheat groats can be soaked in advance and then used to make porridge, a seasoned side dish, or crackers. Kasha is toasted buckwheat. Millet: This versatile, gluten-free grain is a staple crop in India and Africa. Mildly sweet and nutty, it can be used in both main dishes and desserts. Depending on the length of time it is cooked, it can be slightly crunchy or soft and creamy. Serve it with stir-fried dishes, add it to salads, or make a breakfast porridge with cooked millet, nuts, seeds, and fruit. Quinoa: Although quinoa is usually considered a whole grain, it is actually a seed. It is a good protein source and cooks in just ten to fifteen minutes. Rinse quinoa before cooking because it is coated with a bitter compound called saponin. Quinoa tastes great by itself, or for a substantial salad, toss it with veggies, nuts, and a flavored vinegar or light dressing. It makes a great addition to veggie burgers and even works well in breakfast or dessert puddings.

Here are a few notable things that can spark inflammation and depress the function of your liver: Alcohol overload—This is relatively well-known. Your liver is largely responsible for metabolizing alcohol, and drinking too much liquid courage can send your liver running to cry in a corner somewhere. Carbohydrate bombardment—Starches and sugar have the fastest ability to drive up blood glucose, liver glycogen, and liver fat storage (compared to their protein and fat macronutrient counterparts). Bringing in too many carbs, too often, can elicit a wildfire of fat accumulation. In fact, one of the most effective treatments for reversing NAFLD is reducing the intake of carbohydrates. A recent study conducted at KTH Royal Institute of Technology and published in the journal Cell Metabolism had overweight test subjects with high levels of liver fat reduce their ratio of carbohydrate intake (without reducing calories!). After a short two-week study period the subjects showed “rapid and dramatic” reductions of liver fat and other cardiometabolic risk factors. Too many medications—Your liver is the top doc in charge of your body’s drug metabolism. When you hear about drug side effects on commercials, they are really a direct effect of how your liver is able to handle them. The goal is to work on your lifestyle factors so that you can be on as few medications as possible along with the help of your physician. Your liver will do its best to support you either way, but it will definitely feel happier without the additional burden. Too many supplements—There are several wonderful supplements that can be helpful for your health, but becoming an overzealous natural pill-popper might not be good for you either. In a program funded by the National Institutes of Health, it was found that liver injuries linked to supplement use jumped from 7 percent to 20 percent of all medication/supplement-induced injuries in just a ten-year time span. Again, this is not to say that the right supplements can’t be great for you. This merely points to the fact that your liver is also responsible for metabolism of all of the supplements you take as well. And popping a couple dozen different supplements each day can be a lot for your liver to handle. Plus, the supplement industry is largely unregulated, and the additives, fillers, and other questionable ingredients could add to the burden. Do your homework on where you get your supplements from, avoid taking too many, and focus on food first to meet your nutritional needs. Toxicants—According to researchers at the University of Louisville, more than 300 environmental chemicals, mostly pesticides, have been linked to fatty liver disease. Your liver is largely responsible for handling the weight of the toxicants (most of them newly invented) that we’re exposed to in our world today. Pesticides are inherently meant to be deadly, but just to small organisms (like pests), though it seems to be missed that you are actually made of small organisms, too (bacteria

A classic example in the nutritional realm is the age-related difference in muscle protein synthesis (MPS) in response to protein feeding. Subjects in their seventies require nearly double the protein dose in a single meal to maximally stimulate MPS compared to subjects in their twenties.40

began eating things like quinoa, beans, lentils, peas, and tofu, a product I ultimately swapped for its more nutritious fermented soy-based cousin, tempeh. I also ate a lot of raw almonds, walnuts, cashews, and Brazil nuts, the latter a natural testosterone booster due to its high selenium content. Also on my dietary plate: spirulina, a blue-green algae that is 60 percent protein, complete with all essential amino acids, the highest per-weight protein content of any food on Earth. In taking in all these whole foods, I discovered absolutely no protein-related impediment to my recovery or to my ability to build lean muscle mass. Now fifty-one years old and eleven years Plantpowered, I continue to get stronger and faster with each successive year.

They found those who reported having negative experiences with friends and acquaintances had a higher level of proteins related to inflammation in the body, compared with those who reported positive interactions with people. These proteins are associated with a number of chronic conditions, including heart disease, cancer, and depression.

It takes energy to shuttle those nutrients in and out of the bloodstream, to power the enzymes that glue them together (into proteins, triglycerides, and glycogen) and the other enzymes that then break them apart, to fuel the liver during that gluconeogenesis trick.

Instead, complex food matter is broken down into its simplest parts (molecules): amino acids (the building blocks of protein), simple sugars like glucose (the building blocks of more complex sugars and of starches [carbohydrates]), and free fatty acids and glycerol (the constituents of fat). This is accomplished in the gastrointestinal tract by enzymes, chemicals that can degrade more complex molecules. The simple building blocks thus produced are absorbed into the bloodstream for delivery to whichever cells in the body need them.

A great marker is turning out to be something called C-reactive protein (CRP).

The other side of this coin is that viruses may be genes who have broken loose from ‘colonies’ such as ourselves. Viruses consist of pure DNA (or a related self-replicating molecule) surrounded by a protein jacket. They are all parasitic.

Etiology l Genetic studies provide evidence that bipolar disorder is strongly heritable and that depression is somewhat heritable. l Neurobiological research has focused on the sensitivity of receptors rather than on the amount of various transmitters, with the strongest evidence for diminished sensitivity of the serotonin receptors in depression and mania. There is some evidence that mania is related to heightened sensitivity of the dopamine receptors and that depression is related to diminished sensitivity of dopamine receptors. l Bipolar and unipolar disorders seem tied to elevated activity of the amygdala and the subgenual anterior cingulate and to diminished activity in the dorsolateral prefrontal cortex and hippocampus during tasks that involve emotion and emotion regulation. During mania, greater levels of activation of the striatum have been observed. Mania also may involve elevations in protein kinase C. l Overactivity of the hypothalamic–pituitary–adrenal axis (HPA), as indexed by poor suppression of cortisol by dexamethasone, is related to severe forms of depression and to bipolar disorder. l Socioenvironmental models focus on the role of negative life events, lack of social support, and family criticism as triggers for episodes but also consider ways in which a person with depression may elicit negative responses from others. People with less social skill and those who tend to seek excessive reassurance are at elevated risk for the development of depression. l The personality trait that appears most related to depression is neuroticism. Neuroticism predicts the onset of depression. l Influential cognitive theories include Beck’s cognitive theory, hopelessness theory, and rumination theory. All argue that depression can be caused by cognitive factors, but the nature of the cognitive factors differs across

But if ncRNAs are so important for cellular function, surely we would expect to find that sometimes diseases are caused by problems with them. Shouldn’t there be lots of examples where defects in production or expression of ncRNAs lead to clinical disorders, aside from the imprinting or X inactivation conditions? Well, yes and no. Because these ncRNAs are predominantly regulatory molecules, acting in networks that are rich in compensatory mechanisms, defects may only have relatively subtle impacts. The problem this creates experimentally is that most genetic screens are good at detecting the major phenotypes caused by mutations in proteins, but may not be so useful for more subtle effects.

Even though these individuals had seemed perfectly healthy at birth, something that had happened during their development in the womb affected them for decades afterwards. And it wasn’t just the fact that something had happened that mattered, it was when it happened. Events that take place in the first three months of development, a stage when the foetus is really very small, can affect an individual for the rest of their life. This is completely consistent with the model of developmental programming, and the epigenetic basis to this. In the early stages of pregnancy, where different cell types are developing, epigenetic proteins are probably vital for stabilising gene expression patterns. But remember that our cells contain thousands of genes, spread over billions of base-pairs, and we have hundreds of epigenetic proteins. Even in normal development there are likely to be slight variations in the expression of some of these proteins, and the precise effects that they have at specific chromosomal regions. A little bit more DNA methylation here, a little bit less there. The epigenetic machinery reinforces and then maintains particular patterns of modifications, thus creating the levels of gene expression. Consequently, these initial small fluctuations in histone and DNA modifications may eventually become ‘set’ and get transmitted to daughter cells, or be maintained in long-lived cells such as neurons, that can last for decades. Because the epigenome gets ‘stuck’, so too may the patterns of gene expression in certain chromosomal regions. In the short term the consequences of this may be relatively minor. But over decades all these mild abnormalities in gene expression, resulting from a slightly inappropriate set of chromatin modifications, may lead to a gradually increasing functional impairment. Clinically, we don’t recognise this until it passes some invisible threshold and the patient begins to show symptoms.

Geneticists experienced a comparable shock when, contrary to their expectations of over 120,000 genes, they found that the entire human genome consists of approximately 25,000 genes. (Pennisi 2003a and 2003b; Pearson 2003; Goodman 2003) More than eighty percent of the presumed and required DNA does not exist! The missing genes are proving to be more troublesome than the missing eighteen minutes of the Nixon tapes. The one-gene, one-protein concept was a fundamental tenet of genetic determinism. Now that the Human Genome Project has toppled the one-gene for one-protein concept, our current theories of how life works have to be scrapped. No longer is it possible to believe that genetic engineers can, with relative ease, fix all our biological dilemmas. There are simply not enough genes to account for the complexity of human life or of human disease.

Reprogramming is what John Gurdon demonstrated in his ground-breaking work when he transferred the nuclei from adult toads into toad eggs. It’s what happened when Keith Campbell and Ian Wilmut cloned Dolly the Sheep by putting the nucleus from a mammary gland cell into an egg. It’s what Yamanaka achieved when he treated somatic cells with four key genes, all of which code for proteins highly expressed naturally during this reprogramming phase. The egg is a wonderful thing, honed through hundreds of millions of years of evolution to be extraordinarily effective at generating vast quantities of epigenetic change, across billions of base-pairs. None of the artificial means of reprogramming cells comes close to the natural process in terms of speed or efficiency. But the egg probably doesn’t quite do everything unaided. At the very least, the pattern of epigenetic modifications in sperm is one that allows the male pronucleus to be reprogrammed relatively easily. The sperm epigenome is primed to be reprogrammed6. Unfortunately, these priming chromatin modifications (and many other features of the sperm nucleus), are missing if an adult nucleus is reprogrammed by transferring it into a fertilised egg. That’s also true when an adult nucleus is reprogrammed by treating it with the four Yamanaka factors to create iPS cells. In both these circumstances, it’s a real challenge to completely reset the epigenome of the adult nucleus. It’s just too big a task. This is probably why so many cloned animals have abnormalities and shortened lifespans. The defects that are seen in these cloned animals are another demonstration that if early epigenetic modifications go wrong, they may stay wrong for life. The abnormal epigenetic modification patterns result in permanently inappropriate gene expression, and long-term ill-health.

Foldit is another game that is making waves. Users solve puzzles for science by designing proteins. It turns out that humans’ pattern-recognition and puzzle-solving abilities are more efficient than existing computer programs at pattern-folding tasks, so the scientists behind Foldit are using players’ answers to teach computers to fold proteins faster and predict protein structures. The combined effort of players actually helped solve a problem related to HIV that had puzzled scientists for more than 10 years.

The type of food you consume directly affects your metabolism and insulin response. Food is composed of three macronutrients: protein, carbohydrate, and fat, and each of these macronutrients affects your metabolism in a different way. One gram of protein or carbohydrate provides four calories, while one gram of fat contains nine calories. A calorie is the base unit of heat measurement related to metabolic rate. It measures how much energy a particular food provides to the body. Of course, if you do eat more calories than your body requires, it doesn’t matter whether those calories come from protein, carbohydrates, or fat—the extra fuel will be stored in the body as fat. Eating too few calories can be equally problematic. When you do not eat enough food, your body’s endocrine, immunological, and nervous systems begin to malfunction. The result is often hormonal imbalances, thyroid problems, and insulin resistance. When you are in a state of extreme caloric restriction, your body does everything possible to return to a state of homeostasis, or equilibrium—including slowing down your metabolic rate. A slow metabolism affects your energy levels, your digestive and hormonal health, and your ability to lose weight. In my case, severely restricting my calories increased my adrenal

Reduced Disease Risk Factors: Ditching grains, sugars, other simple carbs, and processed foods, especially “bad fats” (trans and partially-hydrogenated), will reduce your production of hormone-like messengers that instruct genes to make harmful pro-inflammatory protein agents. These agents increase your risk for arthritis, diabetes, cancer, heart disease, and many other inflammation-related health problems.

Part of this problem lies with how we do ‘science’. The paradigm of ‘modern science’ is that we isolate each individual factor and study it in isolation. This is the ‘reductionist’ approach to discovering scientific truth. This is straight forward and relatively easy to do, so lots of scientists swear by it. But what if a clinical problem like insulin resistance is not due to a single domino, but rather a number of dysfunctional proteins or other structural materials in combination? The answer – the reductionist approach can’t deliver an answer in this situation. If multiple steps in a pathway, working in varying combinations, eventually compromise that pathway’s action, the reductionist paradigm fails. But if one takes a more holistic or cosmopolitan approach to assessing the problem, the cause of the problem might be better appreciated.

how each relates to all the others and to our health. I was reading Dancing Skeletons, a book by nutritional anthropologist Katherine Dettwyler about her time working in Africa, when I found a section about kwashiorkor. Kwashiorkor is a severe form of malnutrition common in young children throughout the tropics. The hallmark diet of this disease is high in calories (from sweet potatoes or other starches) but low in protein. In this case, the low protein is not the problem—other children who eat equally low amounts of protein but fewer total calories are not likely to develop the disease. It’s the ratio of the nutrients that contributes to the development of kwashiorkor. KEGEL EXERCISE A contraction of the pelvic floor often prescribed to prevent the leakage of urine when coughing or running. This section of Dettwyler’s book resonated with me because I recognize that the outcomes of an exercise program depend largely on the ratio of all the movements to each other. Exercise (a repetitive intake of an isolated muscle contraction to fill a hole of missing strength) is often prescribed like vitamins (a capsule ingested to decrease a nutritional void). One of the arguments I am most known for professionally is that the way the Kegel exercise is prescribed can actually be harmful and not helpful at all. A Kegel is like a starch in the case of kwashiorkor: when done excessively and in the absence of other movement vitamins, it can create a negative outcome—too much pelvic-floor tension. The Kegel (as I’ll expand upon in Chapter 10) is not inherently more “bad” than a sweet potato, but neither is a sweet potato (or Kegel) health-making when consumed in isolation.

University, “The traditional Inuit diet is fats and proteins, no sugar at all. It is probably one of the healthiest diets you can have. The human body is built for that. “(2007). If this high-protein, high-fat diet is so healthy, why don’t we hear more about its positive effects? Probably for a lot of reasons, some relating to our “for-profit” health care system,

The official ration that was settled on for Soviet prisoners 539 and Ostarbeiter in December 1941 was clearly inadequate for men intended for hard labour. It consisted of a weekly allocation of 16.5 kilos of turnips, 2.6 kilos of 'bread' (made up of 65 per cent red rye, 25 per cent sugar beet waste and 10 per cent straw or leaves), 3 kilos of potatoes, 250 grams of horse-or other scrap meat, 130 grams of fat and 150 grams of Naehrmittel (yeast), 70 grams of sugar and two and a third litres of skimmed milk. The appalling quality of the bread caused serious damage to the digestive tract and resulted in chronic malnutrition. The vegetables had to be cooked for hours before they were palatable, robbing them of most of their nutritional content. Though this was a diet that was, relatively speaking, high in carbohydrates, providing a nominal daily total of 2,500 calories, it was grossly deficient in the fat and protein necessary to sustain hard physical labour.

Nutrition is relatively simple, actually. It boils down to a few basic rules: don’t eat too many calories, or too few; consume sufficient protein and essential fats; obtain the vitamins and minerals you need; and avoid pathogens like E. coli and toxins like mercury or lead. Beyond that, we know relatively little with complete certainty.

this routine is known as flexible dieting, and it has four steps: 1. Regulate your calories according to your body composition goal. 2. Eat a high-protein diet. 3. Get most of your calories from whole, nutritious, relatively unprocessed foods. 4. Find a balance of carbohydrate and fat intake that works for you.

On Degenerate Templates and the Adaptor Hypothesis: A Note for the RNA Tie Club,” which Crick sent out early in 1955, is the first of his master-works about protein synthesis and the coding problem. By 1966, he had written two dozen papers related to the subject. Six at least were of great and general importance. Two of those included experiments and were written with collaborators. One more paper, of pleasing ingenuity, happened to be wrong: nature turned out to be less elegant than Crick’s imagination. Of the entire run, however, this first was the most unprecedented and original. The paper defined the next questions, and many were new questions. More, it established the way the questions were to be approached, and the terms in which they were to be argued. Most generally, it took for granted that the questions were spatial, physical, logical, easy to apprehend, and therefore tractable and even—in principle—simple. Yet even now, only a few hundred people have ever read the paper—for the surprising reason that it has never been published. It remained a note for the RNA Tie Club: seventeen foolscap pages, typewritten, double-spaced, mimeographed.

bulk n. 1 [mass noun] the mass or size of something large: residents jump up and down on their rubbish to reduce its bulk. large size or shape: he moved quickly in spite of his bulk. [count noun] a large mass or shape. [as modifier] large in quantity: bulk orders of over 100 copies. roughage in food: potatoes supply energy, essential protein, and bulk. cargo in an unpackaged mass such as grain or oil. [PRINTING] the thickness of paper or a book. 2 (the bulk of) the greater part of something: the bulk of the traffic had passed. v. [with obj.] 1 treat (a product) so that its quantity appears greater than it is: traders were bulking up their flour with chalk. [no obj.] (bulk up) build up flesh and muscle, typically in training for sporting events. 2 combine (shares or commodities for sale): your shares will be bulked with others and sold at the best prices available. bulk large be or seem to be of great importance: territorial questions bulked large in diplomatic relations. in bulk 1 (of goods) in large quantities and generally at a reduced price: retail multiples buy in bulk. 2 (of a cargo or commodity) not packaged; loose. Middle English: the senses ‘cargo as a whole’ and ‘heap, large quantity’ (the earliest recorded) are probably from Old Norse búlki ‘cargo’; other senses arose perhaps by alteration of obsolete bouk ‘belly, body’. bulk buying

It’s Thanksgiving, and you’ve eaten with porcine abandon. Your bloodstream is teeming with amino acids, fatty acids, glucose. It’s far more than you need to power you over to the couch in a postprandial daze. What does your body do with the excess? This is crucial to understand because, basically, the process gets reversed when you’re later sprinting for your life. To answer this question, it’s time we talked finances, the works—savings accounts, change for a dollar, stocks and bonds, negative amortization of interest rates, shaking coins out of piggy banks—because the process of transporting energy through the body bears some striking similarities to the movement of money. It is rare today for the grotesquely wealthy to walk around with their fortunes in their pockets, or to hoard their wealth as cash stuffed inside mattresses. Instead, surplus wealth is stored elsewhere, in forms more complex than cash: mutual funds, tax-free government bonds, Swiss bank accounts. In the same way, surplus energy is not kept in the body’s form of cash—circulating amino acids, glucose, and fatty acids—but stored in more complex forms. Enzymes in fat cells can combine fatty acids and glycerol to form triglycerides (table). Accumulate enough of these in the fat cells and you grow plump. Meanwhile, your cells can stick series of glucose molecules together. These long chains, sometimes thousands of glucose molecules long, are called glycogen. Most glycogen formation occurs in your muscles and liver. Similarly, enzymes in cells throughout the body can combine long strings of amino acids, forming them into proteins. The hormone that stimulates the transport and storage of these building blocks into target cells is insulin. Insulin is this optimistic hormone that plans for your metabolic future. Eat

5. Your Muscles Will Get Stronger In one of the most stunning studies of recent years, scientists have linked refined sugar to a condition called sarcopenia—basically, age-related loss of muscle mass. It happens because added sugar actually blocks the body’s ability to synthesize protein into muscle. (Spending big bucks on protein supplements? If they have added sugar, they’re probably hurting, not enhancing, your ability to build lean muscle.) By reducing the impact of sugar, this plan will keep your muscles younger and stronger—protecting you from injury and helping you to burn fat faster and more efficiently.

Researchers found that those who lifted weights had a 46% lower death rate.9 Even after adjusting for other health variables such as body mass index and chronic disease, and lifestyle habits such as smoking and drinking, the weight-lifting group still had a 19% lower mortality rate. Resistance training has even been shown to reduce age-related cognitive decline, slowing down neurodegeneration in people at risk of developing Alzheimer’s.10 Weight training effectively boosts production of brain-derived neurotrophic factor (BDNF), a naturally occurring protein responsible for nerve cell maintenance. Researchers refer to BDNF as “Miracle Grow for the brain.” Despite the dumb weight lifter stereotypes, resistance training is one of the best things you can do for your cognitive function.

In the brain, a storm comes in the form of gunk, or plaque, that builds up to interfere with the connection of cells. That plaque comes from brain waste (yes, all organs have waste). Some of it is called tau protein; some is called beta-amyloid, or sometimes limbic-predominant age-related TDP-43.1 Essentially, this cell waste attracts inflammation; the buildup disrupts the brain’s connections by gobbling them up and reducing their size, as a storm tangles tree branches and makes power lines ineffective.

RNA viruses mutate relatively quickly, and many, like influenza, are able to undergo a process known as antigenic drift, by which the virus is able to alter the surface antigens that are the targets of our antibodies—thus evading our existing immunity. Some viruses, like measles, cannot change their genomic sequence in ways that substantially alter enough of their surface proteins, so measles remains susceptible to our vaccines or the immunity that we get from prior infection. However, for viruses like influenza, as their surface proteins undergo change, the virus is able to dodge the protective antibodies that we’ve developed from past infection or vaccination

Every chemical compound, according to Engels, comes into existence only at a certain time in the development of the universe when the conditions are appropriate for it; and when it does come into existence it manifests this by entering into its characteristic relations. Neither carbon compounds or proteins are ideal forms, but are themselves witnesses of the conditions on a cooling planet. It is here that occurs his celebrated remark that life is the mode of existence of proteins.

The end product of all that evolution is that we are big-brained, moderately fat bipeds who reproduce relatively rapidly but take a long time to mature. We are also adapted to be physically active endurance athletes who regularly walk and run long distances and who frequently climb, dig, and carry things. We evolved to eat a diverse diet that includes fruits, tubers, wild game, seeds, nuts, and other foods that tend to be low in sugar, simple carbohydrates, and salt but high in protein, complex carbohydrates, fiber, and vitamins. Humans are also marvelously adapted to make and use tools, to communicate effectively, to cooperate intensively, to innovate, and to use culture to cope with a wide range of challenges. These extraordinary cultural capacities enabled Homo sapiens to spread rapidly across the planet and then, paradoxically, cease being hunter-gatherers.

Ling’s electrostatically connected water molecules sheathing long, thin protein braids are as easily swayed as Carlyle’s sheeplike critics—a little influence applied in the right place goes a long, long way. Each water molecule shifts the interior balance of its neighbors’ electrons, and every water molecule is able to pivot its electrostatic charge. The result is a typical crowd response: when conditions change, every molecule of H20 swivels in the same direction. The result, in Ling’s words, is a “functionally coherent and discrete cooperative assembly.” If a relatively small but insistent molecule called a cardinal adsorbent*48 steps up to one of the many podiums (docking sites) along the protein chain, it galvanizes attention, making all the water molecules swivel their “heads”—the polarity of the electrons in their shells—simultaneously. This changes the chemical properties of the assembled multitude dramatically.49 But, hey, that’s life—quite literally. When the molecular crowd disperses, a cell is dead.

The reason they’re called high- and low-density lipoproteins (HDL and LDL, respectively) has to do with the amount of fat relative to protein that each one carries. LDLs carry more lipids, while HDLs carry more protein in relation to fat, and are therefore more dense.

The solfeggio is a six-note scale and is also nicknamed “the creational scale.” Traditional Indian music calls this scale the saptak, or seven steps, and relates each note to a chakra. These six frequencies, and their related effects, are as follows: Do 396 Hz Liberating guilt and fear Re 417 Hz Undoing situations and facilitating change Mi 528 Hz Transformation and miracles (DNA repair) Fa 639 Hz Connecting/relationships Sol 741 Hz Awakening intuition La 852 Hz Returning to spiritual order Mi has actually been used by molecular biologists to repair genetic defects.115 Some researchers believe that sound governs the growth of the body. As Dr. Michael Isaacson and Scott Klimek teach in a sound healing class at Normandale College in Minneapolis, Dr. Alfred Tomatis believes that the ear’s first in utero function is to establish the growth of the rest of the body. Sound apparently feeds the electrical impulses that charge the neocortex. High-frequency sounds energize the brain, creating what Tomatis calls “charging sounds.”116 Low-frequency sounds drain energy and high-frequency sounds attract energy. Throughout all of life, sound regulates the sending and receiving of energy—even to the point of creating problems. People with attention deficit hyperactivity disorder listen too much with their bodies, processing sound through bone conduction rather than the ears. They are literally too “high in sound.”117 Some scientists go a step further and suggest that sound not only affects the body but also the DNA, actually stimulating the DNA to create information signals that spread throughout the body. Harvard-trained Dr. Leonard Horowitz has actually demonstrated that DNA emits and receives phonons and photons, the electromagnetic waves of sound and light. As well, three Nobel laureates in medical research have asserted that the primary function of DNA is not to synthesize proteins, but to perform bioacoustic and bioelectrical signaling.118 While research such as that by Dr. Popp shows that DNA is a biophoton emitter, other research suggests that sound actually originates light. In a paper entitled “A Holographic Concept of Reality,” which was featured in Stanley Krippner’s book Psychoenergetic Systems, a team of researchers led by Richard Miller showed that superposed coherent waves in the cells interact and form patterns first through sound, and secondly through light.119 This idea dovetails with research by Russian scientists Peter Gariaev and Vladimir Poponin, whose work with torsion energies was covered in Chapter 25. They demonstrated that chromosomes work like holographic biocomputers, using the DNA’s own electromagnetic radiation to generate and interpret spiraling waves of sound and light that run up and down the DNA ladder. Gariaev and his group used language frequencies such as words (which are sounds) to repair chromosomes damaged by X-rays. Gariaev thus concludes that life is electromagnetic rather than chemical and that DNA can be activated with linguistic expressions—or sounds—like an antenna. In turn, this activation modifies the human bioenergy fields, which transmit radio and light waves to bodily structures.120

Autophagy is essential to life. If it shuts down completely, the organism dies. Imagine if you stopped taking out the garbage (or the recycling); your house would soon become uninhabitable. Except instead of trash bags, this cellular cleanup is carried out by specialized organelles called lysosomes, which package up the old proteins and other detritus, including pathogens, and grind them down (via enzymes) for reuse. In addition, the lysosomes also break up and destroy things called aggregates, which are clumps of damaged proteins that accumulate over time. Protein aggregates have been implicated in diseases such as Parkinson’s and Alzheimer’s disease, so getting rid of them is good; impaired autophagy has been linked to Alzheimer’s disease–related pathology and also to amyotrophic lateral sclerosis (ALS), Parkinson’s disease, and other neurodegenerative disorders.

Processed oils like canola or vegetable oil are polyunsaturated fats, which are molecularly unstable and prone to cell-destroying oxidation. Oxidants are reactive molecules that are used to transfer electrons from one atom to another. They are naturally produced both inside your body and the environment, but in excess they can react with other cellular molecules in your body, such as proteins, DNA, and lipids, often contributing to disease and inflammation in the process. (This is why antioxidants are so important—they help prevent oxidation-related damage.)

BUSTER You may have heard the myth that higher-protein diets lead to kidney dysfunction. The data tell us otherwise. A meta-analysis conducted by prominent protein researcher Stu Philips looked at higher-protein (HP) diets (≥ 1.5 g/kg body weight or ≥ 20% energy intake or ≥ 100 g/day) and their effects on kidney function. The indicator known as glomerular filtration rate (GFR) reflects any change in the efficiency of kidney function. When compared with normal- or lower-protein (≥ 5% less energy intake from protein/day) diets, HP diet interventions did not significantly elevate GFR relative to diets containing lower amounts of protein. Researchers concluded that HP intake does not negatively influence renal function in healthy adults.2 A systematic review of randomized controlled trials and epidemiologic studies conducted by Van Elswyk et al. found that HP intake (≥ 20% but < 35% of energy or ≥ 10% higher than a comparison intake) had little to no effect on blood markers of kidney function (e.g., blood pressure) when compared with groups following US RDA recommendations (0.8 g/kg or 10–15% of energy).

Norepinephrine: The Wake-Up Neurotransmitter One of norepinephrine’s effects on the brain is to sharpen attention. As we saw earlier, norepinephrine (aka noradrenaline) can function as both a neurotransmitter and a hormone. When we perceive stress and activate the fight-or-flight response, the brain produces bursts of norepinephrine, triggering anxiety. But sustained and moderate secretion can also produce a beneficial result in the form of heightened attention, even euphoria, and meditation has been shown to produce a rise in norepinephrine in the brain. A modest dose of norepinephrine is also associated with reduced beta brain waves. 5.11. Norepinephrine: your wake-up molecule. Notice the paradox here. Norepinephrine is associated with both anxiety and attentiveness. How do you get enough to be alert, but not so much you’re stressed? Surrender is the key. Steven Kotler, co-author of Stealing Fire, says that stress neurochemicals like norepinephrine actually prime the brain for flow states. At first, the meditator is frustrated by Monkey Mind. But if she surrenders, despite the perpetual self-chatter of the DMN, she enters the next phase of flow, which is focus. She has hacked her biology, using the negative experience of mind wandering as a springboard to flow. Norepinephrine’s molecular structure is similar to its cousin, epinephrine. While epinephrine works on a number of sites in the body, norepinephrine works exclusively on the arteries. When both dopamine and norepinephrine are present in the brain at the same time, they amplify focus. Attention becomes sharp, while perception is enhanced. Staying alert is a key function of the brain’s attention circuit, which keeps you focused on the object of your meditation and counteracts the wandering mind. It also stops you from becoming drowsy, an occupational hazard for meditators. That’s because pleasure neurotransmitters such as serotonin and melatonin (for which serotonin is the precursor) can put you to sleep if not balanced by alertness-producing norepinephrine. Again, the ratios are the key. Oxytocin: The Hug Drug 5.12. Oxytocin: your cuddle molecule. Oxytocin is produced by the hypothalamus, part of the brain’s limbic system. When activated, neurons in the hypothalamus stimulate the pituitary gland to release oxytocin into the bloodstream. So even though oxytocin is produced in the brain, it has effects on the body as well, giving it the status of a hormone. It is one of a group of small protein molecules called neuropeptides. A closely related neuropeptide is vasopressin. All mammals produce some variant of these neuropeptides. Oxytocin promotes bonding between humans. It is responsible for maternal feelings and physically prepares the female body for childbirth and nursing. It is generated through physical touch but also by emotional intimacy. Oxytocin also facilitates generosity and trust within a group. Oxytocin is the hormone associated with the long slow waves of delta. A researcher hooking subjects up to an EEG found that touch stimulated greater amounts of delta, with certain regions of the skin being more sensitive. The biggest effect was produced by tapping the cheek, as we do in EFT. It produced an 800% spike in delta.

Oxidation burns things gradually and steadily. Just as oxidation causes metal to rust and apple flesh to brown, it damages cells throughout the body by zapping DNA, scarring the walls of arteries, inactivating enzymes, and mangling proteins. Paradoxically, the more oxygen we use, the more we generate reactive oxygen species, so theoretically vigorous physical activities that consume lots of oxygen should accelerate senescence. A related driver of senescence is mitochondrial dysfunction. Mitochondria are the tiny power plants in cells that burn fuel with oxygen to generate energy (ATP). Cells in energy-hungry organs like muscles, the liver, and the brain can have thousands of mitochondria. Because mitochondria have their own DNA, they also play a role in regulating cell function, and they produce proteins that help protect against diseases like diabetes and cancer.29 Mitochondria, however, burn oxygen, creating reactive oxygen species that, unchecked, cause self-inflicted damage. When mitochondria cease to function properly or dwindle in number, they cause senescence and illness.30

What you can afford to eat is dependent upon your fluid availability,” says Professor Michael Tipton. “When you eat protein this creates ammonia in your body, then urea, which is poisonous to your system. To eliminate urea you need liquid to produce urine. So if you eat a lot of protein you raise your fluid requirements . . . these things are intimately related.

You were a child once, too. When you arrived in the world, your only food preferences were milk and buried memories from your mother’s diet. Those early weeks were dominated by meals - the stab of hunger, the sweet contentment of being sated - but you could not yet tell dinner from breakfast. You didn’t yet know - lucky you! - what a trans fat was; or a frappuccino. No one had taught you to worry whether you were getting enough protein, or to feel guilt when your stomach was full. You had never watched a fast-food commercial, and on the relative merits of quinoa and macarons you had no opinion. Food was a wide open for you. The great garden of ingredients - from bitter greens to sweet dates - was all equally unknown: all new, all strange, all waiting to be discovered.

There’s also some indication that replacing carbohydrate with plant rather than animal foods has special health benefits. Among approximately eighty thousand women in the Nurses’ Health Study consuming lower-carbohydrate diets, high consumption of vegetable protein and fat was associated with a 30 percent lower risk for heart disease over twenty years, whereas high consumption of animal protein and fat appear to provide no such protection. One explanation for this finding is that the relative amounts of amino acids in animal protein stimulate more insulin and less glucagon release than those in plant protein – a hormone combination that has detrimental effects on serum cholesterol and fat-cell metabolism. Other possible downsides of a modern, animal-based diet include a less healthful profile of dietary fats, excessive iron absorption (especially for men), and chronic exposure to hormones, preservatives, and environmental pollutants.

It was not until relatively recently, however, that the association between disturbed sleep and Alzheimer’s disease was realized to be more than just an association. While much remains to be understood, we now recognize that sleep disruption and Alzheimer’s disease interact in a self-fulfilling, negative spiral that can initiate and/or accelerate the condition. Alzheimer’s disease is associated with the buildup of a toxic form of protein called beta-amyloid, which aggregates in sticky clumps, or plaques, within the brain. Amyloid plaques are poisonous to neurons, killing the surrounding brain cells. What is strange, however, is that amyloid plaques only affect some parts of the brain and not others, the reasons for which remain unclear. What struck me about this unexplained pattern was the location in the brain where amyloid accumulates early in the course of Alzheimer’s disease, and most severely in the late stages of the condition. That area is the middle part of the frontal lobe—which, as you will remember, is the same brain region essential for the electrical generation of deep NREM sleep in healthy young individuals. At that time, we did not understand if or why Alzheimer’s disease caused sleep disruption, but simply knew that they always co-occurred. I wondered whether the reason patients with Alzheimer’s disease have such impaired deep NREM sleep was, in part, because the disease erodes the very region of the brain that normally generates this key stage of slumber.

The information contained in this eBook does not constitute medical advice. Readers who are in need of medical advice should consult a physician and/or a medical health professional. Readers who are in need of specific dietary advice relating to their condition should consult a dietician and/or a medical health professional.

Every cell in the tree integrates information about the state of the internal environment of the needs then open or close to admit gases or release water vapor. Every cell inside the needle is making similar assessments and decisions, sending and receiving signals, modulating its behavior as it learns about and responds to the environment. When such processes run though animal nerves, we call them “behavior and thought”. If we broaden our definition and let drop the arbitrary requirement of the possession of nerves, then the balsam fir tree is a behaving and thinking creature. Indeed, the proteins that we vertebrate animals use to create the electrical gradients that enliven our nerves are closely related to the proteins in plant cells that cause similar electrical excitation. The signals in galvanized plant cells are languid-they take a minute or more to travel the length of a leaf, twenty times slower than nerve impulses in a human limb-but they perform a similar function as animal’s nerves, using pulses of electrical charge to communicate from one part of the plant to another. Plants have no brain to coordinate these signals, so plant thinking is diffuse, located in the connections among every cell.

For about 60 years type 1 diabetics were treated with insulin extracted from the pancreas of pigs. This wasn’t ideal as the insulin was a relatively minor component of all the proteins in the pig pancreas and required a lot of expensive purification to produce a relatively small amount of the drug. The pig insulin wasn’t quite identical to the normal human version and it wasn’t suitable for some patients. It was also very difficult to ramp up supply quickly when demand increased. In the 1980s, the drug firm Eli Lilly produced and sold human insulin that had been created in genetically modified bacteria. Now, virtually all insulin is made in bacteria or yeast.

It was Wu’s deepest perception that the park was fundamentally sound, as he believed his paleo-DNA was fundamentally sound. Whatever problems might arise in the DNA were essentially point-problems in the code, causing a specific problem in the phenotype: an enzyme that didn’t switch on, or a protein that didn’t fold. Whatever the difficulty, it was always solved with a relatively minor adjustment in the next version. Similarly, he knew that Jurassic Park’s problems were not fundamental problems. They were not control problems. Nothing as basic, or as serious, as the possibility of an animal escaping. Wu found it offensive to think that anyone would believe him capable of contributing to a system where such a thing could happen.

Life relies on digitally coded instructions, translating between sequence and structure (from nucleotides to proteins), with ribosomes reading, duplicating, and interpreting the sequences on the tape. But any resemblance ends with the different method of addressing by which the instructions are carried out. In a digital computer, the instructions are in the form of COMMAND (ADDRESS) where the address is an exact (either absolute or relative) memory location, a process that translates informally into “DO THIS with what you find HERE and go THERE with the result.” Everything depends not only on precise instructions, but also on HERE, THERE, and WHEN being exactly defined. In biology, the instructions say, “DO THIS with the next copy of THAT which comes along.” THAT is identified not by a numerical address defining a physical location, but by a molecular template that identifies a larger, complex molecule by some smaller, identifiable part. This is the reason that organisms are composed of microscopic (or near-microscopic) cells, since only by keeping all the components in close physical proximity will a stochastic, template-based addressing scheme work fast enough. There is no central address authority and no central clock. Many things can happen at once. This ability to take general, organized advantage of local, haphazard processes is the ability that (so far) has distinguished information processing in living organisms from information processing by digital computers.

Estrogen metabolism is the healthy removal or detoxification of estrogen from your body. It’s a two-step process. First, your liver inactivates estrogen by attaching a little molecule or “handle,” which is called conjugation. To do that effectively, your liver needs a good supply of nutrients such as folate, vitamin B6, vitamin B12, zinc, selenium, magnesium, and protein. Your liver also needs to be relatively free from the toxic effects of alcohol or endocrine disrupting chemicals. Even one drink per day can increase your blood level of estrogen.

The DNA molecule is shaped like a twisted ladder, and the rungs of the ladder—the nucleotides—can hold vast amounts of information, the code of life. A gene is a short stretch of DNA, typically about a thousand letters long, that holds the recipe for a protein or a group of related proteins. The total assemblage of an organism’s genetic code—its full complement of DNA, comprising all its genes—is the organism’s genome.

The body’s initial response to a noxious local insult is to produce a local inflammatory response with sequestration and activation of white blood cells and the release of a variety of mediators to deal with the primary ‘insult’ and prevent further damage either locally or in distant organs. Normally, a delicate balance is achieved between pro- and anti-inflammatory mediators. However, if the inflammatory response is excessive, local control is lost and a large array of mediators, including prostaglandins, leukotrienes, free oxygen radicals and particularly pro-inflammatory cytokines (p. 72), are released into the circulation. The inflammatory and coagulation cascades are intimately related. The process of blood clotting not only involves platelet activation and fibrin deposition but also causes activation of leucocytes and endothelial cells. Conversely, leucocyte activation induces tissue factor expression and initiates coagulation. Control of the coagulation cascade is achieved through the natural anticoagulants, antithrombin (AT III), activated protein C (APC) and tissue factor pathway inhibitor (TFPI), which not only regulate the initiation and amplification of the coagulation cascade but also inhibit the pro-inflammatory cytokines. Deficiency of AT III and APC (features of disseminated intravascular coagulation (DIC)) facilitates thrombin generation and promotes further endothelial cell dysfunction. Systemic inflammation During a severe inflammatory response, systemic release of cytokines and other mediators triggers widespread interaction between the coagulation pathways, platelets, endothelial cells and white blood cells, particularly the polymorphonuclear cells (PMNs). These ‘activated’ PMNs express adhesion factors (selectins), causing them initially to adhere to and roll along the endothelium, then to adhere firmly and migrate through the damaged and disrupted endothelium into the extravascular, interstitial space together with fluid and proteins, resulting in tissue oedema and inflammation. A vicious circle of endothelial injury, intravascular coagulation, microvascular occlusion, tissue damage and further release of inflammatory mediators ensues. All organs may become involved. This manifests in the lungs as the acute respiratory distress syndrome (ARDS) and in the kidneys as acute tubular necrosis (ATN), while widespread disruption of the coagulation system results in the clinical picture of DIC. The endothelium itself produces mediators that control blood vessel tone locally: endothelin 1, a potent vasoconstrictor, and prostacyclin and nitric oxide (NO, p. 82), which are systemic vasodilators. NO (which is also generated outside the endothelium) is implicated in both the myocardial depression and the profound vasodilatation of both arterioles and venules that causes the relative hypovolaemia and systemic hypotension found in septic/systemic inflammatory response syndrome (SIRS) shock. A major component of the tissue damage in septic/SIRS shock is the inability to take up and use oxygen at mitochondrial level, even if global oxygen delivery is supranormal. This effective bypassing of the tissues results in a reduced arteriovenous oxygen difference, a low oxygen extraction ratio, a raised plasma lactate and a paradoxically high mixed venous oxygen saturation (SvO2). Role of splanchnic ischaemia In shock, splanchnic hypoperfusion plays a major role in initiating and amplifying the inflammatory response, ultimately resulting in multiple organ failure (MOF). The processes involved include: • increased gut mucosal permeability • translocation of organisms from the gastrointestinal tract lumen into portal venous and lymphatic circulation • Kupffer cell activation with production and release of inflammatory mediators.

Small families are not a new invention. For most of human history, from about one million years ago until as recently as ten to fifteen thousand years ago, all people lived as hunter-gatherers. Men hunted animals and women foraged for fruit and vegetables. Societies were made up of small, scattered bands of people. They had a good, protein-rich diet and most deaths were due to accident, predation and inter-group warfare rather than disease. The children of hunter-gatherers had an excellent chance of survival. Using nothing but the natural, stress-related methods we have discussed, women gave birth to only three or four children in their lifetime. Of these, two or three survived. Large families did not appear until about ten thousand years or so ago, when agriculture brought a change of lifestyle. In the most fertile areas, large and concentrated communities developed, living on a carbohydrate-rich diet. Disease and infant mortality were rife. The average number of children was about seven or eight, but double figures were commonplace. Even so, whole families could be wiped out in days by virulent disease. As with the hunter-gatherers, on average, only two or three in each survived.