It almost seems that a million-and-one books are published everyday touting the secret to rapid and sustained weight loss. But, how many of these diet schemes have been verified to produce the results they advertise? In the latest JAMA (Journal of the American Medical Association) issue, a group of academic centers involved in the Weight Loss Maintenance (WLM) initiative published their results from a three-year study comparing strategies for sustaining weight loss. The project is sponsored by the National Heart, Lung, and Blood Institute (NHLBI), and includes four clinical centers: Duke University, Johns Hopkins University, Pennington Biomedical Research Center, and the Kaiser Permanente Center for Health Research.

The design of the WLM clinical trial involves two phases. Phase 1 comprises a 6-month period where all participants undergo similar intervention to obtain weight loss. Working closely with a trained interventionist, the group strives to achieve a weekly weight loss goal of 1-2 pounds per week through a combination of strategies, such as caloric reduction, dietary modification, and increased physical activity. After having lost weight in phase 1, participants in the 30-month phase 2 trial are randomly divided into three groups, each with a different level of intervention to encourage maintenance of weight loss: 1) minimal intervention; 2) technology-based intervention, with use of an interactive website which sets personal goals, action plans, and provides an online support community; and 3) personal-contact intervention, involving monthly contact with a weight-loss interventionist.

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Imagine this far-fetched hypothetical scenario where an overworked, sleep-deprived, and hypoglycemic post-call resident is driving home (unbelievable, huh?). During a brief moment of weakness, he drifts to the right, but rapidly corrects his driving trajectory. However, a highway patrolman, Officer Poelis, is sitting along the shoulder of the road and notices the momentary lapse in the driver’s control. Sirens blare and the resident stops his car. Given the circumstances, the resident’s erratic driving behavior probably resulted from his prolonged lack of food and sleep. Officer Poelis, however, suspects that alcohol is involved and asks the resident to take a breath test. To the resident’s shock and surprise, he tests positive for alcohol despite not having had any alcoholic beverages since the last Residents Night Out party two weeks earlier.

Although a seemingly stretched hypothetical scenario, it is not beyond the realm of possibility. A Swedish group recently published a case report of a 59 year-old non-drinker who was unable to start a motor vehicle equipped with an alcohol ignition interlock device. A second breath-alcohol test revealed a blood alcohol level of 0.01-0.02 g/dL. These results were shocking, considering the gentleman has remained abstinent from alcohol his entire life.

There is nevertheless a biochemical explanation for the false alcohol reading. In an attempt to lose weight, the patient was on a very low calorie diet (VLCD). People on such diets or prolonged fasting states depend on fat metabolism for energy. Three forms of ketone bodies (acetone, acetoacetate, beta-hydroxybutyrate) subsequently accumulate in the body. The acetone can be metabolized by the liver to form isopropanol. A drawback of the breath-alcohol analyzer is that it cannot differentiate isopropanol from ethanol (the form of alcohol found in liquor). Consequently, despite the lack of substance use, he was recorded to have had an elevated concentration of alcohol in his breath.

Fortunately, blood alcohol tests utilize gas chromatography, which generate more specific results. This method could be used to verify false positives, but I doubt we will see bulky gas chromatograms in squad cars anytime in the near future.

Since this is the first case report of its kind, it is still unclear whether prolonged fasting states relate to a false positive reading. Besides the obvious warning to not drink and drive, I would strongly discourage the use of this excuse if caught. It would be much easier and safer to just find a designated driver. In the case of a resident on q4 call, finding a willing volunteer may be more difficult to accomplish.

• Source
• Jones AW, Rossner S. False-positive breath-alcohol test after a ketogenic diet. Int J Obes 2007;31:559-61.

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In this week’s issue of the journal Nature, researchers at the Washington University in Saint Louis reported on bacteria and their contribution to obesity. The mouse studies indicated that certain bacterial species were more abundant in obese mice than their lean counterparts. The “obese” bacteria were also found to harvest energy from food more efficiently with less calorie content excreted as waste. Bacterial flora from obese and lean mice were introduced in “germ-free” mice, and mice with the “obese” microbiota experienced a significantly greater increase in body fat. The group had published a related study several years ago, so the idea is not completely novel. On the other hand, it is an interesting concept that has not yet reached common knowledge.

Before anybody blames their gut bacteria as the source of obesity, recall that the study was performed on mice. The findings may or may not translate to humans. The authors describe a related study (Webb et al.) that involved human subjects. Obese individuals were noted to excrete less fecal energy than lean subjects. Although the results were not statistically significant, more research is still needed before discounting bacterial involvement in human obesity. Let us also remember that obesity results from a combination of factors. Dietary intake, physical activity, and genetic composition strongly influence body weight. In the study, the authors equalized food consumption among groups to minimize this possible confounder. Five Big Macs in the mouths of “lean” mice can still produce more weight gain than in “obese” mice fed peanuts.

The implications of the study are fascinating. Consider the potential for future gut therapy (e.g., GoLytely and antibiotic bowel prep, followed by customized bacterial inoculation) to treat obesity or promote weight loss. Time to file my patent!

• Sources
• Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 2006;444:1027-31.
• Backhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, Semenkovich CF, Gordon JI. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A 2004;101:15718-23.
• Webb P, Annis JF. Adaptation to overeating in lean and overweight men and women. Hum Nutr Clin Nutr 1983;37:117-31.

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Alzheimer disease is a chronic condition that afflicts more than 14% of the geriatric population. It is the most common cause of dementia, characterized by a progressive decline in cognitive function. Although there are pharmaceutical drugs (i.e., donepezil) that attempt to stave this decline, there is yet no cure.

A recent study published in the American Journal of Clinical Nutrition has correlated green tea consumption with a lower prevalence of cognitive impairment. Although previous animal studies have suggested a protective effect of green tea against neurodegenerative diseases, this is the first study that addresses the topic in humans.

Researchers at the Tohoku University School of Medicine (Sendai, Japan) surveyed 1003 geriatric citizens at ages 70 years or older from the Tsurugaya district of Sendai City. The study examined several variables, including the consumption of certain beverages, the health status, and the social habits of the participants. Their cognitive function was assessed using the Mini-Mental Status Examination (MMSE), a tool commonly used by neurologists and geriatricians.

The study found that participants who routinely consumed greater quantities of green tea generally scored higher on the MMSE. Consumption of black or oolong tea, or coffee did not produce similar trends. The researchers also adjusted the data for several possible confounders, such as presence of different diseases, level of physical activity, educational background, dietary habits, and substance use. The results still demonstrated a positive effect of green tea in cognitive function.

Does green tea hold promise for dementia patients? Can it reverse the cognitive decline in Alzheimer disease? What about using it as prophylaxis by healthy individuals? The findings are exciting, but there is yet much research needed to validate and extend the results of the Tsurugaya Project.

• Source
• Kuriyama S, Hozawa A, Ohmori K, Shimazu T, Matsui T, Ebihara S, Awata S, Nagatomi R, Arai H, Tsuji I. Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya Project. Am J Clin Nutr 2006;83:355-61.

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