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Who Needs Electrolytes and Why?

Many people talk about electrolytes but do you have any idea what electrolyte really is? Being among the smallest of chemicals important to a cell’s function, electrolytes are crucial to the manufacturing of energy, the maintenance of membrane stability, the movement of fluids in the body, and a few other jobs, such as contracting a muscle, like the heart.

No Sweat

You know that you’ll taste salt if you lick the back of your hand after jogging or cutting grass on a hot summer day. Sodium is one of sweat’s main ingredients, along with chloride and potassium. All three are carried to the surface of the skin by the water made in sweat glands and the salt stays after the liquid evaporates. The purpose of sweating is regulation of body temperature, which is achieved by the eccrine glands that cover much of the body. An adult can easily sweat two liters an hour (Godek, 2008), up to eight liters a day (Vukasinovic-Vesic, 2015). It’s the evaporation of the water that has the cooling effect. Some animals do not have efficient sweat glands, such as dogs that have to pant to cool down, or hogs that needs to wallow in mud or cool water.

After exercise — or other cause of heavy perspiration — it’s important to restore fluid balance, especially in hot weather when it is easy to get dehydrated. Rehydration occurs only if both water and electrolytes are replaced. The amount of electrolytes lost through sweat varies from person to person. Accurately matching beverage electrolyte intake with loss through sweat is practically impossible. If you are eating at the same time as drinking plain water, this may suffice for rehydration. Otherwise, inclusion of electrolytes is essential.

What Are They and What Do They Do?

In the body, the electrolytes include sodium, potassium, calcium, bicarbonate, magnesium, chloride, and phosphate. Not all are contained — or needed — in an electrolyte replacement beverage. Sodium, the main cation outside the cell, controls total amount of water in the body, regulates blood volume and maintains muscle and nerve function. You need at least 500 mg a day. The suggested upper level is 2300 mg, but most Americans ingest more than 3000. Chloride, also from table salt, is an anion. Found in extracellular fluids, chloride, in the company of sodium, helps to maintain proper fluid balance and pressure of the various fluid compartments.

Potassium is the major cation inside the cell, where its job is to regulate heart beat and blood pressure while balancing the other electrolytes. Because it aids in transmitting nerve impulses, potassium is necessary for muscle contractions, actually the relaxation half of the contraction. Deficiency of potassium is more common than overdose, and may arise from diarrhea or vomiting, with muscle weakness and cramping being symptoms. Intake of potassium is generally much lower than the recommended 4700 mg a day, which is not surprising in light of the deficits in food caused by insulting agricultural practices. Perhaps the most under-appreciated mineral in the nutrient armamentarium is magnesium, not only a constituent of more than three hundred biochemical reactions in the body, but also a role player in the synthesis of both DNA and RNA. As an electrolyte, magnesium supports nerve and muscle function, boosts immunity, monitors heart cadence, stabilizes blood glucose, and promotes healthy bones and teeth. With half the U.S. population deficient, Mg is the orphan nutrient that is able to prevent elevated markers of inflammation (such as CRP), hypertension (It’s called nature’s calcium channel blocker), atherosclerotic vascular disease, migraines, asthma, and colon cancer (Rosanoff, 2012). Supplementation with magnesium is uncertain because absorption is inverse to intake.

Like the others, calcium is involved in muscle contraction and the transmission of nerve messages, but also in blood clotting. Calcium tells sodium to initiate a contraction so that you can pick up a pencil or scratch your nose. In opposition, magnesium tells potassium to let the pencil go or to move your arm back down. Because the heart needs calcium for a strong beat, it will pull the mineral from bone if dietary sufficiency is missing. After calcium, phosphorus — phosphate — is the most abundant mineral in the body. This anion helps to produce energy inside the cell besides being a bone strengthener. It’s a major building block of DNA and the cell membrane. Bicarbonate keeps pH in balance and is important when muscles make lactic acid from work.

Where Can I Get the Electrolytes I Need?

There are scores of electrolyte replacements on the market and entirely too many with sugar or additives. The issue with electrolytes is, in all honesty, that they taste bitter and salty. The fact that sugar is a carbohydrate hinders the processing of a hydration drink because absorption is slowed. That’s what carbohydrates do. Sugar concentrations in many sports drinks are higher than that of body fluid, so will not be readily absorbed. Plain water passes through too fast; carb-laden drinks pass too slowly. Therefore, an electrolyte balanced drink will do the job better and faster. Sodium and potassium, after all, encourage fluid retention and help to reduce urine output.

It is common knowledge that most of us gravitate to sweetness in times of dehydration; saltiness less so. But when you need rehydration, choose the real stuff, BodyBio’s E-lyte and E-lyte Sport, two electrolyte replacements that copy the mineral balance of the body. Elyte may be used as a daily addition to the diet, and is effective to restore homeostasis in times of virus-induced gastrointestinal distress for adults and children, in electrolyte deficit from uncontrolled diabetes and even for restless leg syndrome. When sodium loss is high from exercise, chose Elyte Sport.

References

Coyle EF.
Fluid and fuel intake during exercise.
J Sports Sci. 2004 Jan;22(1):39-55.

Robert W. Kenefick, PhD and Michael N. Sawka, PhD
Hydration at the Work Site
J Am Coll Nutr. October 2007; vol. 26 no. suppl 5: 597S-603S

Meurman JH, Härkönen M, Näveri H, Koskinen J, Torkko H, Rytömaa I, Järvinen V, Turunen R.
Experimental sports drinks with minimal dental erosion effect.
Scand J Dent Res. 1990 Apr;98(2):120-8.

Noble WH, Donovan TE, Geissberger M.
Sports drinks and dental erosion.
J Calif Dent Assoc. 2011 Apr;39(4):233-8.

Sports Med. 2002;32(15):959-71.
Hydration testing of athletes.
Oppliger RA, Bartok C.

Sawka MN, Montain SJ, Latzka WA.
Hydration effects on thermoregulation and performance in the heat.
Comp Biochem Physiol A Mol Integr Physiol. 2001 Apr;128(4):679-90.

Convertino VA, Armstrong LE, Coyle EF, Mack GW, Sawka MN, Senay LC Jr, Sherman WM.
American College of Sports Medicine position stand. Exercise and fluid replacement.
Med Sci Sports Exerc. 1996 Jan;28(1):i-vii.

Rehrer NJ.
Fluid and electrolyte balance in ultra-endurance sport.
Sports Med. 2001;31(10):701-15.

Maughan RJ, Shirreffs SM.
Dehydration and rehydration in competative sport.
Scand J Med Sci Sports. 2010 Oct;20 Suppl 3:40-7

Gal Dubnov-Raza, Yair Lahavb, and Naama W. Constantinic
Non-nutrients in sports nutrition: Fluids, electrolytes, and ergogenic aids
e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism. 6(4); Aug 2011: pp. e217-e222

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Calorie Restriction Extends Lifespan

calorie restrictionCalorie restriction (CR) in animals extends longevity by a considerable margin. Both primary and secondary aging processes are decelerated by limiting foods to those that are high in nutrients and relatively low in calories. Studies on humans are only now in progress, while those in animals have been unfolding for a few years. One of the boons of CR is a lowered core body temperature, which is that at which all physiological activity is most efficient. Not only this, but also fat reduction and consequent cardiac health can defer the foibles and imperfections of old age.

Studies at Washington University (St. Louis, MO) and the U. of California at San Francisco, sponsored in part by the Calorie Restriction Society, have found that” (calorie) restriction in animals seems to be the fountain of youth…” Studies on people may or may not yield the same results, primarily because free-living humans are not accepting of the same externally imposed restrictions as are endured by the animals. Human variables that need to be addressed include alterations in cognitions, behaviors, responses to stressors, and effects on other markers of health. However, humans have shown some of the same “…adaptations that are…involved in slowing primary aging in rats and mice.” Most notable here is a reduction in the inflammatory markers known as C-reactive protein and Tumor Necrosis Factor-alpha.

Primary aging is the gradual and inevitable process of physical deterioration that occurs throughout life.  You know, the aches and pains, the slowed movements, the loss of 20-20 vision, decreased resistance to infections, impaired hearing, and the rest of the baggage.  Secondary aging results from diseases and poor health practices (read lifestyle) that include smoking, torpor, booze and obesity, all of which can contribute to diseases in the first place.

Does CR work in people?  Yes, as long as it is reasonable…and that varies from person to person.  Decreasing calorie intake by only a few hundred can make a significant difference in health and longevity by reducing body fat, lowering blood pressure and cholesterol, and avoiding degenerative diseases, such as diabetes and heart disease.  Don’t forget about lowered body temperature, where the Washington University researchers learned that life expectancy was increased in animals. (Soare, 2011)  Of course, we can’t definitely tell how this affects people because we don’t know when each is programmed to die.  It is such, however, that family history of salubrious long life can be predictive of an individual’s longevity.

You might be interested to know that a nutritional supplement demonstrates an effect that mirrors calorie restriction.  We advise that you not yet jump for joy without the realization that this needs to be approached sensibly, which means being attentive to calorie intake. You can’t go wild on doughnuts, white flour bagels, ice cream and other culinary nonsense. You see, the mechanism behind calorie restriction’s success is not completely understood, but it is presumed that a protein called sirtuin is responsible for control of the aging process, and that CR directs the activity of sirtuin. Part of the aging procedure involves cellular stress, particularly in the mitochondria, the power plants of the cell that make energy. If we can slow down oxidation by ramping up the mitochondria’s defense mechanisms and simultaneously inhibiting the attack of reactive oxygen species, then we might be able to stave off the pangs of aging.  How do we do that without restriction of calories?  What supplement is held in such high regard? Resveratrol, the red wine polyphenol!

Independent of each other, Zoltan Ungvari (2009) and Thimmappa Anekonda (2006) discovered that resveratrol may have therapeutic value in the treatment of metabolic and neuronal diseases, based at least partially on the activity of sirtuin.  What is known about resveratrol’s mechanism of action is that it encourages the sirtuin homologue SIRT1 to ply its trade as a cellular regulator, where it slows down metabolism and any stimulatory reactions to environmental toxins, thus placing an organism into a defensive state so it can survive adverse circumstances.  Tobacco smoke-induced oxidative stress even becomes minimized.

We are individuals with different needs and responses to interventions, whether dietary or medical.  You will differ in your response to calorie restriction from your twin. You will differ in your response to resveratrol, if that is the route you choose.  But it seems more than likely you will experience a strengthened immune system, heightened energy, a healthier reproductive system, increased stamina…and looser trousers.

References

Exp Gerontol. 2007 Aug;42(8):709-12. Epub 2007 Mar 31.
Caloric restriction in humans.
Holloszy JO, Fontana L.

Toxicol Pathol. 2009;37(1):47-51. Epub 2008 Dec 15.
Caloric restriction and aging: studies in mice and monkeys.
Anderson RM, Shanmuganayagam D, Weindruch R.

Aging (Albany NY). 2011 Apr;3(4):374-9.
Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans.
Soare A, Cangemi R, Omodei D, Holloszy JO, Fontana L.

Free Radic Biol Med. 2011 Apr 22. [Epub ahead of print]
The controversial links among calorie restriction, SIRT1, and resveratrol.
Hu Y, Liu J, Wang J, Liu Q.

Am J Physiol Heart Circ Physiol. 2008 Jun;294(6):H2721-35. Epub 2008 Apr 18.
Vasoprotective effects of resveratrol and SIRT1: attenuation of cigarette smoke-induced oxidative stress and proinflammatory phenotypic alterations.
Csiszar A, Labinskyy N, Podlutsky A, Kaminski PM, Wolin MS, Zhang C, Mukhopadhyay P, Pacher P, Hu F, de Cabo R, Ballabh P, Ungvari Z.

Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1876-81. Epub 2009 Sep 11.
Resveratrol attenuates mitochondrial oxidative stress in coronary arterial endothelial cells.
Ungvari Z, Labinskyy N, Mukhopadhyay P, Pinto JT, Bagi Z, Ballabh P, Zhang C, Pacher P, Csiszar A.

Brain Res Rev. 2006 Sep;52(2):316-26.
Resveratrol–a boon for treating Alzheimer’s disease?
Anekonda TS.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

B Vitamins And Energy

happygirlA considerable fraction of the general population reports using one or more vitamin supplements. Reasons include fighting stress and tiredness, and improving mental function. Until recent decades, there was only modest support from the allopathic community that supplements could render any benefit.

Using questionnaires that tracked mood states, levels of perceived stress, and general health, researchers at the Brain Performance and Nutrition Center of Northumbria University, in the UK, discovered a relationship between vitamin supplement intake and overall performance as related to fatigue, mood, and feelings of well-being.  High-dose B-vitamin supplementation “…led to significant improvements in ratings…” in the vigor subscale of the subjective assessments.  (Kennedy. 2010)  Cognitive and executive function improved in parallel fashion as a result of physical reinvigoration.  The authors concluded that, “Healthy members of the general population may benefit from augmented levels of vitamins/minerals via direct dietary supplementation.”

When questioned about the rationale behind supplementation, the answer should list poor dietary choices, processed food, depleted soil, chemical fertilizers and biocides, synthetic additives, malabsorption, careless food preparation, haphazard storage and shipping, and the use of medications and alcohol.  Feel free to add a few.

Because the vitamin B complex is water-soluble and relatively delicate, it responds to whatever insults include boiling or steaming, heat, and prolonged exposure to light.  Not only that, but the complex is vulnerable to the aerosol pesticides used by the produce brokers who store foods prior to over-the-road shipping.

The B vitamins comprise a group that plays a vital role in cell metabolism.  They were once thought to be a single vitamin, but later were found to have distinct functions in the body, although they coexist in the same foods.  They received their numbers based on the order in which they were isolated.  In conjunction, the B complex is helpful to combat most symptoms and causes of conditions such as depression, stress, coronary heart disease and other cardiovascular concerns.  Working together, the B’s are able to support metabolic homeostasis, the immune system, and the nervous system, while simultaneously maintaining healthy skin, muscle tone, and promoting cell growth and division.  Neat, eh?

The water-solubility of B vitamins helps them disperse throughout the body, but also means that they need replacement every day.  Excess is excreted in urine, which explains the dark yellow-orange color that occurs after taking the supplement.  (That would be riboflavin, B2.)  One of the B group’s claims to fame is its role in the burning of carbohydrates for energy.  If this metabolic purpose is impaired, fatigue strikes, often with a vengeance.  Thiamine in particular, or one of its derivatives, is known to improve energy metabolism during physical fatigue (Nozaki.  2009), and is a reputed activator of carbohydrate processing (Masuda. 2010).

If taken as an isolated supplement, a singular B vitamin may act as a drug, even though there are few adverse reactions, with the possible exception of very high-dose pyridoxine (B6) being associated with sensory neuropathy.  (Scott. 2008)  Alcohol of any type, even the comparatively innocuous beer, will result in a net deficit of the B vitamins.

The stress that characterizes the Western lifestyle takes a physical, as well as psychological, toll.  The mood changes and testiness that follow physical exhaustion are shared with family and friends.  B-vitamin supplementation has shown itself to attenuate the causes and effects, either one at a time or together.  (Stough. 2011)  People with the lowest levels of the B vitamins in their diets usually have the poorest memories and cognitive abilities.  Those with gastric dysfunction, such as that characterized by low stomach acid or deficit of intrinsic factor, will absorb the least vitamin B12 from their foods, so are well-advised to supplement.

The interaction of the body’s chemistry is complex.  We need vitamin B2 to metabolize B6.  We need B6, B12, and folate to clear homocysteine, a marker for cardiac involvement.  But taking an isolated B vitamin without the rest of the family upsets the apple cart.  The RDA is a poor guide because it recommends only that dose of a nutrient that will prevent deficiency disease, such as beriberi or pellagra.  Meeting with a health care professional can help you to figure what’s what.

References

Kennedy DO, Veasey R, Watson A, Dodd F, Jones E, Maggini S, Haskell CF.
Effects of high-dose B vitamin complex with vitamin C and minerals on subjective mood and performance in healthy males.
Psychopharmacology (Berl). 2010 Jul;211(1):55-68.

SUPPORTING ABSTRACTS
Nozaki S, Mizuma H, Tanaka M, Jin G, Tahara T, Mizuno K, Yamato M, Okuyama K, Eguchi A, et al
Thiamine tetrahydrofurfuryl disulfide improves energy metabolism and physical performance during physical-fatigue loading in rats.
Nutr Res. 2009 Dec;29(12):867-72.

Masuda H, Matsumae H, Masuda T, Hatta H.
A thiamin derivative inhibits oxidation of exogenous glucose at rest, but not during exercise.
J Nutr Sci Vitaminol (Tokyo). 2010;56(1):9-12.

Scott K, Zeris S, Kothari MJ.
Elevated B6 levels and peripheral neuropathies.
Electromyogr Clin Neurophysiol. 2008 Jun-Jul;48(5):219-23.

Stough C, Scholey A, Lloyd J, Spong J, Myers S, Downey LA.
The effect of 90 day administration of a high dose vitamin B-complex on work stress.
Hum Psychopharmacol. 2011 Sep 8.

Bassett JK, Hodge AM, English DR, Baglietto L, Hopper JL, Giles GG, Severi G.
Dietary intake of B vitamins and methionine and risk of lung cancer.
Eur J Clin Nutr. 2011 Aug 31.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Athletes And Fuel – Feeling Fuelish?

runnerWhen it comes to fueling an athlete, there had been as many approaches as there are sports to play. Several respected bodies have merged philosophies to incorporate and publicize nutritional recommendations that can be adapted to most athletic pursuits. There is much about diet that is common sense, but the habits cultivated from family traditions just might fly in the face of that. Ethnic or regional cuisines may feature foods that upset the balance of both macro- and micro-nutrient intake. There is no doubt that the physiological needs of serious athletes have to be the first consideration in finding and combining the right fuels.

Optimal nutrition is mandatory if an athlete wants to realize his full potential during an event. Not only performance, but also recovery, is enhanced by food intake. A position paper issued jointly by the American Dietetic Association, the Dietitians of Canada, and the American College of Sports Medicine, states, “Energy and macronutrient needs, especially carbohydrate and protein, must be met during times of high physical activity to maintain body weight, replenish glycogen stores, and provide adequate protein to build and repair tissue,” continuing that, “Adequate food and fluid should be consumed before, during, and after exercise to help maintain blood glucose concentration during exercise, maximize exercise performance, and improve recovery time. Athletes should be well hydrated before exercise and drink enough fluid during and after exercise to balance fluid losses.”  (Rodriguez. 2009)

Your performance will be affected by genetics (over which you have zero control), training (over which you have total control), and diet (ditto). If you fail to consume enough energy, the body will use both fat and lean tissue as fuel. Strength and endurance will then suffer, and the immune system and endocrine glands will pay a stiff price. If you’re trying to lose weight, you still have to pay attention to energy intake. It takes calories to burn calories. This is especially true for women, who may experience amenorrhea and osteoporosis if they aren’t careful.

You can store about 400 to 600 grams of carbohydrates, or 1600 to 2400 calories’ worth. These glycogen stores can be burned in 1 ½ to 2 hours, after which fat is mobilized and you “hit the wall.”  You don’t want to get more than about 60 grams of carbohydrates (CHO) an hour while in a marathon, for example, or you might cramp, but your daily intake could be 5-7 grams per kilogram a day (about 3 grams per pound) for moderate exercise that lasts less than 1 ½ hours. For more intense exercise, like that marathon or a cycling event, that lasts more than a couple hours, you’ll need 8-12 grams of CHO a day per kilogram of body weight. Do this prior to, not during, an event. (Burke. 2011)  You might as well convert your body weight to kilograms now. Divide pounds by 2.2 and you’ll have it.

Eating before an event will enhance performance compared to fasting. Common sense says to eat lesser amounts an hour before an event than you would eat four hours ahead of a strenuous workout. Traditional wisdom says that consuming up to 1 gram of CHO per kg is fine one hour before the start; Consuming 4.5 gm/kg is O.K. four hours before. Take it easy on the fiber and fat, though, or you might experience GI distress. During practice sessions is the time to experiment with different foods to come up with effective refueling strategies that fit you.

Protein intake depends on the type and duration of exercise. 0.8 gm/kg/day is fine for the general public, but you’ll probably need more. An endurance athlete will need 1.2-1.4 gm/kg/day, while a weight lifter needs up to 1.7 gm/kg/day. More than 2.0 mg/kg can tax the kidneys and won’t make much physiological difference. It’s important to get protein right after exercise. There’s a 15 minute to 2-hour window during which muscle balance can be increased and muscle tissue can be repaired. Protein supplements are nothing more than a convenience. Besides, such supplements can become delivery systems for things you neither want nor need, like steroids and other illicit substances.

At the end of your performance you need to refill your buckets. That’s called recovery. Adding protein to your carbohydrate intake at a ratio of 3:1 or 4:1, CHO:Pro, can enhance recovery. (Ivy. 2001)  We know of a few marathoners who eat tuna sandwiches with chocolate milk. You might opt for a bowl of Cheerios and a banana, or a yogurt-fruit smoothie and pretzels. Listen to your body. You might end with steak and potatoes. Lemon meringue pie, and carrot cake, and oatmeal cookies, and…  Dream on….PSST, you can do without the sugar.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Off-Season Fitness

group-fitnessThe off-season is the time for a well-deserved break, yet it might be viewed as a chance to get ready for next season.  As each day passes you’ll lose the fitness that you worked so hard to get if you fail to do something to keep it.  There’s no need to go to extremes, though.  Looking at the off-season as part of your overall training cycle will keep you focused on maintaining the fitness level you need to get the job done.  Nutrition is part of that plan.

For a high-school athlete, a summer with no training is a missed opportunity that guarantees a hard return to the rigors of structured sports.  Just as during the season, it’ll help to set goals, such as reducing body fat, adding muscle mass, maintaining aerobic fitness, improving speed, and developing techniques specific to your sport.  Any attempt to alter body composition must be planned over a significant time period, making it absolutely necessary to start a program weeks before the season opens.  It isn’t safe to increase or decrease a body component in a short time.  Because of this, be careful to avoid fads and misinformation from the non-credentialed sources that pop up on the internet and from friends of friends’ friends.

Since you’re on your own during the off-season, or are hangin’ with the guys at best, you’ll be separated from the atmosphere that lends itself to motivation and drive.  If you’re totally idle, you’re detraining, and that’ll reverse the training-induced physiological adaptations you need to excel at your sport.  You’ll lose strength, power, endurance, and aerobic power and capacity.  Within days or only a few weeks you’ll see these qualities diminish.  If you‘re a runner, fifteen days’ inactivity will award you with a 25% decrease in performance.  (Houston et al. 1979)  If you’re a strength-trained athlete, strength or power will decline almost immediately after the cessation of training.  (Kraemer. 2002)  Since you’re on your own, you’re also unlikely to train as you would under supervision, and the results will show it.  (Mazzetti. 2000)  It came as a surprise, however, when researchers announced that if frequency of training is reduced by two thirds, endurance capacity can be maintained for as long as three months.  (Hickson. 1982)  (Neufer. 1987)  So, now you have some slack time.

Simple things like walking, taking the stairs instead of the escalator, and even stretching contribute to your fitness plan.  And there’s nothing wrong with cross-training.  But there are some things you can’t do all at once, like lose weight and increase muscle mass.  These need to be tackled separately, mostly because the body isn’t very adept at doing both at the same time.  Lose the weight, and then build the muscle.

The off-season doesn’t mean you can eat what you want.  The high-calorie energy bars that got you through the season won’t do you any good if you don’t burn ‘em.  You still need to keep an eye on calories in and calories out, as well as on hydration.  Your nutrition goals will include maintaining the physique that is suited to your sport, so balancing energy needs is important.  This is an individual venture that requires a different carbohydrate to protein ratio from that during the active season, particularly if your off-season training sessions are of shorter duration.  Once you find your competition weight, stick to it, even if you have to monitor yourself a few times a week to find any changes you didn’t cause on purpose.  (Smith. 1984)  If you’re trying to lose weight, be watchful not to over-restrict your eating.  Sports dietitians are available to help you with this.  It might be worth your while to sit down with a pencil and paper and figure out how many calories you need to train and how many you need for normal body functions, and work from there.  If you’re trying to drop a few pounds, keep in mind that you need about 30 calories of energy per kilogram of lean body mass to keep you going.  Otherwise you risk metabolic and hormonal insult, and if you’re a girl, you need to watch for menstrual disorders.

When it comes to protein intake, the total amount is not as important as the timing.  Consuming protein before and right after a session will enhance protein synthesis and net protein balance.  1.2–1.6 grams per kilogram of body mass will serve you well in both endurance and strength.   If you lay off completely for a few weeks, you can lower those numbers to 0.8–1.0.  (Colombani. 2011)

Different activities have different fuel needs, so carbohydrate intake is not one-size-fits-all.  For light training, you need about 5 grams of carbohydrate per kilogram of body mass, while heavier, prolonged, or strenuous work that demands optimal synthesis of glycogen might call for 7–10 grams per kilogram.  You’ll need the higher amounts for events that last longer than one hour.  You should be able to fine tune intake according to your specific needs.  (Burke. 2011)

The off-season needn’t be a season off.  A serious athlete will take care of business so that getting back into the groove is not a monumental feat.  In light of this, it’s O.K. to have a cheat day once in a while, where you can eat pizza on a Friday night, or a bowl of ice cream, or a chocolate éclair after a meal.  But don’t do all these at the same time.  Nine to thirteen servings of fruits and vegetables a day, even during the off-season, will supply nutrient density to help offset prandial sins.  That sounds like a lot, but really isn’t.  Besides, eating this much produce can displace the potential to eat empty calories during the off-season.

Staying properly hydrated is a matter of common sense, but that faculty is ignored too often.  Losing 2% of body weight to sweat impairs performance on the field or in the gym.  More than that risks serious after effects that may include hospitalization. On the other hand, overhydration will dilute electrolytes and backfire.  Don’t drink at rates that are greater than sweat losses.  You might actually gain weight during the competition period.  Get hydrated before an event with 8-16 ounces of fluid a couple of hours prior.  Drink ½-1 cup every fifteen to twenty minutes, if you can, during an event.  Afterwards, replace any fluids you have lost at a rate of about two cups for every pound of body weight lost.  If you’re not exercising regularly, you still need three liters—or more—of water a day, some of which comes from food.  Use it or lose it.

References

Burke LM, Hawley JA, Wong SH, Jeukendrup AE.
Carbohydrates for training and competition.
J Sports Sci. 2011 Jun 8:1-11.

Colombani PC, Mettler S.
Role of dietary proteins in sports
Int J Vitam Nutr Res. 2011 Mar;81(2):120-4.

R. C. Hickson, C. Kanakis Jr ,J. R. Davis, A. M. Moore, and S. Rich
Reduced training duration effects on aerobic power, endurance, and cardiac growth
Journal of Applied Physiology July 1982 vol. 53 no. 1 225-229

Holway FE, Spriet LL.
Sport-specific nutrition: Practical strategies for team sports.
J Sports Sci. 2011 Aug 11. [Epub ahead of print]

Houston ME, Bentzen H, Larsen H.
Interrelationships between skeletal muscle adaptations and performance as studied by detraining and retraining.
Acta Physiol Scand. 1979 Feb;105(2):163-70.

Kraemer WJ, Koziris LP, Ratamess NA, Hakkinen K, TRIPLETT-McBRIDE NT, Fry AC, Gordon SE, Volek JS, French DN, Rubin MR, Gomez AL, Sharman MJ, Michael Lynch J, Izquierdo M, Newton RU, Fleck SJ.
Detraining produces minimal changes in physical performance and hormonal variables in recreationally strength-trained men.
J Strength Cond Res. 2002 Aug;16(3):373-82.

Mazzetti SA, Kraemer WJ, Volek JS, Duncan ND, Ratamess NA, Gómez AL, Newton RU, Häkkinen K, Fleck SJ.
The influence of direct supervision of resistance training on strength performance
Med Sci Sports Exerc. 2000 Jun;32(6):1175-84.

Montain SJ.
Hydration recommendations for sport 2008.
Curr Sports Med Rep. 2008 Jul-Aug;7(4):187-92.

Mujika I, Padilla S.
Detraining: loss of training-induced physiological and performance adaptations. Part I: short term insufficient training stimulus.
Sports Med. 2000 Aug;30(2):79-87.

Mujika I, Padilla S.
Muscular characteristics of detraining in humans.
Med Sci Sports Exerc. 2001 Aug;33(8):1297-303.

Neufer PD, Costill DL, Fielding RA, Flynn MG, Kirwan JP
Effect of reduced training on muscular strength and endurance in competitive swimmers.
Med Sci Sports Exerc. 1987 Oct;19(5):486-90.

Smith NJ.
Weight control in the athlete.

Clin Sports Med. 1984 Jul;3(3):693-704.

Staron RS, Hagerman FC, Hikida RS
The effects of detraining on an elite power lifter. A case study.
J Neurol Sci. 1981 Aug;51(2):247-57.

Taaffe DR, Marcus R
Dynamic muscle strength alterations to detraining and retraining in elderly men.
Clin Physiol. 1997 May;17(3):311-24.

Willis KS, Peterson NJ, Larson-Meyer DE.
Should we be concerned about the vitamin D status of athletes?
Int J Sport Nutr Exerc Metab. 2008 Apr;18(2):204-24.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Sleep and Weight

sleeping-manAhh, yes, that state of rest for body and soul.  It’s the time when will power and consciousness are suspended, and when body functions are mostly in neutral. Most sleep scientists agree that sleep has considerable value as a recuperative and adaptive function in humans.   Because it takes work for the body to maintain a constant temperature in an environment with temperature ranges, the eight-hour respite affords a chance to reconstitute cells and tissues.  While the body slows down, the brain, on the other hand, revs up its metabolic activity during the REM phase of sleep to get ready for the input of the next day.  Complicated stuff, for sure.

The negative consequences of too little sleep can rattle your chain with fanfare.  Falling asleep at the wheel is scary.  Falling off the pew in church is embarrassing.  Dozing during a business call gets expensive.  And being cranky all day gets you no favors.  But guess what.  Lack of sleep can make you fat, too.  Try to figure that out, since nobody eats when they’re asleep.  Do they?

Just because body functions slow down, it doesn’t mean they stop.  Hormones and other body chemicals are still at work.  Two of those, ghrelin and leptin, are responsible for turning appetite on and off, respectively.  Sleep deprivation seems to crank up the ghrelin and stimulate appetite.  When that happens, you crave more food while losing the sensitivity—or even the common sense—to know when to stop eating.  This problem could well be a circuitous matter:  does fatness cause lack of sleep or is it the other way around, or do they share a common factor?  Hmm.  Michael Breus, sleep researcher extraordinaire, addresses this conundrum in his recently published, “The Sleep Doctor’s Diet Plan:  Lose Weight Through Better Sleep” (Rodale, 2011).  And Dr. Marie-Pierre St-Onge, researcher at the New York Obesity Nutrition Research Center at St. Luke’s-Roosevelt Hospital, adds her expertise by pointing out that sleep-deprived people burn the same number of calories during the day as sound sleepers, but, she adds, eat about three hundred more calories a day.  Since there are 3500 calories in a pound, a person will add that pound to his repertoire in a little less than two weeks (St-Onge, 2011)

The interest in the association of lousy sleep to weight problems is international.  Even in Japan, there’s a St. Luke’s Hospital.  Here, doctors checked out more than 21,000 middle-aged guys’ sleep habits and compared them to individual body mass index, finding that the variability of sleep duration is related to weight gain.  And these participants thought that 6 hours’ sleep was enough (Kobayashi, 2012).  Guess they were wrong.  A year earlier, the same docs at the same hospital compared ~7-hour sleepers to ≤5-hour sleepers, and found weight gain and obesity in the deprived group.  It was interesting to note that there was little difference between the 7-hour and 8-hour subjects (Kobayashi, 2011).  The kicker in the 2011 study is that the investigators also found metabolic syndrome to be related to poor sleep (Kobayashi, Takahashi, et al 2011).

In experimentally-induced sleep loss, insulin sensitivity decreases without compensation in beta-cell function, resulting in impaired glucose tolerance and increased risk for diabetes.  Sleep loss down-regulates leptin function, lowers satiety, and up-regulates the appetite enhancing ghrelin.  Increased appetite = increased food intake=weight gain  (Morselli, 2010) (Chamorro, 2011).  Sleep fragmentation—waking every couple hours—causes daytime sleepiness (Mavanji, 2012). We need a study to show that?   In the valiant effort to revitalize, we turn to sugary foods in the hope they’ll provide bursts of energy lasting long enough to get us through the rest of the day.  Empty calories here.  And the energy high is soon followed by an almost audible crash.

With all the studies being performed in this area, you’d think somebody would be working on a remedy.  Maybe we already have one, but don’t know it.  Have you spoken to your doctor about poor sleep?  If you’d rather do it alone, consider a few simple steps.  Go to bed at the same time every night.  The body needs to know when to go to sleep.  Exercise a little bit every day.  That’ll reduce anxiety, one of the biggest reasons for poor sleep.  But don’t do it just before bed.  Do it a few hours beforehand.  If you’re a worrier, keep a journal.  That helps to identify things that aren’t likely to happen, anyway, so you don’t have to worry about them in the first place.  Try not to delay what needs to be done to prepare for the next day.  You’ll only add to the worry list.  Coffee will try to keep you awake for several hours after the last cup in the afternoon, so don’t drink any after, say, 2 or 3 o’clock.  Alcohol will not improve sleep.  It might make you fall asleep faster, but almost certainly will interrupt restorative sleep.  In the AM, drink water before anything else, and get fifteen minutes of sunlight to help reset your circadian clock.

Although the link between sleep loss and weight gain is convincing, the exact science behind the connection is to be determined.  You can always stay up all night and try to catch the leather fairy cutting your belt a little shorter.  Or you can try an alternative sleep aid, such as valerian, melatonin, or a hops sachet under your pillow.  But check with a healthcare professional before you embark.

References

Chamorro RA, Durán SA, Reyes SC, Ponce R, Algarín CR, Peirano PD.
[Sleep deprivation as a risk factor for obesity].  [Article in Spanish]
Rev Med Chil. 2011 Jul;139(7):932-40.

Knutson KL.
Does inadequate sleep play a role in vulnerability to obesity?
Am J Hum Biol. 2012 Jan 24. doi: 10.1002/ajhb.22219. [Epub ahead of print]

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Relation between metabolic syndrome and sleep duration in Japan: a large scale cross-sectional study.
Intern Med. 2011;50(2):103-7. Epub 2011 Jan 15.

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Association between weight gain, obesity, and sleep duration: a large-scale 3-year cohort study.
Sleep Breath. 2011 Sep 3. [Epub ahead of print]

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Association between weight gain, obesity, and sleep duration: a large-scale 3-year cohort study.
Sleep Breath. 2011 Sep 3. [Epub ahead of print]

Kobayashi D, Takahashi O, Shimbo T, Okubo T, Arioka H, Fukui T.
High sleep duration variability is an independent risk factor for weight gain.
Sleep Breath. 2012 Feb 22. [Epub ahead of print]

Mavanji V, Billington CJ, Kotz CM, Teske JA.
Sleep and obesity: a focus on animal models.
Neurosci Biobehav Rev. 2012 Mar;36(3):1015-29. Epub 2012 Jan 16.

Morselli L, Leproult R, Balbo M, Spiegel K
Role of sleep duration in the regulation of glucose metabolism and appetite.
Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):687-702.

Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.
Insufficient sleep undermines dietary efforts to reduce adiposity.
Ann Intern Med. 2010 Oct 5;153(7):435-41.

Patel SR, Malhotra A, White DP, Gottlieb DJ, Hu FB.
Association between reduced sleep and weight gain in women.
Am J Epidemiol. 2006 Nov 15;164(10):947-54. Epub 2006 Aug 16.

St-Onge MP, Roberts AL, Chen J, Kelleman M, O’Keeffe M, RoyChoudhury A, Jones PJ.
Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals.
Am J Clin Nutr. 2011 Aug;94(2):410-6.

St-Onge MP, McReynolds A, Trivedi ZB, Roberts AL, Sy M, Hirsch J.
Sleep restriction leads to increased activation of brain regions sensitive to food stimuli.
Am J Clin Nutr. 2012 Apr;95(4):818-24.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Why Bother Exercising?

lower-back-painIn our earnest attempts to maintain physical fitness and overall wellness, we occasionally overdo it.  Strengthening the muscles and the cardiovascular system, fine tuning athletic skills for a particular sport, trying to lose weight, or only having fun, humans have forgotten the concept of moderation.  So have couch potatoes, but that’s another story.  Well-orchestrated workouts yield benefits beyond six-pack abs and improved self-image.  They can boost immunity, practically eliminate Type 2 diabetes, improve mental health, and even prevent depression (Colberg, 2012) (Jazaieri, 2012) (Callaghan, 2004) (Venjatraman, 1997).

Both aerobic and anaerobic exercises are good for the heart. Aerobic improves the oxygen system and increases cardiac volume; anaerobic works to improve cardiac muscle strength. Not everyone benefits equally from exercise, though. Genes, diet, and testosterone have significant impact on exercise outcomes, especially in resistance training that anticipates muscle hypertrophy (Brutsaert, 2006). In aerobic exercise, glycogen is broken down to get glucose, which reacts with oxygen to produce carbon dioxide and water while producing energy. If there are no carbohydrates available for this process, fat is used, in which case the process slows down and performance declines. This gradual switch to fat as fuel results in “hitting the wall.” Where glycogen is burned without oxygen, there is anaerobic exercise, an inefficient process that makes the athlete “hit the wall” sooner. Short bursts of intense exertion are characteristic of this type of exercise.

Hey, That Hurt!

In either of these ventures, muscle needs to recover. And tomorrow morning you’ll discover muscle in places you didn’t know existed. Recovery time should be built into an exercise regimen, for this is the time the body adapts to the stress it just endured, and it reaps the benefits of the training. This is where energy stores are replenished and damage control gets to work. Then, there’s the fluid loss that needs to be addressed.  Overtraining without recovery can cause malaise, depressed affect, and increased risk of injury (Vetter, 2010) (Szovak, 2012).

Active recovery, or short-term, is that which occurs in the hours right after a workout, a time to perform low-intensity cool-down activities. This could continue into the next day.  Energy stores need to be rebuilt now to maximize protein synthesis, to prevent muscle breakdown and to increase muscle size. This is the time for the branched-chain amino acids (BCAA), leucine, isoleucine, and valine, three essential amino acids that share a common membrane transport system and account for almost thirty-five percent of the amino acids in muscle proteins.  Since muscle mass in a human is about forty percent of body weight, the reserve of BCAA’s is sizeable. Not only are BCAA’s helpful in recovery, but also they have a place in decreasing muscle soreness if used before a strenuous workout ( Shimomura, 2006). Leucine alone, consumed during steady exercise, was found to improve muscle protein synthesis during recovery (Pasiakos, 2011) (Blomstrand, 2006). Differing from short-term, long-term recovery is built into seasonal exercise programs and includes cross training, modified workouts, and changes in intensity or time.

Recovery?  How? 

During recovery it’s important to restock the stores of nutrients that were sacrificed to performance. You have to repair and recondition muscle. After endurance exercise, like running or cycling, glycogen is the most important factor in determining recovery time, and for this carbohydrates are required. One gram of carbohydrate per kilogram of body mass per hour is needed for recovery. That’s 68 grams for a 150-pound person. Adding protein at this time, at a ratio of 1 to 4, protein to carbs, results in a synergistic increase in insulin secretion that can possibly accelerate glycogen re-synthesis (Betts, 2010) (Beelen, 2010). It’s long been established that consuming carbohydrates and protein during the early phases of recovery plays an important part in subsequent performance.  Start eating within fifteen minutes to two hours after the game. Look for a quarter gram of protein per pound of body weight right away. More than one gram per pound could tax the kidneys.

Electrolyte replacement is vital to overall health as well as to athletic performance.  In this matter, one size does not fit all.  Instead, the factors that contribute to electrolyte and fluid disturbance need to be considered. The weather, prior hydration status, diet, genetics and physiology play a role in determining needs. Don’t rely on thirst to tell you when to drink.  Losing two percent of body weight to sweat begins dehydration; four percent will probably hospitalize you. It’s prudent to weight yourself beforehand, and to drink 24 ounces per pound of weight lost afterward. During the workout, try to get 20 – 40 ounces of fluid an hour. One cup every fifteen minutes is a start. You don’t want to use an electrolyte that contains sugar because that’ll affect the body’s ability to absorb electrolytes. Sodium is the first electrolyte lost to heavy sweating, so it needs replacement right away to prevent dehydration (Shirreffs, 2011) because it helps to retain water. Another benefit of sugarless electrolytes is that they stimulate thirst, so you will drink during a workout.  Prehydrating with an electrolyte at a rate of about one ounce( of diluted product if concentrated) for each ten pounds of body weight, starting a few hours before an event, will enhance fluid absorption during the game.

Anything Else?

Yep. Stretching after an event can assist recovery and help you cool down. Rest never hurts, and occasionally really helps. Getting a rub down improves blood flow; ice is nice.  Then there’s the alternating hot and cold shower. The theory behind this is that repeated constriction and dilation of blood vessels helps to push toxins out. You’ll see plenty of debate about this. Saving the best for last, we have sleep. You heal during sleep. You produce growth hormones.  Loss of sleep diminishes peak power during exercise, partly because it lowers maximum heart rate. It harms coordination and may adversely affect body temperature. When else can you dream about certain victory?

Referenes

Beelen M, Burke LM, Gibala MJ, van Loon L JC.
Nutritional strategies to promote postexercise recovery.
Int J Sport Nutr Exerc Metab. 2010 Dec;20(6):515-32.

Betts JA, Williams C.
Short-term recovery from prolonged exercise: exploring the potential for protein ingestion to accentuate the benefits of carbohydrate supplements.
Sports Med. 2010 Nov 1;40(11):941-59.

Blomstrand E, Eliasson J, Karlsson HK, Köhnke R.
Branched-chain amino acids activate key enzymes in protein synthesis after physical exercise.
J Nutr. 2006 Jan;136(1 Suppl):269S-73S.

Brutsaert TD, Parra EJ.
What makes a champion? Explaining variation in human athletic performance.
Respir Physiol Neurobiol. 2006 Apr 28;151(2-3):109-23. Epub 2006 Jan 30.

Burke LM, Hawley JA, Ross ML, Moore DR, Phillips SM, Slater GR, Stellingwerff T, Tipton KD, Garnham AP, Coffey VG.
Preexercise Aminoacidemia and Muscle Protein Synthesis after Resistance Exercise.
Med Sci Sports Exerc. 2012 May 22. [Epub ahead of print]

Callaghan P.
Exercise: a neglected intervention in mental health care?
J Psychiatr Ment Health Nurs. 2004 Aug;11(4):476-83.

Colberg SR.
Physical activity: the forgotten tool for type 2 diabetes management.
Front Endocrinol (Lausanne). 2012;3:70. Epub 2012 May 17.

Francis KT.
Effect of water and electrolyte replacement during exercise in the heat on biochemical indices of stress and performance.
Aviat Space Environ Med. 1979 Feb;50(2):115-9.

Howarth KR, Moreau NA, Phillips SM, Gibala MJ.
Coingestion of protein with carbohydrate during recovery from endurance exercise stimulates skeletal muscle protein synthesis in humans.
J Appl Physiol. 2009 Apr;106(4):1394-402. Epub 2008 Nov 26.

Ivy JL.
Dietary strategies to promote glycogen synthesis after exercise.
Can J Appl Physiol. 2001;26 Suppl:S236-45.

Jazaieri H, Goldin PR, Werner K, Ziv M, Gross JJ.
A Randomized Trial of MBSR Versus Aerobic Exercise for Social Anxiety Disorder.
J Clin Psychol. 2012 May 23. doi: 10.1002/jclp.21863. [Epub ahead of print]

Jentjens R, Jeukendrup A.
Determinants of post-exercise glycogen synthesis during short-term recovery.
Sports Med. 2003;33(2):117-44.

Lunn WR, Pasiakos SM, Colletto MR, Karfonta KE, Carbone JW, Anderson JM, Rodriguez NR.
Chocolate milk and endurance exercise recovery: protein balance, glycogen, and performance.
Med Sci Sports Exerc. 2012 Apr;44(4):682-91.

Pasiakos SM, McClung HL, McClung JP, Margolis LM, Andersen NE, Cloutier GJ, Pikosky MA, Rood JC, Fielding RA, Young AJ.
Leucine-enriched essential amino acid supplementation during moderate steady state exercise enhances postexercise muscle protein synthesis.
Am J Clin Nutr. 2011 Sep;94(3):809-18. Epub 2011 Jul 20.

Reitelseder S, Agergaard J, Doessing S, Helmark IC, Lund P, Kristensen NB, Frystyk J, Flyvbjerg A, Schjerling P, van Hall G, Kjaer M, Holm L.
Whey and casein labeled with L-[1-13C]leucine and muscle protein synthesis: effect of resistance exercise and protein ingestion.
Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E231-42. Epub 2010 Nov 2.

Shimomura Y, Yamamoto Y, Bajotto G, Sato J, Murakami T, Shimomura N, Kobayashi H, Mawatari K.
Nutraceutical effects of branched-chain amino acids on skeletal muscle.
J Nutr. 2006 Feb;136(2):529S-532S.

Shirreffs SM, Sawka MN.
Fluid and electrolyte needs for training, competition, and recovery.
J Sports Sci. 2011;29 Suppl 1:S39-46.

Szivak TK, Hooper DR, Kupchak BK, Apicella JM, Saenz C, Maresh CM, Denegar CR, Kraemer WJ.
Adrenal Cortical Responses to High Intensity, Short Rest, Resistance Exercise in Men and Women.
J Strength Cond Res. 2012 May 3. [Epub ahead of print]

Venjatraman JT, Fernandes G.
Exercise, immunity and aging.
Aging (Milano). 1997 Feb-Apr;9(1-2):42-56.

Vetter RE, Symonds ML.
Correlations between injury, training intensity, and physical and mental exhaustion among college athletes.
J Strength Cond Res. 2010 Mar;24(3):587-96.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Sleep Deprivation may Lead to Impaired Insulin Response in Fat Cells

insomniaInsulin response? Huh? It’s just what it says, the way the body responds to insulin and the challenges that excite it in the first place. Insulin, as you recall, is a polypeptide hormone secreted by the islets of Langerhans in the pancreas. (A polypeptide, by the way, is made of two or more amino acids and becomes part of a protein.) Its job is to regulate metabolism of carbohydrates and fats, especially the conversion of glucose to glycogen, which lowers blood glucose levels. Glycogen is the chief carbohydrate storage material in animals, tucked nicely away mostly in the liver and partly in muscle, and can be liberated on demand. With insulin resistance the cells become less sensitive to the effects of insulin. If this happens, the pancreas is provoked to work harder and to release more of the hormone. Thus far, no disease is recognized, only a state wherein the body fails to respond. Sensitivity to insulin is widely different within the general population, so much so that the most insulin-sensitive people might be six times more so than those identified as most resistant. The prevalence of insulin resistance in the United States is about a fourth of the general population.

 The most common condition related to insulin resistance is obesity, now a public health concern in its own right and a risk factor for type 2 diabetes, hypertension, and coronary artery disease.  Losing weight increases the body’s sensitivity to insulin. Just a ten percent drop in weight can make a big difference. Of course, exercise enters the picture because it encourages the muscles to use glucose and gets rid of the spare tire. A high-fiber diet reduces levels of blood insulin and lowers risk of developing high blood pressure. Then there are drugs, decidedly the last resort. But there is now another factor that enters the scene, one to which we pay too little attention and take for granted—sleep, that marvelous cyclical event that restores body, mind and spirit.

A very recent study announced that fat cells need sleep as much as the cells in the brain.  Lack of sleep and limited sleep have a direct and harmful effect on fat, a state that could lead to major health issues, including obesity and type 2 diabetes by increasing risk for insulin resistance. Under conditions controlled for calorie intake and physical activity, subjects in a cross-over study (where they change places after an allotted time) were allowed 4.5 or 8.5 hours of sleep. Insulin response in the fat cells was measured afterward. It was found that response to insulin after sleep restriction was 30% lower, dropping fat cell function to that of an obese or diabetic person, despite being physically fit (Broussard, 2012). Because many of us are sleep deprived, this is a significant finding, portending obesity, diabetes and other metabolic concerns.

Fat, or adipose tissue, serves an important function as an energy depot, and also prevents body heat loss and provides an elastic padding between organs. Having a density of about 0.9 kilogram per liter compared to muscle’s 1.06 kg/L, fat will float quite easily. Weight loss does not automatically make fat cells disappear; they merely shrink, waiting to balloon again under the right conditions. Fat may even become an active organ that sends chemical signals to other parts of the body, possibly triggering sickness and disease (ACS, 2010). Two of those signalers are leptin, which controls appetite, and adiponectin, a protein hormone that regulates glucose and fatty acid catabolism.

A single night of sleep deprivation may evoke hepatic insulin resistance and decrease glucose disposal rate, thereby affecting peripheral insulin sensitivity and disturbing more than one metabolic pathway (Donga, 2010). This upset of energy balance likewise presages disease manifestations that include thyroid dysregulation and weight gain (Bosy-Westphal, 2008). Where does weight gain fit in here? It seems that sleep deprivation stimulates the activity of ghrelin, a hormone produced by stomach cells that turns hunger on. Leptin is its counterpart. A French analysis of sleep-deprived men noted their consumption of as much as twenty-two percent more calories on the day after sleep restriction than they did with ample sleep (Brondel, 2010). These reports demonstrate a link between sleep loss and risk for chronic disorders (Chamorro, 2011).

The feverish pitch of world citizenship compromises our sleeping hours.  Instead of the eight we need, many of us are lucky to see five or six. What used to be a complaint of college students has become a contagion that affects an increasing number of us.  Medications and defined sleep disorders aside, the time for sleep needs to be assigned and followed, lest we open the door to the unwelcomed guests that accompany deprivation. One of the simplest steps to restore the time for sleep is to learn to say “no” so you can eliminate the other gremlins of sleep loss that include acne, insomnia and a sensitive stomach.  If work worries keep you awake at night, look for ways to stop taking a fortune out of your bank of well-being, since renegade glucose metabolism is not a sweet deal.

References

ACS News Service Weekly PressPac: October 13, 2010
New evidence that fat cells are not just dormant storage depots for calories

Bosy-Westphal A, Hinrichs S, Jauch-Chara K, Hitze B, Later W, Wilms B, Settler U, Peters A, Kiosz D, Muller MJ.
Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women.
Obes Facts. 2008;1(5):266-73.

Brondel L, Romer MA, Nougues PM, Touyarou P, Davenne D.
Acute partial sleep deprivation increases food intake in healthy men.
Am J Clin Nutr. 2010 Jun;91(6):1550-9.

Broussard JL, Ehrmann DA, Van Cauter E, Tasali E, Brady MJ.
Impaired insulin signaling in human adipocytes after experimental sleep restriction: a randomized, crossover study.
Ann Intern Med. 2012 Oct 16;157(8):549-57.

Orfeu M. Buxton, Milena Pavlova, Emily W. Reid, Wei Wang, Donald C. Simonson, Gail K. Adler
Sleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men
Diabetes. Sep 23 2010;59(9):2126-2133.

Chamorro RA, Durán SA, Reyes SC, Ponce R, Algarín CR, Peirano PD.
Sleep deprivation as a risk factor for obesity
Rev Med Chil. 2011 Jul;139(7):932-40.

Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, Romijn JA.
A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8. Epub 2010 Apr 6.

Knutson KL, Van Cauter E.
Associations between sleep loss and increased risk of obesity and diabetes.
Ann N Y Acad Sci. 2008;1129:287-304.

Reynolds AC, Dorrian J, Liu PY, Van Dongen HP, Wittert GA, Harmer LJ, Banks S.
Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men.
PLoS One. 2012;7(7):e41218. Epub 2012 Jul 23.

Sebastian M Schmid, Manfred Hallschmid, Kamila Jauch-Chara, Britta Wilms, Hendrik Lehnert, Jan Born, Bernd Schultes
Disturbed glucoregulatory response to food intake after moderate sleep restriction.
Sleep (impact factor: 5.05). 01/2011; 34(3):371-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Sweet Sweep of Sleep

sleepy-womanAhh, the sweet balm that soothes the nerves and restores the soul at the end of the day. Sadly, for some of us it is elusive, and its intangible rewards sporadic. Sleep. It can get interrupted, disrupted and corrupted. Even in its worst state, sleep can be the most desired gift for the time.

There have been thousands of sleep studies over the years, but science still isn’t completely sure why we need it. “Completely” is the key word. One goofy answer is that we sleep to cure sleepiness. It’s agreed that sleep gives the body a chance to rejuvenate. That we know about rapid eye movement sleep (REM) shows that sleep is not a totally static process for the brain. Asleep, it still needs calories. The amount of sleep a person needs is purely singular, and depends on his or her circadian rhythm, which is that twenty-four-hour cycle of biological activities that occur regularly and dependably regardless of illumination. What sleep experts look for are maximum melatonin levels and minimum core body temperature, reporting that one should be asleep at least six hours before lowest temp is achieved. When these occur just after the middle of the sleep cycle, the timing is deemed to be just right (Wyatt, 1999) (Dijk, 2002) (Taillard, 2011).

Too much sleep can be as unhealthy as too little. Where lack of sleep can increase the chance of accidents and CVD issues, a plethora might increase risk of other-cause mortality (Ferrie, 2007). Because animals with brains sleep, we might infer that it’s a needed pastime. Regardless of who and how much, the fact is that we heal better when we sleep, the immune system gets a chance to recoup, memory and cognitive function improve, and a general restoration takes place. And now there’s another reason to cut Z’s…the prevention of Alzheimer’s disease and related cognitive disorders.

Whether it’s more hypothetical than proven, a new study released by the University of Rochester hints that a good night’s sleep can ward off Alzheimer’s disease (Xie, 2013). Lead author, Maiken Nedergaard, notes that sleep serves a vital function, a collective term that includes washing debris out of the brain. The brain produces toxic waste as it works every day. This new study says that while we sleep the brain shrinks in size, allowing the spaces between brain cells to enlarge so that junk can be washed out by the cerebral spinal fluid that is pumped around it (Underwood, 2013).

Researchers in Nedergaard’s lab noticed that mice whose brains were probed while conscious would sometimes fall asleep. When that happened, cerebrospinal fluid would rush into the brain’s interstitial space and wash away cellular debris. Delving into the phenomenon, they observed that the brain’s glial cells, a web of connective tissue that supports neurons, expand during wakefulness to reduce the space between cells and shut off the movement of fluid. During sleep, the interstitial volume changes again.

Interstitial fluid is a solution that bathes the area around cells with a concoction that contains sugars, salts, fatty acids, amino acids, coenzymes, hormones, and neurotransmitters. Different areas of the body have different concentrations of these substances. Little attention was paid to the area between cells before Nedergaard’s investigation because that was considered just space (Herculano-Houzel, 2013).  The brain’s drainage system was termed the glymphatic system, a functional waste management setup that removes extracellular proteins and metabolic waste products from the pathway, but reliant upon the glia instead of a dedicated, albeit absent, lymphatic network.

To double-check their findings, scientists injected the mouse brains with proteins that parallel those implicated in Alzheimer’s disease (AD)—the amyloids. These were washed away faster from the brains of sleeping mice than their awake peers. It is the accumulation of these soluble proteins at the synapses that is believed by some to initiate the disease (Tomiyama, 2010) (Esparza, 2013).

Fragmented sleep is that which does not include much slow-wave sleep and is not refreshing. Total time asleep is less than normal, affecting about a third of all adults. Unfragmented-consolidated sleep is divided into two periods with a gap between. This “bi-phasic” sleep is common and is something people can adjust to. Fragmented sleep is characteristic of Alzheimer’s and Parkinson’s patients, though it is common to the aging process. However, there is debate about whether increased fragmentation is a normal part of aging or indicative of an underlying pathology. Regardless, it is associated with cognitive performance (Lim, 2013). In any case, it’s unpleasant to experience the next day’s sleepiness. There are pharmaceutical sleep aids, but the natural ones, such as valerian and melatonin, are safer.

Melatonin is produced in the brain, but decreases with age and in those with Alzheimer’s disease. There are data from clinical trials demonstrating that melatonin can slow the progression of cognitive impairment in AD patients by protecting neural cells from amyloid-mediated toxicity and by arresting the formation of plaques in the first place (Lin, 2013). As a noted anti-oxidant, melatonin is able to scavenge the free radicals that are likewise implicated in AD etiology (He, 2010), and to improve mitochondrial energy metabolism (Cheng, 2006) (Liu, 2013). Produced in the pineal gland from tryptophan, melatonin, as a sleep aid, lowers body temperature and blood pressure, a condition required for sound sleep.

If sleep can clear the abnormal accumulation of neurotoxins (Rothman, 2012), and if melatonin can help resolve dysfunctional sleep patterns, then this bag of ideas might just hold more than water.

References

Orfeu M. Buxton, Sean W. Cain, Shawn P. O’Connor, James H. Porter, Jeanne F. Duffy,
Wei Wang, Charles A. Czeisler and Steven A. Shea
Adverse Metabolic Consequences in Humans of Prolonged Sleep Restriction Combined with Circadian Disruption
Sci Transl Med. 11 April 2012; Vol. 4 Issue 129: p. 129ra43

Cheng Y, Feng Z, Zhang QZ, Zhang JT.
Beneficial effects of melatonin in experimental models of Alzheimer disease.
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Daniel A. Cohen, Wei Wang, James K. Wyatt, Richard E. Kronauer, Derk-Jan Dijk, Charles A. Czeisler and Elizabeth B. Klerman
Uncovering Residual Effects of Chronic Sleep Loss on Human Performance
Sci Transl Med. 13 January 2010; Vol. 2 Issue 14: p. 14ra3

Dijk DJ, Lockley SW.
Integration of human sleep-wake regulation and circadian rhythmicity.
J Appl Physiol. 2002 Feb;92(2):852-62.

Dragicevic N, Copes N, O’Neal-Moffitt G, Jin J, Buzzeo R, Mamcarz M, Tan J, Cao C, Olcese JM, Arendash GW, Bradshaw PC.
Melatonin treatment restores mitochondrial function in Alzheimer’s mice: a mitochondrial protective role of melatonin membrane receptor signaling.
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Feeling Anxious? Maybe Not

anxious-womanGood for you. You’re going to Disney World. But don’t say you’re anxious about it. It’s okay to be anxious about going to the dentist. It’s understandable that you’d be anxious about your debut at an IRS audit. Unless you‘re terrified by the characters, you’re eager, not anxious, about visiting Walt’s place. To be anxious is to be afraid, apprehensive, uneasy, or distressed, but not enthusiastic. Anxiety is a disorder with more than one characterization. It can display as panic disorder, obsessive-compulsive disorder, post-traumatic-stress disorder, social anxiety, and a few others, including various phobias. It’s even possible to be anxious about being anxious, to the point that the subsequent distress precludes a normal life.

A common emotion, anxiety is felt by most humans once in a while. Taking a test, facing a novel problem at the office, or making a difficult decision is enough to get you anxious. Being lost in a strange town makes you feel like a rat in a laboratory maze. These little upsets are supposed to go away. If they cause a lingering burn, it’s time to talk about it. Frustration with a task can cause anxiety, and anxiety about doing it in the first place can cause frustration, which then perpetuates the cycle. Replacing uncomfortable cognitions with calming thoughts—something you can learn to do yourself—is one path to serenity.  The Roman Emperor Marcus Aurelius wrote about dealing with frustration and anxiety two thousand years ago. So, this isn’t a new challenge. However, what is new is the discovery that the ninety percent of the cells that compose the body have the potential to respond to anxiety. These would be the intestinal bacteria that have the uncanny ability to communicate with the brain, a conclusion attributed to evolution but more than likely decided at the ontogeny. That a bidirectional communication system between the gut and the cerebrum exists has been established, and that it influences brain development and behavior through complex signaling mechanisms is amply defined (Diaz-Heijtz, 2011) (Collins, 2012) (Chen, 2013).

The connection between gut and brain is controlled by the vagus nerve, which is the longest cranial nerve, passing through the neck and thorax into the abdomen, where it directs motor and secretory impulses of the viscera—your innards. Stimulation of this nerve can instigate activity in a body process known as the HPA axis (Hosoi, 2000) (O’Keane, 2005), the hypothalamic-pituitary-adrenal axis, the control center for most of the body’s hormones, one of which is the steroid hormone cortisol. Cortisol is used as a biomarker for psychological stress (Djuric, 2008).  In response to physical or mental stress, the hypothalamus produces corticotropin-releasing factor, which binds to specific receptors in the pituitary gland, where adrenocorticotropic hormone (ACTH) is made. ACTH then moves to the adrenals to direct the secretion of cortisol. The idea behind cortisol is to break down body tissue to be used as energy. When rampant, it breaks down lean tissue to liberate amino acids that can be used to raise blood sugar. In adipose tissue, cortisol breaks fats into fatty acids and glycerol, which also elevate blood sugar.

To calm this activity in a kind of physiological riot control, the body enlists the major inhibitory neurotransmitter, called gamma-aminobutyric acid—GABA—to slow down the firing of nerve cells in the brain. Emily Dean, M.D., a psychiatrist practicing in Massachusetts, likens GABA to a glass of wine in front of a fire, to restful sleep, or to tranquility and yoga (http://www.psychologytoday.com/blog/evolutionary-psychiatry/201206/do-probiotics-help-anxiety). Paints a nice picture, eh? Negative alterations in GABA receptor expression are implicated in the development of anxiety and depression, which are comorbid with functional bowel disorders.

It’s been hypothesized that probiotics are able to make compounds that enhance the brain-gut link by acting as delivery vehicles for neuroactive substances, with each neurochemical being related to a specific strain of intestinal flora (Lyte, 2011). The strain Lactobacillus rhamnosus is known to modulate the immune system by manipulating tumor necrosis factor alpha (TNFa) and Interleukin 8 (Ma, 2004), two cytokine signaling molecules related to immunity and inflammation. In mouse studies performed in Ireland a couple years back, those animals preloaded with L. rhamnosus were spared a frantic response to physiological insult and stress, contrasted to their cage mates denied the probiotic, whose cortisol levels were extreme (Bravo, 2011). As expected, mice whose vagus nerves were severed had no similar neurochemical and behavioral effects, indicating the vagus nerve as the major thoroughfare between gut bacteria and the brain (Ibid). Even in the absence of insult, mice treated with lactobacillus presented with higher levels of anxiety-reducing receptors, the observation of which could not be made until their sacrifice. A lactobacillus, then, reduces stress-induced levels of corticosterone (the rodent equivalent of cortisol) by normalizing the HPA axis (Gareau, 2007).

The HPA axis helps to regulate physiological processes that include temperature, digestion, immunity, mood, sexuality and energy usage, besides controlling your response to stress, trauma and injury. If, as believed, the hypothalamus is involved with fibromyalgia and the adrenals with chronic fatigue syndrome, the use of a probiotic to tend to the HPA axis should ameliorate these assaults. If GABA plays a major role in the HPA stress response (Herman, 2004) (Cullinan, 2008), and if GABA production is enhanced by lactic acid bacteria (Dhakal, 2012), then a five-dollar treatment for anxiety is at hand.  Not only L. rhamnosus, but also L. brevis (Li, 2010), L. reuteri (Ma, 2004), and strains of Bifidobacteria (Barrett, 2012) work to produce GABA. This should settle once and for all that not all bacteria are bad.

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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.