Categories:

Ray Peat, PhD on Brewer’s Yeast

Also see:
Collection of Ray Peat Quote Blogs by FPS
Collection of FPS Charts
Master List – Ray Peat, PhD Interviews
Diabetes: Conversion of Alpha-cells into Beta-cells
The Streaming Organism
The Randle Cycle
Bisphenol A (BPA), Estrogen, and Diabetes
Insulin Inhibits Lipolysis
Aldosterone, Sodium Deficiency, and Insulin Resistance

“Many people with diabetes have used brewer’s yeast and DHEA to improve their sugar metabolism. In diabetes, very little sugar enters the cells, so fatigue is a problem.”

“Brewer’s yeast has been used successfully to treat diabetes. In the 1930s, my father had severe diabetes, but after a few weeks of living on brewer’s yeast, he recovered and never had any further evidence of diabetes. Besides its high B-vitamin and protein content, yeast is an unusual food that should be sparingly used, because of its high phosphorous/calcium ratio, high potassium to sodium ratio, and high estrogen content. The insulin-producing beta cells of the pancreas have estrogen receptors, but I don’t know of any new research investigating this aspect of yeast therapy.”

“Zinc, as in oysters, and potassium and the B vitamins, as in brewer’s yeast, are sometimes necessary. Many people get gas from the complex carbohydrates in yeast. This can be prevented by steeping a tablespoonful in a cup of boiling water, and drinking only the yellow liquid and throwing away the sediment. Protein is lost, but the other nutrients are highly soluble.”

“Since early in this century, brewer’s yeast was used for treating diabetes. The pancreas has an estrogen receptor, and estrogen promotes insulin secretion. Since reading of yeasts’ responsiveness to sex hormones about 15 years ago, I have encouraged people to use liver when they need a vitamin-mineral supplement, and to restrict the use of brewer’s yeast mainly to treatment of diabetes.”

“Brewer’s yeast has been used traditionally to correct diabetes, and its high content of niacin and other B vitamins and potassium might account for it beneficial effects. However, eating a large quantity of it is likely to cause gas, so some people prefer to extract the soluble nutrients with hot water. Yeast contains a considerable amount of estrogen, and the water extract probably leaves much of that in the insoluble starchy residue.”

Posted in General.

Tagged with , , , , , , , , , , .


Why Shoes Make “Normal” Gait Impossible

Also see:
Shod versus Unshod
High Heeled Shoes: A Real Pain
The Effects Of Shoes On Foot Strike, Performance

Why Shoes Make “Normal” Gait Impossible: How flaws in footwear affect this complex human function.
By William A. Rossi, D.P.M.

Dr. Rossi, a frequent contributor to this magazine, serves as a consultant for the footwear industry, and resides in Marshfield, MA.

Each year, consumers spend hundreds of millions of dollars for “walking shoes” promising to help the wearer walk “right” or more comfortably. Each year, additional hundreds of millions of dollars are spent for orthotics designed to “normalize” foot balance, stability, and gait. Podiatrists and other medical practitioners are constantly applying therapies and ancillary products to correct gait faults and re-establish “normal” gait.

While such therapies provide some relief from gait-induced distress symptoms, they are largely ineffectual in re-establishing natural gait. Why? Because natural gait is biomechanically impossible for any shoe-wearing person. Natural gait and shoes are biomechanically incompatible because all shoes automatically convert the normal to the abnormal, the natural to the unnatural. And no therapy or mechanical device, no matter how precisely designed or expertly applied, can fully reverse thc gait from wrong to right.

Let’s now see if these seemingly presumptuous statements can be substantiated by the evidence of the shoe/gait conflict.

Gait is the single most complex motor function of the human body. So complex, in fact, that it is the only motor function for which a definition or standard or “normal” does not exist. It involves half of the body’s 650 muscles and 200 bones, along with a large share of the joints and ligaments. And despite all the serious gait studies that have been done since Hippocrates to the present, all the mysteries at human gait have yet to be revealed.

First, it’s important to distinguish between “normal” and “natural.” Normal is defined as an accepted standard, a mean or average. For example, everyone occasionally catches a cold, hence the common cold is “normal,” though it is neither healthy nor natural. Conversely, natural means the pristine, ideal state, the ideal of form and function stemming from nature itself. Hence the difference between normal and natural is essentially the difference between what is and what can or ought to be.

Applying this to human gait, we can say that in shoe-wearing societies many people have what appears to be “normal” gait, while in shoeless societies they have “natural” gait. And there are pronounced differences between the two both in torn and function.

In shoe-wearing societies a visibly faulty gait can often be corrected and made normal, but it can never be made natural as long as conventional shoes are worn. It is biomechanically impossible because of the forced alterations from the natural in foot stance, postural alignment, body balance, equilibrium, body mechanics and weight distribution caused by shoes.

Let’s now see some of the specifics of how these inevitable gait faults are caused by shoes.

The Role of Heels

The role of heels or heel heights has been given much attention in the literature because their influence is so obvious, especially on heels two or more inches in height.

Barefoot, the perpendicular line of the straight body column creates a ninety degree angle with the floor. On a two-inch heel, were the body a rigid column and forced to tilt forward, the angle would be reduced to seventy degrees, and to fifty-five degrees on a three-inch heel. Thus, for the body to maintain an erect position, a whole series of joint adjustments (ankle, knee, hip, spine, head) are required to regain and retain the erect stance.

In this reflex adjustment scores of body parts — bones, ligaments and joints, muscles and tendons — head to foot must instantly change position. If these adjustments are sustained over prolonged periods, or by habitual use of higher heels, as is not uncommon, the strains and stresses become chronic, causing or contributing to aches of legs, back and shoulders, fatigue, etc.

But the alterations are internal and organic, as well. For example, when standing barefoot, the anterior angle of the female pelvis is twenty-five degrees; on low, one-inch heels it increases to thirty degrees; on two-inch heels to forty-five degrees; on three-inch heels to sixty degrees. Under these conditions, what happens to the pelvic and abdominal organs? Inevitably, these must shift position to adapt.

Does the wearing of low, one-inch “sensible” heels prevent these problems of postural adaptation? No. All the low heel does is lessen the intensity of the negative postural effects. Hence, the wearing of heels of any height automatically alters the natural erect state of the body column. (Note: millions of men habitually wear boots or shoes with heels one and a half to three inches in height, such as on western boots or elevator shoes.)

But shoe heels have other, lesser-known influences on gait. For example, any heel, low to high, requires a compensatory alteration or forward slant on the last, which is translated to the shoe. This slant is known as the “heel wedge angle.” This is the slope or slant of the heel seat, rear to front, to compensate for the shoe heel height. The higher the heel, the greater the angle.

On the bare foot there is no wedge angle. The bottom of the heel is on a level one hundred and eighty degrees, with body weight shared equally between heel and ball. Inside the heeled shoe the wedge angle shifts body weight forward so that on a low heel body weight is shared forty percent heel, sixty percent ball; and on a high heel ninety percent ball and ten percent heel.

Under these conditions the step sequence is no longer heel-to-ball- to toes and push-off, as with the bare foot. On heels two or more inches in height little weight is borne by the heel of the foot, an step push-off is almost wholly from the ball.

On medium to higher heels, due to the reduced base of the heel top-lift, the line of falling weight shifts, causing a wobbling of the less-secure ankle, which tilts medially. The shift in the body’s center of gravity alters the equilibrium of the body column and prevents a natural step sequence,

One consequence is that heel strike moves to the lateral-rear corner of the heel top-lift. This is not natural. The heel of the shoeless foot receives its initial heel strike not at the lateral-rear corner but in the center at the site of the plantar calcaneal tuberosity. The natural plantar path of the step sequence — heel to lateral border to ball to hallux and push-off — is forced to shift, further affecting natural gait.

Let’s add one further influence of shoe heels, low to high. The shoe’s elevated heel shortens the Achilles tendon and accompanying shortening of the calf muscles. Both the tendon and the muscles are, of course, vital to step propulsion and gait stamina — which may help to explain the performance dominance of marathon runners from nations where the barefoot state is common from infancy to adulthood.

The heeled shoe “steals” much of this propulsive power from the tendon and leg muscles. This not only places more stress on them to achieve needed propulsion, but power must be borrowed from elsewhere — knees, thigh muscles, hips, and trunk. A small army of anatomical reinforcements must come to the rescue of the handicapped tendon and calf muscles.

Thus a shoe heel of any height sets in motion a series of gait-negative consequences, making natural gait — meaning the barefoot form — impossible. But this is only the beginning.

Toe Spring

If you rest a shoe, new or old, on a table and view it in profile from the side, it reveals an up-tilt of the toe tip varying from five-eighths to one inch or more. More on worn shoes. This is known as “toe spring” and is built into the last.

On the bare, natural foot the digits rest flat, their tips grasping the ground as an assist in step propulsion. Inside the shoe, the digits are lifted slantwise off the ground, unable to fulfill their natural ground-grasping function.

So why is toe spring built into the last and shoe? To compensate for lack or absence of shoe flexibility at the ball. The toe spring creates a rocker effect on the shoe sole so that the shoe, instead of full flexing as it should, forces the foot to “roll” forward like the curved bottom of a rocking chair. The thicker the sole, such as on sneakers or work boots, or the stiffer the sole (such as on men’s Goodyear welt wingtip brogues), the greater the toe spring needed because of lack of shoe flexibility.

With toe spring, the toes of the foot are constantly angled upward five to twenty degrees, depending upon the amount of shoe toe spring. Functionally, they are “forced out of business,” denied much or all of their natural ground-grasping action and exercise so essential to exercising of the whole foot because 18 of the foot’s 19 tendons are attached to the toes.

The combination of the up-tilted toes caused by the toe spring, and the down-slanted heel and foot caused by the heel wedge angle, create an angle apex at the ball where the two angles converge. The angle apex has a dagger-point effect on the ball. This is certainly an important contributing cause of metatarsal stress symptoms and lesions.

But equally important, the natural gait mechanics are affected. Because the hallux and other digits are largely immobilized by their uptilted position, the step propulsion must come almost wholly from the metatarsal heads. This not only imposes undue stress on the heads, but forces an unnatural alteration of the gait pattern itself.

Gait Hazards of the Last

The shoe’s last, the form of mold over which the shoe is made, is not visible to the consumer. but it bears much influence on the shoe and gait. There are several built-in design faults with most commercial lasts, but two in particular have relevant influence on gait.

First, almost all shoe lasts are designed with inflare, whereas almost all feet are designed on a straight axis. This automatically creates a biomechanical conflict between foot and last (or shoe). This is the prime reason why virtually all shoes go out of shape with wear — because foot and shoe are mismated. If, because of this conflict, the foot cannot function naturally inside the shoe, it cannot take a normal or natural step.

A second common fault of the last is the concavity at most lasts under and across the ball, which is automatically “inherited” by the shoe at the same site.

Why are lasts made with a concavity under the ball? Tradition. About 80 years ago a shoe manufacturer discovered that the foot could be made to look smaller and trimmer by allowing it to “sink” into a cavity in the shoe n a cavity that no one would see — thus reducing the amount of foot volume n n visible above. It was so successful in its mission of smaller-looking feet that it was quickly adopted by other manufacturers. It has long since become a standard part of last design.

This cavity is further accentuated by the construction of the shoe itself, wherein the space between outsole and insole must be filled with a special filler material (ground cork, foam rubber, fiberglass, etc.). However, the combination of the foot’s heat, moisture, and pressure forces the filler material to compress and “creep,” deforming its original flat surface.

The combination of the concave-bottom last at the ball an the compression and creep of the filler material sinking into the cavity, creates a sinkhole into which the three middle metatarsal heads fall as the first and fifth heads rise on the rim. We thus have the classic “fallen” metatarsal arch. The application of a metatarsal pad, whether in the shoe or via an orthotic or strapping, provides relief — not because it “raises” the arch but simply by filling in the cavity and returning the heads to their natural level plane.

Thus the important role of the metatarsal heads as a fulcrum and the toes as grasping-gripping mechanisms for step propulsion is seriously diminished. The step push-off is now almost entirely from the ball, and weakly so because the metatarsal heads are pushing from a cavity rather than from a flat surface. A propulsive energy must now be drawn from other sources –legs, thighs, hips, the forward tilt of the trunk and shoulders — with undue strain on all those body sectors. The gait loses natural form and function.

Shoe Flexibility

On taking a step, the foot normally flexes approximately 54 degrees at the ball on the bare foot.

But all shoes flex 30 to 80 percent less than normal at the ball. This obviously creates flex resistance for the foot by the shoe. The foot must now work harder to take each or its approximately eight thousand daily steps. The required extra energy imposes undue strain and fatigue on the foot.

Why are most shoes inflexible? First, the average shoe bottom consists of several layers or materials or components: outsole, midsole, insole, sock liner, filler materials, cushioning. This multiple-layered sandwich poses a formidable challenge to bending or flexing. Second, many types of footwear — athletic, sneakers, work and outdoor boots, walking, casual, etc. — have thick soles which add further to inflexibility.

Many elderly people whose feet have lost elasticity and flexibility over the many years of shoe wearing have difficulty climbing or descending stairs. They must use stair rails for pull-up power and security.

The National Safety council reports that in 1994 (latest figures) 13,500 fatalities occurred from stair falls — and 2,500 of the victims were over age 65. An even greater number or casualties from stair falls resulted in serious injuries (fractures, sprains, etc.), occurring with people of all ages. Climbing and descending stairs requires both foot flexibility and the lift power from the Achilles tendon and calf muscles. If both have been diminished and handicapped by habitual shoe wearing, then the stability and security of the gait itself are diminished and handicapped.

Most people, including medical practitioners and shoe people, test for shoe flexibility in a wrong manner, by grasping the shoe at both ends and bending the sole. But that flexes the shoe behind instead of at the ball. If the foot were flexed in the same manner, the five metatarsals would be fractured.

To properly test for flexing, rest the shoe sole down on a table or counter. Insert one hand inside, using a couple of fingers to press down on the ball. With a finger of the other hand, lift the toe tip of the shoe. If the toe end, tip to ball, lifts easily, the shoe is flexible. The degree to which it resists toe lift is the degree to which it is inflexible.

The more inflexible the shoe, the more flat-footed the gait manner. With inflexible or semi-flexible shoes (which include most) the step push-off is almost wholly from the ball, thus fulfilling only half to three-fourths of the natural step sequence.

Shoe Weight

Most shoes weigh too much. The average pair of dress shoes weighs about 34 ounces; a pair of wingtip brogues about 44 ounces; some work and outdoor boots up to 60 ounces or more. Women’s dress and casual shoes average 16-24 ounces a pair; women’s boots about 32 ounces.

A lightweight pair of 16-ounce shoes amounts to a cumulative four tons of foot-lift load daily (16 ounces times 6,000 foot-lift steps). If the shoes weigh 32 ounces, daily foot-lift load is eight tons; 44 ounces adds up to 11 tons a day. every added four ounces of shoe weight adds another one ton to foot-lift load.

These foot lift loads impose an energy drain not only on the foot but the whole body. It is a common though little recognized source of foot and body fatigue — which is why, after a lone day on one’s feet, one arrives home feeling “dog-tired” and kicks off one’s shoes.

You can walk several miles carrying a four-pound weight on each shoulder. But you can barely manage 100 yards with the same weight attached to each foot. The reason is simple physics: the farther the load from the center of gravity, the heavier the energy and “lift” strain.

No footwear, with certain exceptions, should weigh more than 12 ounces a pair for women, 16-18 ounces for men.

Excessive shoe weight forces an alteration of natural gait form. The drag effect and energy drain of the shoes creates alterations in the natural step sequence — a smooth, easy movement heel to lateral border to ball to toes is disrupted. The common descriptive expression “dragging one’s feet” aptly applies here.

Shoe Fit

There is substantial and incontestable evidence that no commercial footwear fits properly, regardless of type, brand, style, or price. This is because of a combination of inherent faults in the lasts, shoe design and construction. Even the shoe sizing system itself is riddled with faults (we are, incredibly, still using the “system” introduced 630 years ago and “updated” 117 years ago).

One example is width fit. A recent study was conducted by Dr. Francesca M. Thompson, chief of the Adult Orthopedic Clinics at St. Luke’s Hospital, New York, involving several hundred women. The average measurement across the ball of the foot was 3.66 inches, but the shoe measurement at the same site measured less than three inches. Thus, almost all were wearing shoes 20 percent too narrow at the ball.

Too-narrow or “snug” width fit occurs with about 90 percent of men’s and women’s shoes alike. In the stores it has long been the contention that snug fit is right because the foot needs “support” and also because the snug fit allows the shoe to “conform” to the foot with wear. It is also regarded as proper fit by most doctors and consumers.

Snug or narrow fit has a negative effect on gait because the natural expansion of the foot with each weight-bearing step is prevented. The normal plantar surface at the ball is diminished, affecting foot balance and the security of the gait itself.

Reduced Foot Tread

One of the most insidious of the numerous negative effects of footwear on gait is loss of foot tread surface. With the shod foot, 50 to 65 percent of the foot’s natural tread surface is lost, This is easily seen by examining the sole surface of a worn shoe. Most of the wear is concentrated at the rear-outer corner of the heel top-lift and the center or medial undersurface of the ball. The rest of the sole is usually unworn or only slightly worn. A footprint will show 50 to 70 percent greater tread surface.

Under these conditions we automatically have an unbalanced foot receiving excessive strain on small portions receiving the brunt of the wear. It is impossible for such a foot to “walk right,” meaning with natural function and full tread.

A dog (or any other four-footed animal) has a much greater and more stable base beneath its body than does a human. We humans stand erect with a relatively tiny base beneath us and with the center of gravity about hip high. The dog has a much lower center of gravity, plus a much larger base area beneath its body balanced on four legs.

It’s the difference between balancing a small cube in the palm of your hand, then trying to balance a long, thin pencil on its end in the sane manner. This is why half of the body’s 650 muscles and 208 bones (plus most of its joints and ligaments) are required just to stand and walk. They are necessary to keep that long pole of body erect.

To further jeopardize this fragile balance of the body column by denying it half of more of its base tread surface is pushing the biomechanics of gait to extremes of risk. Yet, that is exactly what happens because of the various tread faults of the shoes we wear.

Sensory Response

Podiatry, unfortunately, along with all the other medical specialties, has given little attention to the role of the earth’s bioelectromagnetic forces relative to sensory response of the foot, which bear enormous influence on gait. It is a field begging investigation by podiatry, because the foot is so intimately involved.

The soles and tips of the toes contain over 200,000 nerve endings, perhaps the densest concentration to be found anywhere of comparable size on the body. Our nerve-dense soles are our only tactile contact with the physical world around us. Without them we would lose equilibrium and become disoriented. If the paws or feet of any animal were “desensitized,” the animal could not survive in its natural environment for an hour.

Says orthopedist Philip Lewin, “The foot is the vital link between the person and the earth, the vital reality of his day-to-day existence.” City College of New York anatomists Todd R. Olson and Michael E. Seidel write, “Because the sole is so abundantly supplied with tactile sensory nerve endings, we use our feet to furnish the brain with considerable information about our immediate environment.”

Thus there is a sensory foot/body, foot/brain connection vital to body stability, equilibrium, and gait.

Yet, much of it is denied us because of our thick-layered, inflexible shoes that shut off a considerable amount of this electromagnetic inflow and our sensory response to it. B. T. Renbourne, M.D., of England’s Brookside Hospital, has done considerable research in this field. He writes, “Modern shoes give good wear, but they also impair the foot’s sensory response to the ground and earth, affecting the reflex action of the foot and leg muscles in gait. This sensory foot contact is essential for stable, sure-footed walking.”

It is well known by both common experience and clinical testing that infants are able to walk with much more confidence and stability barefoot than with shoes on. In fact, thc same can be said of adults. This is not only because of the foot’s biomechanics (flexing, toe grasping, heel-to-toe step sequence, etc.), but also because of the neural energy assist from the sensory response.

However, when several layers of shoe bottom materials are packed between foot and ground, a certain amount of sensory blockage is inevitable, and the gait loses some of its natural energies and functional efficiency.

The Role of Orthotics

The foregoing comments concerning natural human gait require a completely fresh perspective concerning the use of foot orthotics — especially those designed to establish or re-establish “normal” foot balance and stability of gait.

To put the conclusion first: natural gait is impossible for the shoe-wearing foot — at least shoes as traditionally designed and constructed. And it is equally impossible for any orthotic to achieve “correct” foot and body balance and gait stability with the orthotic inside the gait-negative shoes, no matter how correct and precise the biomechanical design of the orthotic.

A secure, stable superstructure cannot be erected on a design- defective base or foundation (the Tower of Pisa is a classic example). In regard to “restoring” natural gait, shoe and orthotic are biomechanically incompatible. While orthotics may assist as therapy in more extreme gait faults, they are not suitable therapy to correct or stabilize gait and return it to its natural, unadulterated state.

Summary

We have always assumed that most people in modern shoe-wearing societies walk “normally.” It is true only if we use the term “normal” in its liberal context, meaning to conform to an accepted standard or general average.

But natural walking — the pure manner without faults of form or function — is quite another perspective. All ambulatory creatures in nature walk naturally, hence with maximum efficiency. That includes all shoeless people, who are the only “pure” walkers on the planet. All the rest of us, by grace of the shoes we wear, are defective walkers in varying manner or degree. And who knows how many of our foot problems stem, directly or indirectly, from those shoe-caused postural and gait faults.

Does all this suggest that the only means of retaining or regaining the natural state of gait is to go barefoot? Unfortunately, yes. That is, until the “ideal” shoe, devoid of all the faults of design, construction, and performance of traditional footwear, is made available. But, throughout all history to the present, nobody has yet designed such a shoe while at the sane time providing the esthetics and styling desired by consumers.

But how about modern custom-made, custom-fitted shoes? Certainly they should permit natural gait. Not so, While they provide custom fit they also include the usual biomechanical faults — the use of heels, lack of flexibility, toe spring, excessive weight, etc., which largely nullify the custom fit.

Ironically, the closest we have ever come to an “ideal” shoe was the original lightweight, soft-sole, heel-less, simple moccasin, which dates back more than 14,000 years. It consisted of a piece of crudely tanned but soft leather wrapped around the foot and held on with rawhide thongs. Presto! custom fit, perfect in biomechanical function, and no encumbrances to the foot or gait.

The vital importance of the foot to gait is only too obvious: no feet, no gait; the lower the functional perforuance of the feet, the lower the functional performance of the gait.

But the foot’s role in gait has even greater significance which most podiatrists themselves don’t fully realize or appreciate. The foot’s architectural design and its consequent biomechanical function was responsible for our distinctive erect manner of gait, walking on two feet with a stride.

That accomplishment — perhaps the single most significant development of bioengineering in all evolutionary history — was responsible for making us human in the first place and the spawning of the human species. More than any other distinctive human capacity — the huge brain, language, conceptual thinking, etc.- our unique form of gait, unduplicated in all evolutionary history, was the very seed of our humanity.

The noted anthropologist Frederick Wood-Jones states, “Man’s foot is all his own and unlike any other foot. It is the most distinctive part of his whole anatomical makeup. It is a human specialization; it is his hallmark, and so long as man has been man, it is by his feet that he will be known from all other creatures of the animal kingdom. It is his feet that will confer upon him his only real distinction and provide his only valid claim to human status.” To that, Donald C. Johanson, paleoanthropologist and chief of the Institute of Human Origins, Berkeley, California, adds, “Bipedalism is what made us human,” Thus, man stands alone because only man stands.

It took four million years to develop our unique human foot and our consequent distinctive form of gait, a remarkable feat of bioengineering. Yet, in only a few thousand years, and with one carelessly designed instrument, our shoes, we have warped the pure anatomical form of human gait, obstructing its engineering efficiency, afflicting it with strains and stresses and denying it its natural grace of form and ease of movement head to foot. We have converted a beautiful thoroughbred into a plodding plowhorse.

True, despite all these shoe-induced handicaps or gait, the human species is doing fine. But we might make our lives a shade better if we could find a way to regain our natural manner of walking and at the same time keep our shoes on our feet.

Posted in General.

Tagged with , , , , .


Index to SSRI Stories

Index to SSRI Stories

Posted in General.

Tagged with , , , , , .


Women: Vintage Weight Gain Ads

Also see:
Sugar Ads
Gelatin Ads

Posted in General.

Tagged with , , , , .


Healthy Standing & Seated Posture


Posted in General.

Tagged with , , , , , , , , , , .


Kathleen Porter Videos – Natural Alignment






K. Porter Books:
Ageless Spine, Lasting Health: The Open Secret to Pain-Free Living and Comfortable Aging
Natural Posture for Pain-Free Living: The Practice of Mindful Alignment
Sad Dog Happy Dog: How Poor Posture Affects Your Child’s Health & What You Can Do About It

Website:
Natural Posture Solutions

Posted in General.

Tagged with , , , , , , , , , .


Serotonin in Fruits

Also see:
Estrogen, Serotonin, and Aggression
Fermentable Carbohydrates, Anxiety, Aggression
Anti Serotonin, Pro Libido
Gelatin > Whey
Thyroid peroxidase activity is inhibited by amino acids
Whey, Tryptophan, & Serotonin
Tryptophan, Fatigue, Training, and Performance
Carbohydrate Lowers Free Tryptophan
Protective Glycine
Intestinal Serotonin and Bone Loss
Hypothyroidism and Serotonin
Estrogen Increases Serotonin
Whey, Tryptophan, & Serotonin
Tryptophan, Sleep, and Depression
Intestinal Serotonin and Bone Loss
Linoleic Acid and Serotonin’s Role in Migraine
Gelatin, Glycine, and Metabolism
Serotonin and Melatonin Lower Progesterone
The Serotonin Irritation Syndrome (SIS)
Plant Toxins in Response to Stress
Toxic Plant Estrogens
Dietary Fiber, Bowel Health, and Cancer
Fermentable Carbohydrates, Anxiety, Aggression
Bowel Toxins Accelerate Aging

“Plantains are very proinflammatory, with a high serotonin content; commercial orange juice, especially if it doesn’t separate when standing for a few hours, can produce bowel irritation by supporting bacterial growth because of the suspended modified fiber, and watermelons that aren’t perfectly ripe have enough starch to cause problems, though very ripe watermelon is safe.” -Ray Peat, PhD

Am J Clin Nutr. 1985 Oct;42(4):639-43.
Serotonin content of foods: effect on urinary excretion of 5-hydroxyindoleacetic acid.
Feldman JM, Lee EM.
Using a highly specific radioenzymatic assay we determined the serotonin concentration in 80 types of foods. The following fruits had a high serotonin concentration (mean +/- SEM) expressed in micrograms/g weight: plantain 30.3 +/- 7.5; pineapple 17.0 +/- 5.1; banana 15.0 +/- 2.4; Kiwi fruit 5.8 +/- 0.9; plums 4.7 +/- 0.8; and tomatoes 3.2 +/- 0.6. Only nuts in the walnut or hickory family had a high serotonin concentration expressed in micrograms/g weight; butternuts 398 +/- 90; black walnuts 304 +/- 46; English walnuts 87 +/- 20; shagbark hickory nuts 143 +/- 23; mockernut hickory nuts 67 +/- 13; pecans 29 +/- 4; and sweet pignuts 25 +/- 8. Ingestion of these fruits and nuts resulted in an increase in urinary 5-hydroxyindoleacetic acid excretion with no change in platelet serotonin concentration. The above foods should not be eaten while a urine is being collected for 5-hydroxyindoleacetic acid analysis.

J Chromatogr A. 2011 Jun 24;1218(25):3890-9. doi: 10.1016/j.chroma.2011.04.049. Epub 2011 Apr 27.
Simultaneous analysis of serotonin, melatonin, piceid and resveratrol in fruits using liquid chromatography tandem mass spectrometry.
Huang X, Mazza G.
An analytical method was developed for the simultaneous quantification of serotonin, melatonin, trans- and cis-piceid, and trans- and cis-resveratrol using reversed-phase high performance liquid chromatography coupled to mass spectrometry (HPLC-MS) with electrospray ionization (ESI) in both positive and negative ionization modes. HPLC optimal analytical separation was achieved using a mixture of acetonitrile and water with 0.1% formic acid as the mobile phase in linear gradient elution. The mass spectrometry parameters were optimized for reliable quantification and the enhanced selectivity and sensitivity selected reaction monitoring mode (SRM) was applied. For extraction, the direct analysis of initial methanol extracts was compared with further ethyl acetate extraction. In order to demonstrate the applicability of this analytical method, serotonin, melatonin, trans- and cis-piceid, and trans- and cis-resveratrol from 24 kinds of commonly consumed fruits were quantified. The highest serotonin content was found in plantain, while orange bell peppers had the highest melatonin content. Grape samples possessed higher trans- and cis-piceid, and trans- and cis-resveratrol contents than the other fruits. The results indicate that the combination of HPLC-MS detection and simple sample preparation allows the rapid and accurate quantification of serotonin, melatonin, trans- and cis-piceid, and trans- and cis-resveratrol in fruits.

J Pharm Pharmacol. 1960 Jun;12:360-4.
A note on the presence of noradrenaline and 5-hydroxytryptamine in plantain (Musa sapientum, var. paradisiaca).
FOY JM, PARRATT JR.
Noradrenaline, 5-hydroxytryptamine and dopamine are present in the fruit of Musa sapientum, var. paradisiaca (Plantain), which forms a staple food of many inhabitants of West Africa. The amounts of 5-hydroxytryptamine and noradrenaline are highest when the fruit is ripe. An estimated daily intake of 10 mg. of 5-hydroxytryptamine by West Africans has little apparent effect on the normal functioning of the intestinal tract.

J Assoc Off Anal Chem. 1980 Jan;63(1):19-21.
Spectrofluorometric determination and thin layer chromatographic identification of serotonin in foods.
García-Moreno C, Nogales-Alarcon A, Gómez-cerro A, Marine-Font A.
A method is described for determining serotonin in foods, based on alkaline butanol-sand column elution followed by spectrofluorometric and spectrofluorometric determination with thin layer chromatographic confirmation. The method has been applied to fresh bananas, banana-based baby food, and fresh and canned tomatoes. The average recovery was 91%. The amounts of serotonin found were 10–30 ppm in bananas, 0.1–1.9 ppm in banana-based baby foods, 4.4–5.6 ppm in fresh tomatoes, and 2.8–5.6 ppm in canned tomatoes.

J Assoc Off Anal Chem. 1983 Jan;66(1):115-7.
Improved method for determination and identification of serotonin in foods.
García-Moreno C, Rivas-Gonzalo JC, Peña-Egido MJ, Mariné-Font A.
A previously described method to identify and quantitate serotonin in foods has been improved. The extraction and separation of serotonin from interfering substances has been improved, and the scope of material to which the method may be applied has been widened. The relative standard deviation (RSD) for repeated determinations of serotonin in canned fried tomato purée and the average recovery of serotonin added to the same sample was 6.25 and 89.9%, respectively. The method showed the presence of serotonin in apricots, cherries, and peaches.

Posted in General.

Tagged with , , , , , , , , , , , , , .


The Serotonin Irritation Syndrome (SIS)

Also see:
THE EFFECTS OF AIR QUALITY ON THE SEROTONIN IRRITATION SYNDROME
TREATMENT OF ACUTE MANIA WITH AMBIENT AIR ANIONIZATION: VARIANTS OF CLIMACTIC HEAT STRESS AND SEROTONIN SYNDROME
Estrogen, Serotonin, and Aggression
Fermentable Carbohydrates, Anxiety, Aggression
Anti Serotonin, Pro Libido
Gelatin > Whey
Thyroid peroxidase activity is inhibited by amino acids
Whey, Tryptophan, & Serotonin
Tryptophan, Fatigue, Training, and Performance
Carbohydrate Lowers Free Tryptophan
Protective Glycine
Intestinal Serotonin and Bone Loss
Hypothyroidism and Serotonin
Estrogen Increases Serotonin
Whey, Tryptophan, & Serotonin
Tryptophan, Sleep, and Depression
Intestinal Serotonin and Bone Loss
Linoleic Acid and Serotonin’s Role in Migraine
Gelatin, Glycine, and Metabolism
Serotonin and Melatonin Lower Progesterone

“The Serotonin Irritation Syndrome is defined as a significant disturbance of normal nervous system activity and/or the malfunction of various metabolic processes which is characterized by abnormally high levels of serotonin (5-Hydroxytrlptamine or 5-HT, a highly active neurochemical) in the human bloodstream.” -Charles Wallach, Ph.D

Int J Psychiatry Med. 1978-1979;9(2):199-204.
Serotonin irritation syndrome: an hypothesis.
Giannini AJ.
Two patients were seen with multisystememic complaints and anxious feelings. Their history was similar for chronic exposure to potentially ionized atmospheric environments–a waterfall and high-voltage equipment. Physical examination showed various signs sometimes associated with hyperserotonergic states. Laboratory testing showed increased levels of serum serotonin and decreased levels of its metabolite, urinary 5-hydroxyindoleacetic acid (5-HIAA). Removal of the patients from these environments or the use of a serotonin-blocker ameliorated all symptoms and reestablished normal serotonin and 5-HIAA levels. A literature-review disclosed a similar symptom-complex reported with air-ionization during the sweep of hot winds across desert lands. Animal studies are cited in which cation aerosols are used to block serotonin metabolism, producing clinical and laboratory results some of which are similar to those seen in the patients described. It is suggested that a “serotonin irritation syndrome” might be related to cation-induced serotonin metabolic dysfunctions.

J Clin Psychiatry. 1986 Jan;47(1):22-5.
The serotonin irritation syndrome–a new clinical entity?
Giannini AJ, Malone DA, Piotrowski TA.
The literature on the possible existence of a “serotonin irritation syndrome” is examined. This syndrome is an anxiety state occurring in the presence of elevated levels of atmospheric or ambient cations and is associated with elevated central and peripheral serotonin levels. Investigation of these cations’ effects on microbes, insects, and mammals, including humans, shows a disruption of normal activity. It is suggested that clinicians become acquainted with the potential relationship between cation exposure and serotonin in their treatment of anxious patients. Further research exploring the etiology and diagnostic definition of this entity is urged.

J Clin Psychiatry. 1983 Jul;44(7):262-4.
Anxiety states: relationship to atmospheric cations and serotonin.
Giannini AJ, Castellani S, Dvoredsky AE.
Five cases are described that offer evidence for the existence of the “serotonin irritation syndrome,” an anxiety state associated with high cation environments, elevated serum serotonin, and decreased urinary 5-hydroxyindoleacetic acid. The therapeutic response and reduction in serum serotonin after treatment with methysergide and/or removal from the high-cation environment support a serotonergic basis of the anxiety.

Int J Psychiatry Med. 1986-1987;16(3):243-8.
Anxiogenic effects of generated ambient cations–a preliminary study.
Giannini AJ, Jones BT, Loiselle RH, Price WA.
The existence of the putative “serotonin irritation syndrome” (SIS) was tested in a human population. Volunteers were exposed to a highly cationized environment for two hours. Symptoms of anxiety and excitement significantly increased. During the time of exposure serum serotonin levels also increased significantly. These results support the existence of SIS as a clinical entity.

J Clin Psychiatry. 1986 Mar;47(3):141-3.
Reversibility of serotonin irritation syndrome with atmospheric anions.
Giannini AJ, Jones BT, Loiselle RH.
Clinical reports and animal studies support the existence of a “serotonin irritation syndrome.” This is a putative anxiety state caused by a rise in atmospheric cations and reversed by a corresponding rise in anions. Volunteers were exposed to generated ambient cations and anions under controlled conditions. Cations were found to increase anxiety, excitement, and suspicion. Anions reversed the effects of cations and, in addition, reduced suspicion and excitement to levels below those occurring before cationization. Implications of these findings and the possible mediation of effects by serotonin are discussed.

J Gen Physiol. 1960 Nov;44:269-76.
The biological mechanisms of air ion action. II. Negative air ion effects on the concentration and metabolism of 5-hydroxytryptamine in the mammalian respiratory tract.
KRUEGER AP, SMITH RF.
Negative air ions are shown to decrease 5-hydroxytryptamine concentrations in extirpated strips of rabbit trachea and in the respiratory tracts of living mice. An initial exposure of guinea pigs to (-) air ions causes a transient rise in urinary 5-hydroxyindoleacetic acid excretion which is not observed upon subsequent exposures. These findings are compatible with the hypothesis advanced earlier that (-) air ion effects depend on the ability of (-) ions to accelerate enzymatic oxidation of 5-hydroxytryptamine.

J Gen Physiol. 1960 Jan;43:533-40.
The biological mechanisms of air ion action. I. 5-Hydroxytryptamine as the endogenous mediator of positive air ion effects on the mammalian trachea.
KRUEGER AP, SMITH RF.
Intravenous administration of 5-hydroxytryptamine to rabbits and guinea pigs is shown to bring about changes very similar to those produced by (+) air ions, including (1) decreased ciliary rate, (2) contraction of the posterior tracheal wall, (3) exaggerated response of the tracheal mucosa to trauma, (4) marked vasoconstriction in the tracheal wall, and (5) increased respiratory rate. These effects are reversed by (-) air ions. Iproniazid, which raises 5-hydroxytryptamine levels in the animal by blocking monamine oxidase, produces similar but non-reversible effects. Reserpine, which depletes 5-hydroxytryptamine in the animal, causes changes that resemble those produced by (-) air ions, including (1) increased ciliary rate, (2) relaxed posterior sulcus, (3) hyperemia of the tracheal mucosa, (4) lowered respiratory rate, and (5) increased volume and rate of mucus flow. On the basis of these facts, the hypothesis is advanced that (+) air ion effects are mediated by the release of free 5-hydroxytryptamine, while (-) air ion effects depend on the ability of (-) ions to accelerate the enzymatic oxidation of 5-hydroxytryptamine.

Int J Biometeorol. 1978 Mar;22(1):53-8.
Absence of harmful effects of protracted negative air ionisation.
Sulman FG, Levy D, Lunkan L, Pfeifer Y, Tal E.
The absence of harmful effects of protracted negative air ionisation was studied in 5 weather-sensitive women and 5 normal men chosen at random. Negative ions were generated by the Modulion of Amcor-Amron (Herzliya, Israel). The patients were exposed separately during 8 sleeping hours and 8 working hours to the apparatus at 1–2 m distance in a 4 × 4 m room, for 2 months. Thus they were exposed to a daily uptake of 1 × 104 negative ions/cm3 for 16 h/day during 2 months. Urinary 17-KS, 17-OH, adrenaline and noradrenaline excretion was not affected by the negative ionisation. However serotonin, 5-HIAA, histamine and thyroxine excretion — if increased before — diminished by 50% on an average. There were no changes in body weight, blood pressure, pulse, respiratory rate, oral morning temperature, dynamometer grip strength, routine liver function tests, urinary pH, albumen, glucose, ketones, bilirubin, or occult blood, red and white blood count and ECG records. The EEG revealed the typical changes due to negative air ionisation: stabilising of frequency, increased amplitudes, spreading of brainwaves from the perceptive occipital area to the conceptive frontal area and synchronisation of both hemisphere tracings.

Int J Biometeorol. 1973 Sep;17(3):267-75.
Effect of negative air ions upon emotionality and brain serotonin levels in isolated rats.
Gilbert GO.
The effect of small negative air ions on the emotional behavior and brain serotonin content of isolated rats was studied. The results indicate that isolated subjects were more reactive to handling and had larger levels of serotonin than did isolated subjects undergoing continuous ion treatment. Group housed subjects were less reactive to handling than were either isolated subjects or isolated subjects intermittently exposed to ions. Thus ions were effective in reducing both emotionality and serotonin. Only continuous ion treatment was effective.

International Journal of Biometeorology, Volume 7, Issue 1, pp.3-16
The biological mechanism of air ion action: The effect of CO2+ in inhaled air on the blood level of 5-hydroxytryptamine in mice (1963)
Krueger, Albert P.; Andriese, Paul C.; Kotaka, Sadao
Abstract Mice inhaling positively ionized air exhibited a significant rise in the blood level of 5-hydroxytryptamine [5-HT]BL. This effect was duplicated by non-ionized air to which CO2 + was added but did not occur when the same amount of either nonionized CO2 or CO2 − replaced CO2 +. The rise in [5-HT]BL was associated with physiological changes that parallel those appearing after the injection of 5-HT or after administration of iproniazid. Some of the animals exposed to CO2 + in air became ill and suffered tissue damage attributable to excessive concentrations of 5-HT. A few of the mice died and at autopsy pulmonary and enteric lesions were found which also were reasonably ascribed to the increased 5-HTBL.The physiological,pathological and biochemical changes described furnish additional support for the 5-HT hypothesis of air ion action presented in earlier publications. There is good reason to believe that some of the known biological effects of gaseous ions involve other mechanisms.

International Journal of Biometeorology July 1966, Volume 10, Issue 1, pp 17-28
The effects of inhaling non-ionized or positively ionized air containing 2–4% CO2 on the blood levels of 5-hydroxytryptamine in mice
A. P. Krueger, P. C. Andriese, S. Kotaka
An animal chamber was constructed which made possible the exposure of small animals for long periods of time to uniform controlled atmospheres containing a given number of cluster ions. Monitoring of the microenvironment was made possible by the fabrication of a minaturized ion collector. Using these two developments mice were exposed to non-ionized or to positively ionized air containing either 2% or 4% CO2. Non-ionized 2% or 4% CO2 produced a fall in the blood level of 5-HT.Positively ionized 2% or 4% CO2 elicited a rise in 5-HT providing the ionic density was sufficiently great.

Posted in General.

Tagged with , , , , , , , , , , , , , , , , , , , , , .


Lactic Acidosis and Diabetes

Also see:
Aldosterone, Sodium Deficiency, and Insulin Resistance
Diabetes: Conversion of Alpha-cells into Beta-cells
Women, Estrogen, and Circulating DHA
Insulin Inhibits Lipolysis
The Randle Cycle
Comparison: Carbon Dioxide v. Lactic Acid
Carbon Dioxide Basics
Carbon Dioxide as an Antioxidant
Comparison: Oxidative Metabolism v. Glycolytic Metabolic
Promoters of Efficient v. Inefficient Metabolism
Trauma & Resuscitation: Toxicity of Lactated Ringer’s Solution
Enzyme to Know: Pyruvate Dehydrogenase
Glycolysis Inhibited by Palmitate
Insulin Inhibits Lipolysis
PUFA Breakdown Products Depress Mitochondrial Respiration
PUFA Decrease Cellular Energy Production
Free Fatty Acids Suppress Cellular Respiration

“Diabetics typically have elevated lactate, which shows that glucose doesn’t have a problem getting into their cells, just getting oxidized.” -Ray Peat, PhD

“Diabetics are relatively unable to oxidize glucose, they produce lactate in the presence of O2, and may synthesize fat inappropriately. Diabetes is relevant to cancer exactly because of their shared inability to oxidize sugar and lactic acid.” -Ray Peat, PhD

“The presence of lactic acid in our tissues is very meaningful, but it is normally treated as only an indicator, rather than as a cause, of biological problems. Its presence in rosacea, arthritis, heart disease, diabetes, neurological diseases and cancer has been recognized, and recently it is being recognized that suppressing it can be curative, after fifty years of denial.

Lactate contributes to diabetes, inhibiting the ability to oxidize glucose.

A focus on correcting the respiratory defect would be relevant for all of the diseases and conditions (including heart disease, diabetes, dementia) involving inflammation and inappropriate excitation, not just for cancer.” -Ray Peat, PhD

Glucose is said to not be able to enter the cell in diabetes, but the presence of lactic acid suggest glucose is entering the cell but is being wasted, producing lactate via inefficient and stress promoting glycolytic metabolism.

Clin Endocrinol (Oxf). 2011 Feb;74(2):191-6. doi: 10.1111/j.1365-2265.2010.03891.x.
Diabetes, metformin and lactic acidosis.
Scale T, Harvey JN.
OBJECTIVE:
Metformin has long been thought to cause lactic acidosis (LA) but evidence from various sources has led researchers to question a direct causative relationship. We assessed the relationship of metformin prescription and other factors to the incidence of LA.
METHODS:
All cases of LA at a single hospital were identified from laboratory lactate measurements. We compared patients classified as Cohen and Woods class A and B, patients with and without diabetes, and those taking metformin or not.
RESULTS:
LA was more common than in published analyses based on hospital coding of diagnoses. The incidence of LA was greater in diabetes than in the nondiabetic population but with no further increase in patients taking metformin. Lactate levels were no greater in patients on metformin than in patients with type 2 diabetes not on metformin even if patients with acute cardiorespiratory disturbance (Cohen and Woods class A) were excluded. Acidosis was greater in diabetes (hydrogen ion 94·9 ± 4·6 vs 83·2 ± 2·3 10(-9) m, P = 0·027) but factors besides lactate contributed. Acute cardiorespiratory illness, acute renal impairment and sepsis were the most common of the recognized precipitating factors. Age (P = 0·01), acute renal failure (P = 0·015) and sepsis (P = 0·005) were associated with mortality.
CONCLUSIONS:
Diabetes rather than metformin therapy is the major risk factor for the development of LA. Lactic acidosis occurs in association with acute illness particularly in diabetes. Current guidance for the prevention of lactic acidosis may overemphasize the role of metformin.

Int J Epidemiol. 2010 Dec;39(6):1647-55. Epub 2010 Aug 25.
Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study.
Crawford SO, Hoogeveen RC, Brancati FL, Astor BC, Ballantyne CM, Schmidt MI, Young JH.
BACKGROUND:
Accumulating evidence implicates insufficient oxidative capacity in the development of type 2 diabetes. This notion has not been well tested in large, population-based studies.
METHODS:
To test this hypothesis, we assessed the cross-sectional association of plasma lactate, an indicator of the gap between oxidative capacity and energy expenditure, with type 2 diabetes in 1709 older adults not taking metformin, who were participants in the Atherosclerosis Risk in Communities (ARIC) Carotid MRI Study.
RESULTS:
The prevalence of type 2 diabetes rose across lactate quartiles (11, 14, 20 and 30%; P for trend <0.0001). Following adjustment for demographic factors, physical activity, body mass index and waist circumference, the relative odds of type 2 diabetes across lactate quartiles were 0.98 [95% confidence interval (CI) 0.59-1.64], 1.64 (95% CI 1.03-2.64) and 2.23 (95% CI 1.38-3.59), respectively. Furthermore, lactate was associated with higher fasting glucose among non-diabetic adults.
CONCLUSIONS:
Plasma lactate was strongly associated with type 2 diabetes in older adults. Plasma lactate deserves greater attention in studies of oxidative capacity and diabetes risk.

Diabetes. 1988 Aug;37(8):1020-4.
Measurement of plasma glucose, free fatty acid, lactate, and insulin for 24 h in patients with NIDDM.
Reaven GM, Hollenbeck C, Jeng CY, Wu MS, Chen YD.
Fasting and postprandial plasma glucose, free fatty acid (FFA), lactate, and insulin concentrations were measured at hourly intervals for 24 h in 27 nonobese individuals—9 with normal glucose tolerance, 9 with mild non-insulin-dependent diabetes mellitus (NIDDM, fasting plasma glucose < 175 mg/dl), and 9 with severe NIDDM (fasting plasma glucose > 250 mg/dl). In addition, hepatic glucose production (HGP) was measured from midnight to 0800 in normal individuals and patients with severe NIDDM. Plasma glucose concentration was highest in patients with severe NIDDM, lowest in those with normal glucose tolerance, and intermediate in those with mild NIDDM (two-way ANOVA, P < .001). Variations in plasma FFA and lactate levels of the three groups were qualitatively similar, with lowest concentrations seen in normal individuals, intermediate levels in the group with mild NIDDM, and the highest concentration in those with severe NIDDM (two-way ANOVA, P < .001). Of particular interest was the observation that plasma FFA concentrations were dramatically elevated from midnight to 0800 in patients with severe NIDDM. The 24-h insulin response was significantly increased in patients with mild NIDDM, with comparable values seen in the other two groups. Values for HGP fell progressively throughout the night in normal individuals and patients with severe NIDDM, despite a concomitant decline in plasma glucose and insulin levels. Although the magnitude of the fall in HGP was greater in NIDDM, the absolute value was significantly (P < .001) greater than normal throughout the period of observation. These results demonstrate that there are differences in substrate level between individuals with normal glucose tolerance and patients with NIDDM and differing degrees of glucose intolerance, unrelated to ambient insulin level, and these changes persist over 24 h.

Posted in General.

Tagged with , , , , , , , , , , , , , , .


Carbohydrate Consumption During Exercise

Also see:
Low carb + intensive training = fall in testosterone levels
Low Blood Sugar Basics
Carbohydrate Lowers Serotonin from Exercise
Serotonin, Fatigue, Training, and Performance
Ray Peat, PhD on Low Blood Sugar & Stress Reaction
PUFA Promote Stress Response; Saturated Fats Suppress Stress Response
Belly Fat, Cortisol, and Stress
Sugar (Sucrose) Restrains the Stress Response
Carbohydrate Lowers Exercise Induced Stress
Exercise Induced Stress
The Randle Cycle

J Nutr. 1992 Mar;122(3 Suppl):788-95.
Carbohydrate supplementation during exercise.
Coyle EF.
Muscle glycogen and plasma glucose are oxidized by skeletal muscle to supply the carbohydrate energy needed to exercise strenuously for several hours (i.e., 70% maximal O2 consumption). With increasing exercise duration there is a progressive shift from muscle glycogen to blood glucose. Blood glucose concentration declines to hypoglycemic levels (i.e., 2.5 mmol/L) in well-trained cyclists after approximately h of exercise and this appears to cause muscle fatigue by reducing the contribution of blood glucose to oxidative metabolism. Carbohydrate feeding throughout exercise delays fatigue by 30-60 min, apparently by maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously. Carbohydrate feedings do not spare muscle glycogen utilization. Very little muscle glycogen is used for energy during the 3-4-h period of prolonged exercise when fed carbohydrate, suggesting that blood glucose is the predominant carbohydrate source. At this time, exogenous glucose disposal exceeds 1 g/min (i.e., 16 mg.kg-1.min-1) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mmol/L. However, at this time these cyclist cannot exercise more intensely than 74% of maximal O2 consumption, suggesting a limit to the rate at which blood glucose can be used for energy. It is important to realize that carbohydrate supplementation during exercise delays fatigue by 30-60 min, but does not prevent fatigue. In conclusion, fatigue during prolonged strenuous exercise is often due to inadequate carbohydrate oxidation. This is partly a result of hypoglycemia, which limits carbohydrate oxidation and causes muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

Int J Sports Med. 1992 Oct;13 Suppl 1:S126-8.
Carbohydrate feeding during exercise.
Coyle EF.
During strenuous exercise (i.e. 70% maximal O2 consumption) there is a progressive shift from muscle glycogen to blood glucose oxidation with increasing duration of exercise. By maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously, carbohydrate consumption throughout exercise delays fatigue by 30-60 min in endurance-trained subjects. This requires exogenous glucose supplementation at rates in excess of 1 gram/min (i.e., 16 mg/kg/min) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mM. Exogenous glucose must be infused at a rate of 2.6 gram/min (i.e., 37 mg/kg/min), which is similar to the total rate of carbohydrate oxidation, in order to maintain blood glucose at 10 mM after 2 h of exercise. However, carbohydrate supplementation during intense exercise does not spare muscle glycogen utilization in people. This suggests that over the course of 2-4 hours of exercise at 70% VO2max, muscle glycogen and blood glucose contribute equally to total carbohydrate oxidation. Furthermore, during the latter stages of prolonged exercise, exogenous blood glucose supplementation may be capable of supplying almost all of the carbohydrate requirements of exercise at intensities up to 70% VO2max.

J Appl Physiol. 1986 Jul;61(1):165-72.
Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate.
Coyle EF, Coggan AR, Hemmert MK, Ivy JL.
The purpose of this study was to determine whether the postponement of fatigue in subjects fed carbohydrate during prolonged strenuous exercise is associated with a slowing of muscle glycogen depletion. Seven endurance-trained cyclists exercised at 71 +/- 1% of maximal O2 consumption (VO2max), to fatigue, while ingesting a flavored water solution (i.e., placebo) during one trial and while ingesting a glucose polymer solution (i.e., 2.0 g/kg at 20 min and 0.4 g/kg every 20 min thereafter) during another trial. Fatigue during the placebo trial occurred after 3.02 +/- 0.19 h of exercise and was preceded by a decline (P less than 0.01) in plasma glucose to 2.5 +/- 0.5 mM and by a decline in the respiratory exchange ratio (i.e., R; from 0.85 to 0.80; P less than 0.05). Glycogen within the vastus lateralis muscle declined at an average rate of 51.5 +/- 5.4 mmol glucosyl units (GU) X kg-1 X h-1 during the first 2 h of exercise and at a slower rate (P less than 0.01) of 23.0 +/- 14.3 mmol GU X kg-1 X h-1 during the third and final hour. When fed carbohydrate, which maintained plasma glucose concentration (4.2-5.2 mM), the subjects exercised for an additional hour before fatiguing (4.02 +/- 0.33 h; P less than 0.01) and maintained their initial R (i.e., 0.86) and rate of carbohydrate oxidation throughout exercise. The pattern of muscle glycogen utilization, however, was not different during the first 3 h of exercise with the placebo or the carbohydrate feedings. The additional hour of exercise performed when fed carbohydrate was accomplished with little reliance on muscle glycogen (i.e., 5 mmol GU X kg-1 X h-1; NS) and without compromising carbohydrate oxidation. We conclude that when they are fed carbohydrate, highly trained endurance athletes are capable of oxidizing carbohydrate at relatively high rates from sources other than muscle glycogen during the latter stages of prolonged strenuous exercise and that this postpones fatigue.

J Appl Physiol. 1993 Oct;75(4):1477-85.
Carbohydrate supplementation spares muscle glycogen during variable-intensity exercise.
Yaspelkis BB 3rd, Patterson JG, Anderla PA, Ding Z, Ivy JL.
Effects of carbohydrate (CHO) supplementation on muscle glycogen utilization and endurance were evaluated in seven well-trained male cyclists during continuous cycling exercise that varied between low [45% maximal O2 uptake (VO2 max)] and moderate intensity (75% VO2 max). During each exercise bout the subjects received either artificially flavored placebo (P), 10% liquid CHO supplement (L; 3 x 18 g CHO/h), or solid CHO supplement (S; 2 x 25 g CHO/h). Muscle biopsies were taken from vastus lateralis during P and L trials immediately before exercise and after first (124 min) and second set (190 min) of intervals. Subjects then rode to fatigue at 80% VO2 max. Plasma glucose and insulin responses during L treatment reached levels of 6.7 +/- 0.7 mM and 70.6 +/- 17.2 microU/ml, respectively, and were significantly greater than those of P treatment (4.4 +/- 0.1 mM and 17.7 +/- 1.6 microU/ml) throughout the exercise bout. Plasma glucose and insulin responses of S treatment were intermediate to those of L and P treatments. Times to fatigue for S (223.9 +/- 3.5 min) and L (233.4 +/- 7.5 min) treatments did not differ but were significantly greater than that of P treatment (202.4 +/- 9.8 min). After the first 190 min of exercise, muscle glycogen was significantly greater during L (79 +/- 3.5 mumol/g wet wt) than during P treatment (58.5 +/- 7.2 mumol/g wet wt). Furthermore, differences in muscle glycogen concentrations between L and P treatments after 190 min of exercise and in time to fatigue for these treatments were positively related (r = 0.76, P < 0.05). These results suggest that CHO supplementation can enhance prolonged continuous variable-intensity exercise by reducing dependency on muscle glycogen as a fuel source.

Med Sci Sports Exerc. 1992 Sep;24(9 Suppl):S331-5.
Nutritional manipulations before and during endurance exercise: effects on performance.
Coggan AR, Swanson SC.
1) Ingesting CHO during prolonged, moderate-intensity (60-85% VO2max) exercise can improve performance by maintaining plasma glucose availability and oxidation during the later stages of exercise. 2) Plasma glucose may be oxidized at rates in excess of 1 g.min-1 late in exercise. Athletes therefore need to ingest sufficient quantities of CHO in order to meet this demand. This can be accomplished by ingesting CHO at 40-75 g.h-1 throughout exercise or by ingesting approximately 200 g of CHO late in exercise. Ingesting CHO after fatigue has already occurred, however, is generally ineffective in restoring and maintaining plasma glucose availability, CHO oxidation, and/or exercise tolerance. 3) No apparent differences exist between glucose, sucrose, or maltodextrins in their ability to improve performance. Ingesting fructose during exercise, however, does not improve performance and may cause gastrointestinal distress. 4) The form of CHO (i.e., solid vs liquid) ingested during exercise is unlikely to be important provided that sufficient water is also consumed when ingesting CHO in solid form. 5) Ingesting 50-200 g of CHO 30-60 min before exercise results in transient hypoglycemia early in exercise, but this does not affect the rate of muscle glycogen utilization or, in most people, cause overt symptoms of neuroglucopenia. Whether performance is impaired, unaffected, or enhanced by such pre-exercise CHO feedings remains equivocal. 6) Ingesting 200-350 g of CHO 3-6 h before exercise appears to improve performance, possibly by maximizing muscle and/or liver glycogen stores or by supplying CHO from the small intestine during exercise itself.(ABSTRACT TRUNCATED AT 250 WORDS)

J Appl Physiol. 1983 Jul;55(1 Pt 1):230-5.
Carbohydrate feeding during prolonged strenuous exercise can delay fatigue.
Coyle EF, Hagberg JM, Hurley BF, Martin WH, Ehsani AA, Holloszy JO.
This study was undertaken to determine whether carbohydrate feeding during exercise can delay the development of fatigue. Ten trained cyclists performed two bicycle ergometer exercise tests 1 wk apart. The initial work rate required 74 +/- 2% of maximum O2 consumption (VO2 max) (range 70-79% of VO2 max). The point of fatigue was defined as the time at which the exercise intensity the subjects could maintain decreased below their initial work rate by 10% of VO2 max. During one exercise test the subjects were fed a glucose polymer solution beginning 20 min after the onset of exercise; during the other they were given a placebo. Blood glucose concentration was 20-40% higher during the exercise after carbohydrate ingestion than during the exercise without carbohydrate feeding. The exercise-induced decrease in plasma insulin was prevented by carbohydrate feeding. The respiratory exchange ratio was unchanged by the glucose feeding. Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects. This effect appeared to be mediated by prevention of hypoglycemia in only two subjects. The exercise time to fatigue for the 10 subjects averaged 134 +/- 6 min (mean +/- SE) without and 157 +/- 5 min with carbohydrate feeding (P less than 0.01).

“Many studies have found that sucrose is less fattening than starch or glucose, that is, that more calories can be consumed without gaining weight. During exercise, the addition of fructose to glucose increases the oxidation of carbohydrate by about 50% (Jentjens and Jeukendrup, 2005).” -Ray Peat, PhD

Br J Nutr. 2005 Apr;93(4):485-92.
High rates of exogenous carbohydrate oxidation from a mixture of glucose and fructose ingested during prolonged cycling exercise.
Jentjens RL, Jeukendrup AE.
A recent study from our laboratory has shown that a mixture of glucose and fructose ingested at a rate of 1.8 g/min leads to peak oxidation rates of approximately 1.3 g/min and results in approximately 55% higher exogenous carbohydrate (CHO) oxidation rates compared with the ingestion of an isocaloric amount of glucose. The aim of the present study was to investigate whether a mixture of glucose and fructose when ingested at a high rate (2.4 g/min) would lead to even higher exogenous CHO oxidation rates (>1.3 g/min). Eight trained male cyclists (VO2max: 68+/-1 ml/kg per min) cycled on three different occasions for 150 min at 50% of maximal power output (60+/-1% VO2max) and consumed either water (WAT) or a CHO solution providing 1.2 g/min glucose (GLU) or 1.2 g/min glucose+1.2 g/min fructose (GLU+FRUC). Peak exogenous CHO oxidation rates were higher (P<0.01) in the GLU+FRUC trial compared with the GLU trial (1.75 (SE 0.11) and 1.06 (SE 0.05) g/min, respectively). Furthermore, exogenous CHO oxidation rates during the last 90 min of exercise were approximately 50% higher (P<0.05) in GLU+FRUC compared with GLU (1.49 (SE 0.08) and 0.99 (SE 0.06) g/min, respectively). The results demonstrate that when a mixture of glucose and fructose is ingested at high rates (2.4 g/min) during 150 min of cycling exercise, exogenous CHO oxidation rates reach peak values of approximately 1.75 g/min.

Substrate interaction during exercise (randle cycle at work):
Can J Appl Physiol. 1998 Dec;23(6):558-69.
The role of glucose in the regulation of substrate interaction during exercise.
Sidossis LS.
Glucose and fatty acids are the main energy sources for oxidative metabolism in endurance exercise. Although a reciprocal relationship exists between glucose and fatty acid contribution to energy production for a given metabolic rate, the controlling mechanism remains debatable. Randle et al.’s (1963) glucose-fatty acid cycle hypothesis provides a potential mechanism for regulating substrate interaction during exercise. The cornerstone of this hypothesis is that the rate of lipolysis, and therefore fatty acid availability, controls how glucose and fatty acids contribute to energy production. Increasing fatty acid availability attenuates carbohydrate oxidation during exercise, mainly via sparing intramuscular glycogen. However, there is little evidence for a direct inhibitory effect of fatty acids on glucose oxidation. We found that glucose directly determines the rate of fat oxidation by controlling fatty acid transport into the mitochondria. We propose that the intracellular availability of glucose, rather than fatty acids, regulates substrate interaction during exercise.

Posted in General.