Sodium: How much is right for you?

Sodium’s association with high blood pressure is well known. However, sodium also plays a large role in keeping you healthy. It’s important to know how to strike the right balance.

Along with potassium, sodium is essential for fluid balance, facilitating the flow of water in and out of cells to bring nutrients in and take wastes away. Sodium also has a role in the regulation of blood pressure and helping muscles and the heart relax. Each sodium ion contains an electrical charge, acting as an electrolyte, which allows transmission of nerve impulses to the brain and throughout the body.

Sodium levels in the body are controlled by the kidneys. If the body doesn’t receive enough sodium daily—a chronic problem for our early ancestors—then the kidneys retain sodium. When the body has a high enough amount, then the excess sodium is excreted in the urine.

At times, sodium levels may fluctuate. If a person has a dysfunctional kidney, then the body may retain too much sodium, which can result in edema, or swelling in the legs and feet because sodium attracts water. In contrast, diarrhea or vomiting may result decreased sodium levels, a condition known as hyponatremia.

How sodium regulates blood pressure is not entirely understood, but there is an established link between high sodium intake and high blood pressure. As expected, there is also a link between sodium reduction and lower blood pressure.

The sodium-hypertension relationship may also have to do with how sodium interplays with other minerals such as potassium and calcium. Potassium, for example, appears to assist the kidneys in shedding excess sodium. Lowering sodium intake also helps to conserve calcium, which may affect blood pressure.

Recommendations for Sodium

The Institute of Medicine is recommending an Adequate Intake of sodium at 1,500 mg per day for adults and children 9-13 as well as 1,000 mg and 1,200 mg per day for children ages 1-3 and 4-8, respectively. These levels are considered appropriate for replacing daily losses via sweat and urine. The need for sodium may be slightly greater if exercise produces excessive sweating or if a person has symptoms of vomiting or diarrhea.

On average, however, most adults in the U.S. consume about 3,200 milligrams or more a day. With these figures, it is easy to understand why high blood pressure affects nearly 75 million Americans. The average intake is well above the Institute of Medicine’s Tolerable Upper Intake Level of 2,300 milligrams per day for adults and 1,500mg, 1,900mg and 2,200 mg for children ages 1-3, 4-8 and 9-13, respectively.

Cutting sodium intake daily tor recommended levels is important and it doesn’t have to be difficult with these three simple strategies:

Sodium Strategy #1: Limit processed or prepared foods high in sodium. Most sodium in the diet doesn’t come from the salt shaker, but from processed and prepared foods. Thus, the best way to lower sodium is to reduce intake of processed foods or replace them with low-sodium alternatives. This includes ready-to-eat packaged foods such as potato chips, fast-food meals such as burritos, and highly salted meals prepared at restaurants.

Sodium Strategy #2: Learn to enjoy food without salt. Taste food before salting it; the food may already be salty enough or it may be enjoyed without salt. In fact, salty is an acquired taste. The body and taste buds can easily adjust to less salt. Studies have shown that as people reduce salt intake and stick to a relatively lower intake of sodium, they will naturally begin to prefer foods with less salt. When eating at home, try not having the salt shaker on the table and, if eating out, simply move salt shakers to another table. When preparing food, try using less salt and seasoning food with spices or salt-substitutes instead. Keep an eye on store-bought spice blends, though, as many may contain high amounts of salt.

Sodium Strategy #3: Balance sodium with potassium-rich fruits and vegetables. A clear association exists between higher potassium intake from fruits and vegetables and lower blood pressure regardless of sodium intake. Potassium helps the kidneys in promoting sodium excretion, reduces urinary calcium and magnesium (which influence blood pressure), supports smooth vascular muscle health, and helps with regulation of blood pressure.

Less Sodium in a DASH

Most people who are interested in maintaining healthy blood pressure levels would do best to follow a DASH (Dietary Approaches to Stop Hypertension)eating plan. In the well-known DASH-sodium study, which was conducted by the National Heart, Lung and Blood Institute, people following the diet lowered blood pressure in just 14 days even without reducing salt intake.

The DASH eating plan includes consuming a diet rich in low-fat, low-sodium dairy products, fish, chicken and lean meats as well as large amount of whole grains, fruits and vegetables.

When a person is concerned about blood pressure, the best advice nutritionists can give is to begin following a DASH eating plan combined with regular exercise and weight management. In fact, according to a recent study in Hypertension, this plan helped people reduce blood pressure, lose weight, improve mental function, and improve cardiovascular health.

Taking the Pressure Off of Sodium

It’s extremely easy to place all of the blame for society’s high blood pressure woes and medical costs on sodium, but the mineral’s role in the body should not be ignored. Sodium is essential for good health and too little could lead to other health issues, including deficiencies in iodine, which is mainly provided in the North American diet from iodized salt.

While lowering sodium consumption can lead to a natural preference for foods with less salt, it’s important not to cut salt out completely. Because the body requires some sodium to function properly, avoiding salt entirely might backfire, and cause cravings for high-sodium foods. As with almost all vitamins and minerals, the key to healthy sodium intake is always balance with other nutrients. A DASH eating plan and strategies for maintaining a healthy intake (such as those given above) can help you achieve this balance of nutrients for healthy blood pressure levels and optimal health.

Reference

Dyuff RL, American Dietitic Association. American Dietetic Association Complete Food and Nutrition Guide, 3rd edition. 2006. Wiley.

More reason to love olive oil

I use one particular olive oil for cooking and another extra-virgin olive oil to mix with some balsamic vinegar for my salads. Olive oil, as the staple source of fatty acids in the Mediterranean diet, has also been heavily researched for its health benefits especially in comparison to other sources of fat such as butter, corn or soy oil.

On April 20, a study in BMC Genomics was published that found that olive oil eaten at breakfast modified gene expression in patients with metabolic syndrome (1). The breakfast caused the changes in mononuclear cells after intake of the olive oil and repressed pro-inflammatory genes (1).

The study was performed on 20 patients in a double-blind randomized trial (1). The researchers noted that many of the genes were also implicated in type 2 diabetes, dyslipidemia and obesity (1).

The study adds to evidence that olive oil helps reduce inflammation unlike other oils such as butter (2) and, thereby, adds to the reasons why the Mediterranean diet is associated with lower risk of cardiovascular disease (3).

References

1. Camargo A, Ruano J, Fernandez JM, Parnell LD, Jimenez A, Santos-Gonzalez M, Marin C, Perez-Martinez P, Uceda M, Lopez-Miranda J, Perez-Jimenez F. Gene expression changes in mononuclear cells from patients with metabolic syndrome after acute intake of phenol-rich virgin olive oil. BMC Genomics. 2010 Apr 20;11(1):253. [Epub ahead of print]

2. Bellido C, López-Miranda J, Blanco-Colio LM, Pérez-Martínez P, Muriana FJ, Martín-Ventura JL, Marín C, Gómez P, Fuentes F, Egido J, Pérez-Jiménez F. Butter and walnuts, but not olive oil, elicit postprandial activation of nuclear transcription factor kappaB in peripheral blood mononuclear cells from healthy men.Am J Clin Nutr. 2004 Dec;80(6):1487-91.

3. Bellido C. Perez-Jimenez F, Alvarez de Cienfuegos G, Badimon L, Barja G, Battino M, Blanco A, Bonanome A, Colomer R, Corella-Piquer D, Covas I, Chamorro-Quiros J, Escrich E, Gaforio JJ, Garcia Luna PP, Hidalgo L, Kafatos A, Kris-Etherton PM, Lairon D, Lamuela-Raventos R, Lopez-Miranda J, Lopez-Segura F, Martinez-Gonzalez MA, Mata P, Mataix J, Ordovas J, Osada J, Pacheco-Reyes R, Perucho M, Pineda-Priego M, Quiles JL, Ramirez-Tortosa MC, Ruiz-Gutierrez V, Sanchez-Rovira P, Solfrizzi V, Soriguer-Escofet F, de la Torre-Fornell R, Trichopoulos A, Villalba-Montoro JM, Villar-Ortiz JR, Visioli F. International conference on the healthy effect of virgin olive oil. Eur J Clin Invest. 2005 Jul;35(7):421-4.


David

Fibromyalgia

Fibromyalgia, or chronic fatigue syndrome, has increased by 200 to 400 percent in the last decade and now affects approximately 6-12 million Americans. It's a syndrome with symptoms of hormonal, sleep and autonomic control dysfunctions.

Those with fibromyalgia often suffer from widespread pain in muscles, poor sleep, and low energy levels. Co-existing conditions are food reactivities and irritable bowel syndrome, migraine headaches, chronic sinusitis, restless leg syndrome and sleep apnea.

Medical treatment may include analgesics for pain relief such as with acetaminophen or NSAIDS. Most will require treatment for hypothyroidism with Armour Thyroid. A Cortef prescription or supplementation with adrenal glandulars or licorice is also helpful for adrenal support. Lastly, sex hormone therapy may be needed.

Nutritional support may include supplements of iron to guard against iron-deficiency anemia,which may contribute to lacking energy, as well as coQ10, which is fat-soluble antioxidant needed in the mitochondria for production of energy. In addition, acetyl-l-carnitine may be helpful for supporting mitochondrial energy and d-ribose may help increase energy and reduce pain.
Reference
1. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.

Preventing Lung Cancer

My dear second cousin died of lung cancer last night at midnight. This is a horrible disease and it strikes so quickly. The cancer metasticized and reached his lymph nodes and then I think he and we all knew. It's a sad day for our family. It happened so fast and it pains me that I couldn't have been with him when he passed.

Of course, as a nutritionist, my thoughts turn to what could have been done to prevent this awful day from happening. As you look through the scientific literature, of course, you end up figuring that quitting smoking is key to guarding against risk. I know my cousin had quit, but perhaps it was too late.

The only other way to help prevent this disease is simply to be sure to eat plenty of fruits and vegetables daily. The high amounts of phytonutrients probably either help to upregulate antioxidant enzymes protecting cells or act simply act as antioxidants to cells. The result is less potential damage to cell DNA.

Maybe, however, skip out on the veggies high in beta-carotene because of association with higher risk of lung cancer (the beta-carotene apparently can bind to carcinogens in smoke and potentially increase damage to DNA). That's according to the famous CARET study from Finland where beta-carotene supplements appeared to increase risk of lung cancer in smokers and those with exposure to asbestos.

I'm going to add at my cousin might have been a lot better off without all the stress. He had a high amount of stress in his lifestyle. The stress itself, science is beginning to show, leads to more oxidative stress on cells. Perhaps the constant fight-or-flight response does add stress biochemically, but it should be immediately obvious that stress in our lives leads us to eat poorly, eat less fruits and vegetables, and have have poor habits like smoking.

We all could benefit from less stress in our lives. And it leads me to pause and think, I need some good stress-management techniques. Ones that I choose such as nature walking weekly may not be enough. Sooner rather than later I need to begin a steady exercise program, eating regularly, maybe delegating some projects.

Just some thoughts.

Sent from my iPad

Losing weight easy on the Zone Diet

The power behind Dr. Barry Sears's Zone diet is that it offers people simple techniques to be used as part of their eating plan, which makes lower-calorie eating on a high-protein, moderate-carb plan simply easier to follow. 

I've made a list below of a few of the techniques that I've used successfully  to help "stay in the zone," as Dr. Sears calls it, and keeping to a 40-30-30 ratio of carbs, proteins and fats: 

Protein - Decide on the amount of protein you should have by comparing size (e.g. of a chicken breast) with the thickness of your palm.  

Carbs - If it's a "good" (high-fiber; low-glycemic) source of carbs, then the portion should equal the size of  two fists, but if it's a "bad" source (low in fiber; high-glycemic) the portions should equal the size of one fist

Fats - If the protein has fat, don't add any. If it doesn't, then choose nuts or olive oil.  

Simple, right? Then, just eat frequently throughout the day by never letting five hours pass without a snack or meal. And you can generally apply it to a DASH-style, Mediterranean-style or Paleo-style diet.

The Zone diet ratio of protein/carbs/fats is all about keeping your body working efficiently while keeping blood sugar and calories in check. It's not about being complicated or restrictive -- which ultimately the greatest cause for diet failure because it leads to bingeing.

Cordain vs Campbell

I recently read what is entitled the "Protein Debate" between Loren Cordain, a paleo diet proponent, and Colin Campbell, a plant-based diet proponent. Given that I'm simply a graduate student without any specific adherence to either diet philosophy, i found the debate to be fascinating. Both had strong points to defend their positioning. In short, this is how it goes:

• Loren Cordain argues that because nutritional science is a young, evolving science with little agreement as to what is correct in eating for the general population, they should have a "guiding paradigm" based on the diet of our hunter-gatherer ancestors. The paleolithic diet would be one that include high amounts of protein from lean meats and minimally processed foods of paleolithic resemblance.

• Colin Campbell argues that nutritional science is not young (it's older than many other sciences) and, that, although knowledge of ancestral diets may be helpful, "biological complexity" throws out its use as a reference standard (after all, high calorie intake from meat may have increased likelihood of reproduction, but not guarded against disease). The priority should be given to searching for dietary factors that cause "collective disease and health outcomes" to guide nutritional recommendations.

You decide. They could, in fact, both be right and wrong on different levels. David

What causes Autism

Any connection between autism and childhood vaccines?

I don't really "believe" in much unless backed by science. I realize that the connection of vaccines and autism is a touchy subject and that there are opposing viewpoints. Eventually, however, reason must come into the picture and, despite what our opinions are, we need to rely on evidence to guide decision making.

Just last February, The Lancet retracted the study by Dr. Andrew Wakefield that had linked vaccines with autism. The medical journal cited flaws and unethical activity in connecting autism with vaccines (1). This was the study that had launched the first wave of groups against vaccines like Jenny MccCarthy's Generation Rescue. And I think everyone needs to all get over this and continue to see vaccines for what they are, life-saving medicines.

I know that just discounting vaccines' role in autism is not enough to appease a lot of people who fear for their children. After all, according to the CDC, 1 in 110 children in the U.S. now have autism. If not vaccines, than what is making this happen?

Vitamin D Theory

I, for one (being the vitamin D nut that I am), have high hopes for what's been dubbed the "Vitamin D Theory". The theory suggests that our autism epidemic began at or around the same time as did our epidemic of vitamin D insufficiency (2). If there is a link, then it would explain why there is a higher rate of autism among blacks and there should be a higher rate among children who are not in the sun for sufficient amounts of time.

According to Dr. John Cannell writing in Vitamin D Council's January newsletter, "The 'all autism is caused from vaccinations' crowd cannot accept the Vitamin D possibility as it threatens their core beliefs. They simply cannot change their minds" (3).

Then again, there's not much yet to support the vitamin D link, but Dr. Cannell adds "...organized medicine would say you should stop the vitamin D and watch your son deteriorate, which is why slavery to evidence based medicine is fine for scientists and unethical for practitioners" (3).

References

1. CNN. Medical Journal retracts study linking autism to vaccine. Available at: http://www.cnn.com/2010/HEALTH/02/02/lancet.retraction.autism/index.html

2. Vitamin D Council. http://www.vitamindcouncil.org/health/autism/vit-D-theory-autism.shtml

3. Cannell J. Vitamin D Newsletter. 2010 Jan 30.

Thoughts on High Fructose Corn Syrup

There are some really wacked people on the Internet who try to blame the whole obesity epidemic on HFCS, fructose or agave and are misguiding everyone. I liken it to the same misguidance that occurred in 1980s when everyone was scared of fat.

You shouldn't just cut out HCFS and replace it regular sugar or another caloric sweetener. It's really overeating, the overabundance of calories much of it from sugar, that in general contributes to this obesity problem.

What our real problem is is that our brains are wired for fats, carbs and salt that has led us into this obesity crisis now. As a whole, our species needed this wiring to seek out nutritious foods that helped us survive.

But in this modern world of aplenty, the answer to our obesity problem is to control our brains (or trick them with artificial stuff) and use simple discipline, portion control and balanced, nutritious meals.

Sucralose (Splenda)

Sucralose has been on the market for about two decades now and has been touted as a quite the wonderful artificial sweetener. The safety profile of sucralose has been excellent in adults and it has already helped many with type 2 diabetes to manage blood sugar without having to give up on many of their favorite foods and beverages.

Because of increased use of Sucralose over the years, however, high concentrations of it has been popping up in the environment and there have been worries about how the artificial sweetener may influence infants, children and even animals. One big worry has been potential affects on brain growth.

Two Swedish researchers, Dr Viberg and Dr Fredriksson set out to study the possible neurotoxicity of sucralose in mice. They gave just mice an oral dose of 5-125 mg of sucralose per kilogram bodyweight per day on days 8 through 12 immediately after their birth.

Then, the researchers killed the mice and analyzed their brains. They checked for key proteins and found no alterations that would indicate a disturbance to neuronal development.

Thus, they concluded, sucralose "seems to be a safe alternative for people", and possibly even during pregnancy, as it does not affect growth and development of the brain.

Reference

Viberg H, Fredriksson A. Neonatal exposure to sucralose does not alter biochemical markers of neuronal development or adult behavior. Nutrition. 2010 Jan 27. [Epub ahead of print]

High cola intake may cut sperm count, reports Danish study

Men who drink a few too many Diet Coke or some other cola-like beverages daily may have fewer sperm, according to a new study.

The study, published in the April 15, 2010 issue of American Journal of Epidemiology (1), had examined the semen quality of more than 2,500 young Danish men who had been recruited upon was evaluated for fitness and military service.

They found that those subjects who reported on a questionnaire that they consumed high amounts of caffeine (more than 800 mg per day) or high intakes of cola (more than 14 half-liter bottles per week) had reduced sperm concentration and total sperm count. On the other hand, the consumption of only moderate amounts of caffeine (less than 800 mg per day) or low amounts of cola (less than 14 half-liter bottles per week) were not associated with any similar effect on sperm concentration or count.

There was no association established between caffeine from tea or coffee and influence on sperm count.

The Copenhagen researchers of University of Denmark of Growth and Reproduction concluded that they "cannot exclude the possibility of a threshold above which cola, and possibly caffeine, negatively affects semen quality" (1).

They added, "Alternatively, the less healthy lifestyle of these men may explain these findings" (1).

Still, if you're interested in maintaining your vitality (who isn't?), it may be better to avoid the cola!

Caffeine and Semen Quality

There have been several studies that have investigated caffeine and a possible association with semen quality, which have led to conflicting results.

Previous to this study on high intakes of cola, there had been a pregnancy cohort in 2008 on more than 5,000 males that evaluated semen quality in association with prenatal coffee and caffeine exposure (2).

The study, also from Denmark, found that although high caffeine intake didn't have any significant effect on semen quality, it did lead to increased testosterone concentrations (approximately 14 percent) in the men (2).

So, until more research is conducted, there's still no need to give up on the coffee.

References

1. Jensen TK, Swan SH, Skakkebaek NE, Rasmussen S, Jørgensen N. Caffeine intake and semen quality in a population of 2,554 young Danish men. Am J Epidemiol. 2010 Apr 15;171(8):883-91. Epub 2010 Mar 25.

2. Ramlau-Hansen CH, Thulstrup AM, Bonde JP, Olsen J, Bech BH. Semen quality according to prenatal coffee and present caffeine exposure: two decades of follow-up of a pregnancy cohort. Hum Reprod. 2008 Dec;23(12):2799-805. Epub 2008 Aug 28.

Luo han guo - a source of xylitol

Louo han guo is a fruit that has been recently hyped up and marketed as a natural sweetener. What is it really? It's really just a source of xylitol. Xylitol is a natural sugar alcohol, which is not digested as easily by the body lending fewer calories per gram than regular sugar. The polyol also has a slight cooling effect, which you would recognize while eating sugarless gum like Trident.

Xylitol was first discovered and isolated in Sweden from birch bark. It is also now widely used in Sweden (where it was first isolated) and used in all sorts of candies there.

Regular use of xylitol is associated with significant reduction of cavities and tooth remineralization (1). Why? Because research shows that xylitol doesn't contribute to tooth decay and, unlike other sugar alcohols like erythritol, it may even help fight cavities by a mechanism of confusing cavity-causing bacteria to eat it and basically die.

Reference

1. Mäkinen KK. Sugar alcohols, caries incidence, and remineralization of caries lesions: a literature review. Int J Dent. 2010;2010:981072. Epub 2010 Jan 5.

Summing up Low-carb

Low-carbohydrate diets may do wonders for quick weight loss (mostly from water loss) and to improve glucose and insulin levels, but they are not without their adverse effects (1-2).

The body needs carbs for energy. Without sufficient amounts, muscle catabolism and protein will result, the break down of fat stores for fuel will result in incomplete fat oxidation, and an excess of acidic ketones will be produced. Diets too low in carbs can lead to ketoacidosis (1).

However, moderately low-carb diets such as the Mediterranean diet, which includes plenty of fruits, vegetables and monounsatured oils are a good choice for long-term health (2).

References

1. Nix, S. (2005). Williams' Basic Nutrition & Diet Therapy. Philadelphia: Mosby.

2. Shai, I., Schwarzfuchs, D., Yaakov, H., Sahar, D.R., Witkow, S., et al. (July, 2008). Weight loss with a low-carbohydrate, Mediterranean or low-fat diet. The New England Journal of Medicine, 359:229-241.

Does low-calorie dieting cause you to "yo yo" because of lowered metabolism?

This post came out of a question from someone who asked a question related to whether or not eating a very low calorie diet would lead to a "yo yo" effect caused by lowered metabolism, stoping weight loss and causing weight gain upon eating normally again.

There is no evidence suggesting that a "yo yo" effect would occur from low-calorie dieting, nor would lowering calories too far "stop" weight loss altogether. Truth is, calorie restriction does reduce metabolic rate, you would lose weight at a rate that is lower than normally expected, but if you started eating normally again, your metabolism would speed back up again.

In 2006, Heilbronn et al. studied the effects of calorie restriction (CR) on metabolism. The researchers published in JAMA the results of a six-month randomized controlled trial on CR and how it made an impact on biomarkers of metabolism as well as longevity and oxidative stress in overweight adults.

The subjects were paid and placed in one of the following groups: a control group, a CR group (25% reduction from baseline), a CR group with exercise (12.5% reduction, 12.5% increase activity), and what they called a very-calorie diet (890 kcal/d) followed by weight management at 15 percent weight reduction.

By the third month, metabolism had slowed (measured in part with plasma T3 levels) in both CR and very low-calorie diets. At six months, metabolism had slowed in the CR, CR with exercise, and very low-calorie diet groups.

Everyone lost weight in the intervention groups. Those on the very-low calorie diet lost the most, but they also lost the most muscle. From that same study, the researchers were the first to find reduced oxidative stress and DNA damage from CR in humans.

So, what do we know? We know that if you also drop even to 500-800 kcal per day that, despite slower metabolism (your body's survival mechanism), you still would lose weight albeit at a lower rate (as stated before).

What some researchers have tried to do since then to "trick" the body to not slow metabolism. They do it by staggering the calories with alternate-day CR/fasting or intermittent CR/fasting. These are interesting topics of research and may show up as new weight-loss fads of the future.

I don't recommend people drop calories or lose weight too quickly because it leads to too much loss of hard-earned muscle and, possibly, gallstones (if you're not drinking enough water and eating small meals throughout the day). In my experience, I've also seen quite a few people go lower than 800 calories per day for weeks and end up without energy, getting sick and looking pretty frail.

It's best, I think, to stick with losing only 1-2 pounds per week (by dropping calories steadily and increasing activity to keep muscle up) and then eventually keeping diet within 800-1200 kcal/d range.

Undigested meat in the colon

When you have undigested meat proteins in your colon, they will basically do what they do when thery are outside the colon: they rot. The rotting, or decay, is characterized by a release of foul-smelling chemicals.

One such chemical is cadaverine--the same that gave "cadavers" their name because of the smell they emit--which is the result of protein hydrolysis or the decarboxylation product of lysine. It's similar in structure to putrescine, putrescine itself produced from rotting activity.

Rotting flesh in the colon gives off a horrible odor and the smelly chemicals can become apparent in a person's breath, feces or urine. The person may suffer from the foul odors for a good while as the long process digestion or elimination of the meat continues.

To help speed things along, it's important to maintain a diet high in dietary fiber, specifically insoluble fiber, which helps increase rate of transit in the colon. Insoluble fiber comes from the "woody" parts of plants such as wheat bran and vegetable skins.

No one should have to put up with "the smell of death" after a meal. To avoid offensive gas and bad breath, just eat smaller portions of meat and be sure to also include some salad and extra vegetables.

Reference
Lecture notes by Albert Grazia, M.S.

Green tea EGCG in low doses boosts fat oxidation by amounts comparable to caffeine

Several studies have reported that green tea improves weight loss, which has largely been attributed to its content of caffeine. A pilot study, however, reports that green tea's main antioxidant catechin, epgallocatechin-3-gallate (EGCG), may also have thermogenic potential.

Thielecke et al of Germany report in the April issue of European Journal of Clinical Nutrition that consumption of EGCG at low doses taken after meals may contribute to increased fat oxidation similarly to caffeine (as much as 35 percent). The same effects of EGCG were not demonstrated while fasting.

The German researchers employed by DSM Nutritional Products performed a randomized, double-blind, placebo-controlled trial on 12 men that were screened for health problems, drugs and smoking. They also excluded men that had taken any dietary supplement within a week of the study.

Each male volunteer consumed an encapsulated supplement over three days (weeklong wash out in between) of either a low dose of EGCG (300mg), high dose of EGCG (600mg), caffeine (200mg), a combination of low-dose EGCG and caffeine (300mg EGCG/200mg caffeine), or a placebo.

The subjects were fed a standard meal of bread, butter, cheese, ham, tomato and cucumber according to the individual energy requiremens of each volunteer, calculated as 5 kcal/kg body weight with 50 percent enrgy from carbohydrates, 35 percent from fats, and 15 percent from proteins. They were prohibited from drinking caffeinated drinks during the study.

Fat and carbohydrate oxidation rates were calculated using a relatively new "respiratory quotient" that measures variance of oxygen consumption (VO2) and carbon dioxide production (VCO2). After three days of each treatment, the researchers took anthropometric measurements for body weight and BMI.

Here are their reported findings:

- 10 of the 12 successfully completed all five supplementation periods
- No adverse effects were reported
- There was no significant difference in fasting blood glucose and insulin from the different supplements
- Energy expenditure was not affected by EGCG
- Caffeine alone and in combination with green tea did have a pronounced effect on fat oxidation
- High dose EGCG boosted fat oxidation by a non-significant 20 percent
- Low dose EGCG surprisingly boosted fat oxidation by 33 percent after meals similarly to caffeine, but not before meals
- Low EGCG (300mg) and caffeine (200mg) maximized fat oxidation, increasing it by 49 percent, after meals

The researchers conclude: "This pilot study provides for the first time evidence that a single green tea catechin, EGCG, can increase fat oxidation in obese men, at least within 2 h after meal intake. Within this postprandial phase, EGCG is equipotent with caffeine with regard to fat oxidation."

My thoughts:

Why did the high dose EGCG not exhibit the same effects as the low EGCG? I understand that there may be a threshold point that is reached by caffeine and EGCG and its influence on fat oxidation, but I have a hard time buying that a low dose of EGCG may be more effective than a high dose. To that end, I'd like to see similar studies appear to clarify the relationship of EGCG on fat oxidation.

However, I am definitely glad to learn that we now know that EGCG does influence fat oxidation and that its effects of potentially improving weight loss have been pinned down to this mechanism instead of others such as reducing fat absorption. I am also glad to confirm that EGCG has no effect on body composition by means of influencing energy expenditure (meaning an influence on how many calories a person burns in a day).

I will continue recommending three or more cups of green tea a day, with or without the caffeine, for helping patients improve their weight loss. Despite the study, however, I think that across the board the most important reason why we continually see patients losing greatest amounts of weight while drinking green tea daily is because they are, at the same time, replacing their sugary beverages such as fountain drinks.

Reference

Thielecke F, Rahn G, Böhnke J, Adams F, Birkenfeld AL, Jordan J, Boschmann J. Epigallocatechin-3-gallate and postprandial fat oxidation in overweight/obese male volunteers: a pilot study. European Journal of Clinical Nutrition advance online publication 7 April 2010; doi:10.1038/ejcn.2010.47.

Whole milk better for your heart?

Every nutritionist knows (or should know) that a DASH eating plan is incredibly effective for helping patients to lower their blood pressure. A staple on the plan are low-fat or non-fat dairy foods (think 2 percent or skim milk versus whole milk) because they are considered more heart healthy than full-fat dairy, but the results of a 16-year prospective study just published in the European Journal of Clinical Nutritianare suggesting otherwise.

Bonthuis et al are calling for more studies to assess whether or not full-fat dairy may have more cardioprotective benefits than low-fat or nonfat dairy (1). The researchers found that among more than 1,500 adult Australians regularly consuming dairy products, those with highest consumption of full-fat dairy had reduced mortality when compared with those who ate low-fat dairy (1). This was after adjusting for possible confounders such as calcium and vitamin D. Most of the deaths of the participants in the study were related to cardiovascular disease and cancer (1).

The study overall confirms that dairy deserves to continue to be part of DASH and a previously published cohort from Australia that dairy could lower all-cause mortality (2). The study also questions recommendations of avoiding full-fat dairy for long-term protection against chronic disease.

Where did the recommendation to go for the low-fat dairy come from anyway?

The recommendation appeared because of studies that found that low-fat dairy was associated with lower blood pressure, but that full-fat dairy was not. Somewhat recently, the National Heart, Lung, and Blood Institute Family Heart Study in 2006 found an inverse association between prevalent hypertension and consumption of a diet containing dairy low in saturated fat (3).

Given the newest Australian findings, the dairy and blood pressure relationship may be dependent on the fatty acid make-up of the dairy. Could there be something about Australian dairy sources that are cardioprotective? The researchers no doubt must have this data and I imagine less saturated fat and more omega-3s would be involved in their results.

So, don't go switching to whole milk yet. If you like that full-fat flavor, then consider drinking omega-3-fortified dairy.

Just last month in March, a double-blind, cross-over study confirmed that omega-3-fortified dairy foods improved lipid profiles decreasing cardiovascular risk factors (4). The dairy improved omega-3 index, lowered total cholesterol, lowered LDL cholesterol, and lowered triglycerides significantly (4).

Once again, the fact of the matter is that it is the amount of omega-3s in any food that may truly determine how cardioprotective the food really is, as well as its lack of saturated fat and trans fat. Milk is no exception to this nutritional rule.

Reference

1. Bonthuis M, Hughes MC, Ibiebele TI, Green AC, van der Pols JC. Dairy consumption and patterns of mortality of Australian adults. Eur J Clin Nutr. 2010 Apr 7. [Epub ahead of print] Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/20372173.
2. van der Pols JC, Gunnell D, Williams GM, Holly JM, Bain C, Martin RM. Childhood dairy and calcium intake and cardiovascular mortality in adulthood: 65-year follow-up of the Boyd Orr cohort. Heart. 2009 Oct;95(19):1600-6. Epub 2009 Jul 29.
3. Djoussé L, Pankow JS, Hunt SC, Heiss G, Province MA, Kabagambe EK, Ellison RC. Influence of saturated fat and linolenic acid on the association between intake of dairy products and blood pressure. Hypertension. 2006;48:335.
4. Dawczynski C, Marin L, Wagneer A, Jahreis G. n-3 LC-PUFA-enriched dairy products are able to reduce cardiovascular risk factors: A double-blind, cross-over study. Clinical Nutrition. Mar 19. [Epub ahead of print]

Getting to the Bottom of Hemorrhoids

When a patient has hemorrhoids (most prevalent in males over 50) then it is always important to evaluate hydration and dietary fiber intake because constipation contributes to risk (1). Sufficient regular water intake and fiber helps to encourage regular bowel movement and alleviate symptoms of constipation.

One can't get to the bottom (excuse the pun) of hemorrhoids, however, without also evaluating the patient's level of activity. A sedentary lifestyle is a major risk factor (spicy foods and alcohol intake are also risk factors) (2). Sitting too long in an office chair, an automobile, in front of the TV, or on a toilet increases pressure on veins in the anus. Exercise promotes circulation and alleviates pressure on the veins, which helps to shrink hemorrhoids and prevent them in the future.

I am also a fan of flavonoids (in particular, micronized purified flavonoids, or Daflon at 500mg) for use with hemorrhoid therapy. There has been at least a few double-blind, placebo-controlled trial that showed flavonoids relieved symptoms associated with hemorrhoids and reduced frequency and severity of hemorrhoid flare-ups (1-4). The evidence behind use of flavonoids, I realize, is limited because of methodological errors and possible bias (5), but in my experience (which I will not explain) they work well.

References

1. Pigot F, Siproudhis L, Allaert FA. Risk factors associated with hemorrhoidal symptoms in specialized consultation. Gastroenterol Clin Biol. 2005 Dec;29(12):1270-4. Available at http://www.em-consulte.com/article/100126.
2. Jiang ZM, Cao JD. The impact of micronized purified flavonoid fraction on the treatment of acute haemorrhoidal episodes. Curr Med Res Opin. 2006 Jun;22(6):1141-7.
3. Danielsson G, Jungbeck C, Peterson K, Norgren L. A randomised controlled trial of micronised purified flavonoid fraction vs placebo in patients with chronic venous disease. Eur J Vasc Endovasc Surg. 2002 Jan;23(1):73-6.
4. Lyseng-Williamson KA, Perry CM. Micronised purified flavonoid fraction: a review of its use in chronic venous insufficiency, venous ulcers and haemorrhoids. Drugs. 2003;63(1):71-100.
5. Struckmann JR. Clinical efficacy of micronized purified flavonoid fraction: an overview. J Vasc Res. 1999;36 Suppl 1:37-41.
6. Alonso-Coello P, Zhou Q, Martinez-Zapata MJ, Mills E, Heels-Ansdell D, Johanson JF, Guyatt G. Meta-analysis of flavonoids for the treatment of haemorrhoids. Br J Surg. 2006 Aug;93(8):909-20.

Heartburn and Diet

Heartburn is an awful feeling that almost everyone has suffered from at some time in their lives. It's disheartening to hear that in the USA about 44 percent suffer every month and, worse yet, about 10 percent suffer every day (1). There's no need for the continual pain from heartburn (or taking the drugs to avoid it or treat it). With a little knowledge of what causes heartburn and change in diet, anyone can avoid heartburn for life.

GERD

Chronic heartburn, or gastroesophageal reflux disease (GERD), is a result of reflux of gastric acid and gastric contents re-entering the esophagus. Depending on the amount of acid refluxed and heartburn severity, mucosal damage can cause the esophagus to become irritated and painfully inflamed (2). Although the esophagus can heal pretty well, GERD mucosal damage can potentially leads to more serious outcomes such as increased risk for erosive esophagitis, strictures, Barret's esophagus and even adenocarcinoma (1).

Gastric acid amounts, which peak about 2-3 hours after meals, have more of a chance to reflux if a person is in a reclining position (2). Certain foods can also cause the lower esophageal sphincter to relax increasing risk of heartburn, namely alcohol, fatty foods and chocolate. Alcohol and coffee also can cause increased gastric acid secretion increasing risk. As you can imagine or may have experienced, the worst events of heartburn happens to people in the evening after eating a large fatty meal accompanied by alcohol, coffee and chocolate.

Peptic Ulcer

Heartburn can also be the result of a peptic ulcer, or duodenal ulcer that is chiefly caused by infection from Helicobacter pylori or, to a lesser degree, overuse of aspirin or NSAIDs (1). NSAID produces ulcers by blocking the production of prostaglandins in the cyclooxygenase-1 pathways (3). What H. pylori does to cause the ulcers is cause acid to be secreted at higher rates (hypersecretion), which is not good for the gut and produces the discomfort. The rate of secretion also can be corrected by eradicating the H. pylori (1). Whatever can help to modulate acid secretion is also considered therapeutic, which includes H2-receptor antagonists and proton pump inhibitors (1).

Dietary Therapy

Dietary therapy should focus on avoidance of heartburn trigger foods while encouraging healing with other foods as well as improving immune resistance to harmful bacteria such as H. pylori.

A word on low-carb diets

Although there does appear to be a few proponents of a high-protein, low-carb diet as therapeutic for both GERD and peptic ulcer disease, I was not able to find any clinical evidence to back up claims on blogs and Web sites that the diet would help with heartburn, or specifically that a low-carb diet would help eradicate bacterial infection. The interest in low-carb dieting is prevalent, however, and if nutritionists choose to recommend one such as Atkin's, then they should make patients aware of possible unwanted side effect from eating additional fatty foods that may cause increased possibility of heartburn as stated earlier.

Therapeutic Fiber and Probiotics

Dietary therapy for GERD and peptic ulcer disease should begin with a diet higher in fiber, preferably soluble fiber (1-3). According to a prospective cohort study on more than 51,000 male adults in 1986, dietary fiber from beans, tofu, peanuts, and other nuts (all rich in soluble fiber) reduced risk of peptic ulcer disease more than other foods rich in insoluble fiber (3). Dietary fiber helps to normalize gastric motility and soluble fiber can support growth of healthy gut flora (1). To best help prevent both diseases, patients should strive to eat a diet high in fruits, vegetables and legumes.

After antibiotic therapy in peptic ulcer disease, probiotic foods such as yogurt, kefir and sauerkraut can be therapeutic. Probiotics can help support GERD as well by helping to normalize symbiosis. The probiotic bacteria can help repopulate gut flora and they will thrive on prebiotics found in fruits, vegetables and legumes (1). A healthy gut flora can help normalize symbiosis and improve immune resistance to infection.

Avoiding Triggers

What a diet should not do is cause any additional stress to the patient, which include heart burn triggers. GERD patients should limit fatty foods, caffeine, alcohol, chocolate, garlic, onions and peppermint that can relax the lower esophageal sphincter (1). In addition, acidic foods such as peppers, citrus juice and tomato juice should be avoided to limit recurrence of pain from inflammation in the esophagus (1).

On the other hand, there is no evidence for avoiding spicy foods (surprising to me) or milk, alcohol or coffee as they have not been linked as causal factors for peptic ulcer disease (2). Milk, however, can exacerbate symptoms after infection (1). Those with risk of peptic ulcers should also avoid aspirin and NSAIDs with direction from a doctor.

Other advice

GERD therapies
- Avoid large meals, finish eating at least three hours before bedtime, relax, eat slowly, chew food, sleep well, keep their head up during digestion (1;2).
- Because being overweight and smoking are risk factors for GERD, a weight-loss program and quitting the cigarettes can help avoid heartburn (1).
- Try a food allergy elimination diet to determine if there's a challenge from gluten, dairy, eggs, etc (1).
- Take digestive enzymes to avoid maldigestion as necessary (1).
- Take glutamine for as it is the preferred fuel for gut lining and can help encourage faster healing (1).

Peptic ulcer therapies
- Although there is limited evidence on how much it helps, eating broccoli and brussel sprouts may help upregulate antioxidant enzymes and protect and repair gastric mucosa (1;2).
- Cook broccoli and other foods to avoid infection with H. pylori or E. coli (1).
- Drinking green tea, eat berries and drink red wine since they contain catechins, quercetin and other flavonoids that inhibit H. pylori proliferation and have anti-inflammatory effects (1).
- Take zinc-carnosine since it helps to inhibit H. pylori proliferation and shortens duration of treatment with antibiotics (1).

References

1. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
2. Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Baltimore, MD: Lippincott Williams & Wilkins, 2009.
3. Ryan-Harshman M, Aldoori W. How diet and lifestyle affect duodenal ulcers. Review of the evidence. Can Fam Physician. 2004 May; 50:727-732.

Vitamin D and Crohn's disease

Vitamin D deficiency may actually contribute to Crohn's disease because the hormone modulates the immune system. According to endocrinologists at McGill University, vitamin D appears to turn on genes to encode antimicrobial peptides that fight against intestinal invaders (1). The immune support may help avoid inflammation associated with an autoimmune response in Cronh's disease.

This may explain why Crohn's disease is more prevalent in Northern latitude countries. It also suggests that increased vitamin D could assist in avoiding Crohn's disease in the future.

How do these findings affect what we know about ulcerative colitis? I hope we find out soon.

Reference

1. McGill University Health Centre (2010, January 27). Vitamin D supplements could fight Crohn's disease. ScienceDaily. Retrieved March 31, 2010, from http://www.sciencedaily.com­ /releases/2010/01/100127104904.htm

Managing Diverticulitis After Treatment

It is well documented that a diet low in insoluble fiber is considered the main etiological factor in leading to diverticulitis. The intake of insoluble fiber speeds up transit of food and increases bulk reducing pressure on the intestine (1). On the other hand, intake of red meat appears to increase risk (1).

Patients treated for diverticulits are often prescribed antibiotic therapy and recommended to stay on a low-fiber diet and reintroducing insoluble fiber gradually (2). In some cases, surgery is needed (2). Afterward, nutritionists would recommend gradual increases of fiber because a diet high in fiber can lead to high amounts of gas and forceful diarrhea (2-3).

Because of possible damage in the intestine, nutritionists should also evaluate patients are at higher risk of malnutrition. Malnutrition can lead to slow healing and recovery as well as deterioration of muscle, respiratory and immune function (4). To receive adequate nutrients, higher protein intake as well as supplements of certain vitamins such as B12 and minerals such as calcium may be needed (4).

A weight-management program may help to avoid diverticulitis in the future. According to a prospective cohort study, subjects with a BMI, waist circumference and waist-to-hip ratio that categorized them as obese had an increased risk of diverticulitis and diverticular bleeding (5).

Nutritionists may also recommend probiotics along with prebiotics to support growth of healthy intestinal flora after antibiotic therapy (4).

References

1. Korzenik JR. Case closed? Diverticulits: epedemiology and fiber. J Clin Gastroeneterol. 2006 Aug;40 Suppl 3:S1 12-6.
2. Kotzampassakis N, Pittet O, Schmidt S, Denys A, Demarines N, Calmes JM. Presentation and treatment outcome of diverticulitis in younger adults: a different disease than in older patients? Dis Colon Rectum. 2010 Mar;53(3):333-8.
4. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
5. Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL. Obesity increases the risks of diverticulitis and diverticular bleeding 2008;136(1):115-112.

Helping a Patient Manage IBS and Diarrhea

When IBS is diarrhea-predominant, a doctor may prescribe an antimotility agent to assist patients with symptoms (1). He or she may also prescribe an antibiotic if the IBS is a result of small intestinal bacterial overgrowth (1).

As a dietary aid for patients, a nutritionist may suggest soluble fiber such as from oats because it can help act against symptoms such as diarrhea by helping bind fat and slow emptying of food from the stomach into the small intestine (2).

The soluble fiber can include prebiotics such as fructo-oligosaccharides or resistant maltodextrin, which support growth of healthy intestinal bacteria. The prebiotics taken in conjunction with probiotics particularly after antibiotic therpay may help with promoting the growth of the good bacteria. This integrative therapy can help to alleviate symptoms by promoting competition against small intestinal bacterial growth (3).

Nutrionists should recommend suspending intake of insoluble fiber such as from wheat and cereal grains and limiting poorly-digested carbohydrates and sugar alcohols as these can worsen symptoms (4). Patients may find benefit from following an exclusion diet whereas trigger foods are eliminated and then, if thought advisable, reintroduced gradually (4).

References

1. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
2. Bijkerk CJ, de Wit NJ, Muris JWM, Whorwell PJ, Knottnerus JA, Hoes AW. Soluble or insoluble fibre in irratble bowel syndrome in primary care? Randomized placebo controlled trial. Brit Med Jour 2009;339:b3154. Available at http://www.bmj.com/cgi/content/abstract/339/aug27_2/b3154. Accessed on March 31, 2010.
3. American College of Gastroenterology (2008, October 10). How Effective Are Probiotics In Irritable Bowel Syndrome?. ScienceDaily. Available at http://www.sciencedaily.com­ /releases/2008/10/081006092656.htm. Accessed on March 31, 2010.
4. Heizer WD, Southern S, McGovern S. The role of diet in symptoms of irritable bowel syndrome in adults: a narrative view. J Am Diet Assoc. 2009 Jul;109(7):1204-1.

Low-carb diets and dehydration

It is well known that dehydration is a potential adverse effect of a ketogenic diet, which is one higher in fat with adequate protein and lower in carbohydrates.

Nutritionists should be watchful, in particular, of those who use ketogenic diets as therapy for certain conditions such as epilepsy and type 2 diabetes.

A study in epileptic children on ketogenic diets, for example, found dehydration to be the "most common early-onset compllication"and higher in those who fasted (1-2). The dehydration could be partly blamed on the incidence of GI tract adverse effects (1).

When treating those with type 2 diabetes with a ketogenic diet, it is advisable to instruct drinking up to eight 8 oz. glasses of water daily. There may also be need for adjusting those recommendations if certain medications were used such as diuretics.

According to the researchers who performed an intervention trial on those with type 2 diabetes and a ketogenic diet that resulted in a few adverse effects, the following was concluded: "Until we learn more about using low carbohydrate diets, medical monitoring for hypoglycemia, dehydration, and electrolyte abnormalities is imperative in patients taking diabetes or diuretic medications" (1).

The lower carbs can have a diuretic effect on the body, which should lead clinicians to be aware and make recommendations for increased water intake as necessary.

References

1. Duschowny MS. Food for thought: The ketogenic diet and adverse effects in children. Epilepsy Curr. 2005 July;5(4):152-154. Available at: Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1198735/?tool=pmcentrez

2. Kang HC, Chung da E, Kim DW, Kim HD. Epilepsia 2004;45:1116-1123. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1198735/?tool=pmcentrez

Kidneys: Animal vs Veggie Protein

I was curious to know what it is about animal protein in general that would affect kidneys more than vegetable protein. So I went searching for a study.

There was a human intervention trial from the Dept of Internal Medicine in Texas that I found, which had evaluated animal protein-rich diet on kidney stones and calcium. The study took 15 subjects and fed them either vegetable protein, vegetable and egg protein or animal protein for 12 days in three different periods (1). What the study found was that the animal protein diet "conferred an increased risk for uric acid stones" but a lesser risk than the vegetarian diet for "calcium oxalate or calcium phosphate stones" (1).

Because my question really wasn't sufficiently answered by this study, I decided to pursue what National Kidney Foundation had to say. Finally, I found a publication they put out referencing nutrition and speaking to vegetarian diets in which they basically state that the veggie diets aren't "rich in higher quality protein" (2), but that also that the best sources of vegetarian protein may be ones lower in potassium and phosphorus depending on kidney dysfunction.

At best, the main focus on kidney health is a balance between protein and carbs because too few leads to more protein break down as well as protein with sodium (lower is better), phosphorus (lower is better), calcium, potassium (sometimes higher, sometimes low is better) and, of course, water amounts for keeping kidneys functioning well (2).

References

1. Breslau NA, Brinkley L, Hill KD, Pak, CY. J Clin Endocrinol Metab. 1988 Jan;66(1):140-6. Available at: http://www.ncbi.nlm.nih.gov/pubmed/2826524

2. National Kidney Foundation. Nutrition and Early Kidney Disease. Available at: http://www.kidney.org/atoz/pdf/NutriKidFail_Stage1-4.pdf

Why Evidence-based Nutrition

As a result of my profession in science communications, it is a fact of life that I come in to work to find 1-2 papers to read every morning on my desk. I must read an average of between 10 new scientific papers weekly. They can range from culture studies, animal studies, human clinical trials, epidemiological studies, meta-analyses or simply review articles.

As a writer who specializes in topics of nutrition, I am continually faced with the labor of assessing just how “big” the news coming from the study really is, whether or not it merits more attention by our research and sciences team, and whether or not we should communicate it to the public.

If I had any special talent for pointing out flaws or problems in studies, I would be thrilled. I don’t. Not at all. Lucky for me, however, I work with a few knowledgeable scientists with a keen awareness for what’s hot and what’s definitely not.

I doubt that many of my own colleagues share the same luxury that I have for being able to pass a study by an experienced nutritionist to help me place it in proper perspective for our audiences. This is simply evident by an Internet search for nutrition articles and a judgment of how other health writers handle their material.

Relying on experts to sift through the journals has been a unique experience, one that has been inspiring—which is why I now have hopes of ultimately gaining expertise of evidence-based nutrition (EBN) myself. EBN is simply true science and research, after all, and it informs decisions and practice.

It is my view that nutrition is a young science that is maturing quickly. I share a similar positive optimism for the field as Walter Willet, who has written of a merge of nutritional sciences with epidemiology to provide greater knowledge more quickly (1).

I follow with Willet’s assertion that nutritional research approaches are improving (that it won’t take us 100 years to discover flaws in dietary recommendations such as partially hydrogenated oils, for example(1)), and my interest is piqued in learning, as I would expect, that the study of genomics will further influence the future of nutrition.

While evidence-based nutrition and medicine may appear controversial to a few, I cannot see any other way for me, as I long to live in a world where science and statistics (even if we don’t “get” them) govern our understanding, not our often-flawed personal judgments.

I welcome the new process of nutritional epidemiology referenced by Willet that he expects will provide “vast and unprecedented information” (1). For that matter, I expect to be intensely studying as continual information appears over the next decade or so.

To achieve what Trisha Greenhalgh advises in her wonderful primer on evidence-based medicine, How to Read a Paper, it is my expectation to come away with the ability “not only to read papers, but also to read the right papers at the right time” (2) to best guide my decision making.

References

1. Willet WC. Nutritional epidemiology issues in chronic disease at the turn of the century. Epidemiol Rev. 2000;22(1):85-86. Available at: http://epirev.oxfordjournals.org/cgi/reprint/22/1/82.pdf

2. Greenhalgh T. How To Read A Paper: The Basics of Evidence Based Medicine. Malden, MA: Blackwell, 2006, p. 2.

How much water do I drink?

I've been perusing through Dr. Batmanghelidj's book Your Body's Many Cries for Water. Yes, I'm well aware that it does not entirely scientific and does have a few claims that could be regarded as sensationalism for water (excess cholesterol is a result of too little water intake, really?).

I was intrigued, however, at some of the references to the possibility of chronic dehydration as an influence on disease and the beginnings of cellular aging, which can fuel chronic disease.

Plus, anyway, I needed to write a paper on water.

So, of course, I had to ask myself, "How much water do you drink?"

So here goes my diet for today:

8am: 1 cup of green tea (with 1 yogurt/protein shake/fruit)

10am: 1 cup of yerba maté (a habit passed from Argentine mom)

12pm: 1 cup iced tea (with chicken salad lunch)

2pm: 1 shot espresso

4pm: 1 cup yerba maté

6pm: 1 glass red wine (with 1 cup lentil-asparagus soup dinner)

9pm: 1 cup green tea

(Plenty of liquid, but no straight glasses of purified H2O.)

I suppose that from a nutritional standpoint, it appears I did pretty OK for the day and plenty of antioxidants from fruit, veggies, tea, maté, coffee, and red wine. I am simply trying to stick to a relatively decent DASH eating plan.

Although I didn't feel dehydrated (I drank about 7 cups of liquid), given what I have now read about water I'll probably have to reconsider what I'm doing.

I'm especially alarmed at the possible effects of chronic caffeine diminishing ATP and alcohol's influence on vasopressin causing dehydration. (And here I thought the regular tea, coffee and occasional red wine were pretty OK habits.)

It does make sense to me that cells would best function when well-hydrated. After all, as stated in the materials, life began in water, or an ancient primordial swamp.

No doubt in my mind that given our origins from the sea that it's water intake that is truly necessary for entire body's proper function (along with a bit of salt).

As the water-relationship makes common sense to me, I can see how I might recommend it as integrative therapy in certain situations, although I would hang back from calling it "prevention" or "cure" of disease without some considerable evidence-based research.

I admit I had no idea something like a low-grade "chronic dehydration" existed and could exist despite food and liquid intake and affected directly by caffeine and alcohol.

It seems to me that, since water represents pretty much the starting point of nutrition (at least from a cell's and ancient fishapod ancestor's standpoint), the topic of water intake definitely should be part of all nutrition programs.

My thoughts,

David

What's the most dangerous item on a fast food menu?

When I first saw the movie Super Size MeI was first pretty shocked that someone would actually risk his own body this way. Then, I was shocked at how quickly this guy was able to gain weight. This may simply be because I don't tend to gain any weight even after stuffing myself day after day. Of course, I've never tried to stuff myself with McDonald's day after day. Maybe that would do it. It did for this guy. And it does for our children. Sure opened my eyes.

What's the most dangerous item on the fast food menu?

I remember a time when I was younger I would go off with my grandpa to Burger King. He'd say, "Let's get you a Whopper. They're only a buck." I'd gush with enthusiasm. He'd buy me one. He'd buy himself too.

My grandpa died of heart disease. I blame it on those Whoppers. I blame them because they're cheap and because the name itself, like the Big Mac, suggest that you're getting a lot of meat for your money. What you're really getting is a gimmick and a lot of saturated and trans fat. I have no doubt that Burger King Whoppers (they ate them all the time) are what killed both my grandfather and my grandmother.

Why Statins May Require You Take Extra CoQ10 and Vitamin E

Statins are drugs used to lower cholesterol by blocking cholesterol synthesis in the liver (1). By lowering total and LDL cholesterol, in effect, they help lower risk of heart disease and death (1). The most commonly known statin drugs are simvastatin (Zocor), lovastatin (Mevacor), pravastatin (Pravachol), and rosuvastatin (Crestor).

Currently, it is theorized that as statins block cholesterol synthesis, they also block synthesis of coenzyme Q10 (2). This is unfortunate because coenzyme Q10 plays a key role in the mitochondria in the electron transport chain, as an antioxidant and as a regenerator of vitamin E (3).

Statin therapy, then, could potentially lead to deficiencies of both coenzyme Q10 and, possibly, increase the need for vitamin E in cells (4). It has been theorized that deficiencies in both coenzyme Q10 and vitamin E are why statins cause statin-related muscle pain and statin-related myopathy (3-4).

References

1. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. JAMA. 1999 Dec 22-29;282(24):2340-6. Available at: http://www.ncbi.nlm.nih.gov/pubmed/10612322
2. Schaars CF, Stalenhoef AF. Effects of ubiquinone (coenzyme Q10) on myopathy in statin users. Curr Opin Lipidol. 2008 Dec;19(6):553-7.
3. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
4. Galli F, Iuliano L. Do statins cause myopathy by lowering vitamin E levels? Med Hypotheses. 2010 Apr;74(4):707-709. Epub 2009 Nov 6.

What are blood thinners and how do they work?

Blood thinners, or anticoagulants and antiplatelet agents, are drugs to thwart blood clotting of which could block flow of blood to your heart causing a heart attack or your brain causing a stroke.

Common anticoagulants are Coumadin, Warfarin and Heparin. It controls the rate in which clotting can occur and prevents them from forming inside blood vessels and the heart. It can also help prevent existing clots from enlarging.

Common antiplatelet agents are Aspirin, Plavix (clopidogrel bisulfate) and Ticlid (ticlopidene hydrochloride). As the name suggests, they keep platelets from aggregation to prevent possible clotting, specifically where an injury to a blood vessel may have occurred.

Blood thinners aren't associated with any specific nutrient deficiency, but are contraindicated taken with foods and supplements high in vitamin K1 (a clotting factor) or large amounts of vitamins E and C. They are also contraindicated with alcohol, certain herbs and teas, and other dietary agents that cause thinning of blood.

Reference

http://www.nlm.nih.gov/medlineplus/bloodthinners.html

Bone Turnover Biochemical Markers

With estimates that one out of two white women in North America will suffer from an osteoporotic fracture sometime in their life, prevention of osteoporosis should be a major health objective for all women (and men). In addition, especially in post-menopausal women it is useful to predict the rate of bone loss and to further monitor how bone therapies are assisting over time.

Biochemical markers for bone turnover have improved over the last few years (1) and may help with prediction of rate of bone loss. Serum bone alkaline phosphatase, total osteocalcin and procollagen type 1 N-terminal propetide assays are best markers for bone formation (1). N- and C-terminal crosslinked telopeptides in urine and C-terminal telopeptides in serum are sensitive for bone resorption (1). Deoxypiridinoline in urine is another measurement of bone resorption, primarily useful during treatment (2).

Monitoring these biochemical markers can be useful for predicting rate of bone loss thereby can be supportive of recognizing osteoporosis or how effective antiresorptive or hormone-replacement therapies are on a patient. Depending on the rate status, a clinician can decide what therapies are most useful and make adjustments as seen fit.

A disadvantage is that biomarkers may not be as specific as needed to adequately detect rates of bone turnover, because any significant increase in resorption or formation results in increases in all biochemical markers (3). The markers are also not indicative of any certain disease, only reflecting on bone metabolism despite reason for changes (3).

Reference List

1. Eastell R, Hannon RA. Biomarkers of bone health and osteoporosis risk. Proc Nutr Soc 2008;67:157-62.
2. Kitatani K, Nakatsuka K, Naka H, Miki T, Morii H, Nishizawa Y. Clinical usefulness of measurements of urinary deoxypyridinoline (DPD) in patients with postmenopausal osteoporosis receiving intermittent cyclical etidronate: advantage of free form of DPD over total DPD in predicting treatment efficacy. J Bone Miner Metab 2003;21:217-24.
3. Srivastava AK, Vliet EL, Lewiecki ML, Abdelmalek A, Gluck O, Baylink DJ. Clinical Use of Serum and Urine Bone Markers in the Management of Osteoporosis [Abstract and Introduction]. Curr Med Res Opin 2005;21(7):1015-1026. Available at: http://www.medscape.com/viewarticle/508542_print. Accessed on 22 Jan 2010.

Detecting Levels of Iron Storage

Ferritin is the body's major iron-storage protein and its levels in serum are parallel to iron stores. Normally, 1 ng/mL of serum ferritin is related to about 8 mg  of iron in storage. It rises somewhat in males and post-menopausal females. Any rise or decrease in levels of serum ferritin indicates available iron stores in the body. 

As a diagnostic tool, serum ferritin is the most sensitive test of iron-deficiency anemia in a patient. In presence of iron deficiency, ferritin is generally the first sign followed by decreased iron levels and changes noted in red blood cells such as size, color and number. Low levels of ferritin indicate reduced iron stores or, rarely, malnutrition due to protein depletion. A decrease can also result from hemodialysis. Levels below 10 mg/100 mL is a diagnosis of iron-deficiency anemia. 

Higher levels, in contrast, indicate hemochromatosis, hemosiderosis, iron poisoning, or a recent blood transfusion. A higher level of ferritin can also be found in patients with megaloblastic anemia, hemolytic anemia and chronic hepatitis. It is also elevated in those with chronic disease states such as chronic liver disease, uremia, alcoholism, collagen diseases or neoplasm. 

The serum ferritin study is limited because ferritin may act as an acute-phase reactant protein such as in states of inflammatory diseases, infections, metastatic cancer and lymphomas. In these cases, ferritin levels may increase one or two days after onset and peak at three to five days. To classify anemias, tests of serum ferritin should be accompanied with serum iron levels and total iron-binding capacity. 

There are also interfering factors with serum ferritin, mainly blood transfusions, recent dietary intake of red meat, hemolytic diseases, iron storage disorders like hemochromatosis, menstruation (women will have decreased ferritin levels after menstruation), and drugs that increase ferritin levels.

Summarized from

Pagana, K.D., Pagana, T.J. Mosby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006, pp 249-50.

Heavy Metal Biochemical Assessments

Mercury

Mercury’s recent presence in the body can be assessed with blood and urine samples because the initial half-life of blood mercury elimination is 3 days. The half-life of elimination for whole body mercury is between 60 and 90 days. Generally, the levels of mercury are below 10 mcg per liter in urine and below 40 mcg per liter in blood. Hair analysis can be useful as an estimate of long-term exposure to mercury.

To diagnose acute mercury toxicity, symptoms of respiratory distress are evaluated along with lab evaluation with a complete blood count and differential, serum electrolytes, glucose, liver and renal function tests, and urinalysis. Chest readiography and serial ABG measurements should be used for patients with severe inhalation exposure.

Reference: http://www.atsdr.cdc.gov/MHMI/mmg46.html

Lead

Blood lead levels can assess recent exposure to lead. It’s the primary screening method for lead exposure. It can also be measured with erythrocyte protoporphoryn, but this test is not sensitive enough to determine if children have levels below 25 mcg per deciliter. Because lead later travels to soft tissues and eventually to bones and teeth after several weeks, long-term exposure can be measured in bones and teeth with x-ray techniques.

Reference: http://www.atsdr.cdc.gov/toxprofiles/phs13.html

Cadmium

Cadmium in urine is best for determining level of recent and past exposure in the body. Analysis of hair and nails is not as useful because of factors of contamination from environment. Blood calcium can be useful to determine recent exposure in the body.

Reference: http://www.atsdr.cdc.gov/tfacts5.html

What's wrong with hair zinc analysis?

Hair used for nutritional status of a mineral can be flawed because of exogenous contamination--from water, dust, cosmetics, shampoos, etc--and because of endogenous, nonnutritional factors such as hair growth rate, color, sex, pregnancy and age.

However, I do find it quite interesting that hair analysis could indicate a history of nutrition. Historical measurements would be otherwise difficult to get, but hair grows lsowly and so hair can reflect levels of zinc and other elements over time. Plus, it's an easy test since hair is easy to get.

Better non-invasive indicators of zinc deficiency are Bryce-Smith taste and sweat analysis. Loss of taste is one of the first symptoms of a deficiency because zinc is needed for an enzyme, gustin, present in saliva that modulates sense of taste. And sweat analysis may be even more sensitive as an index than blood biomarkers.

NSI Determine Checklists - Grandma and me

Grandma

My grandma, 79, scored a 6 on the NSI Determine Checklist, which puts her at “high nutritional risk.” Her eating habits are affected by GERD and she tries to avoid any processed foods high in sodium because of hypertension. She also eats alone most of the time and eats fewer than two meals per day. Although she dislikes eating fruits and vegetables, she does manage to obtain some of them in her diet. She drinks plenty of milk and uses dairy products liberally. She doesn’t drink alcohol, has enough money for food she needs (although she said she could use more), and only takes one prescription medication. She has not gained or lost 10 pounds without wanting to in the last six months. She shops and cooks for herself and reports that she also picks at food throughout the day.

Me

I, 31, scored a 0 on the NSI Determine Checklist. I have no conditions that affect my diet, I eat balanced meals along with vegetables, fruits and milk products, and don’t drink more than one glass of wine daily. I have no mouth problems, have money to buy food, eat with others most of the time, don’t take any prescriptions, have maintained the same weight for years, and often shop and cook for myself.

Thoughts

Although there is a stark contrast between my nutritional risk and that of my grandmother’s, it doesn’t escape me that in 48 years I could be in the same situation as she is now. I realize that when I eat too much I too am susceptible to GERD symptoms such as reflux and heartburn. This may affect my nutritional risk in the future unless I am conscientious enough to make change in my diet to reduce inflammation in my esophogaus. As for my grandma, her high nutritional risk concerns me greatly because at her age, she should be more focused on nutrition than I am. We will need to change that.

Use of Organic Acids as Detoxification Markers

Environmental toxins, or xenobiotics, are foreign chemicals that enter our bodies and can potentially cause harm to our organs, tissues and cells. There are more than 60,000 known everyday chemicals that we are exposed to of which at least 200 are found in newborns at moment of birth. The most prevalent pollutants nowadays are phthalates and plasticizers, of which have been determined to be endocrine disruptors, and have been linked to thyroid diseases and various health conditions such as insulin resistance, metabolic syndrome, obesity, osteoporosis and arteriosclerosis. Other toxins are implicated in depleting folic acid leading to digestive disorders such as colitis or are known carcinogens.

Organic acids, of which are compounds used in metabolism, can be measured to assess how the body responds to toxins in the body or to evaluate nutrients related to processes of detoxification. For example, methylation is a vital step in the facilitation of converting homocysteine to methionine and in detoxifying chemicals. Without B12, methylation would be suppressed; thus, a resulting methylmalonic acid could be measured in urine at this point. If folic acid deficiency results, then the organic acid formiminoglutamate will accumulate and can be measured. A second example of an organic acid that can be used to evaluate nutrient deficiency resulting from toxins is xanthurenic acid. This acid appears in urine when chemicals deplete B6 (pyridoxine). A third example is measurement of fatty acids. When pthalates interfere with carnitine synthesis, then beta-oxidation in the mitochondria is impaired. THis, in turn, can result in elevated adipate, suberate, and ethylmalonate.

As markers of impaired detoxification or nutrient deficiency resulting from toxins, organic acids can help the clinical practitioner determine nutritional needs as well as possible nutrient or bioactive therapies. These therapies may include supplementation with B12, folic acid, n-acetyl cysteine, glutathione, CoQ10 and glycine. By correcting deficiency or otherwise, these nutrients potentially restore or boost detoxification in efforts to improve health of patients.

Summarized from

Rogers SA. Using Organic Acids to Diagnose and Manage Recalcitrant Patients. Alternative Therapies; July/Aug;12,4, 2006. Available at: http://blackboard.bridgeport.edu/@@437EB59FF6DF953742043192DBAC3894/courses/1/NUTR-560E-DLB-2009NF/content/_22128_1/OrganicsAcidCME.pdf

How to differentiate between a B12 and a folate deficiency

Despite whether or not megaloblastic anemia is caused by a deficiency of folate or vitamin B12 (cobalamin), large doses of folate will correct the anemia (1). Because this is the case, the extra folate can potentially "mask" symptoms of vitamin B12 deficiency such as from pernicious anemia.

Unfortunately, an undiagnosed chronic vitamin B12 deficiency can lead to irreversible neuropathy. The cobalamin in methyl derivative form is necessary to methylate homocysteine to methionine (2). It's also necessary to convert methylmalonyl CoA to succinyl coA. In the absence of B12, then, leads to accumulation of both methylmalonic acid and homocysteine levels (2). As they accumulate, they lead to possible neuropathy via irreversible demyelination of nerves (3).

The mechanism by which this occurs is thought to be related to methylmalonyl CoA acting as an inhibitor of malonyl CoA's role in biosynthesis of fatty acids, which leads to myelin sheath degeneration (3). However, because this does not explain why both homocysteine and methylmalonic acid must be elevated for demyelination, more research is needed.

Correct treatment can depend on telling the difference between a deficiency of B12 from folate. It can be achieved through an assessment of both methylmalonic acid and homocysteine blood levels (2 & 4). A clinician can determine that an elevated level of both will indicate a B12 deficiency in tissues (4). Further, if both are normal, no B12 deficiency exists; and if only homocysteine levels are elevated, then a possible folate deficiency may exist (4).

References

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002
3. Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006
4. Lab tests online. Methylmalonic acid. Available at: http://www.labtestsonline.org/understanding/analytes/mma/test.html

Female Athlete Triad

When I was in high school, one of my best friends was a long-distance runner and a dancer. After only a few months of training, I knew something was wrong. She changed her diet to one of protein and almost no other calories. She was obsessed with exercise leading to a loss of many of her friends. Later on she lost a lot of weight and, to me, instead of becoming healthier she appeared to look pretty unhealthy.

What I didn't know then was that my friend may have suffered from the "female athlete triad". It is a three-part syndrome that affects the health and performance of female athletes and includes osteoporosis, disordered eating and menstrual disorders. Each of these are inter-related and inter-play. Together they can cause serious illness or death.

Writing in a review in British Medical Journal, Dr. Karen Birch explains that the syndrome can be caused by pressures psychological and physiological associated with a sports requirements to perform optimally, which can lead to a perception of needing a "low body mass, result of high-volume training" (1).

Being somewhat controversial, at least one medical researcher has called for abandonment of the syndrome. Dr. Michael Cullen of the British Association of Sport and Exercise Medicine points out that the term "blurs the concepts of a true eating disorder with that of a driven athlete who is simply ignorant of nutritional demands" and that osteoporosis in atheletes is rare (2).

Despite whether a syndrome should be recognized or not, clinicians should continue to recognize which women are most at risk, which are teen girls and female athletes of many kinds, especially where body image counts: gymnasts, figure skaters, ballerinas, swimmers, endurance runners, and so on (3).

The first signs of the female athlete triad may be low-calorie dieting or exercising to excess or obsession (3). The low-calcium diet contributes to low bone density. If amenorrhea results, it may be linked to decreased estrogen levels (3). It has also been my experience that smoking usually is another sign of an eating disorder among teens. The reasons why is because the teens see it as an effective method to control appetite and weight (4). Unfortunately, for a teen suffering already from female athlete triad, smoking can cause an exacerbated loss of bone (5 & 6). The impact of female athlete triad can lead to infertility and stress fractures in the future (1).


References

1. Birch K. Female athlete triad. ABC of sports and exercise medicine. British Medical Journal. Available at: http://www.bmj.com/cgi/content/extract/330/7485/244.

2. Cullen M. et al. 10 Feb 2005. The Female Athlete Triad. Available at: al.http://www.bmj.com/cgi/content/extract/330/7485/244.

3. WebMD. The Female Athlete Triad. Available at: http://www.webmd.com/a-to-z-guides/female-athlete-triad.

4. http://www.ncbi.nlm.nih.gov/pubmed/17056404

5. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

6. http://www.ausport.gov.au/participating/women/issues/osteo

Family influence on meals

My thoughts after reading "A Review of Family Meal Influence on Adolescents' Dietary Intake" by Sarah Woodruff and Rhona Hanning:

It's pretty easy to imagine why having dinner with one's family would instill positive nutritional habits. Even the word family exudes in its meaning what goes further to credit an environment of caring and, above all, nurturing.

When mother and father are at the table, they are naturally given to see to it that their children are eating well. At the same time, they must also set the right example. Thus, it's clear why the authors of the article found that the studies reviewed found that those adolescents who ate with their families had a higher intake dairy, fruits and vegetables.

I would further suggest that family influence comes with wisdom as to healthy eating pattens. For example, when grandma or grandpa or mom or dad make a meal, they themselves are passing on food traidtions that may have well sustained generations with better health. When family is not available and adolescents are left to choose their own eating patterns, one could imagine they're much more inclined to make poorer choices as they have to "reinvent the wheel" so to say.

One element I would have liked to have seen the article address with more detail was actual preapartion of food. It's my own experience that a personal relationship with food can go a long way in how nutritious it is to a person. You might call it a greater food consciousness--more understanding of what's about to be eaten. Food consciousness is often lost on teens when going out to eat or when leaning on the microwave meals. When a teen prepares his or her own food, just the creativity itself involved by choice and cooking is likely to play a factor in actual nutrition.

What's an ALT test?

Alanine aminotransferase (ALT) is an enzyme that is concentrated in the hepatocytes. When the liver is injured or affected by disease, the enzyme is released into the bloodstream. When jaundice occurs, for example, elevated ALT levels can distinguish a liver injury or disease instead of red blood cell hemolysis.

The test is performed on a patient by collecting 7-10 mL of blood in a red-top tube, then sending it to a lab for analysis. If a patient does have liver dysfunction, then the clinician should note that bleeding times may be longer.

Significantly elevated ALT levels may indicate hepatits, hepatitis necrosis or hepatits ischemia. Moderately increased levels may indicate cirrhosis, cholestatis, a hepatic tumor, a hepatotoxic drug, obstructive jaundice, severe burns or trauma to striated muscle. Drugs that may elevate ALT levels include acetaminophens, clofibrate, codeine, salicylates, tetracyclines among many others.

ALT levels may also increase to a lesser extent due to myositis, acute pancreatitis, myocardial infarction, mononucleosis or shock.

Summarized from the following:

Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006, pp. 40-42.

Lee RD, Nieman DC. Nutritional Assessment. New York: McGraw-Hill, 2007.

When You Have an Abnormal Lipid Profile

An abnormal lipid profile is a consistent indicator of atherosclerosis and cardiovascular disease (CHD). Blood lipids include total cholesterol, LDL-C, HDL-C and triglycerides. Because each of these factors are ultimately affected by diet, it serves to reason to recommend dietary strategies to help lower total cholesterol and LDL-C, increase HDL-C and reduce triglyceride levels.

ATP III uses the term therapeutic lifestyle changes (TLC) for recommendations that can help to improve abnormal lipid profiles and reduce risk of CHD. TLC makes recommendations for saturated fat (less than 7% of total calories), polyunsaturated fat (up to 10% of total calories), monounsaturated fat (up to 20% of total calories), total fat (25-35% of total calories, fiber (20-30g/d), protein (approx. 15% of total calories), and cholesterol (less than 200 mg/d). The total calories recommendation, in addition, is based on a balance of energy intake and expenditure to maintain a healthy weight (1).

Because it is often difficult for patients to adhere to specific percentages, a nutritionist can help patients by summarizing recommendations as eating less to lose weight as appropriate, exercising regularly as appropriate, avoiding animal fats in keeping to a low-cholesterol diet, replacing saturated fats with polyunsaturated fats whenever possible, and eating more fruits and vegetables.

A nutritionist could also approach patients with a Mediterranean-style diet. Recent research is showing that this diet is appropriate because it represents many of the same diet recommendations included in TLC. This diet may also have lipid-lowering effects and cardio-protective benefits from the regular intake of red wine, olive oil and fish (2).

Reference List

1. Lee RD, Nieman DC. Nutritional Assessment. New York: McGraw-Hill, 2007.
2. Cheskin LJ, Kahan S. Low-carbohydrate and Mediterranean diets led to greater weight loss than a low-fat diet in moderately obese adults. Evid Based Med 2008;13:176.

When should prevention of atherosclerosis start?

I have three children, one boy, 13 and two girls, 10 and 11. As far as I’m concerned prevention of atherosclerosis should begin as early as possible. That means yesterday. However, I understand that there exists some uncertainty of exactly what age to begin prevention. It has to do partly with juvenile fatty streaks. What may appear unimaginable is that the occurrence of juvenile fatty streaks somehow may have an importance in child development.

Most North American children develop fatty streaks in their aortas by age 3 and in coronary arteries along with macrophage foam cells by age 10 (1); by the time children are reaching puberty, they may already have developed fatty streak lesions. Fatty streaks are nothing new. As offered by McGill et al, our hominin forebears likely developed them as do current non-human Old and New World primates even when living in natural habitats. Studies of other mammals reveal that many of them also develop fatty streaks.

From an evolutionary perspective, then, fatty streaks may have provided a selective advantage to pre-human or human ancestors. Or, as in most cases, there are “trade-offs” in evolution. What may have been a cause of poor health in the long run for human ancestors may have been important part of early development. Fats and calories, for example, may have helped a child's brain or muscle development (3). It also stands to reason that while fatty streaks are normal, they may not necessarily lead to atherosclerosis. Wild mice develop fatty streaks, for example, but won’t develop lesions. Caged mice on a high-fat/cholesterol diet, however, will develop lesions and atherosclerosis as they age (2). When comparisons are given of mice and men (or women), our modern “caged” sedentary lifestyles and high-fat/cholesterol diets suggest humans are a burden to their own health.

Long-range prevention, then, should be focused on encouraging an improved diet early. How early? The American Heart Association’s guidelines suggest starting children on a widely varied diet low in fat and calories by age 2 (4). The amounts of fats and calories, however, must take child development into consideration. Even once children reach puberty this should be the case. As with my own children, who I have on a Mediterranean-style DASH diet rich in fats from olive oil and fish, it is important to give the body a holistic approach.

Reference List

1. McGill HC, Jr., McMahan CA, Herderick EE, Malcom GT, Tracy RE, Strong JP. Origin of atherosclerosis in childhood and adolescence. Am J Clin Nutr 2000;72:1307S-15S.
2. Li Y, Gilbert TR, Matsumoto AH, Shi W. Effect of aging on fatty streak formation in a diet-induced mouse model of atherosclerosis. J Vasc Res 2008;45:205-10.
3. Mitchell MK. Nutrition Across the Life Span. "Chapter 9: Nutrition During Growth: Preschool through Preadolescence". Second Edition. Waveland Press: Long Grove, Illinois, 2003, pp. 271-300.
4. Lee RD, Nieman DC. Nutritional Assessment. New York: McGraw-Hill, 2007.

When to use a C-peptide test

Normally, measuring insulin directly is more accurate with diabetics. But C-peptide levels more accurately reflect islet cell function in situations of insulinomas as well as cases of diabetics taking exogenous insulin (for treatment or secretly).

C-peptide, short for "connecting peptide" is the protein connecting beta/alpha chains of proinsulin. The chains are separated when proinsulin becomes insulin and C-peptide. C-peptide ends up in equal amounts to insulin in the portal vein, lasts longer than insulin so can be found more readily in peripheral circulation, and correlates with insulin levels.

Summarized from

Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006, p. 197.

Why get a glycosylated hemoglobin test?

Measuring blood glucose periodically is critical for staying off the blood sugar rollercoaster. But how can a clinician be sure a patient hasn't gotten on board the rollercoaster? This is when glyosylated hemoglobin comes into the picture.

What happens is that when a person is diabetic and doesn't adequately control blood glucose, her or his blood glucose becomes elevated. The hyperglycemia that results begins to affect certain proteins in the blood as well as hemoglobin. Blood glucose bonds to the hemoglobin and it becomes "glycosylated". The glycosylation mainly happens to hemoglobin A (HbA, the major form of hemoglobin, and it's pretty much irreversible.

After a few weeks, the amount of glycosylated hemoglobin will decline, but only if blood sugar is controlled. If it's not controlled, then a physician can order a glycosylated HbAIC test, or AIC test. A person without diabetes should have about 4-8% HbAIC and the American Diabetes recommends diabetics to stay below at least 7%. The glycosylated hemoglobin test is meant to evaluate how well treatment is going and how well a patient is following recommendations. It also serves as a method to individualize programs, compare therapys, differentiate short-term hyperglycemia in nondiabetics and diabetics, and also to offer as a reward for patients who do well in their control.

Summarized from

Lee, R.D. & Nieman, D.C. Nutritional Assessment, 4th ed. McGraw Hill Higher Education. Boston, 2007, p. 307.

Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006, p. 282.

Baby Steven

John and Susan are both prone to being overweight. They are concerned that their infant son, Steven will also have weight problems. They are referred to you when Steven is 5 months old. Steven's growth data are as follows

Age Weight Length
Birth 8lb 20inches
1 week 8lb 1oz 20 inches
1 month ll lb. 21.5 inches
2 month 12lb 8oz 23 inches
3 month 14lb 8oz 23.5 inches
4 month 16lb 25.5 inches
5 month 18lb 26.5 inches

Steven breast feeds six times daily for about 20-25 minutes at each feeding. He is not presently receiving any other sources of nourishment. Answer the following questions for John and Susan:

Their pediatrician told them that Steven's weight is above average. Is he gaining too much weight?

When charted, Steven’s birth weight and weight gain for the next two months is at about the 50th percentile (1 p. 566). His weight gain afterward appears to be higher than average and he is at the 90th percentile by 5 months (1 p. 566). Steven’s birth length for four months is at about the 50th percentile and then flows upward slightly closer to the 75th percentile (1 p. 567).

Because Steven’s length is slightly higher than average, I would judge that it is the extra growth that may also explain the extra weight gain. The weight gain, then, is probably not at a level that should be worried about. I will agree with others who have replied that at this moment the primary concern should be making sure Steven’s fed well to best support his physical and neurodevelopment that occur in the first year of life (1 p. 216).

Should they delay adding solid foods or add something now? If they should add something, what would recommend?

At Steven’s age of 5 months, the appropriate foods to be supplying him are breast milk or formula, infant cereal and strained fruits and vegetables. He’ll be teething soon, so within two or three months, he’ll be able to enjoy strained meats and breads (1 . Within five to seven months, he’ll be chomping on chopped fruits, vegetables and meats. Steven ca be weaned around 2 to 3 years (1 p. 200).

Should they give Steven juice in a bottle?

No, they should not. According to the American Academy of Pediatrics, there is no reason why juice should be given to Steven at all based on nutritional considerations (2). This is the case even as he grows older. From my own experience with my children, I can tell you that juice, while sure to be fascinating to a baby’s taste buds, would simply turn into a habit whereby breast milk and formula are avoided.

In fact, my own mother tells me all the time that she wishes she never would have given me juice because, as a baby, I immediately stopped breastfeeding when I tried it. The fruit juice also displaced nutrition I could have received otherwise (1 p. 242). Eventually baby bottle tooth decay would also be my fate (1 p. 242).

A neighbor has suggested that Steven could be given skim milk instead of breast milk, Do you recommend this?

Steven’s breastfeeding of six times daily is normal for babies of 2-3 months (1 p. 239). Once reaching 3-6 months, the level normally should drop to 4-5 and he should be introduced to other foods as mentioned above (1 p. 239). Steven should not be given milk at all, be it raw, whole, 2% or skim. Breast milk is best because of its unique properties such as lactoferrin, immunoglobulins and the bifidus factor (1 p. 231-232). These are able to prevent allergies, asthma and infections over time (1 p. 231-232). Infant formula is acceptable, however, and, unlike cow’s milk, can also provide a commonly deficient nutrient in infants: iron (1 p.236). Infant formula is carefully formulated and fortified with vitamins, minerals and essential fats to best support child development (1 p. 235).

References
1. Mitchell MK. Nutrition Across the Life Span. "Chapter 9: Nutrition During Growth: Preschool through Preadolescence". Second Edition. Waveland Press: Long Grove, Illinois, 2003.
2. http://pediatrics.about.com/od/weeklyquestion/a/0806_baby_juice.htm