LETTERS

King Tutankhamuns Family and Demise

To the Editor: In their study, Dr Hawass and colleagues1
reported ancient DNA data from 11 royal Egyptian mummies and used microsatellites to ascertain kinship among
specimens. We question the reliability of the genetic data
presented in this study and therefore the validity of the authors conclusions. Furthermore, we urge a more critical assessment of the ancient DNA data in the context of DNA
degradation and contamination.
The long-term survival of DNA is determined by the
environmental history of the samples, and Gilbert et al2
argued in reference to mitochondrial DNA that in
most, if not all, ancient Egyptian remains, [ancient DNA]
does not survive to a level that is currently retrievable.
The age of the mummies (more than 3300 years before
the present) coupled with their preservation history
suggests that DNA survival is highly unlikely. Longterm survival of nuclear DNA sequences, as accessed by
Hawass et al, is even less likely than mitochondrial DNA,
given lower copy numbers per cell. Success in the
retrieval of putative nuclear DNA sequences is also surprising given the use of traditional polymerase chain
reaction techniques rather than newly developed capture
approaches coupled with second-generation sequencing
that allow for successful capture of degraded (shorter)
DNA sequences.3
Contamination is a major obstacle in human ancient DNA
research.4 Although laboratory members involved in the study
were genotyped, no persons handling the specimens prior
to the study were included, raising a question of the reliability
of the microsatellite profiles. Precautions such as genotyping of associated nonhuman remains and including information on the microsatellite allele frequencies in presentday Egypt would have clarified the issue of modern
contamination.
Another cause for concern is the lack of reported quality
control measures in the genotyping of microsatellites. Potential genotyping errors include allelic stutters, allelic dropout, short allele dominance, and null alleles, all of which
can result in the incorrect identification of alleles. Even small
error rates (0.01 per allele) can lead to high error rates in
downstream applications, such as false paternity exclusion
in kinship testing.5

1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tutankhamuns family. JAMA. 2010;303(7):638-647.
2. Gilbert MT, Barnes I, Collins MJ, et al. Long-term survival of ancient DNA in
Egypt: response to Zink and Nerlich (2003). Am J Phys Anthropol. 2005;128
(1):110-114.
3. Briggs AW, Good JM, Green RE, et al. Targeted retrieval and analysis of five
Neandertal mtDNA genomes. Science. 2009;325(5938):318-321.
4. Willerslev E, Cooper A. Ancient DNA. Proc Biol Sci. 2005;272(1558):
3-16.
5. Hoffman JI, Amos W. Microsatellite genotyping errors: detection approaches,
common sources and consequences for paternal exclusion. Mol Ecol. 2005;
14(2):599-612.

To the Editor: Based on computed tomography (CT), the

study of King Tutankhamuns family by Dr Hawass and colleagues1 purported an age of 35 to 45 years for the KV55
male (Table 1), older than previously thought. Prior studies that refute this claim were dismissed and no substantiation for a much older age range was given in the text or online content.
The KV55 skeletal remains were thoroughly analyzed after their 1907 discovery by Sir Grafton Elliot Smith,2 who
estimated an age of 25 to 26 years based on direct observation of epiphyseal union throughout the skeleton. Reexamination by Ronald Harrison and Ahmed el Batrawi in
1963 augmented macroscopic examination with radiographs to ascertain the degree of fusion in some bones and
assessed morphology of the right pubic symphysis to derive an age of 20 years at death.3 Both anatomists reported
that the epiphyses of the medial clavicle; heads and tubercles of some ribs; and the inferior epiphyses of the fourth
and fifth cervical, fourth thoracic, and superior fifth thoracic vertebrae are unfused, while the iliac crests and most
rib epiphyses are partially fused, cranial sutures are entirely open, and the right maxillary third molar is not fully
erupted (although the others are). These observations indicate an age range of 18 to 23 years. Further documentation, including union of all scapular epiphyses except the
vertebral border, confirms this range.3
Although age estimation from morphology of the pubic
symphysis was not available in Smiths day, Harrisons

Eline D. Lorenzen, PhD

edlorenzen@snm.ku.dk
Eske Willerslev, DSc
Center for GeoGenetics
Natural History Museum of Denmark
Copenhagen, Denmark

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Financial Disclosures: None reported.

Letters Section Editor: Robert M. Golub, MD, Senior Editor.

2010 American Medical Association. All rights reserved.

(Reprinted) JAMA, June 23/30, 2010Vol 303, No. 24

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LETTERS

description and photographs of the right pubic symphysis

supported his estimate.3 Clear billowing (ridges and furrows) with an ossific nodule on the upper extremity but
without delimitation of the upper or lower margins corresponds to phase 1 in the Suchey-Brooks system (the
method most commonly used by osteologists4), yielding a
95% confidence interval of 15 to 23 years for males with a
mean of 18.5 years.5
These age indicators from previously published descriptions and photographs contradict the estimate of 35 to 45
years in the study by Hawass et al, indicating that KV55 is
not old enough at the age of death to be the pharaoh
Akhenaten. Additionally, the purported pathology shared
with Tutankhamun, including a partial cleft palate, deformed maxillary third molar, and scoliosis,1 are not supported by these prior analyses of the KV55 skeleton. This
man must be another son of Amenhotep III based on his
age at death.
Brenda J. Baker, PhD
brendaj.baker@asu.edu
School of Human Evolution and Social Change
Arizona State University
Tempe
Financial Disclosures: None reported.
1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tutankhamuns family. JAMA. 2010;303(7):638-647.
2. Smith GE. Catalogue General Antiquites Egyptiennes du Musee du Caire, Nos
61051-61100: The Royal Mummies: Cairo: Service des Antiquites de LEgypt, Imprimerie de Linstitut Francais Darcheologie Orientale; 1912 [Reprinted]. London, England: Duckworth; 2000.
3. Harrison RG. An anatomical examination of the pharaonic remains purported
to be Akhenaten. J Egypt Archaeol. 1966;52:95-119.
4. Komar DA, Buikstra JE. Forensic Anthropology: Contemporary Theory and
Practice. New York, NY: Oxford University Press; 2008.
5. Brooks ST, Suchey JM. Skeletal age determination based on the os pubis: a comparison of the Acsadi-Nemeskeri and Suchey-Brooks methods. Hum Evol. 1990;
5:227-238.

To the Editor: Based on my review of the radiographic images in the study by Dr Hawass and colleagues,1 I disagree
with the authors conclusion that Tutankhamun had a left
clubfoot. In talipes equinovarus, or clubfoot, the hindfoot
is in equinus, and the navicular is medially displaced on the
talus.2,3 The images in Figure 4 of the article show the left
foot to have a normal hindfoot and a normal talonavicular
relationship. Thus, Tutankhamuns left foot is not in equinus and not in varus, and is not a clubfoot.
However, the relationship of the calcaneus to the
cuboid is consistent with a habitually supinated foot. The
images in Figure 5 show chronic pathology of the second
and third metatarsal heads, so it is reasonable to assume
that Tutankhamun walked with a stick and with his left
foot in supination to relieve pressure on the diseased
metatarsal heads.
Tutankhamun does not have oligodactyly as he has 5 toes.
He does not have hypophalangism as the proximal and distal phalanges are normal and symmetrical with the right side.
It is unclear why he is missing the middle phalanx of the
second toe. It is arguable whether the lateral view of the right
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foot (Figure 4A) represents a pes planus or simply a lowarched variation of normal; however, it is unreasonable to
propose the causation of pes planus to be transferred additional joint load to the right foot in the absence of evidence suggesting either neuromuscular disease or chronic
rupture of the posterior tibial tendon.
James G. Gamble, MD, PhD
jgam@stanford.edu
Department of Orthopaedic Surgery
Stanford University Medical Center
Stanford, California
Financial Disclosures: None reported.
1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tutankhamuns family. JAMA. 2010;303(7):638-647.
2. Ponseti IV. Congenital Clubfoot. Oxford, England: Oxford University Press; 1966:
8-20.
3. Bridgens J, Kiely N. Current management of clubfoot (congenital talipes
equinovarus). BMJ. 2010;340:c355.

To the Editor: Dr Hawass and colleagues1 assessed the relationship between Tutankhamun, Akhenaten, and several
other members of Egypts 18th dynasty. However, some of
their claims regarding possible inherited disorders among
the 11 royal mummies they examined appear to be inconsistent. The Abstract reported that [n]o signs of gynecomastia and craniosynostoses . . . were found, but the text
stated that putative breasts in Tutankhamun and his father Akhenaten (KV55) cannot be determined, because KV55
is a mummified skeleton and Tutankhamun lacks the frontal part of the chest wall.
In their Results section, the authors stated that Akhenaten
has [a cephalic] index of 81.0 and Tutankhamun an
index of 83.9, indicating brachycephaly. . . . Thutmose
II . . . show[s] dolichocephaly, with [a cephalic index] of
73.4. Nevertheless, these skulls are visibly abnormally elongated, having the family head of the 18th dynasty. Threedimensional CT scans of Tutankhamuns skull 2 and
images of Akhenatens skull 3 by these authors show
absent to poorly developed interdigitated cranial sagittal sutures consistent with premature fusion seen in craniosynostosis.
The authors also reported that Macroscopic and radiologic inspection of the mummies did not show . . . deficiency in cytochrome P450 oxidoreductase. However,
such genomic analyses were not described. Therefore, this
study does not exclude the possibility that the elongated
heads and gynecomastia of numerous royal members of
this dynasty were due to a genetic disorder analogous to
Antley-Bixler syndrome,4 in which a single mutant gene
(POR) induces both craniosynostosis and defective steroidogenesis. Classic cases exhibit insufficient estrogen
production leading to deformed, underdeveloped genitalia
in both sexes. We have proposed an as yet undescribed
variant of the syndrome, associated with excess (rather
than deficient) estrogen production as in the aromatase
excess syndrome.5 The observation of Hawass et al that
2010 American Medical Association. All rights reserved.

LETTERS

Tutankhamuns penis was well developed would be

expected in this putative syndrome. This hypothesis could
be tested by appropriate genomic analysis.
Irwin M. Braverman, MD
irwin.braverman@yale.edu
Department of Dermatology
Yale Medical School
New Haven, Connecticut
Philip A. Mackowiak, MD, MBA
Veterans Affairs Medical Center
Baltimore, Maryland
Financial Disclosures: None reported.
1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tutankhamuns family. JAMA. 2010;303(7):638-647.
2. Williams AR. Modern technology reopens the ancient case of King Tut. Natl
Geogr Mag. 2005:2-21.
3. King Tut unwrapped: pharaoh forensics. Discovery Channel Web site. http:
//dsc.discovery.com/videos/king-tut-unwrapped-pharaoh-forensics.html. Accessed March 15, 2010.
4. Flck CE, Tajima T, Pandey AV, et al. Mutant p-450 oxidoreductase causes disordered steroidogenesis with and without Antley-Bixler syndrome. Nat Genet. 2004;
36(3):228-230.
5. Braverman IM, Redford DS, Mackowiak PA. Akhenaten and the strange physiques of Egypts 18th dynasty. Ann Intern Med. 2009;150(8):556-560.

To the Editor: Dr Hawass and colleagues1 suggested Plasmodium falciparum malaria in conjunction with Khler disease II as a possible cause of death for Tutankhamun. Falciparum malaria was endemic in ancient Egypt. Although
detection of plasmodial MSP1, STEVOR, and AMA1 gene fragments in the mummy may prove presence of P falciparum,
we are not convinced that the disease pattern suggested by
the authors was the primary cause of Tutankhamuns early
death. In endemic areas, malaria is a life-threatening disease commonly affecting children until the age of 6 to 9 years,
not semi-immune adults of 18 to 19 years,2 the age that Tutankhamun apparently reached.
In addition, translucent bone areas of 2 metatarsals of the
left foot and shortening of the second toe, likely signs of osteonecrosis, osteomyelitis, or ulcerative osteoarthritis, are
visible in Figure 5 of the article. These radiological signs are
compatible with osteopathologic lesions seen in sickle cell
disease (SCD), a hematological disorder that occurs at gene
carrier rates of 9% to 22% in inhabitants of Egyptian oases.3
The SCD gene HbS may appear homozygously or in combined heterozygosity with -thalassemia mutations, causing disease. Therefore, it is reasonable to include SCD in
the differential diagnosis of Tutankhamuns paleoradiologic findings.
Ischemic osteonecroses, inflamed by osteomyelitis and septicemia (eg, due to Salmonella or Staphylococcus infections), are frequent SCD complications and often triggered
by malaria episodes.4 Heterozygous and homozygous HbS
carriers are not protected from P falciparum infection per
se and may exhibit significant parasitemia.4,5 However, although heterozygous carriers are protected from severe
courses of falciparum malaria, homozygous carriers are prone
to childhood or early adulthood fatality from SCD and its
2010 American Medical Association. All rights reserved.

complications. The age of 25 to 45 years attributed to Tutankhamuns parents and the age of approximately 50 years
of other relatives are reconcilable with segregation of the
HbS trait and, thus, resistance to severe courses of malaria
in the royal pharaonic family. The possible occurrence of
SCD in Tutankhamun is strengthened by the consanguinity suspected in his parents.
We suggest that, if possible, the authors include in genetic testing of their royal mummies the HbS variant on chromosome 11p15.5 (rs334) and common variants causing
-thalassemias.
Christian Timmann, MD
timmann@bni-hamburg.de
Christian G. Meyer, MD
Department of Molecular Medicine
Bernhard Nocht Institute for Tropical Medicine
Hamburg, Germany
Financial Disclosures: None reported.
1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tutankhamuns family. JAMA. 2010;303(7):638-647.
2. Snow RW, Gilles HM. The epidemiology of malaria. In: Warrell DA, Gilles HM,
eds. Bruce-Chwatts Essential Malariology. 4th ed. London, England: Arnold Publishers; 2002:85-106.
3. El-Beshlawy A, Youssry I. Prevention of hemoglobinopathies in Egypt.
Hemoglobin. 2009;33(suppl 1):S14-S20.
4. Makani J, Komba AN, Cox SE, et al. Malaria in patients with sickle cell anemia:
burden, risk factors, and outcome at the outpatient clinic and during hospitalization.
Blood. 2010;115(2):215-220.
5. Williams TN, Mwangi TW, Wambua S, et al. Sickle cell trait and the risk of Plasmodium falciparum malaria and other childhood diseases. J Infect Dis. 2005;
192(1):178-186.

In Reply: Drs Lorenzen and Willerslev are incorrect regarding insufficient contamination prevention and quality control measures during our study. In addition, authentic, adequately preserved DNA can indeed be obtained from
Egyptian mummy tissue (FIGURE 1) but requires specifically adapted extraction protocols.
The following aspects substantiate authenticity. (1) All
generally accepted criteria for ancient DNA authentication1,2 were strictly adhered to before, during, and after genetic analysis experiments, as described in our article. (2)
Putative contamination by people handling the mummies
before the sampling and during the experiments was monitored. (3) All female mummies were negative for Ychromosomal markers. (4) All male mummies showed homozygous (ie, hemizygous) Y-chromosomal profiles. (5) The
profiles and haplotypes of the whole set of mummies showed
individual differences and therefore could not have originated from the same source of putative contaminant DNA.
(6) The combination of nuclear data (Y- and autosomal chromosomerelated markers) complemented each other. (7) Reproducible genotypes were obtained from different biopsies and extractions per mummy. (8) Subsets of the data were
independently replicated in a second, separate ancient DNA
laboratory staffed by a separate group of personnel, who reconfirmed the authenticity of the results. (9) DNA isolated
from Egyptian mummies was highly informative when processed with next generation sequencing.
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LETTERS

Dr Baker questions the accuracy of our CT-based age determination for the KV55 mummy. CT technology allows a
more accurate age determination and depicts bony landmarks more precisely than in previous studies that used inaccurate and vague age estimation methods3 (and also failed
to detect various pathologies of the KV55 mummy described in our study). The cancellous bone distribution of
the femur and humerus heads4; epiphysis ossification of the
vertebrae, long bones, and iliac crests; and osteophyte development on many of the vertebral end plates are typical
of an age at death of 35 to 45 years, ruling out the much
younger age suggested by Baker.
Dr Gamble disagrees with our diagnosis of left clubfoot
and right pes planus in the Tutankhamun mummy. However, the images to which he refers are not sufficient for a
conclusive evaluation when viewed on their own. The dis-

placement of the left navicular and cuboid bone, taken together with the additional adduction and supination of the
left forefoot, indicates a congenital malformation (grade 1
clubfoot) rather than an acquired defect, with the right flatfoot having developed through 1-sided strain (FIGURE 2).
In our opinion, the missing middle phalanx of the left second toe is hypophalangism, as the images show no trace of
glue. Moreover, bearing in mind the extensive damage caused
by the rough and careless handling of the mummy, it seems
improbable that such a painstaking and illogical repair attempt should have been carried out on a toe.
In contrast to the speculations of Drs Braverman and Mackowiak, our conclusions are based on direct examination of
the mummies. Their hypothesis of Antley-Bixler syndrome
or other diseases running in the 18th dynasty royal family5
was refuted by Miller,6 who drew attention to the lack of

Figure 1. Agarose Gel Electrophoresis of 12 Representative DNA Extractions From Egyptian Mummies Described in the Original Article
M

10

11

12

500 bp
500 bp
75 bp
75 bp

Although each aliquot contains only 5 L of extract (which amounts to 5%-10% of a standard extract), the DNA is clearly visible. Lanes 2, 5, 8, 9, and 11 show DNA
extractions that contain fragment sizes up to 500 base pairs (bp) and longer, despite the small volume of the loaded DNA aliquots. Each lane represents a different mummy.

Figure 2. Computed Tomographic (CT) Image of the Left and Right Feet of Tutankhamun From Various Angles
A Axial cross sections
R

B Sagittal CT reconstructions
L

Right foot
Calcaneus
Cuboid

Navicular
Talus

Navicular
Talus

Left foot
Calcaneus
Cuboid

The left cuboid and navicular bones are displaced compared with the normal positioning of the right navicular bone.
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2010 American Medical Association. All rights reserved.

LETTERS

convincing evidence. We agree with Miller6 and reiterate that

none of the 16 examined royal mummies showed any anomalies symptomatic of Antley-Bixler syndrome,7,8 POR deficiency, isolated gynecomastia, or craniosynostoses. Furthermore, the suggestion by Braverman and Mackowiak to
search for a novel disease gene5 would imply positional cloning and a subsequent candidate gene approach, a methodology inapplicable for such a small group of persons of undefined phenotype.
Drs Timmann and Meyer suggest the possibility of SCD
as the origin of the osteopathologic lesions in the mummy
of Tutankhamun. This is an interesting and plausible addition to the palette of potential disease diagnoses in Ancient
Egyptian royalty that we are currently investigating.
Yehia Z. Gad, MD
Ancient DNA Laboratory
Egyptian Museum
Cairo, Egypt
Ashraf Selim, MD
Department of Radiology
Kasr Al Ainy Faculty of Medicine
Cairo
Carsten M. Pusch, PhD
carsten.pusch@uni-tuebingen.de
Institute of Human Genetics
Division of Molecular Genetics
Eberhard-Karls-University
Tbingen, Germany
Financial Disclosures: None reported.
1. Roberts C, Ingham S. Using ancient DNA analysis in paleopathology: a critical
analysis of published papers, with recommendations for future work. Int J
Osteoarcheol. 2008;18(6):600-613.
2. Richards MB, Sykes BC, Hedges RE. Authenticating DNA extracted from ancient skeletal remains. J Archaeol Sci. 1995;22(2):291-299.
3. Hershkovitz I, Latimer B, Dutour O, et al. Why do we fail in aging the skull
from the sagittal suture? Am J Phys Anthropol. 1997;103(3):393-399.
4. Denk W, Szilvassy J, Bauer G. Age determination based on the structure of the
proximal parts of the humerus and femur. Beitr Gerichtl Med. 1990;48:673678.
5. Braverman IM, Redford DS, Mackowiak PA. Akhenaten and the strange physiques of Egypts 18th dynasty. Ann Intern Med. 2009;150(8):556-560.
6. Miller WL. Did Akhenaten have the Antley-Bixler syndrome? Ann Intern Med.
2009;151(12):892.
7. Antley R, Bixler D. Trapezoidocephaly, midfacial hypoplasia and cartilage abnormalities with multiple synostoses and skeletal fractures. Birth Defects Orig Artic Ser. 1975;11(2):397-401.
8. Crisponi G, Porcu C, Piu ME. Antley-Bixler syndrome: case report and review
of the literature. Clin Dysmorphol. 1997;6(1):61-68.

Physical Activity and Preventing Weight Gain

in Women
To the Editor: The observational study by Dr Lee and
colleagues1 found that relatively high levels of physical
activity among overweight or obese women in the Womens Health Study were not associated with protection
against long-term weight gain. On the other hand, among
white women in the US Diabetes Prevention Program,
those exposed to a structured lifestyle intervention (combining exercise, diet, and coping or problem-solving
skills) experienced about 8 kg of weight loss during the
2010 American Medical Association. All rights reserved.

period of their multidisciplinary, structured support.2

The report from the Womens Health Study, therefore, is
consistent with less intensive obesity intervention trials
that found little or no weight loss following exercise or
dietary treatments.
If preservation of cardiometabolic health is a major
objective, these results should not be considered discouraging. A growing body of evidence confirms that adoption of healthy habits can result in reduced abdominal
obesity and improved metabolic risk factors despite minimal change in weight.3 A failure to lose weight or prevent
weight gain does not prove that exercise (or dietary)
interventions were futile. Weight gain under circumstances of high physical activity might reflect accumulation of salutary lean tissue, especially skeletal muscle.
And for adults who gain weight as adipose tissue, a predominant increase in subcutaneous fat may serve to
safely sequester the excessive calorie burden.4 Subcutaneous lipid sequestration (often in the hips and thighs) may
protect such adults from lipotoxic damage to the liver,
muscle, heart, and pancreas. Accumulation of intraabdominal adipose tissue, on the other hand, may indicate increased cardiometabolic risk.
Rather than focus only on weight loss, health promotion
programs might alternatively pursue reductions in abdominal obesity, improved lipid indices, or greater cardiorespiratory fitness. Health benefits might be better estimated,
for example, as improvements in the lipid accumulation product5 (a continuous variable) or as the reduced population
prevalence of a hypertriglyceridemic waist phenotype.
Henry S. Kahn, MD
hkahn@cdc.gov
National Center for Chronic Disease Prevention
and Health Promotion
Centers for Disease Control and Prevention
Atlanta, Georgia
Financial Disclosures: None reported.
Disclaimer: The findings and conclusions in this letter are those of the author and
do not necessarily represent the official position of the Centers for Disease Control and Prevention.
1. Lee IM, Djousse L, Sesso HD, Wang L, Buring JE. Physical activity and weight
gain prevention. JAMA. 2010;303(12):1173-1179.
2. West DS, Elaine Prewitt T, Bursac Z, Felix HC. Weight loss of black, white, and
Hispanic men and women in the Diabetes Prevention Program. Obesity (Silver
Spring). 2008;16(6):1413-1420.
3. Ross R, Bradshaw AJ. The future of obesity reduction: beyond weight loss. Nat
Rev Endocrinol. 2009;5(6):319-325.
4. Unger RH, Clark GO, Scherer PE, Orci L. Lipid homeostasis, lipotoxicity and
the metabolic syndrome. Biochim Biophys Acta. 2010;1801(3):209-214.
5. Kahn HS, Cheng YJ. Longitudinal changes in BMI and in an index estimating
excess lipids among white and black adults in the United States. Int J Obes (Lond).
2008;32(1):136-143.

To the Editor: Dr Lee and colleagues1 examined the relationship between physical activity and weight gain prevention. The study concluded that physical activity is inversely related to weight gain in women of normal weight,
but not in women who are overweight. However, this conclusion may be flawed.
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