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

Gut inflammation and stool tests overview

The gut’s immune system is ultimately responsible for maintaining a healthy gut free of infection or infestation. It must accomplish this task while at the same time being unresponsive to food and helpful bacteria (1).

Gastrointestinal inflammation etiology is largely infection such as via parasite. However, modern lifestyles have increasingly been harassed by new chronic inflammatory diseases such as Crohn’s or ulcerative colitis (1). These are associated mainly with genetic mutations or adaptive immunity affecting immune system recognition as well as by epithelial permeability (1).

Stool tests indicating gastrointestinal inflammation include those for fecal proteins such as eosinophil protein-X (EPX), fecal calprotectin (FC) and fecal myeloperoxidase (MPO):

• FC is a calcium-binding protein found in large amounts in neutrophils and macrophages, which rush into the lumen at onset of inflammation (2-4). FC is considered more sensitive than endoscopy, for example, for evaluating inflammatory bowel disease such as ulcerative colitis and Crohn’s disease. Calprotectin can also be used to determine post-infectious irritable bowel syndrome, NSAID enteropathy or cancer.
  
• MPO is a derivative of neutrophil granulocytes (2). It’s useful diagnostically because it’s found in intestinal mucosa and in feces. Levels of MPO are elevated in active inflammatory bowel disease and mark mucosal inflammation. MPO and FC appear to be better markers in comparison to EPX during the treatment of inflammatory diseases ulcerative colitis or Crohn’s disease (2).
  
• EPX is a glycoprotein that is released when eosinophil granulocytes (white blood cells responsible for battling infectious parasites and bacteria) (2). Its increased levels in feces reflect infection, inflammation and tissue damage relating to food allergies, celiac disease, helminthic infection, inflammatory bowel disease, and cancer (5).

Reference List

1. MacDonald TT, Monteleone G. Immunity, inflammation, and allergy in the gut. Science 2005;307:1920-5.
2. Wagner M, Peterson CG, Ridefelt P, Sangfelt P, Carlson M. Fecal markers of inflammation used as surrogate markers for treatment outcome in relapsing inflammatory bowel disease. World J Gastroenterol 2008;14:5584-9.
3. Savino F, Castagno E, Calabrese R, Viola S, Oggero R, Miniero R. High Faecal Calprotectin Levels in Healthy, Exclusively Breast-Fed Infants. Neonatology 2009;97:299-304.
4. Gaya DR, Mackenzie JF. Faecal calprotectin: a bright future for assessing disease activity in Crohn's disease. QJM 2002;95:557-8.
5. Genova Diagnostics. 2009. "Comprehensive Digestive Stool Analysis 2.0" Gastrointestinal Assessments. Available at: http://blackboard.bridgeport.edu/@@651E45893EFF586CEA74E9CF68D701AA/courses/1/NUTR-560E-DLB-2009NF/content/_22116_1/Comprehensive%20Digestive%20Stool%20Analysis-%20Genova.pdf. Accessed 28 Nov 2009.

Kid Nutrition

Nutritional and energy needs for a child differs profoundly from that of an adult because of a child's continual growth and development. A child is in greater need of nutrient-dense foods--although not to the extent as infants--and requires more energy for basal metabolic rate, physical activity and thermic effect of food. Energy needs are highest during rapid growth and expansion of lean mass.

Each individual child is best understood by first dividing stages of child growth and development into two periods: a preschool period and a school-age period:

• During the pre-school period, from 2-6 years of age, the child grows more slowly in comparison to infancy. A toddler will quadruple birth weight in a full year or so. The brain of the toddler also grows more slowly than as was expected as an infant so head circumference will only increase by a couple of centimeters. A toddler's weight increase can range from 2.5 kg per year for ages 2 and 3 to 2 kg per year for ages 4 and 5. She or he will also grow about 12 cm from age 2 and 3. During that time, body composition will also change as total body water content settles to a comfortable 60-65% and growth of new cells and skeletal muscle causing a decrease in extracellular fluid and increase in intracellular fluid.
  
• The school-age period, or latent growth period, beigns from 6 until puberty of which girls can reach a little earlier at 10 and boys normally at 12. As "baby fat" is lost, the child becomes leaner and mor muscular. The pattern of growth is highly individual. On average, weight increase will be about 3-3.5 kg per year during this period. The child will move beyond the limited vocabulary of three-word-sentences and begin adapting to an environnment of greater language skills, motor skills, as well as personal-social skills. This, of course, will also mean more control over diet through self-feeding.

As both periods represent critical times for growth and development, the focus of recommendations for energy and nutrient intake are based on supporting optimal outcomes. The recommendations are, again, more critical than for adults because of dire long-term consequences. A child, for example, will need special attention to be sure that they receive proteins of high biologic value for growth requirements. Fat and carbohydrate needs will be greater during rapid growth periods as will numerous vitamins and minerals, especially vitamin D and calcium of which are largely deficient in children. Fiber too, which helps normalize bowel movements, is critical for ensuring a child lives free of future risk of disease. All in all the goal is to provide the best support to provide children with bright futures.

Summarized from

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.

Somatic Protein Status

Protein status is assessed by evaluating both somatic and visceral protein status. Somatic protein status is a measure of the protein in skeletal muscle while visceral protein status is a measure of all other proteins (organs, viscera, serum, blood cells, white blood cells).

Evaluation of somatic protein status can generally be performed using muscle circumference or mid-arm muscle area. However, because no single indicator is completely accurate biochemical measures can help better provide perspective for somatic protein status.

Creatinine serves as a useful measure because creatinine is produced in the skeletal muscle. The more skeletal muscle a person has, the more creatinine will be excreted. A 24-hour urinary creatinine excretion test is easily tested in the laboratory. The measure can then be compared to standards based on stature and body weight. The 24-hour urinary creatinine excretion can also be compared to reference values from the creatinine-height index (CHI). The CHI is a ratio of 24-hour urinary creatinine excretion and an expected amount depending on sex and stature. Creatinine measures have their limits samples have to be collected in exactly 24 hours and diet can compromise creatinine measurements and, thus, measures of excretion and CHI.

The amino acid, 3-methylhistidine, is another useful measure of muscle mass because it is found in the contractile proteins of muscle, actin and myosin. It is releasaed when the contractile proteins are catabolized and excreted in the urine. As long as protein synthesis and degradation is steady, the amount of 3-methylhistidine should paint a picture of muscle mass. However, just as 24-hour urinary creatinine excretion, the measure of 3-methylhistine is limited. The value can be affected by diet, age, sex, maturity, hormonal status, physical shape, any recent intense exercise, injury or disease. A significant pool of 3-mehtylhistidine also lies outside of skeletal muscle that also creates complication as an index of skeletal protein breakdown.

Energy needs of healthy term and high-risk infant

The infant, despite whether healthy term or high-risk, will require energy for BMR, thermic effect of food, physical activity, maintenance, growth and for energy lost in feces and urine. There is also energy needed just to maintain body temperature until the early extrauterine period passes. The newborn requires approximately 108 kcal/kg for about six months followed by 98 kcal/kg for the next six.

The high-risk newborn will have the same energy requirements, but Calorie needs will differ in whether or not the infant is enterally fed or parenterally fed. The enterally fed infant needs a greater amount of Calories, at 120/kg, than the healthy infant due to specific dynamic action and cold stress. The parentally fed will need fewer amount of Calories, at about 80-90 kcal/kg, than the healthy infant because of the infant won't use as many calories for activity, cold stress, specific dynamic action or stool losses. Caloric needs for both enterally and parenterally fed high-risk infants will aslo need to depend on medical problems and growth needs.

Assessment methods by which energy needs are determined include anthropometry, biochemical assessment and dietary assessment. Anthropometry assesses weight, length and head circumference. Because weight is most important for the high-risk infant, it will need to be weighed one or more times daily. Biochemcial lab measurements will need to be performed over several days in the high-risk infant to determine development.

The high-risk infant will also need a clinical assessment and a nutrient intake assessment. The clincal assessment will evaluate condition including state of hydration relative to urine and weight gain as well as feeding tolerance including vomiting records. Nutrient intake will evaluate nutrient sources in a qualitative fashion as well as nutrients in terms of quantity. Nutrient sources will need to depend on the condition of the high-risk infant such as state of digestive abilities. Nutrient amounts depends on absorption capacities, whether parenterally or enterally fed and weight.

Reference

Mitchell MK. Nutrition Across the Life Span. Second Edition. Waveland Press: Long Grove, Illinois, 2003.

Protein-deficient diet and teratogenicity

One interesting detail I came across while researching teratogens is that a protein-deficient diet may enhance the effects of xenobiotics in general.

For example, dietary protein deficiency along with exposure to inorganic arsenic through injection in mice was found to increase risk of birth defects, possibly because of lack of methyl donors for arsenic methylation (1). Also, high-dose caffeine teratogenicity is increased when in combination with protein deficiency (2).

Other xenobiotics such as tobacco carcinogens, anticonvulsants and sedatives appear to be teratogenic depending on the status of the cytochrome P450 system of the fetus (1). The effect may or may not be related to protein deficiency. The toxicity is thought to occur due to lack of anitoxidative enzymes such as GSH peroxidase and GSH reductase, which would increased endogenous oxidative stress and cumulative damage (3).

Reference List

1. Lammon CA, Hood RD. Effects of protein deficient diets on the developmental toxicity of inorganic arsenic in mice. Birth Defects Res B Dev Reprod Toxicol 2004;71:124-34.
2. Nehlig A, Debry G. Potential teratogenic and neurodevelopmental consequences of coffee and caffeine exposure: a review on human and animal data. Neurotoxicol Teratol 1994;16:531-43.
3. Wells PG, Kim PM, Laposa RR, Nicol CJ, Parman T, Winn LM. Oxidative damage in chemical teratogenesis. Mutat Res 1997;396:65-78.

Caffeine and pregnancy

I was shocked to learn that FDA in 1980 had determined that caffeine in amounts exceeding 300 mg could potentially be teratogenic (1). Teratogens are agents that cause fetal malformations or birth defects. Good thing caffeine does not harm the fetus when taken in smaller amounts, despite evidence in rats to the contrary (1-2).

However, after digging deeper, I found that the researchers did find that caffeine potentiated teratogenic effect of smoking and alcohol (2). The mechanism appears to be through inducing materno-fetal vasoconstrictions that lead to ischemia (2).

If caffeine potentiates effects of other teratogens in amounts less than 300 mg, I imagine it's still wise of pregnant women to avoid caffeine altogether during pregnancy just in case they are exposed to teratogens of some kind and are unaware of it.

Reference List

1. Mitchell MK. Nutrition Across The Life Span. Long Grove, IL: Waveland Press, 2003.
2. Nehlig A, Debry G. Potential teratogenic and neurodevelopmental consequences of coffee and caffeine exposure: a review on human and animal data. Neurotoxicol Teratol 1994;16:531-43.

Cannabis Teratogenicity

Cannabis sativa’s psychoactive tetrahydrocannabinol (THC) has not been established as a human teratogen (1), but there is a history of teratogenic effects linked to use by expectant mothers (2). The perinatal exposure is thought to interfere with neurodevelopment and affect neurobehavorial outcomes (1-2).

Although the teratogenicity of marijuana is not as catastrophic as other illicit drugs such as cocaine, it’s harm can still lead to problems such as disturbed sleep and attention deficit disorder (2-3). Worth noting is that when cocaine exposure is accompanied by marijuana, the neurological effects can be pronounced (3).

There is also indication that maternal marijuana use may increase risk of acute myeloid leukemia, however, more recent research has not been able to confirm this relationship (4).

Reference List

1. Kozer E, Koren G. Effects of prenatal exposure to marijuana. Can Fam Physician 2001;47:263-4.
2. Reece AS. Chronic toxicology of cannabis. Clin Toxicol (Phila) 2009;47:517-24.
3. Frank DA, Augustyn M, Knight WG, Pell T, Zuckerman B. Growth, development, and behavior in early childhood following prenatal cocaine exposure: a systematic review. JAMA 2001;285:1613-25.
4. Trivers KF, Mertens AC, Ross JA, Steinbuch M, Olshan AF, Robison LL. Parental marijuana use and risk of childhood acute myeloid leukaemia: a report from the Children's Cancer Group (United States and Canada). Paediatr Perinat Epidemiol 2006;20:110-8.