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