Past Views On One Meal A Day (OMAD)

“Eating once a day is angelic, twice a day human, and three, four or more times is bestial.”
~Le Menagier de Paris, The Parisian Household Book, 1393

“Oru velai sapta yogi (if you eat once you’re a yogi);
Rendu velai sapta bogi (if you eat twice you’re a hedonist);
Moonu velai sapta rogi (if you eat thrice you’re a patient).”
~Traditional Tamil wisdom

“And there are men to be found who take but one meal a day, and yet remain quite healthy. The elder Fowler, the phrenologist, is one of them. Such, too, in past years, were Talleyrand of France, and Mr. Taliaferro of Virginia. It is even stated that some of the old Romans ate but one meal a day. Seneca, though worth an estate of $15,000,000, taught the doctrine, and, as it is said, practised it.”
~William Andrus Alcott, 1859

The Laws of Health:
Or, Sequel to The House I Live In

by William Andrus Alcott


636. The question, how often we should eat, has been much agitated, especially within a few years ; and with various results. In general, however, there is a belief that we eat too often, and that a deduction from the number of our meals might very profitably be made. Many incline to the opinion that two meals a day for healthy adults are quite sufficient. A few go farther still, and teach that nature’s purposes are best answered by only one.

637. This subject, like most others pertaining to a connection with the appetite, has been hitherto approached in a wrong way. For, since nature, perverted as she is, ever tends to excess, the great practical question in all these matters should be, not how much we may gratify ourselves without any evil results, but how little gratification will best accord with our usefulness. Instead of inquiring how near the edge of a precipice we can go without falling from it, we should seek to keep at the greatest practicable distance. The proper question is not, Which is the worst or most dangerous road? but, Which is the best?

638. In the present instance, the true physiological inquiry should be, What is the least number of daily meals which will best answer nature’s purposes? What number will preserve us in the most healthy condition, and at the same time give us the firmest appetite, and, in the aggregate, the most pleasure? The true question is not, How often can we eat and not get sick immediately? And yet, more than this, I say, is very seldom asked.

639. Although it should be our first and highest aim to do what is best and most according to truth in all things which concern our appetites, yet we can never keep pleasure entirely out of sight; nor is it the Divine intention that we should. God has kindly united duty, interest, and pleasure; and what he has joined together should not be sundered.

640. There can be little doubt that, the more frequently we eat, the less, as a general rule, we enjoy. At present, it is customary to eat so often that we seldom, if ever, reach the point of having a good appetite; and what of appetite we have, at first, is soon spoiled. The less frequently we eat, on the contrary, even to the comparatively narrow limits of once a day, the more we enjoy.

641. But observe, if you please, I do not say God has united with our duty the highest possible degrees of immediate pleasure, but only the greatest amount in the end. There is room enough left for self-denial, or what is usually called by that name ; by which I mean, a denial of present pleasure, at least in part, for the sake of pleasure in the distance, which is greater in the aggregate.

642. There are certain physiological considerations which aid us in determining how often we should eat ; or, rather, in deter mining how often we should not eat. We have seen (551) that the process of chymification is forwarded, in no small degree, by a species of muscular motion which has a slight resemblance to the churning process among dairy-women.

643. This churning muscular motion generally continues till the stomach is cleared of its contents; i.e., till all, or nearly all, has passed out at its pyloric orifice. The time required for this varies, in the adult, from two or three to four or five hours. (558.) In children, the process, like those of breathing and circulation, is more rapid.*

644. Now, it is a law with all voluntary or willing muscular parts of the body, that they shall have their seasons of rest. But the heart is muscular, and there are muscles in the walls of the thorax to aid in moving the lungs; and then, as we have seen, the stomach is muscular. None of these, it is true, are voluntary or willing muscles. Their motion takes place with out our having much to do with it, directly.

645. Still, it is true, most undeniably true, that these parts need rest. The muscular parts of the heart and lungs have their intervals of rest, though they are short; and is not this the plainest proof that they need it? The muscular parts of the stomach, in all probability, come under the same necessity. Sometimes they obtain this rest; at others they do not. But I have spoken on this subject before. (120-122.)

646. When we breakfast at six, take a lunch at nine or ten, dine at twelve, take another lunch at three, and eat a heavy supper at six, the stomach probably has no rest during the day, and, in consequence, is so much fatigued at night, that the load which is imposed on it at six is not wholly cast off during the night, and we rise in the morning to go again the same round, and with similar results.

647. Then, again, when we rise at seven, breakfast at eight, take a lunch at eleven, or twelve, as in fashionable life, dine at two, take tea at five, and a heavy lunch of the most heavy of all indigestibles at nine or ten, we come to the hour of rest, as before, with a jaded stomach; and in due preparation for a restless and distempered night.

648. And the reward we have so richly earned is sure to be received. Our sleep is too sound on the one hand, or too much disturbed on the other. The latter result is most frequent. We toss out the night in distressing dreams, and wake the next morning to a bad taste in the mouth, a dryness of the throat, a dull headache and loss of appetite, and an unwillingness to rise, except from the most pressing necessity.

649. Such a course of life, persisted in for weeks, months, or years, will bring about, in most persons, a bad state of things in the alimentary canal, which, in its sympathies or effects, some times extends to other parts of the system. Many a tooth-ache, ear-ache, head-ache, and neuralgic attack, and not a few cold feet and sour stomachs, may be fairly charged to the errors of which I have here spoken.

650. Children, no doubt, should eat much more frequently than adults. True, their stomachs are not so strong, nor their digestive powers, though they are generally more active. But even our children eat too often, in most instances. They are trained to it from the very first. Some of them seem to be almost always eating, from morning to night. Little infants, in most instances, are even nursed or fed in the night. And the penalty is but too well known. Half of them, or nearly half, die under ten years of age; and this is one of the causes.’

561. The healthy adult who eats but three times a day, and this at regular intervals of about six hours, gives his stomach a little time for rest; and may hope to proceed on in the journey of life, at least a short time, without disease. He may indulge this hope, I mean, if other things are as they should be.

652. But three meals a day for an adult, whatever may be his habits or circumstances, — except in the rare case of some peculiar disease, — is the maximum number which is admissible. It is running as much risk as we can with safety. It is going as near the edge of the precipice as we can and not fall from it, instead of taking the highest and safest and best road!

653. They who take but two meals a day, especially during the short days of winter, not only give their digestive powers — their stomachs in particular — more time for rest, but actually enjoy more, and find themselves in better general health. Of this habit we have many eminent living examples. In this case the first meal might be profitably taken at ten o’clock in the forenoon, and the second at four in the afternoon.

654. And there are men to be found who take but one meal a day, and yet remain quite healthy. The elder Fowler, the phrenologist, is one of them. Such, too, in past years, were Talleyrand of France, and Mr. Taliaferro of Virginia. It is even stated that some of the old Romans ate but one meal a day. Seneca, though worth an estate of $15,000,000, taught the doctrine, and, as it is said, practised it.

655. It is even told of, Mr. Taliaferro, that he went still farther. When by any unavoidable circumstance he was unable to dine at his usual hour of the day, he deferred it to the next day. This was to eat only once in two days. But this course I think an error. Once a day is the minimum or smallest needful number of our meals.

656. On this point, however, I wish to be understood. I do not say, positively, that three meals a day are incompatible with the maintenance of tolerable health; nor that one a day is sufficient. But I do say that more than three are injurious ; that two would for most persons be preferable to three; and that one for most people may after all be found adequate to every purpose. Indeed, I am inclined to think it would be so.

657. They who take but one meal a day secure at least one important point, that of having always a good appetite. At least they gain this point provided they do not eat too much at this one meal. Most persons, as we have seen, eat so often that they never know what a good appetite is. They always eat before they are truly hungry, in a physiological sense; and hence know neither the blessing of a good appetite or of true gustatory enjoyment.

658. They remind me of a half-idiot, whom I knew in early life, who was always pressing the question, ” Don’t you wish to know the art of never being dry ? “that is, thirsty. ” Always mind to drink before you are dry,” he added, “and you will never be dry.” We have most of us already made a faithful application of the fool’s rule to our eating. We eat always be fore we are hungry, and hence are never hungry.

[Questions. — Is there not a general belief abroad that we eat too often! Have we arrived, as yet, at a settled opinion on this subject?]


659. In the last section I was obliged to encroach a little on the topic assigned to this. I was obliged to allude to the evils of eating too often; and this of course involved the subject of eating between our meals, or, as it is called, of taking lunches or luncheons. But I have not yet said all that the case requires. Eating between our regular meals is a dietetic transgression of no ordinary magnitude.

660. Whether we eat once, twice, thrice, or ten times a day, we should stop with our regular meals, Nothing containing nutriment, whether in a solid or liquid condition, should go down our throats between our meals, except water. To this rule, so far as the healthy are concerned, I know of no exception.

661. May we not eat an apple, it will be asked, or a little fruit, of such kinds as we happen to meet with, or a few nuts? Must we go without all these things, which the kind hand of the great Creator has scattered all along our path — probably not in vain? Would we not be even ungrateful to him, did we do so?

662. No doubt that these things, for the most part, are made to be eaten, either by us or the other animals, or both. But they should be brought to our tables, and, without exception, made a regular part of our meals. Not indeed at the end, after we have eaten enough of something else; nor yet at the beginning, merely to excite an appetite for other food. They should be eaten, as the potato usually is, as a part of our meal.

[Have we not studied the subject in a wrong manner? What is a better way? What should be the true inquiry in prosecuting the study of hygiene? In our inquiries is pleasure to be overlooked, entirely so? Why not? Is our enjoyment in eating in proportion always to the number of our meals? Is he the greatest gainer in point of mere pleasure in eating, who gets the most pleasure immediately?

What are we to infer, in this particular, from the muscular character of the stomach? How may we eat so as to give the stomach and other digestive organs no rest? What are the frequent evidences of abuse during the previous day? What diseases may ensue? Should children eat oftener than adults? What is said, in particular, of the effects of eating three meals a day? What of eating two only? What of eating but one? Are there some eminent examples in both these latter kinds? To what extreme did Mr. Taliaferro go? Who are they that always have a good appetite? What anecdote is related of a certain idiot? What is the application?]

663. It may perhaps be said that our ancestors — puritannical though they were — accustomed themselves not only to lunches in the forenoon and afternoon, but to nuts and cider or apples and cider in the evening, and yet were a healthier people, by far, than their more squeamish descendants; and there will be no want of truth as the basis of the remark.

664. But, remember, that if they were more healthy than we, then we, of course, are less healthy than they. How came we thus? Is it a matter of chance, or hap-hazard? Do these things spring out of the ground? Is there not a cause for every effect? Do we not inherit a deteriorated and deteriorating constitution?

665. Besides, our fathers and grandfathers set out with better constitutions than we, so that, whatever may have been the cause of their better or our inferior stamina, they could most certainly bear up longer under violations of physical law than we, their descendants. It does not then follow, as a necessary inference, that we may eat lunches because they did.

666. May we not take nourishing drinks between our regular meals, such as milk and water, molasses and water, and bread coffee? some will ask. Not a drop. Better, by far, to eat a piece of dry bread; for that will be masticated. But you do not want either. The sediment of nutritious drinks (561) is one of the hardest ordinary things the stomach has to contend with. It is, moreover, a curious fact that a piece of dry bread, well chewed, will often quench thirst better than any liquid, even water. But, I repeat, I do not recommend even that.

667. Anything that contains nutriment must, of course, set the stomach and other digestive organs at work, more or less; even if it is nothing but a strawberry, or a lump of gum or sugar, or some aromatic seeds. I do not say or believe that it takes as long, or tasks the digestive machinery as severely, to work up a lump of sugar or a strawberry into chyle, as a full meal; but I do say that the whole process of digestion, complicated as it is, must be gone through with.

668. Many, who have listened patiently to remarks like these, have at length exclaimed, with some surprise: “But what is the laboring man to do, especially in the long hot days of haying and harvesting, without something to sustain him be tween his meals? You proscribe stimulating drink, and very properly; but what will you propose as a substitute? He, would faint away without something. Or, if he should not faint, there would often be a gnawing at the stomach, which would be insupportable.”

669. It should be distinctly known to everybody, that neither the faintness nor the gnawing here spoken of, indicate any real hunger. They are mere nervous sensations. They indicate, moreover, a diseased condition of the nerves. If any one doubts, let him but make the following experiment. The writer has made it for himself, and that repeatedly.

670. While your fellow-laborers are removing, for the time, their gnawing and faintness by a lunch, just seat yourself at their side, and, instead of adding a new load to the already overloaded and sympathizing stomach, drink slowly a small quantity of pure water, tell a story or hear one, and, if you can, excite a little the risible faculties; and when they return to their labor, join them, as before. Pursue this course a few days, or a few weeks, and see who endures it best, and com plains most of gnawing and faintness.

671. It is no uncommon thing to hear farmers telling how glad they are to be through with their haying and harvesting. But it is they who use lunches, or take other means beyond their regular meals for restoring themselves temporarily at the expense of the future, who complain most. He who eats of plain food twice or three times a day, and drinks nothing but water, endures best the heat and fatigue, and suffers least from gnawing and faintness.

672. Young men in groceries, eating-houses, and inns, as well as clerks in public offices, and in shops and factories, often injure their health very much by a foolish acquired habit of tasting various things which are constantly before them, such as fruits, nuts, confectionery, sugar, dried fish, cordials, etc. Clerks, in addition to all this, sometimes eat wafers.’

673. It is but a few days since I saw a young man about thirty years of age, of giant constitution by inheritance, who was suffering severely in his digestive machinery from the very cause, by his own voluntary confession, of which I am now speaking. And I have before my mind’s eye the painful history of a young man whom I twice cured of dyspepsia from this same cause, but who afterwards went beyond my reach, and fell a victim to it.

674. Perhaps the worst violation of the law which forbids eating between meals, is found in the wretched habit of the young, of eating what are called oyster suppers, at late hours and at improper places. Our cities, and sometimes our large towns, abound with places of resort for those who will not deny their appetites; and it is not surprising that they so often prove, not only a pathway to the grave, but as Solomon says, to hell.


675. There are to be found, among us, a few strong men and women — the remnant of a by-gone generation, much healthier than our own — who can eat at random, as the savages do, and yet last on, as here and there a savage does, to very advanced years. But these random-shot eaters are, at most, but exceptions to the general rule, which requires regularity.

676. For very few things, I am quite sure, can be more obvious to the most careless observer, than that those individuals who are most regular in regard to eating, other things and circumstances being equal, are the most healthy. And, what is of very great importance, too, any one who will take the trouble may soon satisfy himself that it is these regular men and women whose children inherit the best constitutions.

677. I have, indeed, admitted that we are so far the creatures of habit that we can accustom ourselves to almost any hours for eating, and to one, two, three, or more meals a day, as well as to many other things which are generally regarded as objectionable; and yet not suffer much, immediately. But I have also shown and insisted that this does not prove we are wise in forming these habits. We must look a little way into the future, and have regard to the good of the race, as well as to our own present gratification or happiness.

678. It is often said that since the conditions of civic life require occasional irregularities, it is desirable to accustom our selves to such irregularities, betimes. For, if we do not, it is still insisted, we shall be liable, at times, to such derangement and disturbance in our systems, from unavoidable changes, as might subject us to a long and perhaps severe fit of sickness.

[Questions. — Is eating between our meals a light transgression? Should nothing which contains nutriment be swallowed between meals? May we not eat fruits? Why not, if the fruits are made to be eaten? Our ancestors ate lunches; why may not we? What is said of milk and water, molasses and water, etc., between meals? Must the whole work of digestion be gone through with, when we eat but a single nut, or a strawberry? May not the hard laborer have lunches? What then shall we do, when gnawing and faintness arise? Have these sensations nothing to do with real hunger? What experiment is proposed? To what dangers are young men sometimes exposed in groceries, shops, eating-houses, public offices, etc.? Are they apt to yield to the temptations? What case is related by the author? What still more striking case came under his observation? What is the worst violation of the rule for infrequent eating?]

679. This reasoning, by way of objection to the doctrine of regularity in our habits, is certainly specious. The great difficulty with it is, that it is practically untrue. For few things can be more easily shown than that they whose digestive systems hold out best, are precisely those who are most regular in their habits of eating, drinking, etc.

680. It is indeed true that such persons, when subjected to the supposed necessary irregularities of civic life, above alluded to, may be subjected, at times, to a little temporary disturbance, but it quickly passes away. Does not this prove the general integrity of the digestive function? No condition of the human stomach is more to be dreaded than that unresisting state which permits us to make it a complete scavenger for the time; while the abuse awakens slowly, in some remoter part of the human confederacy, a terrible insurrection, and still more terrible retribution.

681. I knew a physician who, at home and abroad, with others, and especially with himself, passed for a wise man. Yet, unable to resist the temptations incident to the life of a country medical practitioner, he gradually fell into the utmost irregularities about his meals. For his morning meal he had no appetite; at the dinner hour he was among his patients, eating at any hour convenient; or, oftener still, refusing to eat at all.

682. On returning to his family, — often late at evening, — , his faithful wife, who knew his habits and expectations, was accustomed to prepare for him as rich and as abundant a meal as possible, of which he almost always partook in excess. But the penalty of his trangression was fearful. Disease, painful and harassing, early followed; and, though blessed with an “iron constitution ” by birthright, he sunk into the grave at sixty-five.

683. The history of this man is, in substance, that of thousands. I have myself witnessed twenty years of the most in tense anguish, ended by a premature and terrible death, which was the obvious result of physical disobedience. The penalty, it has repeatedly been said, does not always fall directly on the suffering organ or function, but sometimes on a part in sympathy with it.

684. It may, to many, seem strange, but it is nevertheless a fact, that they who are most regular with regard to their habits of eating, — whether as it regards times of eating, quality of the food, or quantity, — are the very persons who suffer least, as a permanent thing, when compelled to occasional changes or interruptions of their accustomed habits. Or, if they suffer, the suffering is but temporary. Their stomachs are stomachs of integrity, and their promptitude in meting out justice, and putting to rights injurious tendencies, is as striking as their integrity.

685. Locke, the philosopher, has somewhere told us that when a child asks for food at any other time than at his regular meals, plain bread should be given him — no pastry, no delicacies, but simply plain bread. If the child is really hungry, he says, plain bread will go down; if not, let him go with out till he is so.

686. But why give him anything at all between his regular meals? These, to be sure, should be somewhat more frequent than our own; but this is not to make concessions to irregularity. Is it not truly marvellous to find the best of men — those who in many things have thought for themselves — still yielding to authority when arrayed against the plainest good sense?

687. It is very unfortunate for human health and happiness that the young should be trained from the very first — and to a most lamentable extent — in the way in which they should not go. They are very tenacious of life, — are made to live, — and yet, presuming on their known tenacity of life, we only make them the greater sufferers on account of it. I have known many a child, swept away by summer and autumnal diseases, who, but for his past irregularities in eating, might very probably have escaped.

688. That to train up a child in the way he should go, in every particular, is exceedingly difficult, every parent, master, or guardian well knows. Forbidden trees, on which hang curses, beset everywhere the path of human life, especially that broader division of it which, alas! so many of us travel. How to have our children escape all pitfalls and dangers, — how, even, to escape them ourselves, — is a question not by any means easy of solution ; but its importance is at* the least equal to its difficulties.

689. I wish the young could fully understand that every time they depart from their accustomed usages, and, during the intervals of their meals (be the latter few or many), venture on a little fruit, a little candy, a little confectionery, etc., they are not only impairing their appetite, and contaminating their blood, but impairing the tone of their digestive system, and deranging the action, more or less, of the whole alimentary canal.

690. Every well-directed effort to invigorate the alimentary canal, and increase the tone of that and the greater internal surface of the lungs, is richly repaid in future hardihood and health; while every neglect, or disregard — everything disloyal to the calls and demands of Nature’s conservator — is repaid in near or remote suffering, and perhaps transmitted to yet unborn generations.


691. Nothing is more common than the remark that the greatest dietetic error is with regard to quantity. It is admitted that we often err, as regards quality; that we eat irregularly; and that we eat too fast. And yet the great practical error, after all, we are told, is, that we eat too much.

692. There is truth in the remark, as the subject must necessarily be viewed by those whose standard of hygiene is still low. And yet, bad as excessive alimentation may be, it is but the natural — I had almost said necessary — result of certain errors lying back of it. If the quality of our food, and the modes of preparing and receiving it, and the moral tendencies of our nature, were such, from the very first, as they ought to be, there would be comparatively little among us of excess.

693. The common doctrine of intelligent men is, that we eat about twice as much as nature’s best purposes require. Philosophers, physiologists, chemists, pathologists, dietiticians, and even many of the unenlightened, all agree in this. Not of course that every individual eats twice as much as he ought; but that, as a people, here in the United States, this is true.

694. Most persons, it would seem, eat just about as much as they can and not suffer from it immediately. The inquiry with most who inquire at all, is not how little is best for them and how much they can save, beyond this measure, for “him who needeth”; but how much they can consume, without loss of health or character as the consequence.

[Questions. — What is said of certain random-eaters among us? Are they whose habits of eating are most regular, usually the most healthy? Must we have regard, in the formation of our habits, to the good of our race? What very specious objection is sometimes made to these views and doctrines? Why is it unsound? Relate the anecdote of a medical man, and tell me what it is designed to prove. Is this man’s history substantially that of thousand ? What has the philosopher Locke said? Wherein is he mistaken? What is there especially unfortunate in an early training? Do all our dietetic errors, especially our irregularities in regard to eating, tend to derange the action and motion of the alimentary canal? What important hints does this afford in the education of the young? What equally important hints does it afford to the self-educated?]

695. In truth, the declaration of eighteen hundred years ago, that all seek their own, not another’s (or others’) good, covers the whole ground. To get good and apply it to the gratification of our own propensities, whatever may become of others, is fallen nature’s great law, As John Foster has well said, this not caring for others is the very essence of human depravity.

696. It is frequently asked how much we should eat; and some are unsatisfied till we put in requisition the scales, and tell them exactly how many pounds or ounces they must take, daily. I have even dined, in the city of Boston, with a man otherwise respectable, who had his scales on the table, and proceeded to weigh out, before me, his dinner.

697. Of course I do not intend to question the propriety or the usefulness of weighing out our food, at least, occasionally. Experiments of weighing food, made by scientific or thinking men, for scientific or practical purposes, might be made — no doubt sometimes are made — quite useful.

698. Thus, in experiments made in Glasgow, in Scotland, on laborers, who, from their increased expenditure during their exercises, are very naturally supposed to require as large a supply of food as any other class of men, it has been found that two pounds of good bread, daily, or six pounds of good potatoes, (which in point of nutriment are deemed about equal to two pounds of bread,) is the largest quantity demanded or required.

699. President Hitchcock, late of Amherst College, and Mr. Graham, have taught that the average quantity of nutriment which the best development and support of the body require, is somewhat less than this. They, too, have made their conclusions from observation and experiment. The former would reduce the British standard quantity about one-fourth; the latter, nearly one-half.

700. Much allowance, in this matter, must be made for early training, as will be seen in the next section. I once had the pleasure of sustaining, at college, a most deserving young man, who could not get along, as he believed, without two pounds of bread, or its equivalent, daily. But he had been trained to excess; and for the time seemed to demand it. However, he exhausted his physical capital in a few years, and died bankrupt!

701. Are there, then, you may be disposed to ask, no specific rules for the individual, about quantity? Must we gather up, from abstract or general principles and from facts, a code for ourselves? Like the new-fledged arithmetician at school, must we make our own rules? Is experience in dietetics every thing, and science nothing?

702. Not quite so fast. I have given you the deductions of science already. It has determined, no less surely than experience, that we eat too much. It has told us what is the maximum quantity required. What the minimum or smallest quantity we really need is, we have not yet inquired. And most persons do not choose to make the inquiry, lest they should have to resist, a little, their propensities.

703. To those who have moral courage enough — in other and better words, enough of Christian philosophy — to dare to make the inquiry, a few rules may be given which will enable them to approximate towards the truth in the case, by seeking an answer to the inquiry: How little can we get along with, and at the same time best discharge all our duties and secure all lawful and proper interests?

704. We have been taught, in time past, to leave off hungry; or, as some express it, with a good appetite. Or, as others still, are wont to say, we have been told never to eat quite enough. The rule is a good one, as far as it goes. I have known a few who partly observed it; and they believe they owe to this partial obedience their health and life.

705. Thus, Grant Thorburn, whose writings, over the signature of Laurie Todd, have interested and delighted many, and who, at the age of ninety, or nearly so, is almost as young in his feelings as ever he was, is accustomed to say to his friends that he never ate enough in his whole life.

706. Early in the year 1852, I called to see a man in Ohio, who was eighty-seven years of age. It was one of the severest days of a most severe winter. He was in the woods, at work, for he was a farmer; but he soon came home. Surprised at his power to labor and endure the cold, I inquired about his habits; and, among other things, asked him about the quantity of his food. His answer included just such a statement as that of Mr. Thorburn.

707. Cases of this kind might be multiplied, not, however, to an indefinite extent; for, most unhappily, the world as yet does not abound with them. I will only add to the list, at present, John “Williams, a Baptist minister of Rhode Island, who died at the age of one hundred years or more, and myself.

708. It is quite possible to err, however, under this rule. A person who bolts his food will eat much more without reaching the point of satiety than one who does not. While, therefore, he who bolts food has not reached the stopping-place, so far as he knows, another who masticates well has reached it with far less food. The former may therefore eat too much and yet leave off hungry.

709. It is a better rule still, to eat no longer than the food appears to refresh us, bodily and mentally. This rule, I grant, is liable to the same difficulties with the preceding, nevertheless, it restricts us more. For even Grant Thorburn, who never eats enough, may possibly sometimes eat so long as to become dull in body or mind as the result. I am not without doubt whether he and my Ohio friend always leave off their meal with feelings of merriment, and with a disposition to dance and sing, like children. Yet such, as I believe, should be the effect of our eating. Its main object, I grant, is to secure nourishment for a future hour; but it has a secondary object, too, which is refreshment and gratification.

710. It is recorded of President Jefferson, that he was accustomed to remark that no man, when he comes to die, ever repents of having eaten so little. This remark would be worth more if it were true that men are apt to repent of eating too much. But the truth is, we seldom exercise any genuine repentance at all when we come to die, unless we have begun the work before. Death-beds are not the very honest places some have supposed. Men generally die as they live.

711. The early travellers among the Japanese tell us that a native of that country, especially of the interior, will work all day long on a mere handful of rice and a little fruit. Yet the Japanese are among the stoutest and strongest men of Asia ; and for size and strength almost resemble the German, the Swiss, and the Yankee. Can it be that they suffer for want of food?

712. We come back, then, from our reasonings and facts to the point whence we started, viz., to the affirmation that we generally eat twice as much as we ought, and that retrenchment is loudly and imperiously demanded. Few err on the other side. Inclination, habit, refined cookery, and the customs of society are all against it.

713. I have admitted that the laborer, as a general rule, requires more food than other men, because his expenditure is greater. Yet it does not thence follow, that he who performs two days’ work in one, and who consequently overworks him self, should eat in the same proportion, that is, twice as much. Generally speaking, if he really overworks, he should eat some what less, since the same causes which have overtasked and crippled his general system must have reduced the energies of his digestive system in the same proportion.

Native Americans Feasted Some But Mostly Fasted

“There are to be found, among us, a few strong men and women — the remnant of a by-gone generation, much healthier than our own — who can eat at random, as the savages do, and yet last on, as here and there a savage does, to very advanced years. But these random-shot eaters are, at most, but exceptions to the general rule, which requires regularity.”
~William Andrus Alcott, 1859

Three Squares: The Invention of the American Meal
by Abigail Carroll, pp. 12-14

Encountering the tribal peoples of North America, European explorers and settlers found themselves forced to question an institution they had long taken for granted: the meal. “[They] have no such thing as set meals breakfast, dinner or supper,” remarked explorer John Smith. Instead of eating at three distinct times every day, natives ate when their stomachs cued them, and instead of consuming carefully apportioned servings, they gleaned a little from the pot here and there. English colonists deplored this unstructured approach. They believed in eating according to rules and patterns—standards that separated them from the animal world. But when it came to structure, colonists were hardly in a position to boast. Though they believed in ordered eating, their meals were rather rough around the edges, lacking the kind of organization and form that typifies the modern meal today. Hardly well defined or clean-cut, colonial eating occasions were messy in more ways than one. Perhaps this partially explains why explorers and colonists were so quick to criticize native eating habits—in doing so, they hid the inconsistencies in their own. 3

Colonists found Native American eating habits wanting because they judged them by the European standard. For Europeans, a meal combined contrasting components—usually cereals, vegetables, and animal protein. Heat offered an additional desirable contrast. Swedish traveler Peter Kalm noted that many “meals” consumed by the natives of the mid-Atlantic, where he traveled in the mid-eighteenth century, consisted simply of “[maple] sugar and bread.” With only two ingredients and a distinct lack of protein, not to mention heat, this simplistic combination fell short of European criteria; it was more of a snack. Other typical nonmeals included traveling foods such as nocake (pulverized parched cornmeal to which natives added water on the go) and pemmican (a dense concoction of lean meat, fat, and sometimes dried berries). Hunters, warriors, and migrants relied on these foods, designed to be eaten in that particularly un-meal-like way in which John Williams ate his frozen meat on his journey to Québec: as the stomach required it and on the go. 4

Jerked venison and fat, chewed as one traversed the wilderness, was not most colonists’ idea of a proper meal, and if natives’ lack of sufficient contrasting components and the absence of a formal eating schedule puzzled colonists, even more mystifying was natives’ habit of going without meals, and often without any food at all, for extended periods. Jesuit missionary Christian LeClercq portrayed the Micmac of the Gaspé Peninsula in Canada as a slothful people, preserving and storing only a token winter’s supply: “They are convinced that fifteen to twenty lumps of meat, or of fish dried or cured in the smoke, are more than enough to support them for the space of five to six months.” LeClercq and many others did not realize that if natives went hungry, they did so not from neglect but by choice. Fasting was a subsistence strategy, and Native Americans were proud of it. 5

Throughout the year, Native Americans prepared for times of dearth by honing their fasting skills. They practiced hunger as a kind of athletic exercise, conditioning their bodies for the hardships of hunting, war, and seasonal shortages. According to artist George Catlin, the Mandan males in what are now the Dakotas “studiously avoided . . . every kind of excess.” An anthropologist among the Iroquois observed that they were “not great eaters” and “seldom gorged themselves.” To discourage gluttony, they even threatened their children with a visit from Sago’dakwus, a mythical monster that would humiliate them if it caught them in the act of overeating. 6

Native and European approaches to eating came to a head in the vice of gluttony. Many tribal peoples condemned overeating as a spiritual offense and a practice sure to weaken manly resolve and corrupt good character. Europeans also condemned it, largely for religious reasons, but more fundamentally because it represented a loss of control over the animal instincts. In the European worldview, overindulgence was precisely the opposite of civility, and the institution of the meal guarded against gluttony and a slippery descent into savagery. The meal gave order to and set boundaries around the act of eating, boundaries that Europeans felt native practices lacked. As explorers and colonists defended the tradition of the meal, the institution took on new meaning. For them, it became a subject of pride, serving as an emblem of civilization and a badge of European identity. 7

Europeans viewed Native Americans largely as gluttons. Because whites caught only fleeting glimpses of the complex and continually shifting lives of Native Americans, they were liable to portray the native way of life according to a single cultural snapshot, which, when it came to food, was the posthunt feast. It was well known that natives ate much and frequently during times of abundance. John Smith recorded that when natives returned from the hunt with large quantities of bear, venison, and oil, they would “make way with their provision as quick as possible.” For a short time, he explained, “they have plenty and do not spare eating.” White witnesses popularized the image of just such moments of plenty as typical. 8

Although Native Americans were hardly gluttons, Europeans, fascinated by the idea of a primitive people with a childlike lack of restraint, embraced the grossly inaccurate stereotype of the overeating Indian. William Wood portrayed the natives of southern New England as gorging themselves “till their bellies stand forth, ready to split with fullness.” A decidedly strange Anglo-American amusement involved watching Native Americans relish a meal. “Why,” asked George Catlin, “[is it] that hundreds of white folks will flock and crowd round a table to see an Indian eat?” With a hint of disappointment, William Wood recorded the appetites of tribes people invited to an English house to dine as “very moderate.” Wood was uncertain whether to interpret this reserve as politeness or timidity, but clearly he and his fellow English spectators had not expected shy and tempered eaters. 9

One culture’s perception of another often says more about the perceiver than the perceived. Although settlers lambasted natives for gluttony, whites may have been the real gluttons. According to more than one observer, many a native blushed at Europeans’ bottomless stomachs. “The large appetites of white men who visited them were often a matter of surprise to the Indians who entertained them,” wrote a nineteenth-century folklorist among the Iroquois. Early anthropologist Lewis Morgan concluded that natives required only about one-fifth of what white men consumed, and he was skeptical of his own ability to survive on such a paucity of provisions. 10

Through their criticisms, exaggerations, and stereotypes, colonists distanced themselves from a population whose ways appeared savage and unenlightened, and the organized meal provided a touchstone in this clash of cultures. It became a yardstick by which Europeans measured culture and a weapon by which they defended their definition of it. They had long known what a meal was, but now, by contrast, they knew firsthand what it was not. Encountering the perceived meal-less-ness of the natives brought the colonists’ esteemed tradition into question and gave them an opportunity to confirm their commitment to their conventions. They refused to approve of, let alone adapt to, the loose foodways of Native Americans and instead embraced all the more heartily a structured, meal-centered European approach to eating.

Coffee and Cream, Ketosis and Autophagy

On Twitter, Jerry Teixeira (JT) declared his love of cream in coffee. It led to a long thread where the joys and benefits of creamy vs black coffee were argued.

An interesting side discussion formed over the issue of fasting, ketosis, and autophagy. I must admit that my understanding was always a big hazy about the relationship between the latter two, both of which can be results of fasting. Despite common factors involved in both processes, I didn’t think there was a causal link.

I guess there is a connection, after all (Camberos-Luna et al, The Ketone Body, β-Hydroxybutyrate Stimulates the Autophagic Flux and Prevents Neuronal Death Induced by Glucose Deprivation in Cortical Cultured Neurons.). Even so, that still leaves other benefits of fasting, such as downregulating mTOR (vitamin D3 and Autophagy).

* * *

Patrice Bäumel
My number one reason for drinking black coffee in the morning is to not interfere with IF, which cream does.

Rob W. James
The benefits of IF are overstated in my opinion. Most of the benefits come from calorie restriction, which a splash of milk isn’t going to make much difference too

Patrice Bäumel
The main benefit is clearing out damaged cells. It’s an anti-aging hack. You lose that benefit by breaking fast.

Coffee is still a xenobiotic, you are breaking a fast by drinking coffee and you are breaking a fast by drinking 2 tbsp cream. Regardless, autophagy is stimulated via ketogenesis, neither coffee nor cream Inhibit ketogenesis.

Autophagy doesn’t really hit significant levels until 48hrs though. So benefits are mininal if any during IF

This is not to say autphagy isn’t present until 48hrs, rather it hits full scale around 48hrs.
And if autophagy is why you “fast” an extended fast.. past a normal IF, is necessary to achieve what you’re after.

Autophagy happens downstream via BHB regardless, when you are on a ketogenic diet you have these elevated BHB levels at that point for long periods, where fasting takes 48 hours to get you where a Keto diet keeps you

So if you are IF and eating plenty of carbs I totally agree. It takes longer to get to the higher BHB levels because BHB and carbohydrate are inversely proportional

This is such an important point I don’t see anyone talking about.
That’s why I was talking about fasting a few weeks ago.
No one is talking about needing to be in ketosis to be fasted. So most of these guys doing IF are basically just TRE.. Which is a good enough reason to IF

The contents creators aren’t talking about this though and selling false promises of autophagy and fountain of youth.

I read an article about IF that showed signs of arteriole smoothing with a 16:8 diet. If this is true then autophagy at 48 hours isn’t necessary for sole benefit and daily fasting does have vasculature anti-aging properties.

There are benefits for every hour you fast according to Salk institute researchers . What we will need to see is calorie matched studies between TRE/ IF and CR. But to say there is zero additional benefit if you are healthy is wrong. The amount of benefit is arguable

Beta hydroxy butyrate is an HDAC inhibitor and downstream via that action increases autophagy. Cream doesn’t matter. The longer you fast for the higher the bhb. Or a ketogenic diet can increase the bhb. Ketogenic diet mimics fasting and vice Versa.

They are not synonymous. Of course, however elevated BHB levels are a common thread and a little cream in your coffee is not going to matter at all in that regard.

Myriads research over the last two years and mixing more underway showing the mechanisms by which you still see these benefits from BHB weather or not you fast. I am compiling all the links and will sends them over when done if you would like

Hell, coffee alone (even decaf) induces autophagy.

Yeah, I saw some research that it increases ketogenisis

Human Adaptability and Health

What makes humans unique? There are many answers that can and have been offered. My own dietary experimentation, from paleo to keto to carnivore, has led to certain thoughts. After two months of carnivory (and before reintroducing plant foods), I ended it with an extended fast, three days to be precise, as inspired by Siim Land. There is something impressive about fasting, far beyond its intermittent variety. Yes, ketosis is involved, but lengthening the fasting state steps it up to a whole other level, specifically to be scientific what is called autophagy along with stem cell activation. With autophagy, your body cannibalizes damaged and dead cells in order to build entirely new cells, including in the brain, and in the process of three days of fasting every cell in your immune system will be replaced. That is pretty kick ass!

More basically, fasting simply feels good or it can, assuming one isn’t sick or stressed. It’s not as hard as one might think, assuming one begins it in a state of ketosis and fat-adaptation. That is the way it has been for me, in the several extended fasts I’ve done. I’ve even done part of the time in dry fasting, that is to say not even water. With fasting, energy doesn’t necessarily decline and sometimes there is a boost of energy, specifically when ketones kick into high gear. And even without water, the body shifts into a different mode and one doesn’t get thirsty, at least not for many days (breathing through one’s nose helps as well), since the body stores water similar to how it stores fat. Fasting has been a practice among probably every traditional society that has ever existed, from early Native Americans to early Europeans, and is found in diverse religions, from Buddhism to Christianity — fasting only became uncommon since vast food surpluses were created in recent generations.

I’ve done fasting in the past, but I always limited myself to one-day fasts. It was never difficult and, even though few people ever do it, I never considered it an impressive feat of personal strength and willpower. It simply meant not eating food for a time. More interesting on a personal level was a different kind of fasting. Maybe a couple of decades ago, I got into the habit of jogging before eating and I would sometimes go for hours. I never lacked energy and, if anything, I had more energy than before I began. A strange side effect was that my hunger also decreased for the rest of the day, a rather counter-intuitive result as one would think exercise would make one hungry to make up for the calories lost.

I didn’t understand it at the time, but I had independently discovered ketosis. Once you run out of glucose in your blood and glycogen in your muscles, your body switches to turning fat into ketones. As long as you have enough fat (not a problem for most people), you can continually produce ketones for long periods of time without any food. Even the small amount of glucose your body needs can also be produced by the body without any need of dietary intake of carbohydrates. For a fat person, they literally can go months without food, as the body doesn’t only store energy in body fat but also nutrients. Cole Robinson of Snake Diet fame is an advocate of this method of fat loss — as he puts it, If you want to lose weight, fatty, stop stuffing food in your mouth. While in this state, you can remain active. The Piraha, according to Daniel Everett, would regularly go without eating on some days for no particular reason and at times would dance for several days without stopping for a meal. Cole Robinson talks about continuing his heavy weight lifting routine many days into fasting, not that most modern people with inferior health would want to try this. Under Genghis Khan, Mongol warriors began their war campaigns with an extended period of fasting, maybe to prime their body for ketosis that they maintained with their low-carb and animal-based diet (mostly meat, blood, and milk).

This relates to our evolutionary needs. Early humans survived as a hunting pack. We aren’t the fastest animal, among either predators or prey. We are rather slow actually and our lack of claws and fangs are a disadvantage, but we are endurance runners with the capacity to develop immense tracking skills. Along with ketosis that puts our large brains into overdrive, particularly the use of the pseudo-ketone beta-hydroxybutyrate, we have a special knack for sweating that keeps us cool, partly because of our lack of fur. Also, because of our upright position, our lungs aren’t constricted by our running gait and so our breathing is free to follow it’s own rhythm. Humans did all this while being barefoot for most of our existence, often running across rough ground. In particularly harsh environments such as Australia, the natives would develop thick callouses on the soles of their feet. We run better and more safely without shoes than with them — barefoot running (or using thin footwear such as sandals or moccasins) forces us to use good running form with impact shifted toward the toes rather than the heels. As natives observed, most animals move with the weight put on their toes. This is also what we humans are designed for.

Running is what humans do. Hunter-gatherers can track animals for days without having to stop for food and water and, as long as there is a water supply, could go on for weeks without food. This is natural. This was once the norm. This is how the human species managed to travel across deserts and oceans, how our ancestors survived starvation and ice ages. For hundreds of millennia, humans maintained such high levels of physical strain typically without harm to their health and rarely with injury. Fasting and feasting. Extended activity and periods of rest. And we are able to retain our physical capacities well into old age. Hunter-gathers in their sixties have the same level of running ability as they had in their late teens, with the developmental peak hitting around the late twenties. Many individuals in traditional societies go on running as their normal mode of travel until the day they die and, excluding early deaths from infection (infections, I might add, that mostly were introduced through colonialism), traditional people live as long as do modern Westerners. As said by Geronimo, a man who lived and fought under fierce conditions into older age, “My only friends are my legs. I only trust my legs.”

Even cold weather is not a big issue. An intriguing side of ketosis is that it has a built-in inefficiency. Burning fat produces excess heat, that is to say wasted energy. As Benjamin Bikman has speculated, this is likely because ketosis most often has occurred in the winter. The extra heat was a side benefit. So, fasting will not only give you immense energy from the superfuel of ketones but keep you warmer as well. Cold temperatures, like fasting, also promote autophagy which is healing. The body goes into its most optimal mode of functioning. Humans who are adapted to it can swim in freezing cold water for long periods of time or hike barefoot and half-naked in the snow as Wim Hof has demonstrated and, shown in research, all humans have such capacity for cold adaptation — it’s related to meditation techniques of warming the body where one sits in snow or on ice until it melts. Cold bathing and sleeping out in the open on cold nights, including with little clothing has been done by numerous populations: Australian Aborigines, Native Americans, etc. Make it a practice to take cold showers and you’ll get some small sense of the effect this can have — something I’ve been doing for a while and, to say the least, it is invigorating, but I’ve always been one of those crazy people who will go outside in the winter underdressed. By the way, Wim Hof at the other extreme has also run a half marathon through a desert without water. He has set many other world records, twenty-six in total.

Humans are adaptable, but a too easy and comfortable lifestyle has caused modern people to lose their adaptability. We aren’t meant to always be at the same temperature, always eating, always sedentary, or always anything else. Pushing the biological boundareies is a good thing to do on a regular basis. Consider hormesis — small amounts of stress actually increase our health. A similar thing is seen with exposure to bacteria and parasites when younger that can strengthen the immune system for life and alter how our bodies function. Even in seeking health, we moderns often get it wrong. We aren’t meant to continually do the same exercise in the same way over and over. Variety isn’t only the spice of life for it is also the meat of life. If we don’t use it, we lose it. This is why we should alternate how we exercise.

One method designed for this purpose is high-intensity interval training (HIIT) which is alternating between strenuous activity to exhaustion with periods of rest and repeating this multiple times. It forces the rhythm of your heart rate to expand its variability and that is good thing. Continuous exercise at the same pace, such as typical long distance running does the opposite in decreasing this variability. This is what can sometimes cause seemingly health long distance runners, once reaching the finish line, to drop dead from a heart attack. The lack of heart rate variability strains their heart too much in going from running to stopping. But this could be easily prevented by doing some HIIT exercise such as wind sprints, something I did a lot as a kid during soccer practice. Sometimes walk, sometimes jog, and sometimes run as fast as you can. That is what most of us did as children when playing and often we did it barefoot — I recall running on gravel alley barefoot, walking through the woods barefoot, and climbing trees barefoot. Why do we forget such natural behavior as we become mature, respectable adults? Don’t exercise. Just go play outside.

Our loss of connection to our species inheritance has cost us our health. But this loss isn’t an inevitable fate of modern civilization. We should take advantage of what we now know about human physiology. We humans are amazing creatures. There is a reason we have survived and thrived and spread all over the earth in nearly all environments and ecosystems. Even with all the unnatural strain and harm we put ourselves under, we still somehow manage to keep many of our physiological abilities. Imagine what we could accomplish if, rather than being sickly, our society operated with optimal health.

* * *

Persistence hunting
from Wikipedia

Endurance running hypothesis
from Wikipedia

Endurance Running and Persistence Hunting
by David Carrier

Running After Antelope
from This American Life

Running After Antelope
by Scott Carrier

Born to Run
by Christopher McDougall

Why We Run: A Natural History
by Bernd Heinrich

Becoming the Iceman
by Wim Hof

The Way of the Iceman
by Wim Hof

What Doesn’t Kill Us
by Scott Carney

Science Explains How the Iceman Resists Extreme Cold
by Joshua Rapp Learn

Breathe Like The Iceman: How To Use The Wim Hof Method
by Harry J. Stead

Fasting, Calorie Restriction, and Ketosis

What we eat obviously affects gut health such as the microbiome and through that, along with other mechanisms, it affects the rest of our body, the brain included (by way of permeability, immune system, vagus nerve, substances like glutamate and propionate, and much else). About general health, I might add that foods eaten in what combination (e.g., red meat and grains) is also an issue. Opposite of what you eat impacting neurocognition and mental health, not eating (i.e., fasting, whether intermittent or extended) or else caloric restriction and carbohydrate reduction, ketogenic or otherwise, alters it in other ways.

Fasting, for example, increases the level of neurotransmitters such as serotonin, dopamine, and norepinephrine while temporarily reducing the brains release and use of them; plus, serotonin and its precursor tryptophan are made more available to the brain. So, it allows your reserves of neurotransmitters to rebuild to higher levels. That is partly why a ketogenic diet, along with the brains efficient use of ketones, shows improvements in behavior, learning, memory, acuity, focus, vigilance, and mood (such as sense of well-being and sometimes euphoria); with specific benefits, to take a couple of examples, in cerebral blood flow and prefrontal-cortex-related cognitive functions (mental flexibility and set shifting); while also promoting stress resistance, inflammation reduction, weight loss, and metabolism, and while decreasing free radical damage, blood pressure, heart rate, and glucose levels. Many of these are similar benefits as seen with strenuous exercise.

We know so much about this because the ketogenic diet is the only diet that has been specifically and primarily studied in terms of neurological diseases, going back to early 20th century research on epileptic seizures and autism, was shown effective for other conditions later in the century (e.g., V. A. Angelillo et al, Effects of low and high carbohydrate feedings in ambulatory patients with chronic obstructive pulmonary disease and chronic hypercapnia), and more recently with positive results seen in numerous other conditions (Dr. Terry Wahl’s work on multiple sclerosis, Dr. Dale Bredesen’s work on Alzheimer’s, etc). By the way, the direction of causality can also go the other way around, from brain to gut: “Studies also suggest that overwhelming systemic stress and inflammation—such as that induced via severe burn injury—can also produce characteristic acute changes in the gut microbiota within just one day of the sustained insult [15].” (Rasnik K. Singh et al, Influence of diet on the gut microbiome and implications for human health). And see:

“Various afferent or efferent pathways are involved in the MGB axis. Antibiotics, environmental and infectious agents, intestinal neurotransmitters/neuromodulators, sensory vagal fibers, cytokines, essential metabolites, all convey information about the intestinal state to the CNS. Conversely, the HPA axis, the CNS regulatory areas of satiety and neuropeptides released from sensory nerve fibers affect the gut microbiota composition directly or through nutrient availability. Such interactions appear to influence the pathogenesis of a number of disorders in which inflammation is implicated such as mood disorder, autism-spectrum disorders (ASDs), attention-deficit hypersensitivity disorder (ADHD), multiple sclerosis (MS) and obesity.” (Anastasia I. Petra et al, Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation)

There are many other positive effects. Fasting reduces the risk of neurocognitive diseases: Parkinson’s, Alzheimer’s, etc. And it increases the protein BDNF (brain-derived neurotrophic factor) that helps grow neuronal connections. Results include increased growth of nerve cells from stem cells (as stem cells are brought out of their dormant state) and increased number of mitochondria in cells (mitochondria are the energy factories), the former related to the ability of neurons to develop and maintain connections between each other. An extended fast will result in autophagy (cellular housekeeping), the complete replacement of your immune cells and clearing out damaged cells which improves the functioning of your entire body (it used to be thought to not to occur in the brain but we now know it does) — all interventions known to prolong youthful health, lessen and delay diseases of aging (diabetes, cancer, cardiovascular disease, etc), and extend lifespan in lab animals involve autophagy (James H. Catterson et al, Short-Term, Intermittent Fasting Induces Long-Lasting Gut Health and TOR-Independent Lifespan Extension). Even calorie restriction has no effect when autophagy is blocked (Fight Aging!, Autophagy Required For Calorie Restriction Benefits?). It cleans out the system, gives the body a rest from its normal functioning, and redirects energy toward healing and rebuilding.

As a non-human example, consider hibernation for bears. A study was done comparing bears with a natural diet (fruits, nuts, insects, and small mammals) and those that ate human garbage (i.e., high-carb processed foods). “A research team tracked 30 black bears near Durango, Colo., between 2011 and 2015, paying close attention to their eating and hibernation habits. The researchers found that bears who foraged on human food hibernated less during the winters — sometimes, by as much as 50 days — than bears who ate a natural diet. The researchers aren’t sure why human food is causing bears to spend less time in their dens. But they say shorter hibernation periods are accelerating bears’ rates of cellular aging” (Megan Schmidt, Human Food Might Be Making Bears Age Faster). As with humans who don’t follow fasting or a ketogenic diet, bears who hibernate less don’t live as long. Maybe a high-carb diet messes with hibernation similarly to how it messes with ketosis.

Even intermittent fasting shows many of these benefits. Of course, you can do dramatic changes to the body without fasting at all, if you’re on a ketogenic diet (though one could call it a carb fast since it is extremely low carb) or severe caloric restriction (by the way, caloric restriction has been an area of much mixed results and hence confusion — see two pieces by Peter Attia: Calorie restriction: Part I – an introduction & Part IIA – monkey studies; does intermittent fasting and ketosis mimic caloric restriction or the other way around?). I’d add a caveat: On any form of dietary limitation or strict regimen, results vary depending on specifics of test subjects and other factors: how restricted and for how long, micronutrient and macronutrient content of diet, fat-adaptation and metabolic flexibility, etc; humans, by the way, are designed for food variety and so it is hard to know the consequences of modern diet that often remains unchanged, season to season, year to year (Rachel Feltman, The Gut’s Microbiome Changes Rapidly with Diet). There is a vast difference between someone on a high-carb diet doing an occasional fast and someone on a ketogenic diet doing regular intermittent fasting. Even within a single factor such as a high-carb diet, there is little similarity between the average American eating processed foods and a vegetarian monk eating restricted calories. As another example, autophagy can take several days of fasting to be fully achieved; but how quickly this happens depends on the starting conditions such as how many carbs eaten beforehand and how much glucose in the blood and glycogen stores in the muscles, both of which need to be used up before ketosis begins.

Metabolic flexibility, closely related to fat-adaptation, requires flexibility of the microbiome. Research has found that certain hunter-gatherers have microbiomes that completely switch from season to season and so the gut somehow manages to maintain some kind of memory of previous states of microbial balance which allows them to be re-established as needed. This is seen more dramatically with the Inuit who eat an extremely low-carb diet, but they seasonally eat relatively larger amounts of plant matter such as seaweed and they temporarily have digestive issues until the needed microbes take hold again. Are these microbes dormant in the system or systematically reintroduced? In either case, the process is unknown, as far as I know. What we are clear about is how dramatically diet affects the microbiome, whatever the precise mechanisms.

For example, a ketogenic diet modulates the levels of the microbes Akkermansia muciniphila, Lactobacillus, and Desulfovibrio (Lucille M. Yanckello, Diet Alters Gut Microbiome and Improves Brain Functions). It is the microbes that mediate the influence on both epileptic seizures and autism, such that Akkermansia is decreased in the former and increased in the latter, that is to say the ketogenic diet helps the gut regain balance no matter which direction the imabalance is. In the case of epileptic seizures, Akkermansia spurs the growth of Parabacteroides which alters neurotransmission by elevating the GABA/glutamate ratio (there is glutamate again): “the hippocampus of the microbe-protected mice had increased levels of the neurotransmitter GABA, which silences neurons, relative to glutamate, which activates them” (Carolyn Beans, Mouse microbiome findings offer insights into why a high-fat, low-carb diet helps epileptic children), but no such effect was found in germ-free mice, that is to say with no microbiome (similar results were found in human studies: Y. Zhang, Altered gut microbiome composition in children with refractory epilepsy after ketogenic diet). Besides reducing seizures, “GABA is a neurotransmitter that calms the body. Higher GABA to glutamate ratios has been shown to alleviate depression, reduce anxiety levels, lessen insomnia, reduce the severity of PMS symptoms, increase growth hormone, improve focus, and reduce systemic inflammation” (MTHFR Support, Can Eating A Ketogenic Diet Change Our Microbiome?). To throw out the other interesting mechanism, consider Desulfovibrio. Ketosis reduces its numbers and that is a good thing since it causes leakiness of the gut barrier, and what causes leakiness in one part of the body can cause it elsewhere as well such as the brain barrier. Autoimmune responses and inflammation can follow. This is why ketosis has been found beneficial for preventing and treating neurodegenerative conditions like Alzheimer’s (plus, ketones are a useful alternative fuel for Alzheimer’s since their brain cells begin starving to death for loss of the capacity to use glucose as a fuel).

All of this involves the factors that increase and reduce inflammation: “KD also increased the relative abundance of putatively beneficial gut microbiota (Akkermansia muciniphila and Lactobacillus), and reduced that of putatively pro-inflammatory taxa (Desulfovibrio and Turicibacter).” (David Ma et al, Ketogenic diet enhances neurovascular function with altered gut microbiome in young healthy mice). Besides the microbiome itself, this has immense impact on leakiness and autoimmune conditions, with this allowing inflammation to show up in numerous areas of the body, including the brain of course. Inflammation is found in conditions such as depression and schizophrenia. Even without knowing this mechanism, much earlier research has long established that ketosis reduces inflammation.

It’s hard to know what this means, though. Hunter-gatherers tend to have much more diverse microbiomes, as compared to industrialized people. Yet the ketogenic diet that helps induce microbial balance simultaneously reduces diversity. So, diversity isn’t always a good thing, with another example being small intestinal bacterial overgrowth (SIBO). What matters is which microbes one has in abundance and in relation which microbes one lacks or has limitedly. And what determines that isn’t limited to diet in the simple sense of what foods we eat or don’t eat but the whole pattern involved. Also, keep in mind that in a society like ours most of the population is in varying states of gut dysbiosis. First eliminating the harmful microbes is most important before the body can heal and rebalance. That is indicated by a study on multiple sclerosis that found, after the subjects had an initial reduction in the microbiome, “They started to recover at week 12 and exceeded significantly the baseline values after 23–24 weeks on the ketogenic diet” (Alexander Swidsinski et al, Reduced Mass and Diversity of the Colonic Microbiome in Patients with Multiple Sclerosis and Their Improvement with Ketogenic Diet). As always, it’s complex. But the body knows what to do when you give it the tools its evolutionarily-adapted to.

In any case, all of the methods described can show a wide range of benefits and improvements in physical and mental health. They are potentially recommended for almost anyone who is in a healthy state or in some cases of disease, although as always seek medical advice before beginning any major dietary change, especially anyone with an eating disorder or malnourishment (admittedly, almost all people on a modern industrialized diet are to some degree malnourished, especially Americans, although most not to a degree of being immediately life-threatening). Proceed with caution. But you are free to take your life in your hands by taking responsibility for your own health through experimentation in finding out what happens (my preferred methodology), in which case the best case scenario is that you might gain benefit at no professional medical cost and the worst case scenario is that you might die (not that I’ve heard of anyone dying from a typical version of a diet involving fasting, ketosis, and such; you’re way more likely to die from the standard American diet; but individual health conditions aren’t necessarily predictable based on the experience of others, even the vast majority of others). Still, you’re going to die eventually, no matter what you do. I wish you well, until that time.

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Let me clarify one point of widespread confusion. Talk of ‘diets’, especially of the variety I’ve discussed here, are often thought of in terms of restriction and that word does come up quite a bit. I’m guilty of talking this way even in this post, as it is about impossible to avoid such language considering it is used in the scientific and medical literature. So, there is an implication of deprivation, of self-control and self-denial, as if we must struggle and suffer to be healthy. That couldn’t be further from the truth.

Once you are fat-adapted and have metabolic flexibility, you are less restricted than you were before, in that you can eat more carbs and sugars for a time and then more easily return back to ketosis, as is a common seasonal pattern for hunter-gatherers. And once you no longer are driven by food cravings and addictions, you’ll have a happier and healthier relationship to food — eating when genuinely hungry and going without for periods without irritation or weakness, as also is common among hunter-gatherers.

This is simply a return to the state in which most humans have existed for most of our historical and evolutionary past. It’s not restriction or deprivation, much less malnourishment. It’s normalcy or should be. But we need to remember what normalcy looks and feels like: “People around the world suffer from starvation and malnutrition, and it is not only because they lack food and nutrients. Instead they suffer from immature microbiomes, which can severely impact health” (AMI, The effects of fasting and starvation on the microbiome). Gut health is inseparable from the rest, and these diets heal and rebalance the gut.

We need to redefine what health means, in a society where sickness has become the norm.

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Here is a good discussion that is relevant here, even though the author never discusses ketosis anywhere in his book. He is pointing out that calorie intake and energy usage is approximately the same for urbanized humans as for hunter-gatherers. Yet the former have higher rates of obesity and the latter don’t. As many have noted, not all calories are the same and so calories-in/calories-out is a myth. This data makes more sense once you understand how profoundly different the body functions under ketogenic and non-ketogenic states.

100 Million Years of Food
by Stephen Le
pp.166 -168

At this point, a reader might conclude that the root of modern food-related ailments like obesity and diabetes lies in people eating a lot more food, due to the miracle of nitrogen fixation, and doing a lot less physical activity, due to the miracle of combustion engines and private vehicles. However, it turns out that neither of these common beliefs is supported by the evidence.

First, the food intake myth. The daily energy consumed through food in contemporary industrialized nations runs from about 2,300 kcal (kilocalories) among Japanese men and 1,800 kcal among Japanese women to 2,600 kcal among American men and 1,900 kcal among American women. 21 What is surprising is that the average daily caloric intake of these overweight industrialized societies is about the same as among hunter-gatherer groups, with some hunter-gatherer groups below and others above the calories consumed of industrialized nations. 22 Although hunter-gatherers ate about as much as we do today, they faced much greater variability in their food supply. In northern Australia, among the Anbarra, the daily energy intake dropped to 1,600 kcal during the rainy season and peaked at 2,500 kcal during the dry season. The calorie consumption of the Hiwi in the rainforests of Venezuela bounced between 1,400 and 2,800 kilocalories, depending on the season (plant foods were most plentiful at the end of the wet season). Thus, if any major pattern emerges in terms of caloric intake, it is that our hunter-gatherer ancestors lived on a dramatically varying diet, which swung between feast and famine according to the season and other hazards of fortune.

Another surprising finding concerns physical activity. Although it is commonly believed that people in hunter-gatherer societies expended much more energy than people in industrialized societies today, the evidence so far does not support this assumption. One common measure of physical activity level (PAL) expresses the total energy used in one day as a multiple of a person’s metabolic rate. For example, a PAL of 1 means that a person uses only his/her metabolic energy, i.e., the energy expended by breathing, thinking, digesting, etc. A PAL of 2 means that a person uses twice as much energy as his or her base metabolic rate. PAL allows us to adjust for the fact that people have varying levels of metabolism; a person who has a high metabolic rate can burn up a lot of energy by just sitting in one place compared to a person with low metabolism, so a good measure of physical activity needs to compensate for differences in metabolism. To determine the amount of energy used in a day, the best measure involves giving a person a drink of water that has been “tagged” with isotopes of hydrogen and oxygen. Measurement of these two tags in samples of saliva, urine, or blood allows measurement of exhaled carbon dioxide and hence the degree of respiration from metabolic processes.

Using tagged water, the average PAL among foragers was found to be 1.78 for men and 1.72 for women. Among industrialized contemporary societies with a high human development index (which measures income, literacy, and so on), the PAL of men was 1.79 for men and 1.71 for women. 23 In other words, the energy expenditure of overweight contemporary industrialized societies is roughly the same as that of lean hunter-gatherer societies once metabolism is taken into account; or to put it another way, the cause of obesity is unlikely to be lack of exercise, because people in industrialized societies today use about the same amount of energy as people in hunter-gatherer societies. 24

This finding has important implications for understanding obesity. All of us living in industrialized societies are aware of the stigma associated with obesity, and perhaps the longer-term health consequences of diabetes, high blood pressure, gout, and cancers associated with being overweight. Since food intake and energy expenditure levels today are roughly the same as during ancestral times (using the lifestyles of modern hunter-gatherers as a reasonable model for our ancestors’ lifestyles), why are obesity and diabetes so prevalent among industrialized societies and virtually nonexistent among our ancestors?

The first argument might be an objection that obesity has in fact been with us since the days of our earliest ancestors, so nothing has changed. It has been suggested that figurines of markedly obese women, found in Europe and dating to thirty thousand years ago, are proof that obesity existed at that time. However, no hunter-gatherer or small-scale horticultural group has ever manifested signs of obesity, despite having caloric intake and energy expenditure (adjusted for metabolism) within the range of contemporary industrialized populations. Thus the prehistoric statuettes may be representative of idealized feminine beauty, just as Barbie dolls and Japanese anime characters with huge eyes and exaggerated busts are fantasies more revealing of their creators than of real women.

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Genius Foods:
Become Smarter, Happier, and More Productive While Protecting Your Brain for Life
by Max Lugavere

Baby Fat Isn’t Just Cute—It’s a Battery

Have you seen a baby lately? I’m talking about a newborn, fresh out of the womb. They’re fat. And cute. But mostly fat. Packed with stored energy prior to birth in the third trimester, the fatness of human babies is unprecedented in the mammal world. While the newborns of most mammal species average 2 to 3 percent of birth weight as body fat, humans are born with a body fat percentage of nearly 15, surpassing the fatness of even newborn seals. Why is this so? Because humans are born half-baked.

When a healthy human baby emerges from the womb, she is born physically helpless ad with an underdeveloped brain. Unlike most animals at birth, a newborn human is not equipped with a full catalogue of instincts preinstalled. It is estimated that if a human were to be born at a similar stage of cognitive development to a newborn chimp, gestation would be at least double the length (that doesn’t sound fun—am I right ladies?). By being born “prematurely,” human brains complete their development not in the womb, but in the real world, with open eyes and open ears—this is probably why we’re so social and smart! And it is during this period for rapid brain growth, what some refer to as the “fourth trimester,” that our fast serves as an important ketone reservoir for the brain, which can account for nearly 90 percent of the newborn’s metabolism. Now you know: baby fat isn’t just there for pinching. It’s there for the brain.

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Mitochondria and the Future of Medicine:
The Key to Understanding Disease, Chronic Illness, Aging, and Life Itself
by Lee Know

Ketogenic Diets and Calorie Restriction

Ketone bodies, herein also referred to simply as ketones , are three water-soluble compounds that are produced as by-products when fatty acids are broken down for energy in the liver. These ketones can be used as a source of energy themselves, especially in the heart and brain, where they are a vital source of energy during periods of fasting.

The three endogenous ketones produced by the body are acetone , acetoacetic acid , and beta-hydroxybutyric acid (which is the only one that’s not technically a ketone, chemically speaking). They can be converted to acetyl-CoA, which then enters the TCA cycle to produce energy.

Fatty acids are so dense in energy, and the heart is one of the most energy-intensive organs, so under normal physiologic conditions, it preferentially uses fatty acids as its fuel source. However, under ketotic conditions, the heart can effectively utilize ketone bodies for energy.

The brain is also extremely energy-intensive, and usually relies on glucose for its energy. However, when glucose is in short supply, it gets a portion of its energy from ketone bodies (e.g., during fasting, strenuous exercise, low-carbohydrate, ketogenic diet, and in neonates). While most other tissues have alternate fuel sources (besides ketone bodies) when blood glucose is low, the brain does not. For the brain, this is when ketones become essential. After three days of low blood glucose, the brain gets 25 percent of its energy from ketone bodies. After about four days, this jumps to 70 percent!

In normal healthy individuals, there is a constant production of ketone bodies by the liver and utilization by other tissues. Their excretion in urine is normally very low and undetectable by routine urine tests. However, as blood glucose falls, the synthesis of ketones increases, and when it exceeds the rate of utilization, their blood concentration increases, followed by increased excretion in urine. This state is commonly referred to as ketosis , and the sweet, fruity smell of acetone in the breath is a common feature of ketosis.

Historically, this sweet smell was linked to diabetes and ketones were first discovered in the urine of diabetic patients in the mid-nineteenth century. For almost fifty years thereafter, they were thought to be abnormal and undesirable by-products of incomplete fat oxidation.

In the early twentieth century, however, they were recognized as normal circulating metabolites produced by the liver and readily utilized by the body’s tissues. In the 1920s, a drastic “hyperketogenic” diet was found to be remarkably effective for treating drug-resistant epilepsy in children. In 1967, circulating ketones were discovered to replace glucose as the brain’s major fuel during prolonged fasting. Until then, the adult human brain was thought to be entirely dependent upon glucose.

During the 1990s, diet-induced hyperketonemia (commonly called nutritional ketosis ) was found to be therapeutically effective for treating several rare genetic disorders involving impaired glucose utilization by nerve cells. Now, growing evidence suggests that mitochondrial dysfunction and reduced bioenergetic efficiency occur in brains of patients with Parkinson’s disease and Alzheimer’s disease. Since ketones are efficiently used by brain mitochondria for ATP generation and might also help protect vulnerable neurons from free-radical damage, ketogenic diets are being evaluated for their ability to benefit patients with Parkinson’s and Alzheimer’s diseases, and various other neurodegenerative disorders (with some cases reporting remarkable success).

There are various ways to induce ketosis, some easier than others. The best way is to use one of the various ketogenic diets (e.g., classic, modified Atkins, MCT or coconut oil, low-glycemic index diet), but calorie restriction is also proving its ability to achieve the same end results when carbohydrates are limited.

Features of Caloric Restriction

There are a number of important pieces to caloric restriction. First, and the most obvious, is that caloric intake is most critical. Typically, calories are restricted to about 40 percent of what a person would consume if food intake was unrestricted. For mice and rats, calorie restriction to this degree results in very different physical characteristics (size and body composition) than those of their control-fed counterparts. Regarding life extension, even smaller levels of caloric restriction (a reduction of only 10–20 percent of unrestricted calorie intake) produce longer-lived animals and disease-prevention effects.

In April of 2014, a twenty-five-year longitudinal study on rhesus monkeys showed positive results. The benefit of this study was that it was a long-term study done in primates—human’s closest relatives—and confirms positive data we previously saw from yeasts, insects, and rodents. The research team reported that monkeys in the control group (allowed to eat as much as they wanted) had a 2.9-fold increased risk of disease (e.g., diabetes) and a 3-fold increased risk of premature death, compared to calorie-restricted monkeys (that consumed a diet with 30 percent less calories).

If other data from studies on yeast, insects, and rodents can be confirmed in primates, it would indicate that calorie restriction could extend life span by up to 60 percent, making a human life span of 130–150 years a real possibility without fancy technology or supplements or medications. The clear inverse relationship between energy intake and longevity links its mechanism to mitochondria—energy metabolism and free-radical production.

Second, simply restricting the intake of fat, protein, or carbohydrates without overall calorie reduction does not increase the maximum life span of rodents. It’s the calories that count, not necessarily the type of calories (with the exception of those trying to reach ketosis, where type of calorie does count).

Third, calorie restriction has been shown to be effective in disease prevention and longevity in diverse species. Although most caloric restriction studies have been conducted on small mammals like rats or mice, caloric restriction also extends life span in single-celled protozoans, water fleas, fruit flies, spiders, and fish. It’s the only method of life extension that consistently achieves similar results across various species.

Fourth, these calorie-restricted animals stay “biologically younger” longer. Experimental mice and rats extended their youth and delayed (even prevented) most major diseases (e.g., cancers, cardiovascular diseases). About 90 percent of the age-related illnesses studied remained in a “younger” state for a longer period in calorie-restricted animals. Calorie restriction also greatly delayed cancers (including breast, colon, prostate, lymphoma), renal diseases, diabetes, hypertension, hyperlipidemia, lupus, and autoimmune hemolytic anemia, and a number of others.

Fifth, calorie restriction does not need to be started in early age to reap its benefits. Initiating it in middle-aged animals also slowed aging (this is good news for humans, because middle age is when most of us begin to think about our own health and longevity).

Of course, the benefits of calorie restriction relate back to mitochondria. Fewer calories mean less “fuel” (as electrons) entering the ETC, and a corresponding reduction in free radicals. As you know by now, that’s a good thing.

Health Benefits

As just discussed, new research is showing that judicious calorie restriction and ketogenic diets (while preserving optimal nutritional intake) might slow down the normal aging process and, in turn, boost cardiovascular, brain, and cellular health. But how? We can theorize that the restriction results in fewer free radicals, but one step in confirming a theory is finding its mechanism.

In particular, researchers have identified the beneficial role of beta-hydroxybutyric acid (the one ketone body that’s not actually a ketone). It is produced by a low-calorie diet and might be the key to the reduced risk of age-related diseases seen with calorie restriction. Over the years, studies have found that restricting calories slows aging and increases longevity, but the mechanism behind this remained elusive. New studies are showing that beta-hydroxybutyric acid can block a class of enzymes, called histone deacetylases , which would otherwise promote free-radical damage.

While additional studies need to be conducted, it is known that those following calorie-restricted or ketogenic diets have lower blood pressure, heart rate, and glucose levels than the general population. More recently, there has been a lot of excitement around intermittent fasting as an abbreviated method of achieving the same end results.

However, self-prescribing a calorie-restricted or ketogenic diet is not recommended unless you’ve done a lot of research on the topic and know what to do. If not done properly, these diets can potentially increase mental and physical stress on the body. Health status should be improving, not declining, as a result of these types of diets, and when not done properly, these diets could lead to malnutrition and starvation. Health care practitioners also need to properly differentiate a patient who is in a deficiency state of anorexia or bulimia versus someone in a healthy state of ketosis or caloric restriction.

I’ll add a final word of caution: While ketogenic diets can be indispensable tools in treating certain diseases, their use in the presence of mitochondrial disease—at this point—is controversial and depends on the individual’s specific mitochondrial disease. In some cases, a ketogenic diet can help; in others it can be deleterious. So, of all the therapies listed in this book, the one for which I recommend specific expertise in its application is this diet, and only after a proper diagnosis.

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Grain Brain:
The Surprising Truth about Wheat, Carbs, and Sugar–Your Brain’s Silent Killers

by David Perlmutter

Caloric Restriction

Another epigenetic factor that turns on the gene for BDNF production is calorie restriction. Extensive studies have clearly demonstrated that when animals are on a reduced-calorie diet (typically reduced by around 30 percent), their brain production of BDNF shoots up and they show dramatic improvements in memory and other cognitive functions. But it’s one thing to read experimental research studies involving rats in a controlled environment and quite another to make recommendations to people based upon animal research. Fortunately, we finally have ample human studies demonstrating the powerful effect of reducing caloric intake on brain function, and many of these studies have been published in our most well-respected medical journals. 13

In January 2009, for example, the Proceedings of the National Academy of Science published a study in which German researchers compared two groups of elderly individuals—one that reduced their calories by 30 percent and another that was allowed to eat whatever they wanted. The researchers were interested in whether changes could be measured between the two groups’ memory function. At the conclusion of the three-month study, those who were free to eat without restriction experienced a small but clearly defined decline in memory function, while memory function in the group on the reduced-calorie diet actually increased, and significantly so. Knowing that current pharmaceutical approaches to brain health are very limited, the authors concluded, “The present findings may help to develop new prevention and treatment strategies for maintaining cognitive health into old age.” 14

Further evidence supporting the role of calorie restriction in strengthening the brain and providing more resistance to degenerative disease comes from Dr. Mark P. Mattson, chief of the Laboratory of Neurosciences at the National Institute on Aging (NIA). He reported:

Epidemiological data suggest that individuals with a low calorie intake may have a reduced risk of stroke and neurodegenerative disorders. There is a strong correlation between per capita food consumption and risk for Alzheimer’s disease and stroke. Data from population-based case control studies showed that individuals with the lowest daily calorie intakes had the lowest risk of Alzheimer’s disease and Parkinson’s disease. 15

Mattson was referring to a population-based longitudinal prospective study of Nigerian families, in which some members moved to the United States. Many people believe that Alzheimer’s disease is something you “get” from your DNA, but this particular study told a different story. It was shown that the incidence of Alzheimer’s disease among Nigerian immigrants living in the United States was increased compared to their relatives who remained in Nigeria. Genetically, the Nigerians who moved to America were the same as their relatives who remained in Nigeria. 16 All that changed was their environment—specifically, their caloric intake. The research clearly focused on the detrimental effects that a higher caloric consumption has on brain health. In a 2016 study published in Johns Hopkins Health Review, Mattson again emphasized the value of caloric restriction in warding off neurodegenerative diseases while at the same time improving memory and mood. 17 One way to do that is through intermittent fasting, which we’ll fully explore in chapter 7 . Another way, obviously, is to trim back your daily consumption.

If the prospect of reducing your calorie intake by 30 percent seems daunting, consider the following: On average, we consume 23 percent more calories a day than we did in 1970. 18 Based on data from the Food and Agriculture Organization of the United Nations, the average American adult consumes more than 3,600 calories daily. 19 Most would consider “normal” calorie consumption to be around 2,000 calories daily for women and 2,500 for men (with higher requirements depending on level of activity/exercise). A 30 percent cut of calories from an average of 3,600 per day equals 1,080 calories.

We owe a lot of our increased calorie consumption to sugar. Remember, the average American consumes roughly 163 grams (652 calories) of refined sugars a day—reflecting upward of a 30 percent hike in just the last three decades. 20 And of that amount, about 76 grams (302 calories) are from high-fructose corn syrup. So focusing on just reducing sugar intake may go a long way toward achieving a meaningful reduction in calorie intake, and this would obviously help with weight loss. Indeed, obesity is associated with reduced levels of BDNF, as is elevation of blood sugar. Remember, too, that increasing BDNF provides the added benefit of actually reducing appetite. I call that a double bonus.

But if the figures above still aren’t enough to motivate you toward a diet destined to help your brain, in many respects, the same pathway that turns on BDNF production can be activated by intermittent fasting (which, again, I’ll detail in chapter 7 ).

The beneficial effects in treating neurologic conditions using caloric restriction actually aren’t news for modern science, though; they have been recognized since antiquity. Calorie restriction was the first effective treatment in medical history for epileptic seizures. But now we know how and why it’s so effective: It confers neuroprotection, increases the growth of new brain cells, and allows existing neural networks to expand their sphere of influence (i.e., neuroplasticity).

While low caloric intake is well documented in relation to promoting longevity in a variety of species—including roundworms, rodents, and monkeys—research has also demonstrated that lower caloric intake is associated with a decreased incidence of Alzheimer’s and Parkinson’s disease. And the mechanisms by which we think this happens are via improved mitochondrial function and controlling gene expression.

Consuming fewer calories decreases the generation of free radicals while at the same time enhancing energy production from the mitochondria, the tiny organelles in our cells that generate chemical energy in the form of ATP (adenosine triphosphate). Mitochondria have their own DNA, and we know now that they play a key role in degenerative diseases such as Alzheimer’s and cancer. Caloric restriction also has a dramatic effect on reducing apoptosis, the process by which cells undergo self-destruction. Apoptosis happens when genetic mechanisms within cells are turned on that culminate in the death of that cell. While it may seem puzzling at first as to why this should be looked upon as a positive event, apoptosis is a critical cellular function for life as we know it. Pre-programmed cell death is a normal and vital part of all living tissues, but a balance must be struck between effective and destructive apoptosis. In addition, caloric restriction triggers a decrease in inflammatory factors and an increase in neuroprotective factors, specifically BDNF. It also has been demonstrated to increase the body’s natural antioxidant defenses by boosting enzymes and molecules that are important in quenching excessive free radicals.

In 2008, Dr. Veronica Araya of the University of Chile in Santiago reported on a study she performed during which she placed overweight and obese subjects on a three-month calorie-restricted diet, with a total reduction of 25 percent of calories. 21 She and her colleagues measured an exceptional increase in BDNF production, which led to notable reductions in appetite. It’s also been shown that the opposite occurs: BDNF production is decreased in animals on a diet high in sugar. 22 Findings like this have since been replicated.

One of the most well-studied molecules associated with caloric restriction and the growth of new brain cells is sirtuin-1 (SIRT1), an enzyme that regulates gene expression. In monkeys, increased SIRT1 activation enhances an enzyme that degrades amyloid—the starch-like protein whose accumulation is the hallmark of diseases like Alzheimer’s. 23 In addition, SIRT1 activation changes certain receptors on cells, leading to reactions that have the overall effect of reducing inflammation. Perhaps most important, activation of the sirtuin pathway by caloric restriction enhances BDNF. BDNF not only increases the number of brain cells, but also enhances their differentiation into functional neurons (again, because of caloric restriction). For this reason, we say that BDNF enhances learning and memory. 24

The Benefits of a Ketogenic Diet

While caloric restriction is able to activate these diverse pathways, which are not only protective of the brain but enhance the growth of new neuronal networks, the same pathway can be activated by the consumption of special fats called ketones. By far the most important fat for brain energy utilization is beta-hydroxybutyrate (beta-HBA), and we’ll explore this unique fat in more detail in the next chapter. This is why the so-called ketogenic diet has been a treatment for epilepsy since the early 1920s and is now being reevaluated as a therapeutic option in the treatment of Parkinson’s disease, Alzheimer’s disease, ALS, depression, and even cancer and autism. 25 It’s also showing promise for weight loss and ending type 2 diabetes. In mice models, the diet rescues hippocampal memory deficits, and extends healthy lifespan.

Google the term “ketogenic diet” and well over a million results pop up. Between 2015 and 2017, Google searches for the term “keto” increased ninefold. But the studies demonstrating a ketogenic diet’s power date back further. In one 2005 study, for example, Parkinson’s patients actually had a notable improvement in symptoms that rivaled medications and even brain surgery after being on a ketogenic diet for just twenty-eight days. 26 Specifically, consuming ketogenic fats (i.e., medium-chain triglycerides, or MCT oil) has been shown to impart significant improvement in cognitive function in Alzheimer’s patients. 27 Coconut oil, from which we derive MCTs, is a rich source of an important precursor molecule for beta-hydroxybutyrate and is a helpful approach to treating Alzheimer’s disease. 28 A ketogenic diet has also been shown to reduce amyloid in the brain, 29 and it increases glutathione, the body’s natural brain-protective antioxidant, in the hippocampus. 30 What’s more, it stimulates the growth of mitochondria and thus increases metabolic efficiency. 31

Dominic D’Agostino is a researcher in neuroscience, molecular pharmacology, and physiology at the University of South Florida. He has written extensively on the benefits of a ketogenic diet, and in my Empowering Neurologist interview with him he stated: “Research shows that ketones are powerful energy substrates for the brain and protect the brain by enhancing antioxidant defenses while suppressing inflammation. No doubt, this is why nutritional ketosis is something pharmaceutical companies are aggressively trying to replicate.” I have also done a lot of homework in understanding the brain benefits of ketosis—a metabolic state whereby the body burns fat for energy and creates ketones in the process. Put simply, your body is in a state of ketosis when it’s creating ketones for fuel instead of relying on glucose. And the brain loves it.

While science typically has looked at the liver as the main source of ketone production in human physiology, it is now recognized that the brain can also produce ketones in special cells called astrocytes. These ketone bodies are profoundly neuroprotective. They decrease free radical production in the brain, increase mitochondrial biogenesis, and stimulate production of brain-related antioxidants. Furthermore, ketones block the apoptotic pathway that would otherwise lead to self-destruction of brain cells.

Unfortunately, ketones have gotten a bad rap. I remember in my internship being awakened by a nurse to treat a patient in “diabetic ketoacidosis.” Physicians, medical students, and interns become fearful when challenged by a patient in such a state, and with good reason. It happens in insulin-dependent type 1 diabetics when not enough insulin is available to metabolize glucose for fuel. The body turns to fat, which produces these ketones in dangerously high quantities that become toxic as they accumulate in the blood. At the same time, there is a profound loss of bicarbonate, and this leads to significant lowering of the pH (acidosis). Typically, as a result, patients lose a lot of water due to their elevated blood sugars, and a medical emergency develops.

This condition is exceedingly rare, and again, it occurs in type 1 diabetics who fail to regulate their insulin levels. Our normal physiology has evolved to handle some level of ketones in the blood; in fact, we are fairly unique in this ability among our comrades in the animal kingdom, possibly because of our large brain-to-body weight ratio and the high energy requirements of our brain. At rest, 20 percent of our oxygen consumption is used by the brain, which represents only 2 percent of the human body. In evolutionary terms, the ability to use ketones as fuel when blood sugar was exhausted and liver glycogen was no longer available (during starvation) became mandatory if we were to survive and continue hunting and gathering. Ketosis proved to be a critical step in human evolution, allowing us to persevere during times of food scarcity. To quote Gary Taubes, “In fact, we can define this mild ketosis as the normal state of human metabolism when we’re not eating the carbohydrates that didn’t exist in our diets for 99.9 percent of human history. As such, ketosis is arguably not just a natural condition but even a particularly healthful one.” 32

There is a relationship between ketosis and calorie restriction, and the two can pack a powerful punch in terms of enhancing brain health. When you restrict calories (and carbs in particular) while upping fat intake, you trigger ketosis and increase levels of ketones in the blood. In 2012, when researchers at the University of Cincinnati randomly assigned twenty-three older adults with mild cognitive impairment to either a high-carbohydrate or very low-carbohydrate diet for six weeks, they documented remarkable changes in the low-carb group. 33 They observed not only improved verbal memory performance but also reductions in weight, waist circumference, fasting glucose, and fasting insulin. Now here’s the important point: “Ketone levels were positively correlated with memory performance.”

German researchers back in 2009 demonstrated in fifty healthy, normal to overweight elderly individuals that when calories were restricted along with a 20 percent increase in dietary fat, there was a measurable increase in verbal memory scores. 34 Another small study, yes, but their findings were published in the respected Proceedings of the National Academy of Sciences and spurred further research like that of the 2012 experiment. These individuals, compared to those who did not restrict calories, demonstrated improvements in their insulin levels and decline in their C-reactive protein, the infamous marker of inflammation. As expected, the most pronounced improvements were in people who adhered the most to the dietary challenge.

Research and interest in ketosis have exploded in recent years and will continue. The key to achieving ketosis, as we’ll see later in detail, is to severely cut carbs and increase dietary fat. It’s that simple. You have to be carb restricted if you want to reach this brain-blissful state.

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Power Up Your Brain
by David Perlmutter and Alberto Villoldo

Your Brain’s Evolutionary Advantage

One of the most important features distinguishing humans from all other mammals is the size of our brain in proportion to the rest of our body. while it is certainly true that other mammals have larger brains, scientists recognize that larger animals must have larger brains simply to control their larger bodies. An elephant, for example, has a brain that weighs 7,500 grams, far larger than our 1,400-gram brain. So making comparisons about “brain power” or intelligence just based on brain size is obviously futile, Again, it’s the ratio of the brain size to total body size that attracts scientist’s interests when considering the brain’s functional capacity. An elephant’s brain represents 1/550 of its body weight, while the human brain weighs 1/40 of the total body weight. So our brain represents 2.5 percent of our total body weight as opposed to the large-brained elephant whose brain is just 0.18 percent of its total body weight.

But even more important than the fact that we are blessed with a lot of brain matter is the intriguing fact that, gram for gram, the human brain consumes a disproportionately huge amount of energy. While only representing 2.5 percent of our total body weight, the human brain consumes an incredible 22 percent of our body’s energy expenditure when at rest. this represents about 350 percent more energy consumption in relation to body weight compared with other anthropoids like gorillas, orangutans, and chimpanzees.

So it takes a lot of dietary calories to keep the human brain functioning. Fortunately, the very fact that we’ve developed such a large and powerful brain has provided us with the skills and intelligence to maintain adequate sustenance during times of scarcity and to make provisions for needed food supplies in the future. Indeed, the ability to conceive of and plan for the future is highly dependent upon the evolution not only of brain size but other unique aspects of the human brain.

It is a colorful image to conceptualize early Homo sapiens migrating across and arid plain and competing for survival among animals with smaller brains yet bigger claws and greater speed. But our earliest ancestors had one other powerful advantage compared to even our closest primate relatives. The human brain has developed a unique biochemical pathway that proves hugely advantageous during times of food scarcity. Unlike other mammals, our brain is able to utilize an alternative source of calories during times of starvation. Typically, we supply our brain with glucose form our daily food consumption. We continue to supply our brains with a steady stream of glucose (blood sugar) between meals by breaking down glycogen, a storage form of glucose primarily found in the liver and muscles.

But relying on glycogen stores provides only short-term availability of glucose. as glycogen stores are depleted, our metabolism shifts and we are actually able to create new molecules of glucose, a process aptly termed gluconeogenesis. this process involves the construction of new glucose molecules from amino acids harvested form the breakdown of protein primarily found in muscle. While gluconeogenesis adds needed glucose to the system, it does so at the cost of muscle breakdown, something less than favorable for a starving hunter-gatherer.

But human physiology offers one more pathway to provide vital fuel to the demanding brain during times of scarcity. When food is unavailable, after about three days the liver begins to use body fat to create chemicals called ketones. One ketone in particular, beta hydroxybutyrate (beta-HBA), actually serves as a highly efficient fuel source for the brain, allowing humans to function cognitively for extended periods during food scarcity.

Our unique ability to power our brains using this alternative fuel source helps reduce our dependence on gluconeogensis and therefore spares amino acids and the muscles they build and maintain. Reducing muscle breakdown provides obvious advantages for the hungry Homo sapiens in search of food. It is this unique ability to utilize beta-HBA as a brain fuel that sets us apart from our nearest animal relatives and has allowed humans to remain cognitively engaged and, therefore, more likely to survive the famines ever-present in our history.

This metabolic pathway, unique to Homo sapiens, may actually serve as an explanation for one of the most hotly debated questions in anthropology: what caused the disappearance of our Neanderthal relatives? Clearly, when it comes to brains, size does matter. Why then, with a brain some 20 percent larger than our own, did Neanderthals suddenly disappear in just a few thousand years between 40,000 and 30,000 years ago? the party line among scientists remains fixated on the notion that the demise of Neanderthals was a consequence of their hebetude, or mental lethargy. The neurobiologist William Calvin described Neanderthals in his book, A Brain for All Seasons: “Their way of life subjected them to more bone fractures; they seldom survived until forty years of age; and while making tools similar to [those of] overlapping species, there was little [of the] inventiveness that characterizes behaviorally modern Homo sapiens.”

While it is convenient and almost dogmatic to accept that Neanderthals were “wiped out” by clever Homo sapiens, many scientists now believe that food scarcity may have played a more prominent role in their disappearance. Perhaps the simple fact that Neanderthals, lacking the biochemical pathway to utilize beta-HBA as a fuel source for brain metabolism, lacked the “mental endurance” to persevere. Relying on gluconeogenesis to power their brains would have led to more rapid breakdown of muscle tissue, ultimately compromising their ability to stalk prey or migrate to areas where plant food sources were more readily available. their extinction may not have played out in direct combat with Homo sapiens but rather manifested as a consequence of a simple biochemical inadequacy.

Our ability to utilize beta-HBA as a brain fuel is far more important than simply a protective legacy of our hunter-gatherer heritage. George F. Cahill of Harvard Medical School stated, “Recent studies have shown that beta-hydroxybutyrate, the principle ‘ketone’ is not just a fuel, but a ‘superfuel’ more efficiently producing ATP energy than glucose. . . . It has also protected neuronal cells in tissue culture against exposure to toxins associated with Alzheimer’s or Parkinson’s.”

Indeed, well beyond serving as a brain superfuel, Dr. Cahill and other researchers have determined that beta-HBA has other profoundly positive effects on brain health and function. Essentially, beta-HBA is thought to mediate many of the positive effects of calorie reduction and fasting on the brain, including improved antioxidant function, increased mitochondrial energy production with an increased in mitochondrial energy production with an increase in mitochondrial population, increased cellular survival, and increased levels of BDNF leading to enhanced growth of new brain cells (neurogenesis).


Earlier, we explored the need to reduce caloric intake in order to increase BDNF as a means to stimulate the growth of new brain cells as well as to enhance the function of existing neurons. The idea of substantially reducing daily calorie intake will not appeal to many people despite the fact that it is a powerful approach to brain enhancement as well as overall health.

Interestingly, however, many people find the idea of intermittent fasting to be more appealing. Fasting is defined here as a complete abstinence from food for a defined period of time at regular intervals—our fasting program permits the drinking of water. Research demonstrates that many of the same health-providing and brain-enhancing genetic pathways activated by calorie reduction are similarly engaged by fasting—even for relatively short periods of time. Fasting actually speaks to your DNA, directing your genes to produce an astounding array of brain-enhancement factors.

Not only does fasting turn on the genetic machinery for the production of BDNF, but it also powers up the Nrf2 pathway, leading to enhanced detoxification, reduced inflammation, and increased production of brain-protective antioxidants. Fasting causes the brain to shift away from using glucose as a fuel to a metabolism that consumes ketones. When the brain metabolizes ketones for fuel, even the process of apoptosis is reduced, while mitochondrial genes turn their attention to mitochondrial replication. In this way, fasting shifts the brain’s basic metabolism and specifically targets the DNA of mitochondria, thus enhancing energy production and paving the way for better brain function and clarity . . .

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Ketone bodies mimic the life span extending properties of caloric restriction
by Richard L. Veech Patrick C. Bradshaw Kieran Clarke William Curtis Robert Pawlosky M. Todd King

Aging in man is accompanied by deterioration of a number of systems. Most notable are a gradual increase in blood sugar and blood lipids, increased narrowing of blood vessels, an increase in the incidence of malignancies, the deterioration and loss of elasticity in skin, loss of muscular strength and physiological exercise performance, deterioration of memory and cognitive performance, and in males decreases in erectile function. Many aging‐induced changes, such as the incidence of malignancies in mice 82, the increases in blood glucose and insulin caused by insulin resistance 39, 78, and the muscular weakness have been shown to be decreased by the metabolism of ketone bodies 18, 83, a normal metabolite produced from fatty acids by liver during periods of prolonged fasting or caloric restriction 12.

The unique ability of ketone bodies to supply energy to brain during periods of impairment of glucose metabolism make ketosis an effective treatment for a number of neurological conditions which are currently without effective therapies. Impairment of cognitive function has also been shown to be improved by the metabolism of ketone bodies 84. Additionally, Alzheimer’s disease, the major cause of which is aging 20 can be improved clinically by the induction of mild ketosis in a mouse model of the disease 85 and in humans 86. Ketosis also improves function in Parkinson’s disease 87 which is thought to be largely caused by mitochondrial free radical damage 19, 88. Ketone bodies are also useful in ameliorating the symptoms of amyotrophic lateral sclerosis 89. It is also recognized that ketosis could have important therapeutic applications in a wide variety of other diseases 90 including Glut 1 deficiency, type I diabetes 91, obesity 78, 92, and insulin resistance 20, 39, 93, and diseases of diverse etiology 90.

In addition to ameliorating a number of diseases associated with aging, the general deterioration of cellular systems independent of specific disease seems related to ROS toxicity and the inability to combat it. In contrast increases in life span occur across a number of species with a reduction in function of the IIS pathway and/or an activation of the FOXO transcription factors, inducing expression of the enzymes required for free radical detoxification (Figs. 1 and 2). In C. elegans, these results have been accomplished using RNA interference or mutant animals. Similar changes should be able to be achieved in higher animals, including humans, by the administration of d‐βHB itself or its esters.

In summary, decreased signaling through the insulin/IGF‐1 receptor pathway increases life span. Decreased insulin/IGF‐1 receptor activation leads to a decrease in PIP3, a decrease in the phosphorylation and activity of phosphoinositide‐dependent protein kinase (PDPK1), a decrease in the phosphorylation and activity of AKT, and a subsequent decrease in the phosphorylation of FOXO transcription factors, allowing them to continue to reside in the nucleus and to increase the transcription of the enzymes of the antioxidant pathway.

In mammals, many of these changes can be brought about by the metabolism of ketone bodies. The metabolism of ketones lowers the blood glucose and insulin thus decreasing the activity of the IIS and its attendant changes in the pathway described above. However, in addition ketone bodies act as a natural inhibitor of class I HDACs, inducing FOXO gene expression stimulating the synthesis of antioxidant and metabolic enzymes. An added important factor is that the metabolism of ketone bodies in mammals increases the reducing power of the NADP system providing the thermodynamic drive to destroy oxygen free radicals which are a major cause of the aging process.

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Insights into human evolution from ancient and contemporary microbiome studies
by Stephanie L Schnorr, Krithivasan Sankaranarayanan, Cecil M Lewis, Jr, and Christina Warinner

Brain growth, development, and behavior

The human brain is our defining species trait, and its developmental underpinnings are key foci of evolutionary genetics research. Recent research on brain development and social interaction in both humans and animal models has revealed that microbes exert a major impact on cognitive function and behavioral patterns []. For example, a growing consensus recognizes that cognitive and behavioral pathogenesis are often co-expressed with functional bowel disorders []. This hints at a shared communication or effector pathway between the brain and gut, termed the gutbrain-axis (GBA). The enteric environment is considered a third arm of the autonomic nervous system [], and gut microbes produce more than 90% of the body’s serotonin (5-hydroxytryptamine or 5-HT) []. Factors critical to learning and plasticity such as serotonin, γ-aminobutryic acid (GABA), short chain fatty acids (SCFAs), and brain derived neurotrophic factor (BDNF), which train amygdalin and hippocampal reactivity, can be mediated through gut-brain chemical signals that cross-activate bacterial and host receptors []. Probiotic treatment is associated with positive neurological changes in the brain such as increased BDNF, altered expression of GABA receptors, increased circulating glutathione, and a reduction in inflammatory markers. This implicates the gut microbiome in early emotional training as well as in affecting long-term cognitive plasticity.

Critically, gut microbiota can modulate synthesis of metabolites affecting gene expression for myelin production in the prefrontal cortex (PFC), presumably influencing the oligodendrocyte transcriptome []. Prosocial and risk associated behavior in probiotic treated mice, a mild analog for novelty-seeking and risk-seeking behaviors in humans, suggests a potential corollary between entrenched behavioral phenotypes and catecholamines (serotonin and dopamine) produced by the gut microbiota []. Evolutionary acceleration of the human PFC metabolome divergence from chimpanzees, particularly the dopaminergic synapse [], reifies the notion that an exaggerated risk-reward complex characterizes human cognitive differentiation, which is facilitated by microbiome derived bioactive compounds. Therefore, quintessentially human behavioral phenotypes in stress, anxiety, and novelty-seeking is additionally reinforced by microbial production of neuroactive compounds. As neurological research expands to include the microbiome, it is increasingly clear that host–microbe interactions have likely played an important role in human brain evolution and development [].

Ancient human microbiomes
by Christina Warinner, Camilla Speller, Matthew J. Collins, and Cecil M. Lewis, Jr

Need for paleomicrobiology data

Although considerable effort has been invested in characterizing healthy gut and oral microbiomes, recent investigations of rural, non-Western populations () have raised questions about whether the microbiota we currently define as normal have been shaped by recent influences of modern Western diet, hygiene, antibiotic exposure, and lifestyle (). The process of industrialization has dramatically reduced our direct interaction with natural environments and fundamentally altered our relationship with food and food production. Situated at the entry point of our food, and the locus of food digestion, the human oral and gut microbiomes have evolved under conditions of regular exposure to a diverse range of environmental and zoonotic microbes that are no longer present in today’s globalized food chain. Additionally, the foods themselves have changed from the wild natural products consumed by our hunter-gatherer ancestors to today’s urban supermarkets stocked with an abundance of highly processed Western foodstuffs containing artificially enriched levels of sugar, oil, and salt, not to mention antimicrobial preservatives, petroleum-based colorants, and numerous other artificial ingredients. This dietary shift has altered selection pressure on our microbiomes. For example, under the ‘ecological plaque hypothesis’, diseases such as dental caries and periodontal disease are described as oral ecological catastrophes of cultural and lifestyle choices ().

Although it is now clear that the human microbiome plays a critical role in making us human, in keeping us healthy, and in making us sick, we know remarkably little about the diversity, variation, and evolution of the human microbiome both today and in the past. Instead, we are left with many questions: When and how did our bacterial communities become distinctly human? And what does this mean for our microbiomes today and in the future? How do we acquire and transmit microbiomes and to what degree is this affected by our cultural practices and built environments? How have modern Western diets, hygiene practices, and antibiotic exposure impacted ‘normal’ microbiome function? Are we still in mutualistic symbiosis with our microbiomes, or are the so-called ‘diseases of civilization’ – heart disease, obesity, type II diabetes, asthma, allergies, osteoporosis – evidence that our microbiomes are out of ecological balance and teetering on dysbiosis ()? At an even more fundamental level, who are the members of the human microbiome, how did they come to inhabit us, and how long have they been there? Who is ‘our microbial self’ ()?

Studies of remote and indigenous communities () and crowdsourcing projects such as the American Gut (, the Earth Microbiome Project (, and uBiome ( are attempting to characterize modern microbiomes across a range of contemporary environments. Nevertheless, even the most extensive sampling of modern microbiota will provide limited insight into Pre-Industrial microbiomes. By contrast, the direct investigation of ancient microbiomes from discrete locations and time points in the past would provide a unique view into the coevolution of microbes and hosts, host microbial ecology, and changing human health states through time. […]

Diet also plays a role in shaping the composition of oral microbiomes, most notably by the action of dietary sugar in promoting the growth of cariogenic bacteria such as lactobacilli and S. mutans (). Two recent papers have proposed that cariogenic bacteria, such as S. mutans, were absent in pre-Neolithic human populations, possibly indicating low carbohydrate diets (), while evolutionary genomic analyses of S. mutans suggest an expansion in this species approximately 10,000 years, coinciding with the onset of agriculture (). […]

Ancient microbiome research provides an additional pathway to understanding human biology that cannot be achieved by studies of extant individuals and related species alone. Although reconstructing the ancestral microbiome by studying our ancestors directly is not without challenges (), this approach provides a more direct picture of human-microbe coevolution. Likewise, ancient microbiome sources may reveal to what extent bacteria commonly considered ‘pathogenic’ in the modern world (for example, H. pylori) were endemic indigenous organisms in pre-Industrial microbiomes ().

The three paths to reconstructing the ancestral microbiomes are also complimentary. For example, analysis of the gut microbiome from extant, rural peoples in Africa and South America have revealed the presence of a common, potentially commensal, spirochete belonging to the genus Treponema (). Such spirochetes have also been detected in extant hunter-gatherers (), and in 1,000-year-old human coprolites from Mexico (), but they are essentially absent from healthy urban populations, and they have not been reported in the gut microbiome of chimpanzees (). These multiple lines of evidence suggest that this poorly understood spirochete is a member of the ancestral human microbiome, yet not necessarily the broader primate microbiome. Future coprolite research may be able to answer the question of how long this microbe has co-associated with humans, and what niche it fills.

The Latest in Darwinian Medical Science: 12 Noteworthy New Papers That Shed Evolutionary Light on Health and Disease
by Eirik Garnas

Exposure of the Host-Associated Microbiome to Nutrient-Rich Conditions May Lead to Dysbiosis and Disease Development—an Evolutionary Perspective

The gist of what the paper is about:

We here propose that overfeeding of the host-associated bacterial community, particularly with easily digestible, energy-dense, low-fiber-content foods, likely causes dysbiosis and the development of disease. Overfeeding uncouples natural host-microbe associations, leading to an increased activity and changed functionality of the associated microbiota.

Continue reading…

My comments:
This paper sheds light on an important, yet often overlooked facet of the recent assault on the human microbiome, namely the effects of overfeeding. While it’s widely recognized that fast food doesn’t do the microbiome good, it’s somewhat underappreciated that changes pertaining to our meal pattern and total caloric intake have also undermined human-microbe relations.

Whereas our primal ancestors often did things, like chasing game, on an empty stomach, many humans of the 21st century could be said to almost constantly be in a fed, as opposed to fasted, state. This paper helps draw attention to the microbiome-related implications of this mismatch and suggests that many of the health benefits of intermittent fasting are mediated by gut bacteria.

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Ketogenic Diet and Neurocognitive Health
Spartan Diet
The Agricultural Mind
Malnourished Americans

Can Ketogenic Diets Work for Bodybuilding or Athletics?
by P. D. Mangan

Here’s how I’d summarize the ‘keto for sports’ evidence so far:

  • The longer the study…or the longer its keto-adaptation phase…or the more keto-adapted the subjects are…the more likely the study is to find favorable performance results
  • Keto is worth trying for anyone in any sport (but start in the off-season!)
  • It’s highly unlikely keto is better for high-intensity
  • It’s unlikely that keto is bad for high-intensity
  • It’s likely that keto is neutral for high-intensity
  • It’s likely that keto diets are better for endurance
  • It’s very likely keto diets are better for body composition
  • It’s very likely keto diets are generally healthier than standard high-carb diets for athletes

Neuroscientist Shows What Fasting Does To Your Brain & Why Big Pharma Won’t Study It
by Arjun Walia

Does Fasting Make You Smarter?
by Derek Beres

Fasting Cleans the Brain
by P. D. Mangan

How Fasting Heals Your Brain
by Adriana Ayales

Effect of Intermittent Fasting on Brain Neurotransmitters, Neutrophils Phagocytic Activity, and Histopathological Finding in Some Organs in Rats
by Sherif M. Shawky, Anis M. Zaid, Sahar H. Orabi, Khaled M. Shoghy, and Wafaa A. Hassan

The Effects of Fasting During Ramadan on the Concentration of Serotonin, Dopamine, Brain-Derived Neurotrophic Factor and Nerve Growth Factor
by Abdolhossein Bastani, Sadegh Rajabi, and Fatemeh Kianimarkani

Gut microbiome, SCFAs, mood disorders, ketogenic diet and seizures
by Jonathan Miller

Study: Ketogenic diet appears to prevent cognitive decline in mice
by University of Kentucky

Low-carb Diet Alleviates Inherited Form of Intellectual Disability in Mice
by Johns Hopkins Medicine

Ketogenic Diet Protects Against Alzheimer’s Disease by Keeping Your Brain Healthy and Youthful
by Joseph Mercola

The Gut Microbiota Mediates the Anti-Seizure Effects of the Ketogenic Diet.
by C. A. Olson

Is the Keto Diet Bad for the Microbiome?
by David Jockers

Does a Ketogenic Diet Change Our Microbiome?
by Christie Rice

Can Health Issues Be Solved By Dietary Changes Altering the Microbiome?
by Russ Schierling

Some Benefits of Intermittent Fasting are Mediated by the Gut Microbiome
by Fight Aging!

RHR: Is High Fat Healthy for the Gut Microbiota?
by Chris Kresser

A Comprehensive List of Low Carb Research
by Sarah Hallberg

Randomised Controlled Trials Comparing Low-Carb Diets Of Less Than 130g Carbohydrate Per Day To Low-Fat Diets Of Less Than 35% Fat Of Total Calories
from Public Health Collaboration

Fasting and Feasting.

Someone shared with me a paper on fasting, Intermittent Fasting and Human Metabolic Health (with 11 authors and so I won’t list them). It’s the first time I’ve seen the research discussed in detail. It’s worth a perusal. Here is the conclusion:

“This overview suggests that intermittent fasting regimens may be a promising approach to lose weight and improve metabolic health for people who can tolerate intervals of not eating, or eating very little, for certain hours of the day or days of the week. If proven to be efficacious, these eating regimens may offer promising nonpharmacologic approaches to improving health at the population level with multiple public health benefits.”

I’ve done fasting off and on over the years. I used to do it on a semi-regular basis, just pick a random day and not eat. But I stopped fasting for a number of years, no particular reason. I decided to start fasting again. I’ve been not eating at all in the first part of my day and usually only later have a single meal (or rather an eating period). Besides that, I’ve also been entirely fasting one day a week.

I don’t find fasting all that difficult. It’s been good, actually. I feel better when I’m not constantly eating. And there is no doubt that calorie restriction limits weight gain and can help you lose weight, along with potentially having a healthy influence other aspects of biological functioning (from circadian rhythm to microbiota). I’ve lost some weight and have done so while not starving myself. The one meal I eat a day is still often a relatively larger meal, even if I stretch it out over an hour or so. Slow eating seems to be a useful method, rather than stuffing oneself quickly as most Americans do. Fasting followed by slow eating is a good combination.

Fasting helps me feel less hungry. I’m more likely to eat a lot, if I start eating early and snack all day. Avoiding breakfast, in particular, keeps my hunger down even later on when I do finally eat. This is particularly true if I exercise in the morning. Exercising on an empty stomach gets my metabolism going and oddly makes me less hungry for the rest of the day. That is true for any kind of physical activity, but I find aerobic exercise is most optimal.

Plus, aerobic exercise improves my mood, which is important for reasons of depression. And I know from experience that depression is closely connected to overeating, especially junk food. The whole sugar-serotonin cycle is addictive. I’m sure my blood sugar levels are stay more even throughout the day when I’m following a healthier regimen. When blood sugar levels drop, the immediate experience is craving food. That is what goes away with regular fasting, the cravings that can make it difficult to maintain a healthy lifestyle. Constantly shifting blood sugar levels and serotonin levels causes fluctuating moods and energy levels. It’s rather problematic.

It’s a matter of finding balance. I still eat foods that I enjoy. I’m just more careful about the specifics. I like the taste of sweetness. So, I use a lot of stevia to sweeten drinks. And the sugar I consume tends to come in the form of daily intake of cultured foods (usually kefir or yogurt), but some fruit as well, mostly apples — rather than from soda pop and candy. That was an important change for me, as I used to be a junk food junky. Fasting is a helpful part of this process, especially in resetting one’s metabolism and habits.

It’s taken me years of experimentation to get to this point. I’ve come to the conclusion that fasting is a key part of what works for me.