American Sugar: The Untold Story.

There is a metabolic difference between simple and complex carbohydrates. The simple ones become glucose soon after they are eaten. The complex ones take longer to turn into sugar and are less apt to spike insulin and cause energy crashes down the line. But that isn’t the only difference between the two.

Almost forty years ago scientists had an interest in the relationship of diet to health, specifically of sugar intake to immunity. But their curiosity went past simple sugar to include carbohydrates other than glucose. The cells that are the backbone of the immune system are supposed to kill, swallow, and dispose of alien bodies, including bacteria, viruses and cancer cells. Scientists at Loma Linda University in California examined the activity of neutrophilic phagocytes (cells that dissolve the enemy) after subjects ingested glucose, fructose, sucrose, honey, or orange juice and found that “…all significantly decreased the capacity of neutrophils to engulf bacteria…” (Sanchez, Reeser, et al. 1973). Looking more closely, the researchers also discovered that the greatest effects occurred within the first two hours after eating, but “…the effects last for at least 5 hours.” (Ibid.) If there is any promise, it’s that the effects can be undone by fasting from added sugars for the next two or three days.

At the start of the twentieth century, Americans consumed only about five pounds of sugar a year. By the fifties, that had grown to almost 110 pounds a year, and to more than 152 by the year 2000. Corn sweeteners account for 85 of those pounds. America’s sweet tooth increased 39% between 1950 and 2000 as the use of corn sweetener octupled.

Although the statistics above are decades old, its message is contemporary. High-fructose corn syrup has become the bad boy of the anti-sugar crusade. HFCS began replacing sugar in soft drinks in the 1980’s, after it was portrayed by marketers as a healthful replacement for demon sugar. It didn’t hurt the industry that it cost less, either. The biological effects of sugar and HFCS are the same, however. Neither has any food value — no vitamins, protein, minerals, antioxidants, or fiber — but they do displace the more nutritious elements of one’s diet, and we tend to consume more than we need to maintain our weight, so we gain.

Even though the number of calories from the glucose in a slice of bread or other starch is the same as that from table sugar (half fructose and half glucose), they are metabolized differently and have different effects on the body. While fructose is metabolized by the liver, glucose is metabolized by every cell in the body. When fructose reaches the liver, especially in liquid form (as in soda), it overwhelms the organ and is almost immediately converted to fat. (Taubes. 2011)

Innate immunity is that which occurs as part of your natural makeup and defends you against infection by other organisms. Short-term hyperglycemia, which might come from a pint of vanilla, has been found to affect all the major components of the innate immune system and to impair its ability to combat infection. Reduced neutrophil activity, but not necessarily reduced neutrophil numbers, is one of several reactions to high sugar intake. (Turina. 2005) Way back in the early 1900’s, researchers noted a relationship between glucose levels and infection frequency among diabetes sufferers, but it wasn’t until the 1940’s that scientists found that diabetics’ white cells were sluggish. (Challem. 1997) More recent study has corroborated the diabetes-infection connection, agreeing that neutrophil phagocytosis is impaired when glucose control is less than adequate. (Lin. 2006) Impaired immune activity is not limited to those with diabetes. As soon as glucose goes up, immune function goes down.

Some people think they’re doing themselves a favor by using artificial sweeteners. Once the brain is fooled into thinking a sweet has been swallowed, it directs the pancreas to make insulin to carry the “sugar” to the cells for energy. After the insulin finds out it’s been cheated of real sugar, it tells the body to eat in order to get some, and that creates artificial hunger, which causes weight increase from overeating. Even environmental scientists have a concern with fake sweeteners in that they appear in the public’s drinking water after use. You can guess how that works. (Mawhinney. 2011)

Mineral deficiencies, especially prevalent in a fast-food world, contribute to immune dysfunction by inhibiting all aspects of the system, from immune cell adherence to antibody activity. Paramount among minerals is magnesium, which is part of both the innate and acquired immune responses. (Tam. 2003) Epidemiological studies have connected magnesium intake to decreased incidence of respiratory infections (PDR. 2000). But sugar pushes magnesium — and other minerals — out of the body. (Milne. 2000) This will compromise not only immune function, but also bone integrity. (Tjäderhane. 1998). Mix a sweet alcohol cocktail and find the whammy doubled. (Fuchs. 2002).

Zinc has been touted for its ability to shorten the duration of the common cold. Like magnesium, zinc levels decrease with age, and even tiny deficiencies can have a large effect on immune health, particularly in the function of the thymus gland, which makes the T-cells of the immune system. Zinc supplementation improves immune response in both the young and the old. (Haase. 2009) (Bogden. 2004) (Bondestam. 1985) All the microminerals, in fact, are needed in minute amounts for optimal growth and development…and physiology. Low intakes suppress immune function by affecting T-cell and antibody response. Thus begins a cycle whereby infection prevents uptake of the minerals that could prevent infection in the first place. Adequate intakes of selenium, zinc, copper, iron plus vitamins B6, folate, C, D, A, and E have been found to counteract potential damage by reactive oxygen species and to enhance immune function. (Wintergest. 2007)

Who would have viewed something as sweet as sugar as being so hostile to its host? It likes to let itself in, but has the nasty character of pushing everything else out.


Albert Sanchez, J. L. Reeser, H. S. Lau, P. Y. Yahiku, et al. Role of sugars in human neutrophilic phagocytosis. American Journal of Clinical Nutrition, Nov 1973; Vol 26, 1180–1184

Profiling Food Consumption in America. USDA

Taubes G. “Is Sugar Toxic?” in New York times Magazine, 13 April, 2011

Turina M, Fry DE, Polk HC Jr. Acute hyperglycemia and the innate immune system: clinical, cellular, and molecular aspects. Crit Care Med. 2005 Jul;33(7):1624–33.

Challem J and Heumer RP. The Natural health Guide to Beating the Supergerms. 1997. Simon and Schuster Inc. New York. Pp. 124–125

Lin JC, Siu LK, Fung CP, Tsou HH, Wang JJ, Chen CT, Wang SC, Chang FY. Impaired phagocytosis of capsular serotypes K1 or K2 Klebsiella pneumoniae in type 2 diabetes mellitus patients with poor glycemic control. J Clin Endocrinol Metab. 2006 Aug;91(8):3084–7.

Mawhinney DB, Young RB, Vanderford BJ, Borch T, Snyder SA. Artificial sweetener sucralose in U.S. drinking water systems. Environ Sci Technol. 2011 Oct 15;45(20):8716–22.

Tam M, Gómez S, González-Gross M, Marcos A. Possible roles of magnesium on the immune system. Eur J Clin Nutr. 2003 Oct;57(10):1193–7.

PDR: Physicians’ Desk reference for Herbal Medicines. Magnesium. 2nd edition. Mintvale NJ: Medical Economics Company; 2000: 5340540

Milne David B, PhD and Forrest H. Nielsen, PhD. The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men. J Am Coll Nutr February 2000 vol. 19 no. 1 31–37

Tjäderhane Leo, and Markku Larmas. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. J. Nutr. October 1, 1998 vol. 128 no. 10 1807–1810

Fuchs, Nan Kathryn Ph.D. Magnesium: A Key to Calcium Absorption. The Magnesium Web Site on November 22, 2002.

Haase H, Rink L. The immune system and the impact of zinc during aging.. Immun Ageing. 2009 Jun 12;6:9.

Bogden JD.. Influence of zinc on immunity in the elderly.. J Nutr Health Aging. 2004;8(1):48–54.

Bondestam M, Foucard T, Gebre-Medhin M. Subclinical trace element deficiency in children with undue susceptibility to infections. Acta Paediatr Scand. 1985 Jul;74(4):515–20.

Wintergerst ES, Maggini S, Hornig DH. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 2007;51(4):301–23. Epub 2007 Aug 28.

Smolders I, Loo JV, Sarre S, Ebinger G, Michotte Y. Effects of dietary sucrose on hippocampal serotonin release: a microdialysis study in the freely-moving rat. Br J Nutr. 2001 Aug;86(2):151–5.

Jack Challem, Burton Berkson, M.D., Ph.D., Melissa Diane Smith Glucose and Immunity Accessed 11/2011

Van Oss CJ. Influence of glucose levels on the in vitro phagocytosis of bacteria by human neutrophils. Infect Immun. 1971 Jul;4(1):54–9.

Bernstein J, Alpert S, et al Depression of lymphocyte transformation following oral glucose ingestion. Am J Clin Nutr. 1977; 30: 613

Robert A. Good, Ellen Lorenz. Nutrition and cellular immunity. International Journal of Immunopharmacology. Vol 14, Iss 3, Apr 1992, Pp. 361–366

Diabetes and Omega-3’s

Diabetes, Omega-3 fatty acids Super FoodsReading, interpreting and understanding scientific literature can be tedious because the authors often find that their previous paper on the subject missed its mark or was completely wrong. Easy to do when you are blazing new trails; however, the caution they go through to cover their tracks oftentimes makes for difficult reading. Luc Djousse and his colleagues at the U of Washington reported in the May 18, 2011 edition of the American Journal of Clinical Nutrition that, “With the use of objective biomarkers, long-chain omega 3 Fatty Acids (FAs) and Alpha-Linolenic Acid (ALA) were not associated with a higher incidence of diabetes. Individuals with the highest concentrations of both types of FAs had lower risk of diabetes.”

Speed reading is absolutely out of place. Omega-3 fatty acids in the body help to control the inflammation process, which is a benefit because the start of the healing process—initiated by the omega-6 arachidonic acid—also involves the possibility of getting carried away with the exercise. Say you have a cut or abrasion. The key activity that ensues is to stop the loss of fluids – save the blood.  It is that process which tells the body to start the healing by sending white blood cells and platelets to the site of the wound and to agglomerate and close the exit door by swelling the tissues, which is also another way of looking at inflammation. To inflame can be life saving. The omega-3’s are then involved in the work of modulating the activity helping to ease the inflammation that comes with the correction process.

Fatty acids, especially those that are long and highly unsaturated, increase cell membrane fluidity and functionality. Fatty acids are essential to membrane activity at the location of hormone receptors. Insulin resistance in adult-onset diabetes is directly associated with fewer membrane enhancing long-chain fatty acids, largely due to impaired function of desaturase and elongase enzymes needed for a healthy membrane. Ruiz-Gutierrez 1993, “We have studied the fatty acid composition of erythrocyte membrane phospholipids in nine Type 1 (insulin-dependent) diabetic patients and nine healthy control subjects. Cell membranes from the diabetic patients showed a marked decrease in the total amount of polyunsaturated fatty acids mainly at the expense of docosahexaenoic acid, DHA, and arachidonic acid C20:4n6”.

Cell membrane abnormalities in lipid content are found to be related to poor metabolic control, which is a characteristic of diabetes. Diet is a very important  factor, and interventions with dietary essential fatty acids (EFAs) in the correct ratio (found to be 4:1, omega-6:omega-3), can make a difference. Decsif  T., 2002, “Reduced availability of long-chain polyunsaturates in diabetic children suggests that an enhanced dietary supply of long-chain polyunsaturates may be beneficial”. Children with diabetes demonstrate a deficit of long-chain fatty acids, so incorporating them into a child’s diet is prudent. An unspoken benefit in the application of EFA’s to diabetes treatment is the decrease in triglyceride levels, themselves striking indicators of the potential for cardiovascular issues and very often appearing in persons with diabetes.

Herein resides the prolonged physiological support of the EFAs. For those who lack the efficient conversion of the omega-3 alpha linolenic acid from plant sources (notably flaxseeds and their oil) to EPA and DHA, fish oil may be a viable alternative. In fact the the FA conversion process with diabetes is almost non-existent, but also common with aging.

For quite some time the essential fatty acids have been misunderstood. Of the types of fatty acids, the omega-3’s have received the most publicity, having been applauded for positive health effects, principally, because over the last century the general population ate little fish and had little or no n-3s in the diet. Unless they were more or less health nuts, few did not have any exposure to omega 3s as in flax, and even if they did their ability to elevate up to EPA and DHA was minimal. Fish oil was the answer but the explosion that ensued caused over-consumption and still does.

Hence the comments of Djousse et al that n-3 FAs did not increase diabetes but if both the omega 6s and the 3 s were added together there was marked improvements. There is an inference that n-3s were of no benefit and needed the balance of both EFAs, which we applaud and so should you. Balance is paramount.


Djoussé L, Biggs ML, Lemaitre RN, King IB, Song X, Ix JH, Mukamal KJ, Siscovick DS, Mozaffarian D. Plasma omega-3 fatty acids and incident diabetes in older adults. Am J Clin Nutr. 2011 May 18.

Ruiz-Gutierrez V, Stiefel P, Villar J, García-Donas MA, Acosta D, Carneado J.  Cell membrane fatty acid composition in type 1 (insulin-dependent) diabetic patients: relationship with sodium transport abnormalities and metabolic control.  Diabetologia. 1993 Sep;36(9):850-6.

T. Decsif, H. Minda, R. Hermann, A. Kozári, É. Erhardt, I. Burus, Sz. Molnár and Gy. Soltész  Polyunsaturated fatty acids in plasma and erythrocyte membrane lipids of diabetic children  Prostaglandins, Leukotrienes and Essential Fatty Acids. 67(4); Oct 2002: 203-210

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

Diet Soda is Not A Free Ride

diet soda & weight gainThere is little doubt that obesity in America is on the upswing. Lots of people think that an artificially-sweetened beverage can offset the poor dietary decisions to which they have become accustomed. There has been established a relationship between non-sugar sweeteners and weight gain based on physiological responses to the message of satiety and the perceived need to consume more calories to achieve it. While the perception of sweet taste is supposed to satisfy appetite, the calculated deception to the body just might boomerang and call off all bets.

In the San Antonio Heart Study that ran from 1979 to 1988, researchers examined the association of artificially sweetened beverages with long-term weight gain, and found that, “A significant positive dose-response relationship emerged between baseline ASB (artificially sweetened beverage) consumption and all outcome measures…”  These outcome measures included overweight / obesity, weight gain, and changes in body mass index (BMI).  As with most nutrition research, considerations were made for demographics and behavioral characteristics.  Drinking more than twenty-one ASB’s a week had the most impact, with “…almost double risk of overweight / obesity among 1,250 baseline normal-weight individuals.”  For those with a body mass index already elevated, the changes were more pronounced.  This report concluded with, “These findings raise the question whether AS (artificial sweetener) use might be fueling—rather than fighting—our escalating obesity epidemic.”

That last sentence from the San Antonio Heart Study is quite the incrimination, would you say?
Diet soft drinks have long been thought to be healthier alternatives to their sugary counterparts, but reports like this one have linked increased incidence of weight gain, metabolic syndrome, and even diabetes to frequent intake of diet soft drinks.  Keep in mind, though, that all studies in all areas of health care are subject to scrutiny and critique.    Regardless of the topic, there are always two—or more—sides.  But here it may have been discovered that fooling the body is the instigator behind the concern.

When the body is told that something sweet has been ingested, it launches the production of insulin to carry the sweet to the cells to be burned for energy.  By the time the body finds out that there really is no sugar to be burned—in the form of glucose—the insulin has already been sent on its way to work.  Now the insulin has to find something to do, so it initiates a signal that says, “Feed me.  I need to carry glucose.”  That arouses hunger.  What do we grab for immediate satisfaction?  Carbohydrates, the simpler, the better.  Most of them spike glucose rapidly, which, if it fails to get burned for energy, is stored as fat.  It now appears that a lack of exercise becomes part of the equation.

There’s another tack to look at.  Some artificial sweeteners are alleged to block the brain’s production of serotonin, the neurotransmitter that controls mood, learning, sleep, and…appetite.  When the body experiences low levels of serotonin—and that can affect depressed mood—it seeks foods that can bring the levels back up.   Those foods happen to be the ones that will also bring the belt size up. Real sugar, of course, provides empty calories that can also cause weight gain as excessive energy intake.  But a weight conscious public does what it thinks is right.

Sweet taste enhances appetite.  Aspartame-sweetened water, for example, increased subjective hunger ratings when compared to glucose-sweetened water.  (Yang. 2010)  Other artificial sweeteners were associated with heightened motivation to eat, with more items selected on a food preference list. (Blundell. 1986)  This suggests that the calories in natural sweeteners trigger a response to keep overall energy intake constant, and that inconsistent coupling between sweet taste and actual caloric content can lead to compensatory overeating and consequential positive energy balance.  (This means that more energy came into the body than went out.)  People associate taste with calorie content.  You can tell that a crème brulee has more calories than the eggs from which it is made, but you’d probably eat more of it if made with artificial sweetener than with cane sugar.

Humans have a hedonic component.  We like those things that appeal to the senses and activate our food reward pathways.  That contributes to appetite increase.  But artificial sweeteners fail to provide completeness.  Unsweetening the American diet over the long haul, a little at a time, might just do the trick.  After all, it seems to work with salt.


Obesity (2008) 16(8), 1894–1900.
Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long-term Weight Gain Sharon P. Fowler, Ken Williams, Roy G. Resendez, Kelly J. Hunt, Helen P. Hazuda and Michael P. Stern

Diabetes Care. 2009 Apr;32(4):688-94. Epub 2009 Jan 16.
Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr.
SourceDivision of Epidemiology, University of Texas Health Sciences Center, Houston, Texas, USA. [email protected]

Physiol Behav. 2010 Apr 26;100(1):55-62. Epub 2010 Jan 6.
High-intensity sweeteners and energy balance.
Swithers SE, Martin AA, Davidson TL.

SourceDepartment of Psychological Sciences, Purdue University, 703 Third Street, West Lafayette, IN 47907, United States. [email protected]

Yale J Biol Med. 2010 June; 83(2): 101–108.
Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings
Neuroscience 2010
Qing Yang

The Lancet, Volume 327, Issue 8489, 10 May 1986, Pages 1092-1093

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

Plate and Weight

portion controlPortion control and super-sized everything have taken their toll on the waists of the world, especially in the United States. In every town and city you’ll find an all-you-can-eat buffet within easy driving distance. If not that, how about a diner / restaurant that piles the food so high you can’t see the person across the table? The dining establishments may be feeding the frenzy, but it is the consumers who are getting out of control. And not just when eating out. Dinner plates are larger than ever, and, being good Americans, we feel obligated to empty them.

An article in the July, 2007, edition of the Journal of the American Dietetic Association defines at least one cause of the expanding American waistline:  overeating.  The indictment that, “…portion distortion begins as early as 3 years of age” is quite the slap.  Regardless of gender or hemisphere of residence, education or employment, portion size has the same impact.  “People tend to eat more from larger-sized restaurant portions (in the general range of 30% to 50% more) and they tend to serve themselves and eat more from larger-sized packages (in the general range of 20% to 40% more).”  It really is easy to “make room for more” when your plate is filled, when, all along, you’d have been satisfied with six ounces of spaghetti instead of the ten sitting in front of you.  All of us are unable to estimate the number of calories we’ve just eaten, and it gets harder to do as the pile of food gets taller and wider.   “…even registered nurses and dietitians—are inaccurate at estimating the calories from large portions.”  (Wansink. 2007)

Bigger is better when it comes to the size of the guardian angel that accompanies you through that dark alley downtown on your way home from the late shift.  Besides that, a pile of fifties is better when bigger.  When it comes to food, though, we need to be more aware of bigger.  Early in 2001, the Centers for Disease Control noticed that 61% of Americans are overweight, an increase from the 55% of only a few years earlier.  (Peregrin. 2001)  That can’t be blamed on the food industry, whose job is to sell food, not good nutrition.

Lots of us were taught by Mom to clean our plates.  That wasn’t too much of a concern when the dinner plate was 9 inches in diameter.  Somewhere along the line, though, it grew to ten inches, then to twelve, and, in some venues, fourteen.  We have a friend who bought a farmhouse built in the 1940’s—a real beauty, too.  When his wife tried to put the dinnerware into the built-in cabinets, the plates wouldn’t fit.  They were too big.  A little nosing around found that dinner plates were less than 9 inches in diameter back then.

Since we’re unlikely to change plates at home, we can settle for smaller servings.  But the psychological factor might make us feel deprived.  Using a 10-inch plate instead of a 12-incher will save between 100 and 500 calories a day.  A pound equates to about 3500 calories, so the  math is easy.  By swapping out plates, you can lose between 0.2 and 1.0 pounds a week.  Losing weight slowly gives you ample time to get accustomed to the new regimen…and you likely will not regain what you’ve lost.

Many Americans view eating out as a treat, meant to be a full, rewarding experience.  In a group, it’s difficult to spoil it for others by ordering an appetizer as an entrée.  On the other hand, many restaurateurs disagree, saying an appetizer is perfectly acceptable as a main meal.  Although you can’t order half a meal and expect to pay half the price, you can take it home.  With home cooked meals, in lieu of buying new dinnerware, try using a salad plate.  In a little while your appetite will shrink to fit the size of the dish… and so will your belt.


Journal of the American Dietetic Association. Vol 107, Is 7 , Pp 1103-1106, July 2007
Portion Size Me: Downsizing Our Consumption Norms
Brian Wansink, PhD, Koert van Ittersum, PhD

Journal of the American Dietetic Association. 101(6); Jun 2001: 620
A Super-sized Problem:  Restaurant Chains Piling on the Food
Tony Peregrin

Journal of the American Dietetic Association. 103(2); Feb 2003: 231-234
Expanding portion sizes in the US marketplace: Implications for nutrition counseling
Lisa R Young, PhD, RD and Marion Nestle, PhD, MPH

Arch Intern Med. 2007 Jun 25;167(12):1277-83.
Portion control plate for weight loss in obese patients with type 2 diabetes mellitus: a controlled clinical trial.
Pedersen SD, Kang J, Kline GA.

Plate Size Might Influence Weight Gain

Size of a Diet Plate
Ashley Jacob, RD

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

Medium-Chain Triglycerides Effect Weight Loss

less-weightMedium-chain triglycerides (MCT) are a unique kind of dietary fat that lend a wide range of positive health benefits, weight loss among them. MCT’s have a fatty acid chain length that varies between six and twelve carbon atoms, which is only one characteristic that distinguishes them from the more familiar long-chain fatty acids, such as the highly-celebrated fish oil. MCT’s are transported through the blood by the portal system, which bypasses the usual route of digestion and sends them directly to the liver.

Medium-chain triglycerides do not require the modifications of long-chain and very-long-chain fatty acids.  Neither do they require bile salts for digestion.  These qualities enable them to be less susceptible to hormone-sensitive lipase and to deposition into adipose (fat) tissue storage.  A study from England’s Oxford Brookes University in 2010 announced that, because of their particular character, “MCT’s have been researched for both benefits to exercise performance and health.”  In the former application, MCT’s may be “a means to maximizing an athlete’s ability to maintain their glycogen stores so they can be more competitive.”  From the health angle, these substances “increase fat oxidation and energy expenditure as well as reduce food intake and beneficially alter body composition.”  (Clegg. 2010)

If you watch the lose-weight ads on TV, you might be driven to buy one of the untested, unproven, and maybe even unsafe products that promise the physique of champions.  Read the small print to learn that exercise and diet are part of the program, and your dreams of Roman god-hood (or goddess) are shattered.  Back to the chips and dip, right?  There might be something that’s been tested, and found to be safe and effective for at least a little drop in weight.

Because MCT’s don’t need energy for absorption, utilization or storage, they’ve been used to treat malabsorption conditions.  But weight management has evoked more interest.  The milks from humans, dogs, and guinea pigs contain mostly long-chain fats.  Those from goats, cows, and sheep are primarily short-chain.  Horse milk has lots of medium-chain fatty acids.  Data suggest that the milk of all species depends on a partial resynthesis of pre-formed glycerides. (Breckenridge. 1967)  (Since horses run faster than cows, their milk is hard to bottle, and because they have only two spigots, it takes longer to get it.)

Decades ago, MCT’s had been studied for body fat management in obese persons without diabetes, but more recent work has focused on those with Type 2 diabetes.  The findings showed that a diet containing MCT’s at 18 grams a day (about 2/3 ounce) brought about a reduction in body weight and waist circumference, a decrease in insulin resistance, and a drop in serum cholesterol concentration.  (Han. 2007)  Compared to the subjects ingesting long-chain fatty acids, the results are significant.  The MCT users also enjoyed increased dietary satiety, meaning that they felt full sooner, so they ate less.  Still another welcome benefit was realized by a cohort in 2009, when Chinese investigators noted a significant decline in serum triglycerides and LDL-cholesterol, both markers for cardiovascular complications, in those ingesting 25-30 grams (there are 28 grams in an ounce) of MCT’s a day. (Zhang. 2009).  (Xue. 2009)

The fast rate of oxidation of medium-chain fatty acids leads to greater energy expenditure—almost without doing any hard work.  It’s impressive that such can be the case, especially where weight gain is reduced and the size of body fat deposits diminishes.  Note that fat cells are not normally lost once they appear; they merely shrink in size.  They are, however, prepared to expand again at the drop of a hat.  (Xue. 2009)

Since the 1960’s MCT’s have been advocated for use in weight control.  Back then the research entailed other factors as well, including  the balance of energy intake, the nature of the diet, the ratio of MCT to LCT (long-chain triglycerides), and duration of the protocol.  Nonetheless, the presence of MCT’s as part of the regimen made a difference.  Although the exact mechanism hasn’t been fingered, MCT’s are able to increase energy outgo, hasten satiety at the table, and facilitate weight control when consumed as a replacement for fats containing LCT’s.  ( St-Onge. 2002)  Increased heat production, known as thermogenesis, is one of the activities by which MCT’s burn fat. (Baba. 1982)

Palm oil and coconut oil are major food sources of medium-chain fats.  The fact that these are saturated fats means little because all sat fats are not created equal, displaying differing cholesterolemic effects.  Therefore, when you see them listed on an ingredient label, have no fear.  The less weight you need to lose, the faster you will see results, so it’ll pay to get started now. (St-Onge. 2003)


Clegg ME.
Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance.
Int J Food Sci Nutr. 2010 Nov;61(7):653-79.

W. C. Breckenridge and A. Kuksis
Molecular weight distributions of milk fat triglycerides from seven species
The Journal of Lipid Research. September 1967 (8): 473-478.

Han JR, Deng B, Sun J, Chen CG, Corkey BE, Kirkland JL, Ma J, Guo W.
Effects of dietary medium-chain triglyceride on weight loss and insulin sensitivity in a group of moderately overweight free-living type 2 diabetic Chinese subjects.
Metabolism. 2007 Jul;56(7):985-91.

Zhang YH, Liu YH, Zheng ZX, Wang J, Zhang Y, Zhang RX, Yu XM, Jing HJ, Xue CY, Wu J.
[Medium- and long-chain fatty acid triacylglycerol reduce body fat and serum triglyceride in overweight and hypertriglyceridemic subjects].    [Article in Chinese]
Zhonghua Yu Fang Yi Xue Za Zhi. 2009 Sep;43(9):765-71.

Xue C, Liu Y, Wang J, Zhang R, Zhang Y, Zhang J, Zhang Y, Zheng Z, Yu X, Jing H, Nosaka N, Arai C, Kasai M, Aoyama T, Wu J.
Consumption of medium- and long-chain triacylglycerols decreases body fat and blood triglyceride in Chinese hypertriglyceridemic subjects.
Eur J Clin Nutr. 2009 Jul;63(7):879-86.

Marie-Pierre St-Onge and Peter J. H. Jones
Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity1
J. Nutr. March 1, 2002; 132(3): 329-332

Baba N, Bracco EF, Hashim SA.
Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride
Am J Clin Nutr. 1982 Apr;35(4):678-82.

St-Onge MP, Jones PJ.
Greater rise in fat oxidation with medium-chain triglyceride consumption relative to long-chain triglyceride is associated with lower initial body weight and greater loss of subcutaneous adipose tissue.
Int J Obes Relat Metab Disord. 2003 Dec;27(12):1565-71.

Clegg ME.
Int J Food Sci Nutr. 2010 Nov;61(7):653-79.
Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance

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

Diabetes Prevention: Can We Stop Type 2 Before It Starts?

weigh-inPredictions for an increase in diabetes are dreadful. One in three children born in the United States in the year 2000 are apt to become diabetic unless they change the way they eat and start to move more. The implications of this epidemic are frightening because blindness, amputations, kidney failure and heart disease are in their futures. From the mid 60’s to the mid 90’s, the number of diagnosed diabetes cases has tripled. The type 2 diabetes that appeared at age forty is now showing up at age twelve. Almost all of those kids are overweight.

The Department of Health and Exercise Science at Wake Forest University, in North Carolina, recently concluded a study of the Diabetes Prevention Program that focused on lifestyle influence on type 2 diabetes, and found that overweight and lack of exercise are still principal causes of the disease.  The study included more than three hundred volunteers with body mass indexes (BMI) between 25 and 40, some of whom served as controls, while the others received a diabetes education program that included dietary interventions.  By now, you already figured that the intervention group experienced significantly greater decrease in glucose, insulin, and insulin resistance.  Not only that, but also they lowered their BMI’s and lost about an inch from their waistlines.  (Katula. 2011)  Getting rid of that gut makes a ton of difference.  (Pun intended.)  Parallel studies at Indiana University Medical School yielded similar results, with the additional benefits of improved blood pressure and total cholesterol levels.  (Ackerman. 2011)

In type 1 diabetes, where insulin is required, science is trying to prevent the loss of beta cells, the ones in the pancreas that make insulin.  Examining genetic susceptibility to disease is one step in the process.  Family history is part of that.  Up to now, there are no known pre-diagnosis steps that can be taken to prevent the onset of type 1.  On the other hand, there are several possibilities for helping to save beta cells shortly after a diagnosis of diabetes.  (Wherrett. 2011)  Assiduous effort is put into this area, with the expectation that some factors known to trigger autoimmunity and the eventual destruction of beta cells can be controlled.  Early trials offer promise, but have not yet reached fruition.  (Thrower.  2009)

The list of diabetic complications is long and fearsome:  coronary artery disease, cerebrovascular disease, peripheral vascular disease, retinopathy, and neuropathy, to name a few.  Researchers are looking closely at plants that can offset the costs and side effects of pharmaceuticals, and even obviate their use, but admonish us that diet and lifestyle still need to be reined in.  (Haque. 2011)  Because soy foods are integral to Asian cuisine, it seems appropriate to look for components of soy chemistry that might affect blood glucose.  The soy phytoestrogen, genistein, was reported to protect against glucose-induce pancreas cell death in a study done in China.  (Zhong. 2011)  The applicability of this finding to either type 2 or type 1 diabetes, or both, is yet to be determined, but the prospects have merit.

Patients already diagnosed with type 2, or those who feel themselves candidates, may be comforted to know that alpha lipoic acid, a sulfur compound found in organ meats, spinach and broccoli, and also available as a supplement, prevents a rise in diabetes markers while improving the efficiency of glucose metabolism.  In German studies it was found that administration of alpha lipoic acid for ten days, either orally or intravenously, improves insulin sensitivity in both lean and obese individuals.  (Konrad. 1999)  (Jacob. 1999)  It would be imprudent, though, to expect supplemental alpha lipoic acid to do something we wouldn’t do for ourselves, such as lose weight and exercise.

Dietary fiber gets lots of attention, and is mostly associated with digestive health.  The soluble type is fermented in the gut and makes some physiologically active byproducts.  The insoluble type is comparatively inert and absorbs water to make elimination an efficient process.  Legumes, some cereals and fruits, psyllium, and tuberous vegetables provide soluble fiber.  Wheat and corn bran, whole grains, and nuts and seeds are sources of insoluble fiber.  Psyllium has received considerable interest as an ingredient in high-fiber breakfast cereals, where it’s been reputed to lower cholesterol and to reduce blood glucose response to a meal.  More than one study has reported psyllium to be effective for both.  As little as 5 grams of psyllium taken either with, or just before, a meal has effected improvement in lipid and glycemic control.  At the University of Virginia Diabetes Center, scientists noted a 14% reduction in postprandial glucose at breakfast, and a 20% reduction at dinner, compared to placebo, in people diagnosed with non-insulin-dependent type 2 diabetes.  (Pastors. 1991)  Analyses in Mexico and Texas arrived at the same conclusion, but recorded a pronounced positive effect on total cholesterol, LDL cholesterol and triglyceride levels.  (Rodriguez-Moran. 1998)  (Lee. 1994)

The United States is not alone in the quest to control the diabetes epidemic by recommending lifestyle changes.  The Japanese saw a risk reduction of more than 67% through weight loss, and the Finns realized risk reduction by controlling total and saturated fats and increasing dietary fiber, as well.  (Kosaka. 2005)  (Lindstron.  2006).   Globally, children do not eat enough vegetables.  Those who do, often limit their repertoire to only a few.  French fries don’t count.   What they are missing is magnesium, the prophylactic mineral that is able to improve glucose and insulin balance, especially in obesity.  (Song. 2004)  (Huerta. 2005)  (Lopez-Ridaura. 2004) This mineral is loaded with properties that boost health. The prevention of diabetes is as simple as exercising, losing a few pounds, getting ample fiber, and eating magnesium-rich produce.  Here, an ounce of prevention really is worth a few pounds of cure, not to mention getting stuck with a needle.


Katula JA, Vitolins MZ, Rosenberger EL, Blackwell CS, Morgan TM, Lawlor MS, Goff DC Jr.
One-year results of a community-based translation of the Diabetes Prevention Program: Healthy-Living Partnerships to Prevent Diabetes (HELP PD) Project.
Diabetes Care. 2011 Jul;34(7):1451-7.

Ackermann RT, Finch EA, Caffrey HM, Lipscomb ER, Hays LM, Saha C.
Long-term effects of a community-based lifestyle intervention to prevent type 2 diabetes: the DEPLOY extension pilot study.
Chronic Illn. 2011 Aug 12. [Epub ahead of print]

Wherrett DK, Daneman D.
Prevention of type 1 diabetes.
Pediatr Clin North Am. 2011 Oct;58(5):1257-70.

Thrower SL, Bingley PJ.
Strategies to prevent type 1 diabetes.
Diabetes Obes Metab. 2009 Oct;11(10):931-8.

Haque N, Salma U, Nurunnabi TR, Uddin MJ, Jahangir MF, Islam SM, Kamruzzaman M.
Management of type 2 diabetes mellitus by lifestyle, diet and medicinal plants.
Pak J Biol Sci. 2011 Jan 1;14(1):13-24.

Zhong WW, Liu Y, Li CL.
Mechanisms of genistein protection on pancreas cell damage in high glucose condition.
Intern Med. 2011;50(19):2129-34.

Konrad T, Vicini P, Kusterer K, Höflich A, Assadkhani A, Böhles HJ, Sewell A, Tritschler HJ, Cobelli C, Usadel KH.
Alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes.
Diabetes Care. 1999 Feb;22(2):280-7.

Jacob S, Henriksen EJ, Tritschler HJ, Augustin HJ, Dietze GJ.
Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid.
Exp Clin Endocrinol Diabetes. 1996;104(3):284-8.

Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, Dietze GJ.
Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid.
Arzneimittelforschung. 1995 Aug;45(8):872-4.

Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, Rett K.
Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial.
Free Radic Biol Med. 1999 Aug;27(3-4):309-14.

Pastors JG, Blaisdell PW, Balm TK, Asplin CM, Pohl SL.
Psyllium fiber reduces rise in postprandial glucose and insulin concentrations in patients with non-insulin-dependent diabetes.
Am J Clin Nutr. 1991 Jun;53(6):1431-5.

Rodríguez-Morán M, Guerrero-Romero F, Lazcano-Burciaga G.
Lipid- and glucose-lowering efficacy of Plantago Psyllium in type II diabetes.
J Diabetes Complications. 1998 Sep-Oct;12(5):273-8.

Lee NA, Reasner CA.
Beneficial effect of chromium supplementation on serum triglyceride levels in NIDDM.
Diabetes Care. 1994 Dec;17(12):1449-52.

Kosaka K, Noda M, Kuzuya T.
Prevention of type 2 diabetes by lifestyle intervention: a Japanese trial in IGT males.
Diabetes Res Clin Pract. 2005 Feb;67(2):152-62.

Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J; Finnish Diabetes Prevention Study Group
Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study.
Lancet. 2006 Nov 11;368(9548):1673-9.

Song Y, Manson JE, Buring JE, Liu S.
Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women.
Diabetes Care. 2004 Jan;27(1):59-65.

Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, Patrie JT, Rogol AD, Nadler JL.
Magnesium deficiency is associated with insulin resistance in obese children.
Diabetes Care. 2005 May;28(5):1175-81.

Lopez-Ridaura R, Willett WC, Rimm EB, Liu S, Stampfer MJ, Manson JE, Hu FB.
Magnesium intake and risk of type 2 diabetes in men and women.
Diabetes Care. 2004 Jan;27(1):134-40.

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

USDA vs Healthy Eating

food-pyramid-on-plateThe food pyramids and plates conjured up by the USDA haven’t quite lived up to their expectations. In its attempts to get it right, this august, though somewhat misguided, body has delivered several versions, each one anticipated to be new and improved. So far, none has panned out.

The most visible sign of U.S. nutrition policy is the Food Pyramid, or lately, the Food Plate.  Recognizing that dietary quality plays a role in health and the prevention of chronic disease, the USDA issued a Pyramid revision in 2005 to address the shortcomings of the previous one.  Walter Willett, chair of Harvard’s nutrition department, comments, “…the previous pyramid was in substantial discordance with current scientific evidence.”   If such a guideline is out of harmony with what research concludes to be so, then a critical eye needs to be cast at the base of its formulation.  Willett adds that, “My Pyramid strays from much of the evidence generated through years of research and, in our opinion, fails to provide the public with clear information about healthy food choices.”  (Chiuve. 2007)

The older Food Pyramid had so many carbohydrates at its base that you could have made wallpaper paste for all your friends.  The bread, cereal, rice and pasta food group didn’t mention any difference between refined and whole grains.  Not that it makes much difference, since they’ll spike your insulin, anyhow, with high glycemic factors and initiate metabolic and hyperlipidemic aberrations, including insulin resistance, a precursor to Type 2 diabetes.  The newer 2005 Food Pyramid, with vertical lines instead of horizontal groups, is not only hard to fathom, but also vague.  However, it does mention whole grains.  In June, 2011, with lots of hoopla, the USDA replaced the much-maligned-but-deserving-of-it My Pyramid with a simpler icon, the fruit and vegetable-festooned My Plate.

It needs to be realized that the Department of Agriculture is not in the business of promoting health.  Its job is to promote farmers and foods.  Therefore, your hunt for sage dietary counsel has to travel another direction.  What’s good about the new My Plate is that the flawed My Pyramid has been dismantled.  What’s not so good about My Plate is its misplay in providing all the nutrition advice you need to choose the healthiest diet.  Picky?  Why not?  Who’s paying the freight?

The sections of My Plate don’t give us all the dope we need to make good food choices.  For one thing, it forgets to tell the shopper that whole grains are better for health, since refined grains can contribute to weight gain and elevated triglycerides.
(Hudgins. 2000)  (Parks.  2001)  It also fails to say that all proteins are not created equal.  Some are better for us than others because they have less saturated fat and, like fish, more polyunsaturated essential fats.  Processed meats are harmful to health.  That includes the ubiquitous hot dog.  How about beans and nuts as protein sources?  Good choices.  A hot dog or hamburger on a white-bread bun with fries and a shake can be part of the My Plate cuisine…despite the fact that high red meat and processed meat intake can increase risk for disease.  (Pan. 2011)  (Bernstein. 2010)

My Plate doesn’t distinguish between potatoes and other vegetables.  Potatoes are loaded with rapidly digested starch, having the same effect on blood sugar as refined grains and sweets.  (Hu. 2009)  Sadly, My Plate is silent about fats—the healthy fats, the essential fats.  The good fats can keep cholesterol under control…and the rest of the lipid panel, for that matter.  (Bester. 2010)

The topic of dairy can polarize a community.  Even though it contains a foreign protein, is a poor distributor of calcium, and is allowed to carry a percentage of bovine somatic cells, dairy has its following.  In fact, there is little solid evidence that high dairy intake prevents osteoporosis, but to the contrary, that the countries consuming the most dairy have the highest rates.  (Feskanich. 1997)  (Cumming. 1994)  My Plate recommends dairy at every meal.  It includes nothing about sugary drinks and fiberless juices.

What to do?  For starters, Dr. Willett relates, “If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks, we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases.”  His colleague, Dr. Frank Hu, admits that, “The country’s big low-fat message backfired.  The overemphasis on reducing fat caused the consumption of carbohydrates and sugars to soar.  The shift may be linked to the biggest health problems in America today.”  (LA Times. 2010)  For a better food plate, check out Harvard School of Public Health, at  Then swap carbohydrate and fat percentages in your daily intake.


Chiuve SE, Willett WC. The 2005
Food Guide Pyramid: an opportunity lost?
Nat Clin Pract Cardiovasc Med. 2007 Nov;4(11):610-20.

Hudgins LC.
Effect of high-carbohydrate feeding on triglyceride and saturated fatty acid synthesis.
Proc Soc Exp Biol Med. 2000 Dec;225(3):178-83.

Parks EJ.
Effect of dietary carbohydrate on triglyceride metabolism in humans.
J Nutr. 2001 Oct;131(10):2772S-2774S.

Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Willett WC, Hu FB.
Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis
Am J Clin Nutr. 2011 Aug 10.

Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC.
Major dietary protein sources and risk of coronary heart disease in women.
Circulation. 2010 Aug 31;122(9):876-83.

Hu Y, Block G, Sternfeld B, Sowers M.
Dietary glycemic load, glycemic index, and associated factors in a multiethnic cohort of midlife women.
J Am Coll Nutr. 2009 Dec;28(6):636-47.

Bester D, Esterhuyse AJ, Truter EJ, van Rooyen J.
Cardiovascular effects of edible oils: a comparison between four popular edible oils.
Nutr Res Rev. 2010 Dec;23(2):334-48.

Feskanich D, Willett WC, Stampfer MJ, Colditz GA.
Milk, dietary calcium, and bone fractures in women: a 12-year prospective study.
Am J Public Health. 1997 Jun;87(6):992-7.

Cumming RG, Klineberg RJ.
Case-control study of risk factors for hip fractures in the elderly.
Am J Epidemiol. 1994 Mar 1;139(5):493-503.

Harvard School of Public Health
The Nutrition Source

Marni Jameson
A reversal on carbs: Fat was once the devil. Now more nutritionists are pointing accusingly at sugar and refined grains.
Los Angeles Times.  December 20, 2010

Dina Fitzsimons
Why Milk Won’t Prevent Osteoporosis-And The Protein Myth-

Harvard School of Public Health
The Nutrition Source
Calcium and Milk: What’s Best for Your Bones and Health?

Belin RJ, Greenland P, Allison M, Martin L, et al
Diet quality and the risk of cardiovascular disease: the Women’s Health Initiative (WHI).
Am J Clin Nutr. 2011 Jul;94(1):49-57.

Am J Clin Nutr. 2011 Jul;94(1):247-53. Epub 2011 May 25.
Alternative Healthy Eating Index and mortality over 18 y of follow-up: results from the Whitehall II cohort.
Akbaraly TN, Ferrie JE, Berr C, Brunner EJ, Head J, Marmot MG, et al

Willett WC, McCullough ML.
Dietary pattern analysis for the evaluation of dietary guidelines.
Asia Pac J Clin Nutr. 2008;17 Suppl 1:75-8.

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

Protein Zaps Belly Fat

abdomenIn a sedentary, over-fed, yet undernourished society, the dissolution of abdominal fat with a magic bullet is an incessant quest.  First, we cut out the junk food.  Then we try to eat a balanced diet, the definition of which seems elusive.  After that, we add the foods we think are good for us.  Still, we can’t burn the belly.  Next, we look closer at the ads for products guaranteed to get rid of excess adiposity.  Only after these promises fail do we notice the small print that says the results you see are not typical, and that it must be accompanied by diet and exercise.  Oh, no, I have to work at it.  What happened to the magic bullet?

To be realistic about losing fat, we have to do something actively, not passively.  But that might be as simple as upping the ante on protein.  However, it just isn’t plain, old protein, but the quality of the protein that makes the difference.  Actually it’s the amino acids, the protein building blocks whose chemical properties determine the biological activity of the proteins of which they are a constituent.   Proteins catalyze many of the reactions in living cells—enzymes, hormones, antibodies.  The folding of proteins into three dimensional structures depends upon the information in the amino acid sequences.  Although several hundred kinds of amino acids have been found in nature, only twenty or so apply to human peptides (two or more aminos joined together) and proteins.  Low levels of certain amino acids telegraph as specific problems that include hormone imbalances, lack of concentration, irritability, and even depression.

Based on their individual characteristics, amino acids may be classified as essential, non-essential, or conditionally essential.  Essentiality does not bespeak importance, but acquisition.  The essential ones need to be acquired from diet because they can’t be made by the body.  Here’s a quick rundown of the essential amino acids, with some of their features:

Leucine — a BCAA (branched chain amino), is used for tissue repair after surgery, to build muscle mass, to balance blood sugar, to de-stress, to manufacture HGH (human growth hormone), and for protein synthesis.  It helps to maintain healthy bone, skin, and hemoglobin.

Isoleucine — a BCAA (branched chain amino), addresses mental disorders, tissue rebuild after surgery, energy, muscle, endurance, and blood hemoglobin.

Valine — a BCAA (branched chain amino), is used for mental and emotional disorders, for glycogen production, and in alcohol and drug recovery.  It’s used in muscle metabolism, where it contributes to the structure of proteins.

Lysine — absorbs and conserves calcium and maintains nitrogen balance.  It helps to make collagen, to manage cholesterol and triglycerides, and bolsters the immune system.  (People use this for fever blisters.)

Methionine — has been used to address schizophrenia, and the muscle weakness of Parkinson’s.  It helps to detoxify heavy metals, to form collagen, to prevent brittle hair and nails, to protect against radiation toxicity, and to control histamine levels that may affect cognitions.  Additionally, methionine is a strong antioxidant.

Phenylalanine — addresses chronic pain, helps to make endorphins, assists the manufacture of norepinephrine to direct nerve signals in the brain, promotes alertness and elevates mood, and has been used to treat arthritis, depression, migraines, and Parkinson’s disease.

Threonine — helps to maintain proper protein balance, is important to collagen, elastin, and tooth enamel, aids wound healing, may prevent fatty liver, and assists assimilation.

Tryptophan — is a natural relaxant that helps to alleviate insomnia.  It stabilizes mood, fights migraines and fibromyalgia, and may aid in weight control by reducing appetite.

Histidine — is conditional in adults, but deemed essential to infants and children, and is the immediate precursor to histamine (and carnosine).  Histidine is abundant in hemoglobin, and has been used in the treatment of arthritis, gastric disorders, and the maintenance of the myelin sheath.  It protects against heavy metals and radiation, and aids in the manufacture of red and white blood cells.

The remaining amino acids are non-essential, and are produced from the breakdown of proteins or from the essential ones.  They and a few of their jobs are:

Alanine — (the other component of carnosine) transfers nitrogen from peripheral tissue to the liver in glucose metabolism and guards against the buildup of toxins when muscle tissue is broken down to meet energy needs, as occurs in serious aerobic exercise.

Arginine — is considered the natural Viagra, relaxes blood vessels, supports thymus immunity activity, helps to neutralize ammonia, assists the release of growth hormones, and stimulates the pancreas to release insulin.

Aspartic Acid — from asparagine, is used to treat chronic fatigue and depression, aids the elimination of ammonia, rejuvenates cell activity, and helps to move minerals across the intestinal lining into the bloodstream.

Cysteine — (and cysteine) works as a potent antioxidant and protects against radiation and the toxins of tobacco smoke.  It promotes recovery from burns and promotes the burning of fats. Cystine is formed from the oxidation of two cysteines, but has the same character and activity.

Glutamic Acid — is an excitatory neurotransmitter that is called glutamine after coupling with ammonia, which is carried to the liver for disposal.  Free glutamic acid is important to the metabolism of fats and sugars, and helps to carry potassium into spinal fluid.

Glutamine — is structurally akin to glutamic acid.  It’s the most abundant amino found in muscles, which it helps to build and maintain, where it is useful for those confined to bed for long periods.  It helps to maintain acid-alkaline balance, and might be able to reduce cravings for sugar and alcohol.

Glycine — participates in the biosynthesis of hemoglobin, improves glycogen storage, and is part of the purine component of genetic material.

Ornithine — could be classed with “other” amino acids, helps to release growth hormones, which promotes the metabolism of excess body fat.  It detoxifies ammonia and may help insulin to function as an anabolic agent.  It’s formed from arginine.

Proline — improves skin texture via formation and salvation of collagen.  It works with vitamin C to promote healthy connective tissues.

Serine — is needed for the metabolism of fats and fatty acids, and for participation in the biosynthesis of genetic compounds important to RNA and DNA.

Taurine — is also among the “others.”  It boosts the heart muscle and vision, where it helps to deal with macular degeneration.  Taurine is a key component of bile, and may prevent cardiac arrhythmia.

Tyrosine — is important to overall metabolism, and is a precursor to norepinephrine and dopamine, which regulate mood.  It may suppress appetite and helps to reduce body fat.  Tyrosine affects thyroid hormones.

In a weight management study described in the January, 2012, issue of Nutrition and Metabolism, researchers were able to determine a relationship between the amount of quality protein ingested and central abdominal fat.  They especially paid attention to the number of times that approximately ten grams of essential amino acids (EAA) were consumed in a meal.  Noting that the dietary reference intake (DRI) has no specific recommendations for the types of dietary protein consumed or the distribution of protein throughout the day (Layman, 2009) (Drewnowski, 2001), these scientists drew their conclusion based on maximal stimulation of muscle protein synthesis, thereby arriving at the ~10 gram level, adding that greater amounts do not improve the outcome. (Loenneke, 2012)

Calculating the amount of essential amino acids (EAA) in a meal requires more labor than many of us are able or willing to perform, mostly because we lack the immediate resources needed to find out the base levels of each food in the meal.  There are books and websites that can help with this venture if you are so inclined.  However, eating a quality protein at each meal should do the job.  That usually includes meat, fish, eggs, and dairy, which are complete proteins, meaning that they have all the essential amino acids.   (Egg whites are excellent protein foods.)  Because grains and nuts lack lysine, and legumes lack methionine, it’s a good idea to combine them, as in rice and beans.  Combining essential aminos is not necessary at every meal, but it is in the course of the day.

Whey protein has been shown to stimulate a considerable rise in muscle protein synthesis and results in greater muscle cross-sectional area, especially if combined with a little resistance training—and it enhances recovery after exercise.  (Hulmi, 2010)  Older people show a decreased anabolic sensitivity to essential amino acids, probably because of declining intramuscular expression and receptor activation that are associated with slower anabolic signaling.  (Cuthbertson, 2005)   Among the countermeasures under investigation is regular resistance exercise, regardless of intensity or duration.  In physiological studies at the U. of TX, it was found that the only difference between young and old is the rapidity of the positive response to EAA’s.  (Drummond, 2008)  Timing of EAA ingestion for exercisers makes a difference.  Consume them afterwards.

Stimulating muscle protein synthesis is important to body composition.  If you multiply your body weight in kilograms (2.2 pounds) by 0.8, you’ll arrive at the number of grams of protein you need every day.  (You could also multiply pounds by 0.37.  Why didn’t we say that in the first place?)  More than 30 grams of protein in a single meal does not enhance protein synthesis.  This translates that 113 grams (about 4 oz.) of beef is enough, at 220 calories and 30 grams of protein.  (Symons, 2009)  Therefore, that 12-ounce steak from your favorite eatery isn’t doing much more than filling you up.  While you’re at that restaurant, skip the simple carbs if you’re looking to lose a few inches.  There’s a positive association between girth and consumption of potatoes, refined grains (including alcohol) and simple sugars, but a negative association with protein.  (Halkjaer, 2006)

Protein intake has added benefit—satiety.  If you feel full longer, you’ll eat less and, therefore, consume fewer calories.  Protein increases satiety to a greater degree than fats or carbohydrates (although fats beat carbs), and higher-protein diets result in thermogenesis, which augments energy expenditure.  And, if you have high triglycerides (from eating too many refined and starchy carbohydrates), complete protein is able to attenuate that while you change body composition to something more desirable.  (Clifton, 2009)  (Clifton, 2008)  Don’t forget to choose lean protein, to remove visible fat from your steaks and the skin from poultry, and to add legumes to your regimen.


Clifton PM, Keogh JB, Noakes M.
Long-term effects of a high-protein weight-loss diet.
Am J Clin Nutr. 2008 Jan;87(1):23-9.

Clifton PM, Bastiaans K, Keogh JB.
High protein diets decrease total and abdominal fat and improve CVD risk profile in overweight and obese men and women with elevated triacylglycerol.
Nutr Metab Cardiovasc Dis. 2009 Oct;19(8):548-54.

Cuthbertson D, Smith K, Babraj J, Leese G, Waddell T, Atherton P, Wackerhage H, Taylor PM, Rennie MJ.
Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle.
FASEB J. 2005 Mar;19(3):422-4.

Drewnowski A, Warren-Mears VA.
Does aging change nutrition requirements?
J Nutr Health Aging. 2001;5(2):70-4.

Drummond MJ, Dreyer HC, Pennings B, Fry CS, Dhanani S, Dillon EL, Sheffield-Moore M, Volpi E, Rasmussen BB.
Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging.
J Appl Physiol. 2008 May;104(5):1452-61.

Fujita S, Dreyer HC, Drummond MJ, Glynn EL, Volpi E, Rasmussen BB.
Essential amino acid and carbohydrate ingestion before resistance exercise does not enhance postexercise muscle protein synthesis.
J Appl Physiol. 2009 May;106(5):1730-9.

Halkjaer J, Tjønneland A, Thomsen BL, Overvad K, Sørensen TI.
Intake of macronutrients as predictors of 5-y changes in waist circumference.
Am J Clin Nutr. 2006 Oct;84(4):789-97.

Hulmi JJ, Lockwood CM, Stout JR.
Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein.
Nutr Metab (Lond). 2010 Jun 17;7:51.

Layman DK.
Dietary Guidelines should reflect new understandings about adult protein needs.
Nutr Metab (Lond). 2009 Mar 13;6:12.

Loenneke JP, Balapur A, Thrower AD, Syler G, Timlin M, Pujol TJ.
Short report: Relationship between quality protein, lean mass and bone health.
Ann Nutr Metab. 2010;57(3-4):219-20.

Loenneke JP, Wilson JM, Manninen AH, Wray ME, Barnes JT and Pujol TJ
Quality protein intake is inversely associated with abdominal fat
Nutrition and Metabolism.  Jan, 2012; 9:5

Paddon-Jones D, Westman E, Mattes RD, Wolfe RR, Astrup A, Westerterp-Plantenga M.
Protein, weight management, and satiety.
Am J Clin Nutr. 2008 May;87(5):1558S-1561S.

Sites CK, Cooper BC, Toth MJ, Gastaldelli A, Arabshahi A, Barnes S.
Effect of a daily supplement of soy protein on body composition and insulin secretion in postmenopausal women.
Fertil Steril. 2007 Dec;88(6):1609-17.

Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D.
A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects.
J Am Diet Assoc. 2009 Sep;109(9):1582-6.

Tipton KD, Gurkin BE, Matin S, Wolfe RR.
Nonessential amino acids are not necessary to stimulate net muscle protein synthesis in healthy volunteers.
J Nutr Biochem. 1999 Feb;10(2):89-95.

*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.


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?


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.