Frequent chocolate consumption linked to lower BMI

A recent study showed that frequent chocolate consumption was associated with lower body mass index (BMI), even when adjusting for calorie intake, saturated fat intake, and mood.

Beatrice A. Golomb, MD, PhD, associate professor of medicine at the University of California, San Diego, and colleagues described their findings in a research letter published in the March 26 issue of the Archives of Internal Medicine.

The authors used data from 1018 patients already being screened for inclusion in a widely sampling clinical study evaluating noncardiac effects of statin medications. Of the 1018 participants, 1017 answered the question, "How many times a week do you consume chocolate?" BMI was calculated for 972 participants (95.6%); and 975 (95.8%) answered the validated Fred Hutchinson Food Frequency Questionnaire.

The investigators performed analyses with and without adjustment for calorie intake, saturated fat (satfat) intake, and mood. Fruit and vegetable intake was not associated with chocolate consumption (β, 0.004; P = .55), but satfat intake was significantly related to both chocolate consumption (β, 0.035; P < .001) and higher BMI.

The amount of chocolate consumed was examined, in addition to the frequency of chocolate consumption. Activity (number of times in a 7-day period the participant engaged in vigorous activity for at least 20 minutes) and mood (Center for Epidemiological Studies Depression scale [CES-D]) were also examined.

The relationship between chocolate consumption frequency and BMI was calculated in unadjusted models, in models adjusted for age and sex, and in models adjusted for activity, satfats, and mood.

Study participants consumed chocolate a mean 2.0 (SD, 2.5) times per week and exercised 3.6 (SD, 3.0) times per week. Frequency of chocolate consumption was associated with greater intake of calories and satfats and higher CES-D scores (P < .001 for each of these 3 associations); these all related positively to BMI. Chocolate consumption frequency was not associated with greater activity (P = .41), but it was associated with lower BMI (unadjusted P = .01). This association remained with and without adjustment for age and sex, as well as for calories, satfats, and depression.

Although chocolate consumption frequency was associated with lower BMI, the amount of chocolate consumed was not (eg, per medium chocolate serving or 1 oz [28 g], β, 0.00057 and P = .97, in an age- and sex-adjusted model).

"The connection of higher chocolate consumption frequency to lower BMI is opposite to associations presumed based on calories alone, but concordant with a growing body of literature suggesting that the character — as well as the quantity — of calories has an impact on [metabolic syndrome (MetS)] factors," write the authors.

They further explain that as chocolate products are frequently high in sugar and fat, they are often assumed to contribute to an increased BMI. The authors note that this may still be true in some cases.

"[O]ur findings — that more frequent chocolate intake is linked to lower BMI — are intriguing," write the authors. "They accord with other findings suggesting that diet composition, as well as calorie number, may influence BMI. They comport with reported benefits of chocolate to other elements of MetS," the authors write, noting that a randomized trial studying the metabolic benefits of chocolate in humans may be warranted.


Source: http://www.medscape.com/viewarticle/760920?sssdmh=dm1.771288&src=nldne 


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Ibuprofen lowers risk of altitude sickness

Ibuprofen appears to lower the risk of developing acute altitude sickness, according to a report from Grant S. Lipman, MD, from Stanford University School of Medicine in California, and colleagues, published online March 20 in the Annals of Emergency Medicine.

Approximately 25% of the people who travel to altitudes of 8250 feet or higher suffer from acute mountain sickness, which includes headaches, nausea, dizziness, fatigue, and vomiting> If left untreated, altitude sickness may progress to high-altitude cerebral edema, a potentially fatal condition. Symptoms typically start 6 to 12 hours after reaching the high altitude. Gradual ascent lowers the risk of developing acute mountain sickness.

Dr. Lipman and colleagues propose that an anti-inflammatory drug could counter the brain inflammation that is a response to decreased atmospheric pressure at higher elevations. Although this connection is intuitive, the researchers write, evidence for efficacy has been inconclusive.

To test the hypothesis in a double-blind, placebo-controlled study, the investigators enrolled 58 men and 28 women, all of whom were healthy and who live at low altitudes. The study was conducted over the course of 4 weekends in July and August 2010. Study participants and researchers gathered for the first night at 4100 feet in an area of the White Mountains of California. The next morning, each participant received either 600 mg of ibuprofen or placebo. They were driven to a staging area at 11,700 feet, received a second dose at 2 pm, hiked to 12,570 feet, and received the third dose before spending the night at that elevation.

The participants completed questionnaires asking about symptoms and demographics and had their oxygen saturation measured before receiving the first dose at 4100 feet, and before and after the final ascent.

Nineteen of the 44 participants (43%) given ibuprofen suffered altitude sickness, as did 29 of the 42 control participants (69%). The absolute reduction in incidence was 26% (odds ratio, 0.3; 95% confidence interval, 0.1 - 0.8). The researchers observed a non–statistically significant lower symptom severity in the hikers who took the ibuprofen.

Ibuprofen offers advantages over other medications available to prevent mountain sickness (acetazolamide and dexamethasone), the researchers write. It does not have the adverse effects associated with the other 2 drugs (nausea, dizziness, and fatigue for acetazolamide; delirium depression, insomnia, mania, adrenal suppression, and hyperglycemia for dexamethasone). Moreover, ibuprofen is easily obtained, and can be effective if taken 6 hours before ascension compared with acetazolamide, which must be taken the day before the ascent.

"We found that ibuprofen was effective in reducing the incidence of acute mountain sickness compared with placebo, with the odds of experiencing acute mountain sickness about 3 times greater in participants receiving placebo rather than prophylactic ibuprofen," the researchers conclude.

A possible limitation of the study is acclimatization at 4100 feet, although this is unlikely because of the high incidence of symptoms in the control group. Possible confounders include variability in diet, unreported relevant physiological conditions, and the fact that the participants self-selected and may not represent other groups of hikers.

The researchers caution that they chose the study conditions to represent experiences of recreational hikers, so extrapolation to those hiking at higher altitudes may not be valid.


Source: http://www.medscape.com/viewarticle/760487?sssdmh=dm1.769238&src=nldne

Aspirin reduces cancer mortality and risk for distant metastases

Evidence from 3 new studies demonstrates that aspirin can reduce the risk for cancer-related mortality and can reduce or prevent the risk for distant metastasis.

Peter M. Rothwell, MD, PhD, professor of clinical neurology at the University of Oxford, United Kingdom, was lead author on all 3 studies.

In the first study, published online March 21 in the Lancet, comparing daily aspirin with no aspirin to prevent vascular events, aspirin use reduced the risk for nonvascular death in all 51 trials examined (1021 vs 1173 deaths; odds ratio [OR], 0.88; P = .003). When data from 34 trials were examined (n = 69,224; 89% of total cohort), there were fewer deaths from cancer in the aspirin than in the control group (562 vs 664 deaths; OR, 0.85; P = .008).

Dr. Rothwell and colleagues note that even though the decreased risk for major vascular events in these trials was initially offset by a higher risk for major bleeding, both of these effects diminished over time, leaving only the reduced risk for cancer after 3 years.

"In view of the very low rates of vascular events in recent and ongoing trials of aspirin in primary prevention, prevention of cancer could become the main justification for aspirin use in this setting," they write.

Compelling but no recommendations yet
In an accompanying editorial, Andrew T. Chan, MD, MPH, and Nancy R, Cook, ScD, both from Harvard Medical School in Boston, Massachusetts, note that although these results are compelling, they do have limitations.

These analyses exclude the largest randomized trials in primary prevention, the editorialists point out. The Women's Health Study (WHS) of 39,876 women treated with alternate-day aspirin 100 mg over 10 years and the Physicians' Health Study (PHS) of 22,071 men treated with alternate-day aspirin 325 mg over 5 years were not included in the current study because of possible differences in the biologic effect between alternate-day and daily aspirin intake. However, in these 2 studies, aspirin was not associated with a lower risk for colorectal cancer or overall cancer incidence or mortality.

Another limitation, say the editorialists, is that the researchers only used 6 randomized trials to analyze low-dose aspirin in the primary prevention of cancer.

In these 6 trials (n = 35,535), aspirin was shown to lower the incidence of cancer after 3 years in women (132 vs 176; OR, 0.75; P = .01), in men (192 vs 245; OR, 0.77; P = .008), and in both (324 vs 421; OR, 0.76; P = .0003).

A third limitation is that because the included studies were designed to examine cardiovascular end points, there was no information about cancer screening or surveillance.

Finally, some of the analyses were limited by the quality of available data; some estimates pooled individual-level data with published results.

But "caveats notwithstanding, Rothwell and colleagues show quite convincingly that aspirin seems to reduce cancer incidence and death across different subgroups and cancer sites, with an apparent delayed effect," they write. For most individuals, "the risk–benefit calculus of aspirin seems to favor aspirin's long-term anticancer benefit. These findings are consistent with observational findings and our understanding of the stepwise progression of carcinogenesis."

These data might not be the final word on aspirin, as far as making a population-based recommendation, the editorialists caution, because the WHS and PHS remain "significant counterbalancing trials that have not shown a cancer benefit with alternate-day aspirin up to 10 to 12 years."

Another factor to be considered is the adverse events from daily aspirin. Even though there is a "convincing case" that the vascular and anticancer benefits of aspirin outweigh the harms of major extracranial bleeding, less serious adverse effects on quality of life, such as less severe bleeding, are not accounted for in these analyses, Drs. Chan and Cook write.

Nonetheless, until data from forthcoming trials and longer-term follow-up from the WHS and PHS become available, this "impressive collection of data moves us another step closer to broadening recommendations for aspirin use," they conclude.

Metastasis in randomized trials
In the second study, also published online March 21 in the Lancet, Dr. Rothwell and colleagues analyzed data from 5 large randomized trials of daily aspirin (75 mg or more daily) for the prevention of vascular events in the United Kingdom. The cohort consisted of 17,285 trial participants, 987 of whom had a new solid cancer diagnosed during a mean follow-up of 6.5 years.

Aspirin use reduced the risk for cancer with distant metastasis (hazard ratio [HR] for all cancers, 0.64; P = .001). The risk for cancer with distant metastasis was reduced by 36%, and the risk for adencarcioma was reduced by 46% (P = .0007). Among patients with adenocarcinoma who did not have metastasis at their initial diagnosis and who remained on trial treatment up to or after diagnosis, the use of aspirin reduced the risk for metastasis on subsequent follow-up by about 70%.

Aspirin lowered the cancer mortality rate among patients who developed adenocarcinoma, especially in those without metastasis at diagnosis (HR, 0.50; P = .0006). Aspirin also lowered the overall risk for fatal adenocarcinoma (HR, 0.65; P = .0002), but not the risk for other fatal cancers (HR, 1.06; P = .64). These effects were independent of confounders such as age and sex, but the absolute benefit was greatest in smokers, the authors note.

Observation vs randomized
The third study, published online March 21 in the Lancet Oncology, looked at the effect of aspirin on metastases, but with a different approach. The authors compared the effect of aspirin on the 20-year risk for cancer-specific mortality between observational studies and randomized trials.

They conducted this comparison because although randomized trials can clearly establish the risk for colorectal cancer, other solid tumors, and metastasis, such trials lack the statistical power to establish effects on less common cancers and on cancers in women.

Observational and case–control studies can provide these data if the results are shown to be reliable.

Overall, results from observational studies were similar to those from randomized trials, and showed that regular aspirin use lowered the long-term risk for several cancers and for distant metastasis.

In 6 eligible randomized trials, the aspirin group had a consistently lower 20-year risk for death from colorectal cancer than the control group (OR, 0.58; P = .0002). In the 26 case–control studies, any use of aspirin was associated with a lower risk for colorectal cancer (pooled OR, 0.67; P < .0001).

In 17 case–control studies, the regular use of aspirin was associated with a reduced risk for colorectal cancer (pooled OR, 0.62; P < .0001). In the randomized trials, there was good correlation between the effect of daily aspirin use and the 20-year risk for death from colorectal cancer (OR, 0.58; P = .0002).

The authors observed the same consistent reductions in risks for esophageal, gastric, biliary, and breast cancers, and estimates of the effect of aspirin on individual cancers in case–control studies were highly correlated with those seen in randomized trials (P = .0006). The largest effects were observed for gastrointestinal cancers.

In 5 studies, the regular use of aspirin was associated with a reduced proportion of cancers with distant metastasis (OR, 0.69; P < .0001); in 7 studies, it was not associated with a reduction in regional spread (OR, 0.98; P = .71). This was consistent with the findings from the randomized trials.

The authors note that "there is an urgent need for more data for effects on metastasis when aspirin is started after diagnosis of cancer."

More data are also needed for the effects of nonaspirin nonsteroidal anti-inflammatory drugs, they write, adding that "new case–control studies...have the potential to provide data quickly for each of these issues, with reasonable reliability and good statistical power."


Source: http://www.medscape.com/viewarticle/760565?sssdmh=dm1.769238&src=nldne

Vitamin D deficiency: Sun exposure not enough

"The 'epidemic' in vitamin D deficiency is clearly not from too little sun exposure," and dermatologists can be confident in insisting that their patients continue their sun protection efforts, said Richard Gallo, MD, PhD, here at the American Academy of Dermatology (AAD) 70th Annual Meeting.

"Clearly solar exposure is an influence — there is no doubt about that — but you cannot predictably say that a certain amount of exposure will normalize vitamin D deficiency," said Dr. Gallo, chief of dermatology and professor of medicine and pediatrics at the University of California, San Diego, in an interview with Medscape Medical News.

Speaking to an overcapacity audience at the meeting's "Hot Topics" symposium, Dr. Gallo, who was involved in the 2010 Institute of Medicine's (IOM's) consensus report on updated dietary vitamin D intake recommendations, said that although "sunlight is a very reliable source of vitamin D, nutritional sources are clearly required and are, of course, much safer."

He said although there is strong evidence that vitamin D is "absolutely necessary" for bone health, other potential health benefits such as protection from cardiovascular events, cancer, and infection are, as yet, unproven.

Although some physicians advocate universal screening for vitamin D deficiency or insufficiency, Dr. Gallo said there is no evidence to support this approach, and there is a lack of consensus on the definition of these conditions.

The IOM report recommends that patients should have serum vitamin D levels above 20 ng/mL, but the American Endocrine Society sets this level at 30 ng/mL, Dr. Gallo said.

There is evidence to support screening in high-risk individuals, he added, and noted that this is an extensive list including all dark-skinned, pregnant or lactating, elderly, and obese individuals, as well as those with malabsorption syndromes, rickets, osteomalacia, osteoporosis, chronic kidney disease, granulomatous disorders and lymphomas, and patients receiving chronic antifungal therapy.

"This is a pretty broad spectrum of individuals, and it's kind of left up to the individual practitioner right now to use their common sense regarding who should be screened and who shouldn't," Dr. Gallo noted. Physicians who do find a deficiency on screening should consider checking parathyroid hormone, which can sometimes have a compensatory rise, he said.

"An elevated parathyroid hormone paired with low vitamin D and potentially low calcium could be high risk for bone disease. So those kinds of individuals on the severe [low] end you might be best to refer to an endocrinologist," he said in the interview.

"For individuals on the borderline, at 15 ng/mL (and a lot of individuals are there) a simple thing to do is to just suggest a vitamin supplement and rescreen them perhaps 3 to 6 months later."

Winter blood tests will naturally reflect lower levels than in the summer, he added.


Source: http://www.medscape.com/viewarticle/760456?sssdmh=dm1.768201&src=nldne

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Vitamin E may prevent memory deficits caused by lack of sleep

Sleep-deprived individuals who stumble through the day in a mental fog may be encouraged by the results of a new study conducted in rats. The findings suggest that daily doses of vitamin E may help prevent memory impairment caused by chronic lack of sleep.

Sleep deprivation causes oxidative stress in many regions of the brain that may, in turn, blunt our ability to learn and remember. Sleep provides the opportunity for cells to combat oxidative stress and promotes the formation of memories. We typically need a solid 7-9 hours of slumber to reap the maximum benefits. However, many of us fall short of this mark, sometimes on a daily basis, which makes us vulnerable to a slew of mental and physical health woes including poor memory.

Vitamin E is a fat-soluble antioxidant that halts the production of some harmful free radicals that can damage cells. Vitamin E exists in eight different forms: alpha-, beta-, gamma-, and delta-tocopherol; and alpha-, beta-, gamma-, and delta-tocotrienol. However, the most active form in humans is alpha-tocopherol, which is stored in the fatty tissues of the body and provides ongoing antioxidant protection.

A growing body of research indicates that the potent antioxidant properties of vitamin E may help to protect the brain, which is made up of about 60% fats. Now, a new study from the Jordan University of Science and Technology lends further support to the potential neuroprotective effects of vitamin E in the setting of chronic sleep deprivation.

To conduct the study, the researchers deprived lab rats of sleep for 6 weeks. Half of the rodents received 100 mg/kg of vitamin E per day over the 6-week period, whereas the other half did not. At the end of the 6-week period, both groups of sleep-deprived rats, as well as normal "control" rats that slept as much as they wanted, were released into a maze to evaluate their spatial learning and memory abilities. After several trial runs to learn how to navigate the maze, the animals were then tested 30 minutes, 5 hours, and 24 hours later to gauge their short- and long-term ability to remember the correct route.

Compared with the well-rested control rats, the sleep-deprived animals showed significant impairment of both short- and long-term memory in the absence of vitamin E. However, the sleep-deprived animals that received vitamin E demonstrated a preserved ability to remember the correct maze path on par with that displayed by the well-rested control rats.

Closer examination of the brains of the animals revealed that chronic sleep deprivation decreased antioxidant defense mechanisms in the absence of vitamin E, as noted by paltry levels of several antioxidant enzymes. However, sleep-deprived animals that were given daily vitamin E showed normal levels of the antioxidant enzymes, again at concentrations equivalent to those found in control mice.

Giving vitamin E to well-rested control mice did not boost their memory or further increase the levels of the tested antioxidants. Thus, the investigators believe that vitamin E protects memory but does not enhance it, suggesting that vitamin E might only work in this context if there is impairment in memory functions.

The investigators concluded that "sleep deprivation induces memory impairment, and vitamin E prevented this impairment probably through its antioxidant action in the hippocampus" of the brain.


 Source: 1. Alzoubi, K. H., O. F. Khabour, et al. (2012). "The neuroprotective effect of vitamin E on chronic sleep deprivation-induced memory impairment: the role of oxidative stress." Behav Brain Res 226(1): 205-210.

Gastric H pylori infection linked to hemoglobin A1c

Gastric Helicobacter Pylori infection is associated with elevated hemoglobin A1c (Hb1Ac) levels in adults, according to a large study by Yu Chen, PhD, an associate professor of environmental medicine, and Martin Blaser, MD, a professor of internal medicine, at the New York University School of Medicine in New York City. The results of this study were published online March 14 and in the April 15 issue of the Journal of Infectious Diseases.

The researchers conducted cross-sectional analyses of data from 7417 participants in the National Health and Nutrition Examination Survey (NHANES) III (aged 18 years or older) and 6072 participants in NHANES 1999-2000 (aged 3 years or older) whose H pylori status was obtained, to study the association between H pylori infection and type 2 diabetes mellitus.

H pylori/diabetes status, HbA1c measurement
In 1996, participants in the NHANES III phase 1 study who were aged 18 years or older were tested for H pylori immunoglobulin G (IgG) antibodies with 2 tests: the H pylori IgG enzyme-linked immunosorbent assay (Wampole ELISA), and the cagA IgG ELISA.

According to those results, study participants were classified into 3 groups:
H pylori–positive and cagA-positive,
H pylori–positive and cagA-negative, or
H pylori–negative and cagA-negative.

H pylori status was established in NHANES 1999-2000 study participants with the Wampole ELISA. An immune status ratio (ISR) was calculated for each specimen by dividing the specimen optical density by the mean optical density of the cutoff controls. Specimens were given a negative value if the ISR was from 0 to 0.90, and a positive value if the ISR was higher than 0.90.

Participants received a positive diabetes status if they reported insulin use or a physician diagnosis of diabetes. HbA1c assays for both study groups were standardized to the reference method used in the Diabetes Control and Complications Trial, a large clinical study funded by the National Institute of Diabetes and Digestive and Kidney Diseases.

Because cagA status was only determined in NHANES III, the researchers only performed analyses of joint H pylori–cagA status in the NHANES III group.

They evaluated the effect of body mass index (BMI) on the association between H pylori status and HbA1c level, and performed stratified analyses using the standard definitions for overweight (≥25 kg/m2) and normal (<25 kg/m2) BMI.

H pylori associated with increased HbA1c levels in adults
In the NHANES 1999-2000 study overall, participants with H pylori had higher mean HbA1c levels (P = .02); this persisted when the researchers excluded those with known diabetes or insulin use (P = .02). The positive relationship was stronger in those 18 years of age or older (P = .01). There was no association in participants who were younger than 18 years.

After the adults were stratified according to BMI (<25 kg/m2 and ≥25 kg/m2), the association between H pylori and HbA1c was only present in participants with a higher BMI. H pylori–associated increases in HbA1c were greater in those with a higher BMI (P for interaction < .01).

In NHANES III, the association between higher HbA1c levels with positive H pylori status was only apparent in participants without diabetes (P < .01). As in NHANES 1999-2000, H pylori–positivity was associated with higher HbA1c levels in participants with a high BMI who did not have diabetes (P < .01). Unlike in the earlier study, however, the association was also seen in participants with lower BMIs and no diabetes (P < .01).

H pylori cagA associated with increased HbA1c in adults
Overall, there was a progressive increase in HbA1c when comparing participants who were H pylori–negative, H pylori–positive/cagA-negative, and H pylori–positive/cagA-positive (P = .02), especially after excluding participants who had diabetes or used insulin (P < .01). Positive H pylori cagA status was positively associated with HbA1c levels in both BMI groups after excluding people with a history of diabetes.

Association between H pylori and diabetes unclear
In NHANES 1999-2000, H pylori was positively associated with diabetes (odds ratio [OR], 1.30; 95% confidence interval [CI], 0.94 - 1.80). This association was significant in people with higher BMIs (OR, 1.43; 95% CI, 1.00 - 2.03). There did not appear to be a difference between BMI levels (P for interaction = .21).

In NHANES III, H pylori was not associated with diabetes in either BMI group. CagA positivity was not associated with diabetes overall or in stratified analyses based on BMI. Neither H pylori nor H pylori cagA positivity was associated with current insulin use in the total population, or in participants stratified by BMI, although the sample size for this analysis was small.

The authors suspect that H pylori directly or indirectly increases HbA1c levels in adults, particularly those who are obese, as H pylori regulates leptin and ghrelin, which play a key role in energy homeostasis and metabolism.

In addition, H pylori causes gastric inflammation, which may be related to the development of metabolic syndrome, according to recent data.

"Given that the prevalence of H. pylori is decreasing, the proportion of diabetes that could be attributable to H. pylori is likely to also decrease," write the authors. "However, among older individuals and especially those with a higher BMI, glucose intolerance associated with H. pylori could remain significant."

In an accompanying editorial, Dani Cohen, PhD, from Tel Aviv University in Israel, and Khitam Muhsen, PhD, from the University of Maryland School of Medicine, Baltimore, write, "Chen and Blaser utilized two independent large national samples of the general population. In addition, the use of a reliable biomarker of diabetes as a dependent variable confers originality to the article because prior studies on the association between H. pylori and HbA1c have been limited."

Noting that some adults might benefit from H pylori treatment, Dr. Cohen and Dr. Muhsen write, "Helicobacter pylori–infected adults with higher BMI, even if asymptomatic, may need anti–H. pylori therapy to control or prevent diabetes mellitus. With the continuous trend in the decline in H. pylori infection rates in developed countries, the relative importance of H. pylori in the etiology of diabetes mellitus will probably decrease. Nevertheless, there will be still many years in which older individuals, especially those with a higher BMI and glucose intolerance, will benefit from this new information," they write.


Source: http://www.medscape.com/viewarticle/760225?sssdmh=dm1.767383&src=nldne

A soda a day raises CHD risk by 20%

Sugary drinks are associated with an increased risk of coronary heart disease (CHD) as well as some adverse changes in lipids, inflammatory factors, and leptin, according to a new analysis of men participating in the Health Professionals Follow-up Study, reported by Dr Lawrence de Koning (Children's Hospital Boston, MA) and colleagues online March 12, 2012 in Circulation [1].

"Even a moderate amount of sugary beverage consumption — we are talking about one can of soda every day — is associated with a significant 20% increased risk of heart disease even after adjusting for a wide range of cardiovascular risk factors," senior author Dr Frank B Hu (Harvard School of Public Health, Boston, MA) told heartwire . "The increased risk is quite substantial, and I think has important public-health implications given the widespread consumption of soda, not only in the US but also increasing very rapidly in developing countries."

The increased risk is quite substantial, and I think has important public-health implications given the widespread consumption of soda.

The researchers did not find an increased risk of CHD with artificially sweetened beverages in this analysis, however. "Diet soda has been shown to be associated with weight gain and metabolic diseases in previous studies, even though this hasn't been substantiated in our study," says Hu. "The problem with diet soda is its high-intensity sweet taste, which may condition people's taste. It's still an open question whether diet soda is an optimal alternative to regular soda; we need more data on this. "

Hu says water is the best thing to drink, or coffee or tea. Fruit juice is "not a very good alternative, because of the high amount of sugar," he adds, although if diluted with water, "it's much better than a can of soda," he notes.

And Hu says although the current results apply only to men, prior data from his group in women in the Nurses' Health Study [from 2009] were comparable, "which really boosts the credibility of the findings."

Inflammation could be a pathway for impact of soda upon CHD risk
Hu and colleagues explain that while much research has shown a link between the consumption of sugar-sweetened beverages and type 2 diabetes, few studies have looked at the association of these drinks with CHD.

Hence, they analyzed the associations of cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal CHD (MI) in 42 883 men in the Health Professionals Follow-up study. Beginning in 1986 and every two years until December 2008, participants answered questionnaires about diet and other health habits. A blood sample was provided midway through the study.

There were 3683 CHD cases over 22 years of follow-up. Those in the top quartile of sugar-sweetened-beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (RR 1.20; p for trend < 0.001) after adjustment for age, smoking, physical activity, alcohol, multivitamins, family history, diet quality, energy intake, body-mass index, preenrollment weight change, and dieting.

Adjustment for self-reported high cholesterol, high triglycerides, high blood pressure, and diagnosed type 2 diabetes only slightly attenuated these associations, which suggests that drinking soda "may impact on CHD risk above and beyond traditional risk factors," say the researchers.

Consumption of artificially sweetened drinks was not significantly associated with CHD (multivariate RR 1.02; p for trend=0.28).

Intake of sugar-sweetened drinks, but not artificially sweetened ones, was also significantly associated with increased triglycerides and several circulating inflammatory factors — including C-reactive protein, interleukin 6 (IL-6), and tumor-necrosis-factor receptor 1 (TNFr1) — as well as decreased HDL cholesterol, lipoprotein (a) (Lp[a]), and leptin (p < 0.02).

"Inflammation is a key factor in the pathogenesis of cardiovascular disease and cardiometabolic disease and could represent an additional pathway by which sugar-sweetened beverages influence risk," say Hu et al.

Cutting consumption of soda is one of easiest behaviors to change
Hu says that one of the major constituents of soda, high-fructose corn syrup, is subsidized in the US, making such drinks "ridiculously cheap" and helping explain why consumption is so high, particularly in lower socioeconomic groups.

Doctors should be advising people with heart disease or at risk to cut back on sugary beverages; it's almost a no-brainer.

"Doctors should set an example for their patients first," he stresses. "Then, for people who already have heart disease or who are at high risk, physicians should be advising them to cut back on sugary beverages; it's almost a no-brainer, like recommending that they stop smoking and do more exercise. The consumption of sugary beverages is a relatively easy behavior to change."

And although this particular study included mostly white subjects and there are few data on the risk of cardiovascular disease associated with the consumption of soda in people of other ethnicities, there are data on its effect on type 2 diabetes in these groups, he says.

"It has been shown for minority groups — such as African Americans and Asians — that they are more susceptible to the detrimental effects" of sugary drinks on diabetes incidence, he notes.


Source: http://www.medscape.com/viewarticle/760100?sssdmh=dm1.766570&src=nldne