|
NUTRITION:
The Food Pushers
A review by Walter Willett*
------------------------------------------------------------------------------
--
Food Politics How the Food Industry Influences Nutrition and Health
Marion Nestle
University of California Press, Berkeley, 2002. 469 pp. $29.95, £19.95. ISBN
0-520-22465-5.
------------------------------------------------------------------------------
--
National statistics document an explosive increase in obesity in the United
States during the last two decades; its prevalence in adults has increased by
more than 50%, and over half of American adults are now overweight or obese.
Obesity is only the most conspicuous manifestation of the sorry state of
American diets, which are characterized by high amounts of refined starch,
sugar, and hydrogenated fats. Other consequences include skyrocketing rates
of type 2 diabetes and stagnation in the decline in coronary heart disease
incidence. An analysis of the origins of the obesity epidemic and our diets
is thus timely, and Marion Nestle's Food Politics: How the Food Industry
Influences Nutrition and Health is a valuable contribution to this effort.
Nestle, currently a professor in the Department of Nutrition and Food
Sciences at New York University, is well positioned to have written this book
because she has worked in the U.S. Surgeon General's office, served on
dietary guideline committees and advisory committees to the Food and Drug
Administration, and acted as a consultant to the food industry. Her well-
documented book draws together information from many sources, including some
that are not easily accessible through usual literature reviews.
A central theme of the book is that the food industry's fundamental goal is
to induce the public to eat more, which inevitably contributes to the
epidemic of obesity. As Nestle points out, this effort to increase food
consumption is appropriate, legal corporate behavior in an unfettered
capitalist economy. However, as she documents in great detail, the effort
does not merely consist of advertising to informed adults. She describes the
industry's behind-the-scenes efforts in Congress, federal agencies, the
courts, universities, and professional organizations to limit public access
to relevant information and to promote consumption of products designed for
profit rather than health.
Among the most troublesome topics discussed by Nestle is the dual role of
U.S. Department of Agriculture, which both promotes higher consumption of
American agriculture products and provides dietary guidance to Americans
(primarily through the food pyramid). The inherent conflict of interest is
obvious because the USDA defines its primary stakeholders as the groups that
represent major producers in the dairy, beef, sugar, and other sectors. In
this context, advice to eat less food--either in general or with regard to
specific foods--inevitably meets resistance by powerful forces.
The commercial exploitation of children by the food industry, well described
by Nestle, is particularly egregious. Recognizing that children are not fully
mature with regard to making informed decisions, we control the promotion of
alcohol, firearms, and tobacco. Yet we assume that young children can
rationally decide about food choices that have important health consequences,
and we expose them to intense marketing of products that are largely devoid
of nutritional value but replete with calories. Nestle documents in great
detail the billions of dollars spent to develop junk foods that are
increasingly seductive to children, and the additional billions spent
promoting these products. Particularly troublesome are contracts for "pouring
rights," whereby cash-strapped school systems are paid by Coca-Cola or Pepsi
for exclusive rights to promote their products intensively within schools. As
Nestle describes, companies find such contracts lucrative for current sales
but also regard the arrangements as an opportunity to train children to be
consumers of their products. Because colas and some other beverages link a
mildly addicting substance (caffeine) with large amounts of sugar, these
drinks are likely to be particularly effective means of promoting childhood
obesity. If this were not enough, food services in some schools are being
replaced by fast food franchises.
Nestle does not leave readers burdened with an array of problems lacking
remedies. She has clearly given considerable thought to ways by which the
current failings might be rectified. For example, she suggests that
governmental responsibility for dietary advice be transferred from the
Department of Agriculture to the Department of Health and Human Services.
Given her description of agroeconomic influences through Congress, however,
placing this responsibility as far from politics as possible--perhaps with
the Institute of Medicine--would seem even better. The author makes a strong
case for protecting children from exploitation by the food industry; she
advocates banning from schools commercials for foods of minimal nutritional
value and sales of soft drinks and other junk food. To counter the low levels
of physical activity that also contribute to obesity, Nestle favors requiring
schools to provide daily opportunities for physical education and sports and
expanding development of parks, sidewalks, and bicycle paths to encourage
physical activity by all. This will require public investment, but the costs
will be small compared with the annual costs of obesity, which are already on
the order of $150 billion and increasing rapidly.
The book contains a wealth of thought and analysis on the ways the food
industry often facilitates excessive consumption and poor diets, but the
industry is far from monolithic. One could point to many positive examples
where healthy products have been successfully promoted. Also, Nestle largely
ignores the complicity of the nutrition community itself. She characterizes
the message from our field as "consistent but dull" advice to increase
consumption of fruits, vegetables, and grains. However, our advice has hardly
been consistent. On the basis of unpublished and flawed data, the 1990 U.S.
Dietary Guidelines even encouraged midlife weight gain; though this advice
was reversed in 1995, it seriously distracted attention from the developing
obesity epidemic. And the nutrition community has almost certainly
contributed to the obesity problem by conveying the notion that only fat
calories lead to weight gain and that grains and other starches can be eaten
with impunity. Throughout the book, Nestle repeatedly equates low-fat diets
with healthy diets, a conclusion for which there is no scientific support and
which may mislead readers. Clearly, real progress can be expected only if
nutritionists and policy-makers alike strive to develop and act on sound data
rather than beliefs, even well-intended ones.
Food Politics is essential reading for anyone seriously interested in
addressing the nutritional dilemma facing the United States. Its greatest
value lies in the detailed documentation of the ways in which the food
industry operates, and nearly everyone will find information that is new and
useful. Nestle's account does not make for light reading, but it will
certainly contribute to informed discussion and, hopefully, effective actions
to reduce the burdens of obesity and related conditions.
------------------------------------------------------------------------------
--
The author is in the Department of Nutrition, Harvard University, Building
II, Room 309, 655 Huntington Avenue, Cambridge, MA 02115, USA. E-mail:
wwillett@hsph.harvard.edu |
|
|
NEJM Jan 2003
Hypervitaminosis A and Fractures
Paul Lips, M.D., Ph.D.
The toxicity of certain foods that contain high amounts of vitamin A has been
recognized for centuries. The 1597 diary of Gerrit de Veer, which he wrote
while taking refuge in the winter in Nova Zembla during an attempt to reach
Indonesia by the northern passage, states that he and his men became gravely
ill after eating polar-bear liver. They feared for their lives but ultimately
recovered. De Veer's diary also notes widespread and striking desquamation
during recovery.1
Vitamin A retinol is present in food sources such as liver, kidney, and
milk. Dairy foods are fortified with small amounts of vitamin A and D in many
countries. The provitamin beta carotene is widely distributed in plants and
is cleaved to form retinol. The liver stores retinol primarily as retinyl
esters. Symptoms may occur with either too little or too much vitamin A. The
first symptom of vitamin A deficiency is maladaptation to darkness (night
blindness), followed in later stages by dryness of the conjunctiva
(xerophthalmia), corneal ulceration (keratomalacia), and blindness. Vitamin A
deficiency in children is a major cause of blindness in some developing
countries. Hyperkeratosis and dry skin may also occur with vitamin A
deficiency. Acute vitamin A toxicity is characterized by the severe illness
that de Veer described, whereas chronic vitamin A toxicity, caused by a high
intake of vitamin A (25,000 to 50,000 IU per day or more) over a long period,
is characterized by bone and joint pain, anorexia, nausea and vomiting, and
weight loss. Benign intracranial hypertension and hepatosplenomegaly may
ensue.2
Chronic vitamin A toxicity affects bone and mineral metabolism. Retinoic
acid, an active metabolite of vitamin A, stimulates osteoclast formation and
activity, leading to increased bone resorption and periosteal bone
formation.3 Hypercalcemia may also be observed. Increased bone resorption has
been associated with fractures in rats.4 Periosteal bone formation causes
characteristic hyperostoses in metacarpals, metatarsals, and other tubular
bones such as the ulna, tibia, and fibula.5 The periosteal apposition of
coarse woven bone with large osteocyte lacunae, a characteristic feature of
chronic vitamin A toxicity, was observed in an early Homo erectus skeleton
found in Kenya and was attributed to high dietary intake of carnivore liver.6
Several groups of investigators have examined the possibility that excessive
dietary intake of vitamin A is associated with decreased bone mineral density
and an increased risk of hip fracture. Melhus and coworkers evaluated such an
association in an effort to identify the cause of the high incidence of hip
fractures in Sweden and Norway.7 An earlier epidemiologic survey had shown
that vitamin A intake was six times as high in Scandinavia as in southern
Europe. The study by Melhus et al.7 included a cross-sectional examination of
bone mineral density and a nested casecontrol study of the incidence of hip
fracture. In a multivariate analysis adjusted for the body-mass index, energy
intake, level of physical activity, smoking status, estrogen status, and use
of estrogen, vitamin A intake was significantly associated with the bone
mineral density of the lumbar spine, femoral neck, and trochanter, as well as
total-body bone mineral density. The bone mineral density was 10 percent
lower in persons with a vitamin A intake that exceeded 1.5 mg per day than in
those with an intake of 1.5 mg per day or less. The relative risk of hip
fracture was 2.1 for persons with a vitamin A intake that exceeded 1.5 mg per
day, as compared with those whose intake was less than 0.5 mg per day.
These data were confirmed by a report from the Nurses' Health Study,8 in
which a total vitamin A intake equal to or greater than 1.5 mg per day was
associated with a relative risk of 1.64 for hip fracture, as compared with an
intake of less than 0.5 mg per day. On the other hand, beta carotene intake
had no significant influence on the risk of hip fracture.8
In the Rancho Bernardo Study,9 an inverse U-shaped association was found
between vitamin A intake and bone mineral density. In that study, bone
mineral density was optimal when the vitamin A intake was 2000 to 2800 IU per
day (0.6 to 0.9 mg per day), indicating that both low and high intakes of
vitamin A may compromise bone health. The current recommended intake of
vitamin A is 0.7 mg per day for women and 0.9 mg per day for men10 amounts
that are similar to the optimal intake in the Rancho Bernardo Study.9 The
maximal intake considered to be safe is 3 mg per day. In the Nurses' Health
Study, 21 percent of the participants had a vitamin A intake that exceeded
this amount.8
In this issue of the Journal, Michaėlsson and his colleagues in Sweden
provide further data on the possible deleterious effects of vitamin A on
bone,11 from a long-term, prospective study of 2322 men in whom serum retinol
and beta carotene levels were measured at base line.11 During the 30-year
follow-up period, fractures were reported in 266 men. The relative risk was
1.64 for any fracture and 2.47 for hip fracture among men in the highest
quintile for serum retinol (more than 75.62 µg per deciliter [2.64 µmol per
liter]), as compared with the middle quintile (62.16 to 67.60 µg per
deciliter [2.17 to 2.36 µmol per liter]). The relative risk of any fracture
was 7.14 among men with a serum retinol level that exceeded 103.12 µg per
deciliter (3.60 µmol per liter).
Although this group's earlier report7 described a relatively small sample of
women, the current study involved a population-based sample of men. This
larger study shows a direct link between the serum retinol level and the risk
of fracture, although retinol levels were measured only once. As in earlier
studies, the beta carotene level was not associated with the risk of
fracture. Michaėlsson and colleagues conclude that high serum retinol levels
(above 86 µg per deciliter [3 µmol per liter]) may increase the risk of
fracture and should thus be avoided. They suggest that hypervitaminosis A may
explain, in part, the high incidence of hip fractures in Scandinavia and the
United States, countries where vitamin supplements are commonly used.
What are the implications of the present study with respect to vitamin A
intake, food fortification, and the use of supplements? Multiple
environmental and ethnic factors should be considered in reaching a
conclusion. The third National Health and Nutrition Examination Survey
(NHANES III) showed that low serum retinol levels (less than 20.05 µg per
deciliter [0.70 µmol per liter]) were rare in children and adults but that
suboptimal levels (less than 30.08 µg per deciliter [1.05 µmol per liter])
were more common in black and Mexican-American children than in white
children.12 High serum retinol levels (more than 74.48 µg per deciliter [2.60
µmol per liter]) were reported in 5 to 10 percent of the NHANES III
participants and were particularly common in men over the age of 30 years and
in women over the age of 50 years.
Serum retinol increases with age, probably because of reduced metabolic
clearance, and older persons may be at increased risk for hypervitaminosis A.
Supplements containing vitamin A were used by 28 percent of the NHANES III
participants and by 46 percent of the women and 38 percent of the men in the
Baltimore Longitudinal Study of Aging.13 The proportion of participants in
the Nurses' Health Study who used multivitamin supplements increased from 34
percent in 1980 to 53 percent in 1996.8
One may conclude from such data that supplements containing vitamin A should
not be routinely used by men or women and that fortification of cereals with
vitamin A should be questioned.10 On the other hand, vitamin A deficiency and
xerophthalmia occur frequently in African and Asian countries and are
associated with malnutrition in children.14 Vitamin A supplemention and
fortification of food with vitamin A have been used to prevent xerophthalmia
in these countries. Although there are occasional reports of xerophthalmia in
Western countries, it is usually associated with a markedly insufficient
diet. Thus, the therapeutic window for vitamin A is narrow. Osteoporotic
fracture due to excessive intake of vitamin A is a risk among adults,
especially older persons, whereas eye disease due to vitamin A deficiency is
a risk primarily among malnourished children. The study by Michaėlsson and
colleagues11 suggests that vitamin A supplementation and fortification of
food with vitamin A may be harmful in Western countries, where the life
expectancy is high and the prevalence of osteoporosis is increasing.
Source Information
From the Department of Endocrinology, Vrije Universiteit Medical Center,
Amsterdam.
References
Roeper V, Wildeman D, eds. Om de Noord: De tochten van Willem Barentsz en
Jacob van Heemskerck en de overwintering op Nova Zembla zoals opgetekend door
Gerrit de Veer. Nijmegen, the Netherlands: Uitgeverij SUN, 1996.
Hathcock JN, Hattan DG, Jenkins MY, McDonald JT, Sundaresan PR, Wilkening VL.
Evaluation of vitamin A toxicity. Am J Clin Nutr 1990;52:183-202.[Abstract]
Scheven BAA, Hamilton NJ. Retinoic acid and 1,25-dihydroxyvitamin D3
stimulate osteoclast formation by different mechanisms. Bone 1990;11:53-59.
[ISI][Medline]
Hough S, Avioli LV, Muir H, et al. Effects of hypervitaminosis A on the bone
and mineral metabolism of the rat. Endocrinology 1988;122:2933-2939.
[Abstract]
Frame B, Honasoge M. Kottamasu PR. Osteosclerosis, hyperostosis and related
disorders. New York: Elsevier, 1987.
Walker A, Zimmerman MR, Leakey REF. A possible case of hypervitaminosis A in
Homo erectus. Nature 1982;296:248-250.[ISI][Medline]
Melhus H, Michaėlsson K, Kindmark A, et al. Excessive dietary intake of
vitamin A is associated with reduced bone mineral density and increased risk
for hip fracture. Ann Intern Med 1998;129:770-778.[ISI][Medline]
Feskanich D, Singh V, Willett WC, Colditz GA. Vitamin A intake and hip
fractures among postmenopausal women. JAMA 2002;287:47-54.[ISI][Medline]
Promislow JHE, Goodman-Gruen D, Slymen DJ, Barrett-Conner E. Retinol intake
and bone mineral density in the elderly: the Rancho Bernardo Study. J Bone
Miner Res 2002;17:1349-1358.[ISI][Medline]
Anderson JJB. Oversupplementation of vitamin A and osteoporotic fractures in
the elderly: to supplement or not to supplement with vitamin A. J Bone Miner
Res 2002;17:1359-1362.[ISI][Medline]
Michaėlsson K, Lithell H, Vessby B, Melhus H. Serum retinol levels and the
risk of fracture. N Engl J Med 2003;348:287-294.[Abstract/Full Text]
Ballew C, Bowman BA, Sowell AL, Gillespie C. Serum retinol distributions in
residents of the United States: third National Health and Nutrition
Examination Survey, 1988-1994. Am J Clin Nutr 2001;73:586-593.[Abstract/Full
Text]
Hallfrisch J, Muller DC, Singh VN. Vitamin A and E intakes and plasma
concentrations of retinol, -carotene, and -tocopherol in men and women of the
Baltimore Longitudinal Study of Aging. Am J Clin Nutr 1994;60:176-182.
[Abstract]
Schemann JF, Banou AA, Guindo A, Joret V, Traore L, Malvy D. Prevalence of
undernutrition and vitamin A deficiency in the Dogon Region, Mali. J Am Coll
Nutr 2002;21:381-387.[Abstract/Full Text]
---------------------------------------------------
--
HOME | SEARCH | CURRENT ISSUE | PAST ISSUES | COLLECTIONS
| HELP
Comments and questions? Please contact us.
The New England Journal of Medicine is owned, published, and copyrighted ©
2003 Massachusetts Medical Society. All rights reserved. |
|
