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December 2009 Highlights of This Issue
Systematic Review Finds Higher Protein Intake May Benefit Bone Density
Background Increasing lifespans are accompanied by increases in chronic diseases, such as osteoporosis, which some experts consider to
be at epidemic proportions: 1 in 4 women will experience a bone fracture in her lifetime. Consequently, measures to enhance bone health are of great
importance, and diet tends to take center stage. Although it is tempting to think of bone as being an inert structure made up of minerals, it is living
tissue that changes as we age. Protein makes up about half its volume, and adequate dietary protein across the lifespan is critical in the development and
maintenance of healthy bones. Considerable research has been done to look at the relation between dietary protein and bone health, but the results from
these studies have not been systematically reviewed. A recently conducted research project at the University of Surrey and the University of York, however,
did just this. The results, as well as a complementary editorial by Kerstetter, are published in the December 2009 issue of The American Journal of
Clinical Nutrition.
Study Design To conduct this investigation, the researchers searched several scientific databases to identify all human studies
published since 1966 on protein intake and bone. To be included, studies had to have collected relatively rigorous data concerning indexes of bone health,
such as bone mineral density, bone mineral content, bone turnover, or fracture risk. Both epidemiologic (observational) and intervention (experimental)
studies were considered. Of the 2180 studies initially identified, 61 met the criteria for inclusion in this systematic review.
Results When all studies were considered together, the data suggested a very small, positive relation between protein intake and bone
mineral density. Variation in protein intake accounted for 1–2% of variation in bone strength. Similarly, the researchers found that increased protein
intake was related to greater bone mineral density at the lumbar spine region. They found no association between protein consumption and risk of bone
fracture.
Conclusions The authors concluded that there may be a small benefit of higher protein consumption on bone health, but this does not
necessarily translate into reduced fracture risk in the long term. In her accompanying opinion piece, Kerstetter reminds us that these data can be looked at
another way as well. That is, they support the contention that, contrary to what we often hear, higher dietary protein consumption (including animal protein)
is not detrimental to bone health. In fact, the opposite may be true. The highest risk group may be the frail elderly because their protein and calcium
intakes may be low and their risk of osteoporosis is high. For those individuals, Kerstetter recommends “let us make it a goal to add a small protein
source to their tea and toast meals.” This certainly seems to be safe and prudent advice.
Reference Darling AL,
Millward DJ, Torgerson DJ, Hewitt CE, Lanham-New SA. Dietary protein and bone health: a systematic review and meta-analysis. American Journal of Clinical
Nutrition 2009;90:1674–92.
Kerstetter JE. Dietary protein and bone: a new approach to an old question. American Journal of Clinical Nutrition 2009;90:1451–2.
For More Information For the complete article, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1674
To contact the corresponding author, Andrea Darling, please send an e-mail to:
a.darling{at}surrey.ac.uk.
For the complete editorial, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1451
To contact the corresponding author, Jane Kerstetter, please send an e-mail to:
jane.kerstetter{at}uconn.edu.
Vitamin B-12 Deficiency Difficult To Assess in Era of Folate Fortification
Background Folate and cobalamin (vitamin B-12) are essential, water-soluble vitamins, both being required for the conversion of
homocysteine to the amino acid methionine. Without adequate vitamin B-12, homocysteine concentrations build up in the blood (a risk factor for cardiovascular
disease), and folate becomes “trapped” in its inactive form. However, amidst vitamin B-12 deficiency, high consumption of folate can “mask” some of the
vitamin B-12 deficiency signs (such as macrocytic anemia) and thus make diagnosis of vitamin B-12 deficiency difficult. Because vitamin B-12 deficiency can
cause memory loss and depression, this can have serious consequences. The recent fortification of the US food supply with folic acid (a synthetic form of
folate) has caused some scientists to be concerned that vitamin B-12 deficiency might be underdiagnosed—especially in the elderly, in whom it is common.
A study reported in the December 2009 issue of The American Journal of Clinical Nutrition looks at this question, as does an accompanying editorial
by Ralph Carmel from New York Methodist Hospital.
Study Design This study involved 1535 Latino subjects enrolled in the Sacramento Area Latino Study on Aging (SALSA) (mean age: ~70 y).
Fasting blood samples were collected and analyzed for a variety of substances indicative of folate and vitamin B-12 status. Tests assessing cognitive
function and symptoms of depression were also administered. Subjects were then classified as having high folate or not and/or adequate vitamin B-12 or
not.
Results The data indicated that individuals with low vitamin B-12 accompanied by high folate concentrations had the highest circulating
concentrations of homocysteine and methylmalonic acid and the lowest concentration of holotranscobalamin (all indicators of vitamin B-12 deficiency).
However, there were no apparent differences between groups in terms of cognitive scores or depressive symptoms.
Conclusions The results suggest that high folate intake (most likely from supplements and fortified foods) in combination with vitamin
B-12 malabsorption or low vitamin B-12 intake may be especially dangerous in increasing risk of vitamin B-12 deficiency. These data bring into question
whether there might be important unintended consequences of national folic acid fortification programs. In his companion editorial, Carmel reminds us that
there are limitations to the conclusions that can be drawn from studies such as this, but for ethical reasons more conclusive studies cannot be done. He also notes that only 22 (1.4%) of the subjects in this study were classified as having low
vitamin B-12 and high folate, the combination of interest. Even more information likely lies within a smaller subset of these 22 subjects, for example
those with pernicious anemia. Nonetheless, Carmel concludes that these findings highlight the challenges that lie ahead in the contemporary era of folic
acid fortification—challenges that will take additional, detailed clinical studies to overcome.
Reference Miller JW, Garrod
MG, Allen LH, Haan MN, Green R. Metabolic evidence of vitamin B-12 deficiency, including high homocysteine and methylmalonic acid and low holotranscobalamin,
is more pronounced in older adults with elevated plasma folate. American Journal of Clinical Nutrition 2009;90:1586–92.
Carmel R. Does high folic acid intake affect unrecognized cobalamin deficiency, and how will we know it if we see it? American Journal of Clinical
Nutrition. 2009; 90:1449–50.
For More Information For the complete article, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1586
To contact the corresponding author, Ralph Green, please send an e-mail to
ralph.green{at}ucdmc.ucdavis.edu.
For the complete editorial, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1449
To contact the corresponding author, Ralph Carmel, please send an e-mail to
rac9001{at}nyp.org.
Fetal and Infant Nutrition and Growth May Influence Timing of Puberty
Background Nutrition and its effect on growth during early life (including gestation) can likely have profound influences on later
health and wellbeing. For instance, being born small and/or experiencing rapid growth during early infancy can predispose a person to later obesity and
cardiovascular disease. These same nutrition-related factors have also been shown to be associated with timing of puberty, especially in girls. Because
early onset of puberty has been linked with increased risk of several diseases including cancer, type 2 diabetes, and adiposity, there is considerable
interest in understanding modifiable factors such as nutrition that influence the timing of puberty. In a study published in the December 2009 issue of
The American Journal of Clinical Nutrition, a group of German researchers led by Anja Kroke report the results of a study they conducted to
investigate the association between early life, nutrition-related factors, and pubertal timing. They also went one step further and examined whether any
relations they found might be explained via variations in prepubertal body composition.
Study Design This investigation was part of the DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study, which
began to enroll infants in 1985 and is a detailed study of diet, growth, development, and metabolism. Each year since its start, 40–50 infants join
the study, and to date information on >1100 infants has been longitudinally collected. For the present study, only full-term singleton infants classified as
having a healthy weight at birth (>2500 g) were included in the analyses. In all, 215 boys and girls were included, and a variety of factors, such as birth
weight and length, early feeding characteristics, infant weight gain velocity, and prepubertal body composition, were assessed to determine which factors
were related to the timing of puberty.
Results The results painted a relatively consistent picture of factors related to earlier onset of puberty in both boys and girls. For
example, children who weighed between 2500 and 3000 g at birth were ~7 mo younger when they reached their adolescent growth spurt in terms of height than
were children who were heavier at birth. In addition, participants who gained weight the fastest during the first 2 years of life reached their growth
spurt 4 mo earlier than the other children. This rapid, early weight gain was also related to earlier menarche in girls. None of these associations could
be explained by variations in body fatness in the 3 y immediately preceding puberty onset.
Conclusions In summary, these data point to a potentially important relation between early nutritional environment and timing of
puberty in both males and females. The public health relevance of this 4–7 mo difference in age at puberty onset is unknown. More studies are needed to
identify the physiological mechanisms by which these early life experiences influence a person’s reproductive maturity.
Reference Karaolis-Danckert N,
Buyken AE, Sonntag A, Kroke A. Birth and early life influences on the timing of puberty onset: results from the DONALD (DOrtmund Nutritional and
Anthropometric Longitudinally Designed) Study. American Journal of Clinical Nutrition 2009;90:1559–65.
For More Information For the complete article, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1559
To contact the corresponding author, Anja Kroke, please send an e-mail to
anja.kroke{at}he.hs-fulda.de.
Slight Genetic Alterations Can Influence Relation between Dietary Fat and Health
Background Scientists have long been aware that genetic and lifestyle factors interact to influence health. For example, small genetic
differences (polymorphisms) can cause some people to respond one way to a certain dietary pattern, whereas others may respond differently or not at all.
Furthermore, various dietary patterns can influence health by stimulating different parts of our genetic code. One area of particular interest is how
differences in dietary fat intake can modulate health by altering gene expression. Metabolic syndrome (MetS) is a condition characterized by pre-diabetes,
abnormal blood lipids, abdominal obesity, and hypertension that can eventually lead to type 2 diabetes and cardiovascular disease. Many studies have
investigated the relation between dietary fat intake (eg, monounsaturated, polyunsaturated, and saturated fats) and risk of MetS, but the results of these
studies have not been consistent. It is possible that these inconsistencies are, in part, due to different types of lipids as well as polymorphisms and
variations in gene expression. The results of 3 studies all examining this complex issue are published in the December 2009 issue of The American Journal
of Clinical Nutrition.
Study Designs In one study, a group of Dutch researchers conducted a controlled feeding trial in which 20 overweight or obese men and
women were randomly assigned to 1 of 2 treatment groups for 8 wk: a high saturated fatty acid (SFA) diet or one enriched with monounsaturated fatty acids
(MUFA). Effects on insulin sensitivity and expression of all genes in adipose/fat tissue were then examined. In the second study, an international team of
scientists followed 1754 French men and women for 7.5 y to see whether polymorphisms in the complement component 3 (C3) gene interacted with
dietary polyunsaturated fatty acid (PUFA) to predict risk of MetS. The C3 protein is an important component of the body’s immune system. Lastly, researchers
studied 1100 American men and women to examine the interactions between polymorphisms in the Circadian Locomotor Output Cycles Kaput (Clock)
gene, dietary fat intake, and MetS.
Results Data from the Dutch study suggested that the high-SFA diet increased expression of genes involved in inflammation—a
response related to MetS; the high-MUFA diet had the opposite effect. Results from the French study confirmed that certain polymorphisms in the C3
gene were associated with decreased risk of MetS and that this was even more pronounced in people consuming a diet high in omega-3 fatty acids (such as
those found in fish). The final study also showed that polymorphisms, this time in the Clock gene, could interact with dietary fatty acids
(specifically MUFAs) to modulate MetS traits.
Conclusions In conclusion, these studies bring us slightly closer to understanding what we have long known to be true: nature and
nurture interact to influence our health. As nutrition scientists continue to deepen their understanding of these complex interrelationships, the public
gets closer to the possibility of “personalized diets” devised to complement each of our unique genetic profiles.
Reference Garaulet M, Lee Y-C,
Shen J, et al. CLOCK genetic variation and metabolic syndrome risk: modulation by monounsaturated fatty acids. American Journal of Clinical
Nutrition 2009;90:1466–75.
Phillips CM, Goumidi L, Bertrais S, et al. Complement component 3 polymorphisms interact with polyunsaturated fatty acids to modulate risk of metabolic
syndrome. American Journal of Clinical Nutrition 2009;90:1665–73.
van Dijk SJ, Feskens EJM, Bos MB, et al. A saturated fatty acid–rich diet induces an obesity-linked proinflammatory gene expression profile in adipose
tissue of subjects at risk of metabolic syndrome. American Journal of Clinical Nutrition 2009;90:1656–64.
For More Information For the complete article by Garaulet et al, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1466
To contact the corresponding author, Marta Garaulet, please send an e-mail to
garaulet{at}um.es.
For the complete article Phillips et al, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1665
To contact the corresponding author, Helen Roche, please send an e-mail to
helen.roche{at}ucd.ie.
For the complete article by Van Dijk et al, please go to the following URL:
http://www.ajcn.org/cgi/content/full/90/6/1656
To contact the corresponding author, Lydia Afman, please send an e-mail to
lydia.afman{at}wur.nl.
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