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Context.-Annexin II is a calcium-dependent phospholipid binding protein that plays a role in many cellular functions, including apoptosis, signal transduction, and cellular motility. The protein is strongly expressed in normal prostatic epithelial glands, but its expression in benign prostatic lesions has not been reported. Although commonly underexpressed in prostate cancer, the association of reduced expression with pathologic grade and stage is unknown.

Objective.-To compare annexin II expression in benign prostatic lesions with expression in high-grade prostatic intraepithelial neoplasia and prostate cancer, as well as to correlate expression levels with pathologic grade and stage.

Design.-A semi-quantitative assessment of annexin II expression was performed in radical prostatectomy specimens from 74 patients and prostate needle core biopsy specimens from 13 patients. Foci with normal prostatic glands, atrophic glands, basal cell hyperplasia, high-grade prostatic intraepithelial neoplasia, and prostatic adenocar-cinoma were evaluated.

Results.-Annexin II expression was present in more than 50% of glands in most (>85%) samples of benign prostatic epithelium, atrophic glands, and basal cell hy-perplasia. In high-grade prostatic intraepithelial neoplasia, annexin II staining was markedly reduced in epithelial cells but not in basal cells. Annexin II was absent or focally present in moderately differentiated adenocarcinoma but was retained in poorly differentiated adenocarcinomas.

Conclusions.-Reduced annexin II expression may be a useful diagnostic biomarker to help identify small foci of moderately differentiated adenocarcinoma on needle core biopsy specimens since it is consistently expressed in benign prostatic glands. Re-expression of annexin II in poorly differentiated adenocarcinoma may provide prognostic information.

Annexin II is a member of a family of calcium-dependent phospholipid membrane-binding proteins that contain a conserved repeating domain of approximately 70 amino acids.1,2 Annexins have roles in diverse cellular functions, including apoptosis, membrane trafficking, signal transduction, cellular motility, and cell-cell interactions. 3-6 In particular, annexin II has been shown to concentrate in lipid rafts7 and probably participates in ion channel regulation and formation of tight junctions.8 An-nexin II is up-regulated in response to physiologic stress.6 It inhibits cellular mobility when levels are restored in prostate cancer cells in culture.1

Several annexin family protein members are underex-pressed in prostate cancer.9-13 Down-regulation of annexin I protein expression in prostate cancer was first demonstrated by molecular profiling studies of human prostate cancer samples.14,15 Subsequent studies evaluating more than 100 radical prostatectomy specimens demonstrated that annexin I expression is reduced in more than 90% of high-grade intraepithelial neoplasia (HGPIN) lesions and early-stage prostate cancers.12,13 Annexin II is also reduced in human prostate cancer,12 and biological studies in which annexin II expression was restored suggest that dysregulation of annexin II expression may be an important early event in prostate cancer initiation.1 Although reduced annexin II (lipocortin II, p36) expression in human prostate cancer has previously been demonstrated, expression levels in prostatic atrophy and basal cell hy-perplasia are not known. Furthermore, the correlation between annexin II expression and Gleason score has also not been reported.10-13

This report confirms the association of reduced annexin II expression and prostate cancer. Both HGPIN lesions and prostate cancer foci demonstrated significant reduction in annexin II expression. In contrast, annexin II was diffusely expressed in benign lesions, including prostatic atrophy and basal cell hyperplasia. Interestingly, annexin II expression was restored in a subset of high-grade prostate cancers (Gleason score, 8-10). Finally, reduced annexin II expression in prostate cancer and HGPIN was observed in prostate needle core biopsy specimens.

Radical prostatectomy specimens were procured from the University of California Irvine Medical Center in Orange after the institutional review board approved the study. Seventy-four patients who had undergone radical prostatectomy and had high-stage lesions and high Gleason scores were randomly selected. The method for pathologic staging was determined according to the College of American Pathologists. Ninety-two foci of acinar-type prostate cancer from these patients were reviewed independently by a urologist and 2 uropathologists. In 1 case, minor disagreement was resolved by consultation. Each focus of cancer was assigned a Gleason score. Annexin II expression in the epithelial cells of prostate cancer, HGPIN, prostatic atrophy, basal cell hyperplasia, and benign prostatic epithelium was assessed semi-quantitatively. The quantitative assessment of staining was as follows: grade 0, 0% to 5% of epithelial cells; grade 1, more than 5% to 50%; and grade 2, more than 50% staining. Each of these foci was also evaluated for the pattern of annexin II staining (ie, membranous, cytoplasmic, or mixed). We did not score all benign prostate and HGPIN foci because of homogeneity of an-nexin II staining in these cell types. In addition, 23 foci of prostate cancer from a random selection of 13 patients undergoing prostate needle core biopsies were assigned a Gleason score and evaluated for annexin II expression.

Prostate cancer is the second leading cause of cancer death among men. Every year, approximately 40,000 American men die of this disease and one out of eight men will develop prostate cancer during his lifetime.

Since prostate cancer does not usually display symptoms in its early stages, researchers are searching for genetic markers to aid in diagnosis and treatment. A new study from the University of Michigan Medical School, published in the August 23, 2001 issue of Nature, gave scientists their first look at the genetic and molecular profile of prostate cancer.

“The potential significance of this research is in three areas–diagnosis, prognosis and therapeutic,” says Mark Rubin, M.D., co-author of the study. “The ultimate goal is to develop tests that could help us identify the presence of prostate cancer and determine which patients have this aggressive disease. More importantly, we hope to identify genes we can target for therapy.”

* The prostate is a gland in the male reproductive system. It contributes to seminal fluid–a milky fluid that nourishes sperm and is released to form part of semen. The prostate surrounds the upper part of the urethra, the tube that transports urine from the bladder. If the prostate grows too large, the flaw of urine con be slowed or interrupted.

* The risk of developing prostate cancer increases with age, with about 60 percent of cases diagnosed in men over age 60. Other risk factors include a family history of prostate cancer or being of African-American descent.

* Men over age 50 should have an annual prostate check-up, consisting of a digital rectal exam and a blood test to measure a protein called prostate-specific antigen (PSA). Men with additional risk factors should begin annual check-ups at age 40.

* Both advanced prostate cancer and benign prostate enlargement can produce the following symptoms: weak or interrupted urine flow, frequent or difficulty urinating, blood in the urine, painful urination or ejaculation, prolonged pain in the lower back, pelvis or upper thighs.

Doctors frequently prescribe an inappropriate drug to men with early prostate cancer. Though the consequences of this treatment are severe, most men reported a high degree of satisfaction with their care. These paradoxical findings come from the first major study to look at the quality of life for men who were not treated surgically or with radiation therapy.

This study is an important contribution to the debate about whether the prostate-specific antigen (PSA) screening test for prostate cancer causes more harm than good. As its use increased dramatically over the last decade, so too has the diagnosis of early prostate cancer. The blood test is now routinely given to men with no symptoms, though studies show that most prostate cancers remain dormant an entire lifetime. Consequently, many men are treated unnecessarily. Previous studies of men with early disease who remained untreated showed that their prostate cancer death rate was similar to that of men given a prostatectomy. Neither the PSA test, nor any other, can accurately identify the minority of prostate cancers destined to be fatal. And there is no proof that treating the potentially fatal version at an early-stage saves lives.

There is a consensus among researchers, though not among urologists, that the decision to remain untreated is a valid choice. This used to mean: no treatment until symptoms occur (”watchful waiting”). But now it appears that many men who forego a radical prostatectomy or radiation therapy are being treated with a drug that stops their production of the male hormone, androgen. Known as androgen deprivation therapy (ADT), the treatment amounts to a medical castration, usually with the injectable drug, Lupron.

Lupron has been tested and proven useful only as a palliative treatment for men with advanced prostate cancer. A palliative treatment means that the drug can only alleviate symptoms. And now the drug is being prescribed for early-stage cancer in men without symptoms–at a great physical cost, according to the new study published recently in the Journal of the National Cancer Institute (3/20/02). “There is no definitive evidence that early ADT alone improves length or quality of life in men with clinically localized prostate cancer,” according to the study’s authors, Arnold L. Potosky, PhD, and colleagues.

All of the men who agreed to take part in this study had been newly diagnosed in 1994-5 with cancer that had not spread beyond the prostate gland. They are participants in a much larger project called the Prostate Cancer Outcomes Study (PCOS), initiated by the National Cancer Institute to investigate variations in the treatment of prostate cancer and to determine how the men fared afterward. Significantly, the PCOS is primarily following men who were treated at community medical practices, as opposed to a research-based cancer center. The participants include men under 60, as well as African-Americans and Hispanics, represented in higher proportions than white men over the age of 60.

Out of the PCOS database of over 3,000 men, Dr. Potosky and colleagues concentrated on the 661 who had not been treated with surgery, radiation, or cryotherapy (destruction of the gland by freezing it) and were followed for at least one year. They found that an astonishingly high proportion–37%–had been given ADT alone as their primary treatment, which was described as “an indication authoritatively endorsed nowhere in the medical literature,” by James A. Talcott, MD, in an editorial that accompanied the new study.

Compared with men who were just observed–that is, given no treatment, the ADT-treated men were five times more like to have breast swelling and hot flashes. Those who were sexually potent prior to ADT were more than twice as likely to be impotent afterward. The overall physical functioning and vitality tended to be poorer among the men given ADT.

Though no scientific evidence supports the use of ADT for preventing or delaying onset of symptoms, Potosky and colleagues were able to identify a rationale for the doctors’ prescription by going through the men’s medical records. The ADT-treated men were more likely to have palpable tumors, more poorly differentiated tumors and a baseline PSA values over 10 ng/dL. In other words, their condition at diagnosis was viewed as worse than men with non-palpable, well differentiated tumors and a PSA under 10 ng/dL. The characteristics of the ADT-treated men indicate that their cancers could have spread outside the prostate.

Though it seems logical to treat the men whose cancer might be slightly more advanced, it is illogical to prescribe a drug that can only relieve symptoms in men who have none. Surprisingly, despite the distressing side effects, more ADT-treated men (56%) reported that they were “pleased” or “delighted” with their treatment (56%) than men who decided to remain untreated (45%). Additionally, the ADT-treated men believed themselves to be free of cancer at a 12% higher rate.

Although the prostate-specific antigen (PSA) test has been in widespread use as a cancer screening tool for well over a decade, early detection and treatment remain clouded by unresolved questions. The argument over the value of PSA testing in asymptomatic men has been highlighted on several occasions in American Family Physician.

Updated prostate cancer screening guidelines(1) from the American Cancer Society are as follows: (1) The PSA screening test and a digital rectal examination should be offered annually to men, beginning at age 50, who have a life expectancy of at least 10 years. (2) Men at high risk should undergo initial screening at 45 years. (3) Before screening tests are conducted, patients should be given the opportunity to learn about the benefits and limitations of testing for early prostate cancer detection and its subsequent treatment.

The American Academy of Family Physicians supports the need to review with patients the appropriateness of screening for prostate cancer, recommending that men be made aware of the uncertain benefits of and the potential risks associated with screening.(2) The U.S. Preventive Services Task Force(3) does not recommend the use of PSA screening until available evidence indicates that the test saves lives.

Although the recommendations have not been changed, evidence now demonstrates that mortality rates and the incidence of advanced metastatic disease have substantially decreased since the onset of PSA-based prostate cancer screening. Whether this reduction is the result of PSA screening and the subsequent treatment of early disease can be argued; however, the recently identified decline in prostate cancer mortality in white men under 85 years of age to levels below those of the pre-PSA era, combined with a reduction in the incidence of distant disease, is highly suggestive of a positive effect of PSA testing.(4,5) Population-based studies(6,7) demonstrate a decline in mortality related to prostate cancer–apparently associated with PSA testing. A more definitive prospective randomized trial is in progress,(8) but the results will not be available for several more years. Meanwhile, the use of PSA screening continues to expand. As physicians, what are we to do?

We daily offer patients many preventive health interventions; for some of these interventions, effectiveness and mortality reduction are evidence-based (e.g., mammography) and, for other interventions, they are self-evident but not “proved” through randomized, controlled trials (e.g., Papanicolaou smears). Where in our busy schedule does the PSA screening test fit? How much discussion and education are appropriate? Patients no longer accept health care being dictated to them on a “doctor knows best” basis, but they still depend on us for guidance and direction. In light of the current state of the science related to the PSA test, our responsibility is to make our patients aware that the PSA assay is available and to help them understand the associated implications.

Patients should be helped to understand that the PSA assay is not specific for cancer, that some benign conditions can result in an “abnormal” level, and that some cancers may exist despite a PSA value within the normal range. The conversation should also include the “next steps” that would be necessary if the test result is abnormal, including referral for additional tests (e.g., ultrasonography, needle biopsy).

Discussing selection of therapy and choosing among various options, including watchful waiting, can be specifically framed only in the context of a known histologic diagnosis and tumor grade. Patients should, however, have a general understanding that any benefit associated with testing and a reduced risk of mortality from prostate cancer can be obtained only by use of treatment interventions that also have risks.

We should advise our asymptomatic patients when routine consecutive testing most likely will be of little benefit because of advanced age or the presence of serious comorbid conditions. We should advise patients of the need for vigilance when they are at increased risk (because of race or a family history of cancer) of developing or dying of prostate cancer. They should be aware that the PSA test can detect prostate cancer at an earlier and potentially more treatable stage and may improve their chance for survival. This is the essence of an informed decision.

It has been suggested that, given the limited time available to discuss preventive issues, we should focus our efforts on interventions with known efficacy. A decision on our part not to present patients with the option of PSA testing is tantamount to placing patients who may have asymptomatic prostate cancer into treatment with watchful waiting without their consent. However, this is not an informed decision, and the patient may not be pleased with the outcome.

While counseling is time-consuming, it seems that the best option is to provide patients with the most current information and allow them to select the best course of action. We are much more likely to have satisfied patients in the future if we make the necessary investment of time to allow them to participate in the decision-making process today.

Neurologic complications continue to pose problems in patients with metastatic prostate cancer. From 15 to 30 percent of metastases are the result of prostate cancer cells traveling through Batson’s plexus to the lumbar spine. Metastatic disease in the lumbar area can cause spinal cord compression. Metastasis to the dura and adjacent parenchyma occurs in 1 to 2 percent of patients with metastatic prostate cancer and is more common in those with tumors that do not respond to hormone-deprivation therapy. Leptomeningeal carcinomatosis, the most frequent form of brain metastasis in prostate cancer, has a grim prognosis. Because neurologic complications of metastatic prostate cancer require prompt treatment, early recognition is important. Physicians should consider metastasis in the differential diagnosis of new-onset low back pain or headache in men more than 50 years of age. Spinal cord compression requires immediate treatment with intravenously administered corticosteroids and pain relievers, as well as prompt referral to an oncologist for further treatment. (Am Fam Physician 2002;65:1834-40. Copyright[C] 2002 American Academy of Family Physicians.)

Prostate cancer is second only to lung cancer as the leading cause of cancer-related deaths in men.(1) Histologic evidence of prostate adenocarcinoma is present in 30 percent of men more than 50 years of age and in 70 percent of men more than 80 years old. About 9.5 percent of men will have a clinical diagnosis of prostate cancer in their lifetime, and 2.9 percent will succumb to this malignancy.(2,3)

Although most men with prostate cancer have asymptomatic, indolent disease, central nervous system (CNS) complications often occur with advanced metastatic disease(4,5) (Table 1).(4-6) CNS involvement may present as back pain caused by spinal cord compression resulting from bone metastasis via the paravertebral venous plexus or, less commonly, as headache or neurologic changes caused by the hematogenous spread of prostate cancer to the brain. Paraneoplastic syndromes, including neuropathies (sensory, peroneal, etc.), cerebellar ataxia, and limbic and brain-stem encephalitides, may also occur; discussion of these rare complications is beyond the scope of this article.

TABLE 1

More Common Neurologic Complications in Patients with Metastatic
Prostate Cancer[*]

Complication
(incidence, %)      Clinical clues (incidence, %)

Spinal cord         Localized back pain
compression         (90 to 95)
caused by         Weakness (75 to 80)
metastasis (7)    Autonomic dysfunction (57)

Sensory changes (50)

Brain metastasis    No symptoms (?)
(1 to 2)          Headaches (34)
Motor deficits (26)
Altered mental status (23)
Seizures (8)

Complication
(incidence, %)      Treatment options

Spinal cord         Dexamethasone sodium phosphate (Decadron):
compression         16 to 100 mg administered as an intravenous
caused by           bolus; then 4 mg given intravenously four times daily
metastasis (7)      for 3 days; tapered over about 14 days
Morphine, hydromorphone (Dilaudid),
fentanyl (Duragesic), or oxycodone
(Roxicodone) for pain management
Oncology referral

Brain metastasis    Dexamethasone, as above, if magnetic
(1 to 2)            resonance image shows edema
Anticonvulsants (not as prophylaxis, and
not phenytoin [Dilantin] if radiotherapy
is anticipated, because of the risk
of Stevens-Johnson syndrome with
concomitant treatment)
Oncology referral

? = unknown.

[*]–The rarer neurologic complications include paraneoplastic syndromes
such as peroneal neuropathy (peroneal nerve palsy related to local
metastasis), cerebellar ataxia, limbic encephalitis and brain-stem
encephalitis.

Information from references 4, 5, and 6.

Lesions in the brain and spinal cord require prompt treatment. Hence, family physicians need to consider metastatic prostate cancer in the differential diagnosis of new-onset back pain or headache in men more than 50 years of age.

Anatomy and Metastasis of Prostate Cancer

The pudendal nerve innervates the few striated muscles within the prostatic capsule. The parasympathetic nerves emanate from S2 to S4 and form the pelvic nerve. The sympathetic preganglionic nerves, which reside in the thoracolumbar region between T6 and L2, provide the major neural input to the prostate and reach the pelvis through the hypogastric nerve .

Prostate cancer has been shown to metastasize by following the venous drainage system through the lower paravertebral plexus, or Batson’s plexus. Although hematogenous spread of other malignancies is most commonly to the lungs and liver, 90 percent of prostatic metastases involve the spine, with the lumbar spine affected three times more often than the cervical spine. Prostate cancer also spreads to the lungs in about 50 percent of patients with metastatic disease, and to the liver in about 25 percent of those with metastases.

A 62-year-old man with androgen-independent metastatic prostate cancer that had failed to respond to multiple treatment regimens stopped all conventional therapy and began 10 mg/day of lycopene and 300 mg of saw palmetto 3 times per day. The prostate-specific antigen (PSA) level decreased from 365 ng/ml to 140 ng/ml after 1 month and to 8.1 ng/ml after 2 months. A repeat bone scan revealed an improvement of bony metastases. He has continued the lycopene and saw palmetto and has remained asymptomatic for an unspecified period of time.

Comment: Androgen-independent prostate cancer is difficult to treat and has a relatively poor prognosis. This case report, which demonstrates a partial remission, is therefore quite promising. The authors of the study attributed the benefit solely to the lycopene, since saw palmetto does not typically reduce PSA levels in men with BPH. However, it is not possible to rule out an anti-cancer effect of saw palmetto in this patient. Moreover, it is difficult to believe that such a small amount of lycopene, which can be obtained from less than 3 tablespoons of spaghetti sauce per day, could by itself have such a profound impact on a patient with advanced, treatment-resistant prostate cancer. Clearly, additional trials with these natural compounds are warranted.

Residents of the Lower Mississippi River Delta are linked by the muddy waters flowing through the region and by a common culture, including unique music, literature, and food. Though lower Delta states share a rich heritage, they also form one of our nation’s most impoverished and poorly nourished regions.

On average, diets in Arkansas, Mississippi, and Louisiana include 20 percent fewer vegetables and fruits, less dairy products and more added sugar and calories from fat than the national average. Obesity and chronic diseases, such as heart disease, stroke, and cancer, affect people living in Mississippi Delta states more than other U.S. residents.

Congress created the Lower Mississippi Delta Nutrition Intervention Research Initiative (NIRI) to address the health problems of residents in the three states. Before NIRI was established, research on the dietary habits of this population was lacking. Since 1995, researchers at NIRI headquarters in Little Rock, Arkansas, have been working with their cooperators to find ways to improve the nutrition and health of the men, women, and children of the Delta.

Better Lifestyles Through Science

The Agricultural Research Service is partnered with six universities, state cooperative extension services, rural communities, and other partners in the three-state region. NIRI researchers have conducted and will continue conducting a series of surveys to assess the nutrition and health needs of the Delta region.

Over time, NIRI partners selected three communities in the Delta region for the initial intervention research efforts. NIRI will help guide these communities for the next several years, while tracking changes in their members’ nutrition and health. these communities–Marcell, Arkansas, and its surrounding public school district; Franklin Parish in Louisiana; and the city of Hollandale, Mississippi–were chosen because of the high levels of enthusiasm community leaders have shown in the past towards the NIRI program and the dedication community members previously demonstrated towards their ability to work together at improving their overall fitness and health.

“These communities are each unique. They happen to include a school district, a parish, and a city because they each define themselves differently,” says Beverly McCabe-Sellers, a nutrition scientist and NIRI’s research coordinator. “Not only do they have different geographic boundaries, but they each define ‘community’ differently.”

Part of the problem Delta residents face when searching for healthy food items is the distance they must travel to find full-service grocery stores. A NIRI study of 228 stores chosen at random in the three-state region found that convenience stores outnumber supermarkets and smaller grocery stores. They found most convenience stores have fewer healthy foods and higher prices.

Currently, NIRI communities are enthusiastically implementing intervention research to improve individual residents’ health and nutrition. Using the community-based participatory research model as the basis for carrying out the Delta NIRI mission, schools and community organizations in each state are using intervention research to address such concerns as food choices, eating patterns, food insecurity, and maintaining healthy weights.

At the same time, NIRI scientists and communities are analyzing the success of the intervention research and will determine which methods can be used to carry out these programs in other rural communities of the Lower Mississippi Delta.

According to Margaret L. Bogle, a nutritionist and Delta NIRI’s executive director, “NIRI partners will share what they’ve learned about which interventions are successful, while improving the communities’ capabilities to carry out these types of programs in the future.”

Communities Choose Their Paths

Marvell is one of the three communities chosen for the initial nutrition intervention research, and it serves as a good example of the persistence and dedication that will be required to make this ambitious program successful. Though the school district of Marvell is rural and contains a small town, NIRI was able to find local residents with the knowledge, experience, and enthusiasm needed to organize and run the program.

Marvell initiated a walking club in which dozens of residents are now taking part. Participants strap on pedometers and don their club T-shirts each week to get in a good workout with friends. Once a month, the Marvell Walking Club meets over a healthy breakfast. Health professionals are invited to give them health, nutrition, and physical fitness advice.

“Community members say they have more energy, sleep better and feel better, and have less joint pain,” says Willie Allen, NIRI’s community coordinator and representative from the University of Arkansas Cooperative Extension Service.

Marvell already had a walking trail, but NIRI and the city recently received a state grant to refurbish it. Adding benches, lights, new pavement, trees, and a water fountain will help create a more appealing environment for exercisers. The city also received a grant to create a farmer’s market, which will bring fresh produce closer to residents.

The College Student’s Guide To Eating Well On Campus by professional nutritionalist Ann Selkowitz Litt is the ultimate guide to helping the college student around the campus maintaining affordable and healthy eating. A “must-read” for all college students, Litt enlightens the readers to the limitless possibilities of the general students eating pallet consist of and what of that is healthy for the individual. Enhanced with nutritional information of many popular restaurants around campuses, summaries of weight-loss diets popular with college students and many more informative and helpful facts of the college life, The College Student’s Guide To Eating Well On Campus is a highly recommended read to all college students, especially newcomers to the college atmosphere.

Despite the popularity of the low-carbohydrate, high-protein, high-fat diet, no randomized, controlled trials have evaluated its efficacy. The conventional dietary approach to weight management, recommended by the leading research and medical societies, is a high-carbohydrate, low-fat, energy-deficit diet. The Atkins diet, originally published in 1973 and again in 1992 and 2002, may be the most popular of the low carbohydrate diets. More than 10 million copies of Atkins’s diet book have been sold, and four times as many dieters have read one of the Atkins books as have read any other diet book. Despite its longevity and popularity, no randomized trials evaluating the efficacy of the Atkins diet have been published.

The researchers of the current study conducted a one-year, multicenter, randomized, controlled trial to evaluate the effect of the low-carbohydrate, high-protein, high-fat Atkins diet on weight loss and risk factors for coronary heart disease in obese persons. The subjects were randomly assigned to follow either a low-carbohydrate, high-protein, high-fat Atkins diet or a high-carbohydrate, low-fat, energy-deficit conventional diet. Professional contact was minimal, so as to approximate the approaches used by most dieters.

A total of 63 persons (43 women and 20 men) participated in the study. All subjects completed a comprehensive medical examination and routine blood tests. Subjects in both test groups were instructed to take a daily multivitamin supplement and met with a registered dietitian for 15 to 30 min during the third, sixth, and twelfth months to review dietary issues.

The 33 subjects who were assigned to the low-carbohydrate, high-protein, high-fat diet met individually with a registered dietitian before beginning the program to review the central features of the diet, which involves limiting carbohydrate intake without restricting consumption of fat and protein intake. For the first two weeks, carbohydrate intake is limited to 20 g per day and is then gradually increased until a stable and desired weight is achieved. Each subject was given a copy of Dr. Atkins’ New Diet Revolution.

The 30 subjects who were assigned to the conventional diet also met with a registered dietitian before beginning the program to review the components of a high-carbohydrate, low-fat, low-calorie diet (1200 to 1500 cal per day for women and 1500 to 1800 cal per day for men, with approximately 60% of cal from carbohydrate, 25% from fat, and 15% from protein) and to receive instructions about calorie counting. Subjects were given a copy of the Learn Program for Weight Management, which provides 16 lessons covering various aspects of weight control.

A total of 49 subjects completed three months of the study (28 on the low-carbohydrate diet and 21 on the conventional diet), 42 subjects completed six months (24 on the low-carbohydrate diet and 18 on the conventional diet), and 37 subjects completed twelve months (20 on the low-carbohydrate diet and 17 on the conventional diet). The percentage of subjects who had dropped out of the study during the third, sixth, and twelfth months was higher in the group following the conventional diet, but the difference was not statistically significant. Subjects on the low-carbohydrate diet lost significantly more weight than did the subjects on the conventional diet during the third and the sixth months, but the difference in weight loss was not statistically significant at during the twelfth month. During the first three months, the percentage of patients who tested positive for urinary ketones was significantly greater in the group on the low-carbohydrate diet than was in the group on the conventional diet, but there was no significant difference between the groups after three months. Systolic blood pressure did not change significantly in either group during the study. Diastolic blood pressure decreased in both groups, but there was no significant difference between the groups. The area under the glucose curve did not change significantly during the oral glucose-tolerance test throughout the study. The area under the insulin curve decreased in both groups, without significant difference between the groups.

There were no significant differences between groups in the total or LDL cholesterol concentration, except on the third month, when values were significantly lower in the group on the conventional diet than in the group on the low-carbohydrate diet. In contrast, the relative increase in HDL cholesterol concentrations and the relative decrease in triglyceride concentrations were greater in the group on the low-carbohydrate diet than in the group on the conventional diet throughout most of the study.

The results of this multicenter, randomized, controlled trial demonstrate that the low-carbohydrate, high-protein, high-fat Atkins diet produces greater weight loss (an absolute difference of approximately 4%) than a conventional high-carbohydrate, low-fat diet for up to six months, but that the differences do not persist at one year. These data suggest that long-term adherence to the low-carbohydrate Atkins diet may be difficult. The differences in weight loss between the two groups in the first six months demonstrate an overall greater energy deficit in the low-carbohydrate group. The mechanism responsible for the decreased energy intake induced by a low-carbohydrate diet with unrestricted protein and fat intake is not known, but may be related to the monotony or simplicity of the diet, alterations in satiety factors, or other factors that affect appetite and dietary adherence.

I am not exactly health-obsessed. Although I’ve been married for six months, I still order pizza twice a week, and the drive-through guys at In-N-Out Burger know me by my first name. My job as a magazine writer with never-ending deadlines leaves little time for the gym, beyond the odd free-weight routine and maybe 20 minutes on the treadmill. Even so, I was OK with my 5′7″ 162-pound frame, and so was my wife. My only real worry, health-wise, was holding on to my teeth.

But recently I found myself obsessing over every calorie, every carb. At the suggestion of Men’s Fitness, I went on a diet that cut my calorie intake from around 2,700 to a meager 1,200 a day. For two weeks, I ate nothing but cabbage soup, steamed greens, and jicama. In other words, I deprived myself–extremely. Why would anyone do this? Because it just might help you live forever.

The Calorie Restriction Diet, as it’s called, is rooted in a 70-year-old Cornell University study, in which rats were fed at least two-thirds less than they normally would be and rived some 30% longer and appeared younger than their well-fed counterparts. Whether this translates into a longer life in humans remains a subject of debate, though an unusually high number of people in places where low-calorie living is the norm–Okinawa, Japan, for example–live past the century mark. More recent studies have argues that by eating the minimum number of calories to keep the body functioning, the metabolism rate is severely slowed, and with it the rate of cellular and genetic disrepair. In addition to helping you live longer, the theory goes, a low-calorie life could improve everything from eyesight to memory, while lessening the chances of cancer, diabetes, and heart failure. Not even the mega-popular Atkins Diet promises that.
.
But calorie restriction is meant for the zealous, not the masses. The 1,200 or so members of the Calorie Restriction Society (calorierestriction.org) take the benefits of CR as a kind of gospel. “Your life is just better on this diet,” said Warren Taylor, a 58-year-old Californian, when I first asked him to guide me through a CR diet. “You have a much greater feeling of peace, self-confidence, and control. You’re not nervous, you don’t fidget, and you don’t wory.” A former powerlifter and long-distance runner, Taylor gave them up four years ago when he joined the group, since the calorie restriction life doesn’t include much exercise. Even sex is an iffy proposition. For anyone doing CR, the diet slows your metabolism to a crawl, and it has roughly the same effect on your libido as a Kirstie Alley film festival.

While I wondered how my 33-year-old body could survive on CR, Taylor delivered one of the pep talks that I would come to crave and loathe during the next two weeks: “Sure your energy level will be lower than what you’re used to. But when you realize all the benefits, you’ll be hooked.”

DAY 1 Taylor faxes me what he calls a CR free-choice diet, meaning I could eat anything I wanted from the list as long as I stayed within the calorie limit. I decide to consume all the nutrients I can muster based on his plan–collard greens, spinach, Belgian endive–to make up for the lack of beer, sausage, and everything else I enjoy. I am to avoid starchy vegetables like corn and squash and skip fruits altogether, save berries, where the sugar content is balanced by a bounty of dietary fiber. I go through two bags of bitter-tasting dandelion and turnip greens before noon. A few hours later, I graduate to Brussels sprouts–more peppery and flavorful than I remember. Dinner is frozen okra, which tastes less like snot when you dust it with curry powder. I go to bed hungry but not Survivor-level hungry. This is going to be easy.

DAY 2 I wake up at 6 a.m. with such hunger pangs, I’m convinced I’m giving birth. So as the sun rises, I begin to make the soup that is to sustain me for the next two weeks. Although my version of the recipe for “CR 3 Day Soup” is pretty austere–three 32-ounce cartons of organic chicken broth (60 calories total), equal parts water, and a pound each of cabbage, carrots, and onions–it does include the only meat I will have in the next 13 days, which today is a little less than a pound of chopped lean turkey breast. I eat soup for breakfast, lunch, and dinner. That night, I worry that this may be the last chance to make love to my wife for the next 12 days, so I insist we give it a go. Afterward, I find myself craving roast beef.

DAY 3 One of the drawbacks of my job is a regular 6 a.m. deadline, which typically means I’m writing until about 5:57. With nothing but soup and collard greens to go on, I find my typing speed is cut nearly in half. The real problem is revealed when I read over my story the next day about a Hollywood event: ME: So what are you wearing tonight? STARLET: A vintage hunger from the house of Hunger. And I thought this diet was supposed to make me think more clearly.