Research - Smoking
Nicotine exposure of male mice produces behavioral impairment in multiple generations of descendants
- Deirdre M. McCarthy,
- Thomas J. Morgan Jr.,
- Sarah E. Lowe,
- Matthew J. Williamson,
- Thomas J. Spencer,
- Joseph Biederman,
- Pradeep G. Bhide
Use of tobacco products is injurious to health in men and women. However, tobacco use by pregnant women receives greater scrutiny because it can also compromise the health of future generations. More men smoke cigarettes than women. Yet the impact of nicotine use by men upon their descendants has not been as widely scrutinized. We exposed male C57BL/6 mice to nicotine (200 μg/mL in drinking water) for 12 wk and bred the mice with drug-naïve females to produce the F1 generation. Male and female F1 mice were bred with drug-naïve partners to produce the F2 generation. We analyzed spontaneous locomotor activity, working memory, attention, and reversal learning in male and female F1 and F2 mice. Both male and female F1 mice derived from the nicotine-exposed males showed significant increases in spontaneous locomotor activity and significant deficits in reversal learning. The male F1 mice also showed significant deficits in attention, brain monoamine content, and dopamine receptor mRNA expression. Examination of the F2 generation showed that male F2 mice derived from paternally nicotine-exposed female F1 mice had significant deficits in reversal learning. Analysis of epigenetic changes in the spermatozoa of the nicotine-exposed male founders (F0) showed significant changes in global DNA methylation and DNA methylation at promoter regions of the dopamine D2 receptor gene. Our findings show that nicotine exposure of male mice produces behavioral changes in multiple generations of descendants. Nicotine-induced changes in spermatozoal DNA methylation are a plausible mechanism for the transgenerational transmission of the phenotypes. These findings underscore the need to enlarge the current focus of research and public policy targeting nicotine exposure of pregnant mothers by a more equitable focus on nicotine exposure of the mother and the father.
Source PLOS Biology
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Renoprotective effect of Spirulina platensis extract against nicotine-induced oxidative stress-mediated inflammation in rats
Walid E.ZahranManal A.Emam
Background: Nicotine is an important factor in the pathogenesis of renal injury in smokers. Purpose: The purpose of the present study was to investigate the renoprotective effect of Spirulina platensis extract (SP) against chronic nicotine administration in rats.
Methods: Nicotine intoxication was induced with 0.5 mg/kg BW. Rats received 500 mg SP/kg BW by gastric gavage over 4 weeks.
Results: Our data revealed that nicotine induced renal dysfunction manifested by significant abnormal levels of kidney function markers (creatinine and urea) accompanied by increased levels of oxidative stress biomarker (malondialdehyde) and inflammatory markers (nitric oxide, Interleukin-6 and tumor necrosis factor-α) while antioxidant status as glutathione level and glutathione S-transferase activity were found to be decreased significantly as compared with controls. It is worthy to note that nicotine toxicity induced significant increments in the protein expression levels of nuclear factor kappa B as well as caspase-3. Histopathological observations showed tubular necrosis and congestion in the endothelial lining glomerular tuft and epithelial lining renal tubules with nicotine intoxication. Interestingly, our data demonstrated that SP supplementation significantly improved the nicotineinduced kidney dysfunction, alleviated the induced-lipid peroxidation, inflammatory, apoptotic protein markers, and boosted the enzymatic/non-enzymatic antioxidants. Moreover, it attenuated the nicotineinduced histopathological alterations of the kidney architecture.
Conclusion: Thus, it is tempting to recommend dietary approaches with Spirulina platensis extract for smokers to minimize the deleterious effect of chronic nicotine consumption and exposure-related problems towards kidney injury via its antioxidant, anti-inflammatory and antiapoptotic properties.
Source : Journal Phytomedicine
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Aqueous Extract of Semen Ziziphi Spinosae Exerts Anxiolytic Effects during Nicotine Withdrawal via Improvement of Amygdaloid CRF/CRF1R Signaling
Changhong Gu,1 ZhengLin Zhao,1,2 Xiaodong Zhu,3 Tong Wu,1 Bong Hyo Lee,2 Yu Jiao,1 Chul Won Lee,2 Dae Hwa Jung,2 Chae Ha Yang,2Rongjie Zhao,1,2,3 and Sang Chan Kim2
Anxiety during nicotine withdrawal (NicW) is a key risk factor for smoking relapse. Semen Ziziphi Spinosae(SZS), which is a prototypical hypnotic-sedative herb in Oriental medicine, has been clinically used to treat insomnia and general anxiety disorders for thousands of years. Thus, the present study evaluated the effects of the aqueous extract of SZS (AESZS) on NicW-induced anxiety in male rats that received subcutaneous administrations of nicotine (Nic) (0.4 mg/kg, twice a day) for 7 d followed by 4 d of withdrawal. During NicW, the rats received four intragastric treatments of AESZS (60 mg/kg/d or 180 mg/kg/d). AESZS dose-dependently attenuated NicW-induced anxiety-like behaviors in the elevated plus maze (EPM) tests and 180 mg/kg/d AESZS inhibited NicW-induced increases in plasma corticosterone. Additionally, the protein and mRNA expressions of corticotropin-releasing factor (CRF) and CRF type 1 receptor (CRF1R) increased in the central nucleus of the amygdala (CeA) during NicW, but these changes were suppressed by 180 mg/kg/d AESZS. A post-AESZS infusion of CRF into the CeA abolished the attenuation of anxiety by AESZS and 180 mg/kg/d AESZS suppressed NicW-induced increases in norepinephrine and 3-methoxy-4-hydroxy-phenylglycol levels in the CeA. The present results suggest that AESZS ameliorated NicW-induced anxiety via improvements in CRF/CRF1R and noradrenergic signaling in the CeA.
Source : Evidence Based Complementary and Alternative Medicine
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Smoking Worsens Inflamed Joints
Important in the transition from genetic risk to symptomatic disease
Age and cigarette smoking increase the risk of inflammatory joint signs among first-degree relatives of patients with rheumatoid arthritis (RA), U.S. researchers have found.
Smoking at younger ages increased this risk more than four-fold, they reported online inArthritis & Rheumatology.
"Our findings add to the literature that smoking is an important, and potentially modifiable, risk factor during pre-clinical transitional phases of RA pathogenesis," wroteJeffrey A. Sparks, MD, Brigham and Women's Hospital, Boston, and co-investigators. "In our study, those who smoked more than 10 pack-years as well as current smokers had significantly increased odds for tender and swollen joints both at baseline and after 2 years of follow-up."
The Studies of the Etiology of Rheumatoid Arthritis cohort was used to evaluate RA risk factors and inflammatory joint signs in a prospective cohort of 966 non-Hispanic white first-degree relatives without RA. Their mean age was 47.2 years, 70.8% were female, and 43.7% had ever smoked. Most (54.9%) had at least one HLA shared epitope allele.
Inflammatory joint signs were tender or swollen joints on a 68-count joint examination. Only inflammatory joint signs at small joints at RA-specific sites were considered, according to the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria.
At baseline, 23% of the first-degree relatives had at least one swollen/tender joint present at RA-specific sites by physical examination. Eighty (8.3%) had one or more swollen joints and 195 (20.2%) had one or more tender joints at baseline.
Increasing age was significantly associated with any swollen joint (OR 1.04, 95% CI 1.02-1.05), any tender joint (OR 1.03, 95% CI 1.02-1.04), and any swollen/tender joint (OR 1.03, 95% CI 1.02-1.04).
Compared with never smoking, more than 10 pack-years of smoking was associated with any swollen joint (OR 1.89, 95% CI 1.05-3.41), any tender joint (OR 1.87, 95% CI 1.23-2.83), and any swollen/tender joint (OR 1.89, 95% CI 1.26-2.82).
Compared with never smoking, current smoking was associated with swollen joints (OR 2.51, 95% CI 1.28-4.94) and swollen metacarpophalangeal/wrist (OR 1.96, 95% CI 1.14-7.72).
The risk of inflammatory joint signs increased with heavier smoking in all age groups, but this risk was especially high among those with more than 10 smoking pack-years who were younger than 50 years. Among those younger than 50, those who smoked more than 10 pack-years had an odds ratio of 4.39 (95% CI 2.23-8.66) for swollen/tender joints compared with never smokers.
Among those 50 years and older, there was no significant association between smoking pack-years and inflammatory joint signs.
"Our findings provide evidence that smoking is important in the transition from genetic risk to symptomatic and objective inflammatory joint findings prior to RA onset and that this risk is highest for heavy smokers at younger ages," Sparks and colleagues wrote.
"These findings emphasize the public health importance of smoking cessation, particularly among younger family members of patients with RA."
There was no interaction for HLA shared epitope and smoking (P=0.34) or RA-related autoantibodies and smoking (P=0.90) for inflammatory joint signs.
Neither genetic risk score nor RA-related autoantibodies were associated with inflammatory joint signs at baseline.
Age (OR 1.05, 95% CI 1.02-1.08) and smoking >10 pack-years (OR 2.66, 95% CI 1.01-7.03) were associated with incident inflammatory joint signs at 2 years. Environmental RA risk factors, genetic risk score, and RA-related autoantibodies were not associated with inflammatory joint signs after 2 years of prospective follow-up.
The researchers speculated that smoking plays a dual role in the pathogenesis of RA by inducing autoantibody production while also propagating joint inflammation. "Since smoking was associated with inflammatory joint signs even in the absence of autoantibodies, inflammatory joint signs may develop before detectable autoantibodies," they wrote.
"Since few participants in our study were seropositive, our findings provide evidence that smoking promotes inflammatory arthritis independent of the presence of serologic RA-related autoantibodies and independent of the shared epitope."
Among study limitations, the authors listed potential misclassification of inflammatory arthritis by physical examination. Also, the study may have been underpowered to find true associations between other established RA risk factors and inflammatory joint signs, given the low number of outcomes in the study
Source : MedPage Today
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Smoking Cigarettes Can Be a Chronic Pain in Your Neck - Smoking linked to cervical degenerative disc disease
Adding to the already length list of reasons not to smoke, researchers have connected smoking to worsening degenerative disc disease in the cervical spine, according to research presented this week at the Association of Academic Physiatrists Annual Meeting in Sacramento, Calif.
The cervical spine is located in the neck and is made up of bones called vertebrae. Between these bones are cervical discs that absorb shock to the spine. Through the normal aging process, these discs slowly degenerate, which means they become dehydrated and shrink. This may result in a person experiencing chronic neck pain that may be difficult to treat. In some cases, the drying of the disc may result in the formation of cracks and tears, through which some of the jelly-like central portion of the disc may spill out and irritate local nerves, which much of the time results in pain in the shoulders, arms, hands and fingers.
It isn’t only wear and tear over time that can damage these discs. Some unhealthy habits, such as smoking, can add to cervical disc degeneration, according to Mitchel Leavitt, MD; resident physician at Emory University’s Department of Physical Medicine and Rehabilitation and the lead investigator of a new study looking at smoking and cervical disc disease. “Smoking is not healthy for a person’s intervertebral discs given the risk of developing microvascular disease – a disease of the small blood vessels – due to nicotine abuse,” Dr. Leavitt explains. “Intervertebral discs receive their nourishment from the microvasculature that line the endplates on either side of each disc; when these blood vessels are damaged, the discs do not receive nourishment and this may speed up the degenerative process.”
While smoking has been associated with degeneration in the lumbar spine (toward the base of the spine), no studies have been able to make this association with the cervical spine. To address this, Dr. Leavitt’s team evaluated the CT scans of 182 consecutive patients who were scanned for various reasons.
“There are more and more high-quality studies coming out that show an association between healthy lifestyle and improved quality and quantity of life as well as better disease management. Spine health is no different, and this study adds to existing studies that have looked at blood vessel health as it relates to chronic back pain,” Dr. Leavitt says.
The patients evaluated by Dr. Leavitt’s team were mostly female (57 percent), and 34 percent were smokers. The researchers utilized a radiologist with subspecialty training in neuroradiology and a physiatrist – a physician who specializes in physical medicine and rehabilitation – to review the CT scans, and they provided documentation on the severity of cervical degenerative disc disease.
Each disc was rated as normal (no loss of disc height), mild (one to 33 percent loss of disc height), moderate (34 to 66 percent loss of disc height), or severe with (greater than 66 percent loss of disc height or having a condition called vacuum disc where gas has accumulated in the discs). Based on this, scores of zero (normal) to three (severe) were given to each disc, and a cumulative cervical degenerative disc disease score was given for the entire cervical spine with a range of zero to 15.
The researchers considered each patient’s smoking status and his or her number of pack years smoked, which is the number of packs of cigarettes the patient smokes each day multiplied by the number of years he or she has smoked. Finally, the researchers collected and considered other health information such as age, body mass index, high blood pressure (called hypertension), high cholesterol and diabetes.
Current smokers were found to have more cervical degenerative disc disease by one point, on average. Additionally, the researchers found that increased age was associated with worsening cervical degenerative disc disease, but co-existing diseases – such as diabetes, hypertension, high cholesterol and high BMI – were not associated with the disease.
“This is another example of the detrimental effects of smoking. Tobacco abuse is associated with a variety of diseases and death, and there are lifestyle factors associated with chronic neck pain,” explains Dr. Leavitt of the study’s findings. “Pain and spine clinics are filled with patients who suffer chronic neck and back pain, and this study provides the physician with more ammunition to use when educating them about their need to quit smoking.”
Dr. Leavitt suggests more research should be conducted on other lifestyle factors (e.g., diets high in fat vs. plant-based, alcohol use, obesity, etc.) as they relate to chronic back and neck pain, as well as identifying any objective changes on advanced imaging or autopsy.
“As the population continues to get older, more and more patients are wanting, if not demanding, that they be given the opportunity to be as active as they were in their 40s. They want to play golf, run triathlons, work in their garden, etc.; however, chronic pain originating from the spine makes these activities difficult,” says Dr. Leavitt. “Virtually everyone knows that moderate exercise somewhere around four to five times per week is beneficial, plus other lifestyle factors like avoidance of smoking and a proper diet are equally important. However, these topics are usually geared towards heart health, lowering blood pressure, managing diabetes, or controlling other medical conditions, and not specific to the spine. It is one thing to live to the age of 95, and it is another to live to 95 while retaining one's mobility and being free of pain. Lifestyle medicine will likely play a large role in the future of healthcare, and having plenty of data to support lifestyle management is critical for a provider who practices evidenced-based medicine. The lifestyle approach may allow us to not only live longer and healthier lives, but we may also be able to take less medication in the process, thereby sparing us the risk of medication side effects.”
Smoking and Cervical Degenerative Disc Disease as Seen on Computed Tomography
Mitchel Leavitt, MD; William Beckworth, MD
Objectives: This study seeks to evaluate the association between cigarette smoking and cervical degenerative disc disease (DDD) via advanced imaging using computed tomography (CT). This has been reported in the lumbar spine but not in the cervical spine except for an x-ray study suggesting that smoking had no effect.
Design: A radiologist with subspecialty training in neuroradiology along with a physiatrist reviewed 182 consecutive CT scans which had been completed at a university hospital for various reasons. Documentation was done in regards to severity of the cervical DDD. Each disc was rated as normal, mild (0-33% loss of disc height), moderate (33-66% loss of disc height), or severe (>66% loss of disc height or vacuum disc). Scores of 0 (normal) to 3 (severe) were given for each disc. A cumulative cervical DDD score was given for the entire cervical spine (C2-7), with a range of 0-15. Other health information was collected including age, smoking status, pack years smoked, BMI, hypertension, dyslipidemia and diabetes. A linear regression model was used to evaluate for a correlation with cervical DDD while accounting for age.
Results: Of the 182 patients there were 61 smokers (34%) and 103 females (57%). Age correlated with worsening cervical DDD (correlation coefficient 0.636, p < 0.0001). Current smokers were found to have more severe cervical DDD after controlling for age (p=0.0203). Active smokers had a worse cumulative cervical DDD score by one point on average. There was no statistical significance for pack years (p=0.164). Comorbidities including diabetes, hypertension, hyperlipidemia and BMI did not correlate with worsening cervical DDD.
Conclusions: There is a positive correlation between active smoking and cervical DDD after controlling for age, although the effect was small. This has not been previously described in the cervical spine.
Source : Newswise
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Parental smoking during pregnancy and total and abdominal fat distribution in school-age children: the Generation R Study
B Durmuş1,2,3, D H M Heppe1,2,3, H R Taal1,2,3, R Manniesing4, H Raat5, A Hofman3, E A P Steegers6, R Gaillard1,2,3 and V W V Jaddoe1,2,3
Objective: Fetal smoke exposure may influence growth and body composition later in life. We examined the associations of maternal and paternal smoking during pregnancy with total and abdominal fat distribution in school-age children.
Methods:We performed a population-based prospective cohort study among 5243 children followed from early pregnancy onward in the Netherlands. Information about parental smoking was obtained by questionnaires during pregnancy. At the median age of 6.0 years (90% range: 5.7–7.4), we measured anthropometrics, total fat and android/gynoid fat ratio by dual-energy X-ray absorptiometry, and preperitoneal and subcutaneous abdominal fat were measured by ultrasound.
Results:The associations of maternal smoking during pregnancy were only present among girls (P-value for sex interaction<0.05). Compared with girls from mothers who did not smoke during pregnancy, those from mothers who smoked during the first trimester only had a higher android/gynoid fat ratio (difference 0.23 (95% confidence interval (CI): 0.09–0.37) s.d. scores (SDS). Girls from mothers who continued smoking throughout pregnancy had a higher body mass index (difference: 0.24 (95% CI: 0.14–0.35) SDS), total fat mass (difference: 0.23 (95% CI: 0.14–0.33) SDS), android/gynoid fat ratio (difference: 0.34 (95% CI: 0.22–0.46) SDS), subcutaneous abdominal fat (difference: 0.22 (95% CI: 0.11–0.33) SDS) and preperitoneal abdominal fat (difference: 0.20 (95% CI: 0.08–0.31) SDS). Similar associations with body fat distribution outcomes were observed for paternal smoking during pregnancy. Both continued maternal and paternal smoking during pregnancy may be associated with an increased risk of childhood overweight. The corresponding odds ratios were 1.19 (95% CI: 0.98–1.46) and 1.32 (1.10–1.58), respectively.
Conclusions:Maternal and paternal smoking during pregnancy are associated with an adverse body and abdominal fat distribution and increased risk of overweight in children. Similar effects of maternal and paternal smoking suggest that direct intrauterine mechanisms and common family-based lifestyle-related factors explain the associations.
Source : International Journal of Obesity
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Nicotine exposure gives baby rats addictive personalities
Results suggest explanation for why people exposed to nicotine in the womb are more likely to become smokers.
Exposure to nicotine in the womb increases the production of brain cells that stimulate appetite, leading to overconsumption of nicotine, alcohol and fatty foods in later life, according to a new study in rats.
Smoking during pregnancy is known to alter fetal brain development and increase the risk of premature birth, low birth weight and miscarriage. Prenatal exposure to nicotine also increases the likelihood of tobacco use and nicotine addiction in later life, but exactly how is unclear.
To understand the mechanisms behind this effect, Sarah Leibowitz, a behavioural neurobiologist at the Rockefeller University in New York, and her colleagues injected pregnant rats with small doses of nicotine — which the researchers say are comparable to the amount a pregnant woman would get from smoking one cigarette a day — and then examined the brains and behaviour of the offspring.
In a paper published today in Journal of Neuroscience1, they found that nicotine increased the production of specific types of neurons in the amygdala and hypothalamus. These cells produce orexin, enkephalin and melanin-concentrating hormone, neuropeptides that stimulate appetite and increase food intake.
Rats exposed to nicotine in the womb had more of these cells and produced more of the neuropeptides than those that were not, and this had long-term consequences on their behaviour. As adolescents, they not only self-administered more nicotine, but also ate more fat-rich food and drank more alcohol.
“These peptide systems stimulate food intake,” says Leibowitz, “but we found that they similarly increase the consumption of drugs and stimulate the brain’s reward mechanisms that promote addiction and substance abuse.”
Leibowitz notes that children whose mothers smoked during pregnancy are more likely to smoke themselves during adolescence and adulthood. Her team's findings suggest a possible mechanism for that.
The use of nicotine patches or e-cigarettes during pregnancy could have a similar effect. “Whether given subcutaneously, as in our study, or via smoking or patches, the same amount of nicotine would still get into the brain to affect neuronal development and function,” Leibowitz says.
The results highlight the toxic effects of nicotine exposure on brain development, says George Koob, a neurobiologist at the Scripps Research Institute in La Jolla, California. He also adds that the study casts new light on the role of these neuropeptides in reward and motivation.
In earlier work, Leibowitz and her colleagues showed that rats exposed to fat and alcohol in the womb likewise overconsume these substances as adolescents. “Our studies make it very clear that neuronal development in utero is highly sensitive to these substances,” she says, “with each promoting their overconsumption and addictive-like behaviour in the offspring.”
She and her collaborators are now comparing the effects of nicotine, fat and alcohol to learn more about how this promotion occurs. They are also exploring ways to reverse the effects of prenatal exposure to these substances, thus preventing their overconsumption in later life, which could lead to addiction and obesity.
Source : Nature
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Quitting smoking in pregnancy tied to benefit for baby
Women who quit smoking immediately before or after becoming pregnant gain more weight during and after pregnancy - but their babies are less likely to be born small than those born to smokers, a new study suggests.
Researchers in Denmark found that women who quit smoking gained about six more pounds during their pregnancies than those who continued to smoke, and a similar amount in the year after giving birth.
On the other hand, women who quit smoking early in pregnancy and nonsmokers gave birth to babies of similar birth weights, on average. Babies of women who kept smoking were more likely to be born at a low weight.
"The big thing to get out of this study is that quitting early in pregnancy is as helpful in respect to the birth weight of your baby as never having smoked while you were pregnant," Dr. Amber Samuel, a maternal-fetal medicine expert at Emory University School of Medicine in Atlanta, said.
"I think that can be an inspiration to moms who are looking to make a change in their lives."
According to the American Cancer Society, between 10 and 15 percent of women smoke during pregnancy. Studies have linked smoking to premature birth and other complications, such as birth defects, low birth weight and stillbirth.
Infants have a three to four times higher risk of dying from sudden infant death syndrome, or "crib death," if their mothers smoke during and after pregnancy. Children exposed to secondhand smoke also have more ear infections, pneumonia, bronchitis, asthma and other health problems.
The new study included 1,774 women who were part of the "Smoke-free Newborn" study conducted in Copenhagen, Denmark, between 1996 and 1999.
Twice during pregnancy, researchers surveyed women about their smoking status. To double-check whether women who said they quit smoking really did, their saliva was checked for cotinine - created when nicotine is broken down in the body.
About 38 percent of women were smokers before becoming pregnant, and half of them quit right before or soon after, Dr. Line Rode of Copenhagen University Hospital and colleagues found.
During pregnancy, nonsmokers gained almost 30 pounds, on average, smokers gained 29 pounds and quitters gained 35 pounds.
Among women who quit smoking, 8 percent had babies born below the 10th percentile for birth weight, based on general Scandinavian records. In comparison, 22 percent of smokers had babies whose weight fell below that cutoff.
Babies with low birth weight are at higher risk for infections, breathing and respiratory disorders, delayed growth and social development and learning disabilities.
One year after giving birth, half of quitters were able to stay off cigarettes. Nonsmokers and relapsed quitters both gained between 1.5 and 2 pounds post-pregnancy, successful quitters gained 7 pounds and smokers lost about half a pound, according to findings published in Obstetrics and Gynecology.
"One strength of the study is that it tried to ferret out whether women who say they quit smoking actually did quit," Samuel, who was not involved in the research, told Reuters Health.
On the other hand, she said the results may not apply to the current U.S. population.
"There were very few obese women in this study," Samuel said.
According to the Institute of Medicine, women with a normal pre-pregnancy weight should gain between 25 and 35 pounds during pregnancy and obese women should gain 11 to 20 pounds.
Excessive weight gain during pregnancy is linked to birth complications and medical problems for the mother, such as gestational diabetes. Extra weight that stays on after pregnancy can increase a woman's risk for obesity, diabetes and heart disease.
Samuel said most women in this study did not gain enough weight to offset the long-term benefits of not smoking.
She said it's not possible to put a time frame on how late into pregnancy a woman can quit smoking and still see benefits for her baby, since the researchers did not analyze their results based on when, exactly, women kicked the habit.
Source : Reuters
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Quit Smoking? Vitamin E May Give Extra Boost to Heart Health
Taking a specific form of a vitamin E supplement can accelerate the health benefits that occur when people quit smoking, new research suggests.In the small study, improvement in blood vessel function associated with the added vitamin E potentially translates into an estimated 19 percent greater drop in future risk for cardiovascular disease.
Smokers were recruited to participate in a study to quit smoking for seven days, with blood markers of inflammation and blood vessel function measured before and after the trial. After seven days of not smoking, participants saw an increase in their vascular function by an average of 2.8 percent. Those who quit smoking and also took the gamma-tocopherol form of vitamin E showed a 1.5 percent additional improvement in vascular function.
While these changes in vascular function may appear to be small, previous large-scale studies suggest that every 1 percent increase in vascular function – or improvement in the blood vessel’s ability to dilate – translates into a 13 percent drop in risk of developing heart disease later in life.
“This is a very short-term study that shows very promising effects,” said Richard Bruno, associate professor of human nutrition at The Ohio State University and senior author of the study.
“The underlying rationale is that we know it takes many years before the risk for cardiovascular disease of a former smoker matches that of a nonsmoker. We hope to develop a therapy to combine with smoking cessation that could accelerate the restoration of vascular function and reduce cardiovascular risk.”
The research was presented Tuesday (4/23) at the annual Experimental Biology meeting in Boston.
The supplement in the study is not the same as the average vitamin E available on most store shelves. Vitamin E occurs in eight forms based on their chemical structure, and the most well-known form belongs to a variety called tocopherols. In this study, researchers tested the effects of the gamma-tocopherol form. The most common form of vitamin E, and the one for which humans have a dietary requirement, is alpha-tocopherol.
Though taking gamma-tocopherol is safe, Bruno noted that longer-term studies with more participants would be required to nail down specific dietary recommendations related to smoking cessation.
A total of 30 smokers in their 20s who had smoked at least half a pack per day for a year participated in the study. All participants stopped smoking, and 16 received 500 milligrams daily of gamma-tocopherol while 14 received a placebo.
In addition to taking blood samples, researchers measured vascular function by obtaining ultrasound images of an artery in the upper arm as the vessel responded to a surge of blood flow after circulation in the arm was stopped for five minutes.
The quality of vascular function is defined by the artery’s ability to dilate in response to the surge of blood – more dilation suggests the vessel has appropriate responses to changes in blood flow.
“Greater dilatory response is an indicator of vascular health. People with a long history of smoking tend to have low vasodilatory responses,” Bruno said.
Participants who took the supplements showed greater improvements in vascular function and also had lower levels of two inflammation-related proteins in their blood than did participants who received a placebo.
Bruno said the lower levels of those two proteins in the supplemented participants’ blood suggest that the gamma-tocopherol form of vitamin E restores vascular function at least in part by lowering inflammation.
Gamma-tocopherol is abundant in the American diet, but is difficult to obtain from low-calorie sources. Food sources include soybean, canola and some other vegetable oils, and certain nuts such as pistachios, pecans, cashews and peanuts. Supplements that are rich in gamma-tocopherol can be found in specialty stores.
Source : Newswise
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Smoking Associated With Worse Back Pain
Patients with spinal disorders who quit smoking may experience substantial improvements in back pain, according to the findings of an analysis of a prospectively maintained database.
Caleb Behrend, MD, from the University of Rochester Medical Center in New York, and colleagues present their findings in an article published in the December issue of the Journal of Bone & Joint Surgery.
The authors mention that smoking has been identified as a modifiable risk factor for chronic pain disorders. "Furthermore, with regard to chronic pain disorders, smokers have reported an increased magnitude of pain when compared with nonsmokers," the authors write. "Glassman et al. found that smoking cessation in patients undergoing spinal arthrodesis was associated with increased patient satisfaction, fusion rates, and return to work."
In the study, the authors reviewed questionnaires for 5333 patients completed at the time of entry into care and at the time of the latest follow-up. Patient-reported pain scores were assessed using a visual analog scale (VAS).
Compared with never-smokers, current smokers reported significantly greater pain scores at the latest follow-up (mean VAS score, 4.49 [95% confidence interval (CI), 4.15 - 4.84] vs 3.59 [95% CI, 3.49 - 3.70]; P < .001).
Patients who quit smoking reported significantly greater improvements compared with current smokers in worst (mean VAS score, −1.56 [95% CI, −1.94 to −1.17] vs −0.70 [95% CI, −0.90 to −0.51]; P = .013), current (mean VAS score, −1.07 [95% CI, −1.44 to −0.70] vs −0.46 [95% CI, −0.66 to −0.28; P < .05), and average (mean VAS score, −1.23 [95% CI, −1.56 to −0.86] vs −0.46 [95% CI, −0.66 to −0.27]; P = .024) weekly pain.
In addition, nearly 2-fold more patients who quit smoking reported a more than 30% decrease in worst pain than current smokers (32.0% vs 16.6%), and never-smokers reported a greater mean improvement in disability as determined by the Oswestry Disability index than current smokers (−7.3 points [95% CI, −8.1 to −6.5 points] vs −4.6 [95% CI, −5.6 to −3.6]).
According to the authors, limitations of the study include their inability to capture the effects of all possible factors that may influence pain and determine when patients stopped smoking or experienced improvements in pain.
They conclude that smoking cessation programs are needed to improve chronic pain among patients with spinal conditions. "The present study supports the need for smoking cessation programs for patients with axial or radicular pain of spinal etiology, given a strong association between improved patient-reported pain and smoking cessation," the authors write.
Asked for independent comment, David O. Werner, MD, from the Mayo Clinic, Rochester, Minnesota, agreed with the authors' conclusion. "This suggests that tobacco use interventions should be an integral part of pain treatment," Dr. Werner told Medscape Medical News. "Given the tremendous health benefits of quitting, clinicians should take every opportunity to help every smoker quit, but if pain is improved, this makes the issue even more urgent for the pain physician."
One coauthor received a grant from the Southwestern Foundation. One coauthor received grants or has grants pending with FOT and Goldstein. The other authors and the commentator have disclosed no relevant financial relationships.
J Bone Joint Surg Am. 2012;94:2161-2166. Abstract
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Cytoprotective Potential of Royal Jelly on Human Umbilical Vein Endothelial Cells against Nicotine Toxicity via Catalase
Roongtawan Supabphol1* and Athikom Supabphol2
1Department of Physiology, Faculty of Medicine, Srinakharinwirot University, Bangkok, Thailand.
2Department of Surgery, Faculty of Medicine, HRH Princess Maha Chakri Sirindhorn Medical Center (MSMC), Srinakharinwirot University, Ongkharak, Nakorn Nayok, Thailand.
Aims: To examine the cytoprotective effects and mechanisms of a royal jelly extract in protecting the human umbilical vein endothelial cells (HUVECs) from nicotine toxicity.
Study Design: Laboratory experimental tests.
Place and Duration of Study: Department of Physiology and Department of Surgery, Faculty of Medicine, Srinakharinwirot University, Bangkok 10110, Thailand, between June 2011 and February 2012.
Methodology: Cytotoxic assay of royal jelly to HUVECs was performed by using the 3-(4,5-dimethylthiazol,2-yl)-2,5-diphenyltetrazolium bromide (MTT) reagent. The cytoprotective effect was then investigated by examining the presence of vacuole-like structures in HUVECs exposed to nicotine 5 or 7.5 mM with and without royal jelly. Cells were stained with crystal violet and photographed under phase contrast microscope. mRNA levels of genes involved in intracellular antioxidant system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GSR) were confirmed by reverse transcription-polymerase chain reaction (RT-PCR). Catalase activity was also determined by examining peroxidative function.
Results: Vacuole-like structures were found in the cytoplasm of HUVECs exposed to 5 mM nicotine and higher. Royal jelly alone at the concentrations lower than 2 mg/ml did not affect the structure or the survival rate of HUVECs after 1, 4, and 7 days of treatment. For cytoprotective effect, royal jelly 1-4 mg/ml mixed with 5 mM nicotine could obviously decrease the numbers of cells containing vacuole-like structures in the cytoplasm of HUVECs with the dose- and time-dependent fashion. The catalase mRNA levels and catalase activity in HUVECs exposed to 5 mM nicotine decreased significantly, but recovered when the cells were treated with royal jelly.
Conclusion: Royal jelly can be safety applied to endothelial cells even at high doses. Royal jelly is able to attenuate the abnormal vacuole-like structures induced in endothelial cell cytoplasm when exposed to nicotine. Further investigation of antioxidant gene expression showed that the mechanism possibly involves a reduction of oxidative stress via an up-regulation of catalase. Besides the supplementary food, royal jelly could be useful for endothelial cell protection from nicotine toxicity found in smoking or nicotine addiction.
Source : European Journal of Medicinal Plants
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Green Tea Could Modify the Effect of Cigarette Smoking On Lung Cancer Risk
Drinking green tea could modulate the effect of smoking on lung cancer.
Results of this hospital-based, randomized study conducted in Taiwan were presented at the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer, Jan. 11-14, 2010.
"Lung cancer is the leading cause of all cancer deaths in Taiwan," said I-Hsin Lin, M.S., a student at Chung Shan Medical University in Taiwan. "Tea, particularly green tea, has received a great deal of attention because tea polyphenols are strong antioxidants, and tea preparations have shown inhibitory activity against tumorigenesis."
However, previous studies of green tea have been inhibited by the flaws of the epidemiologic model with its inherent biases.
Lin and colleagues enrolled 170 patients with lung cancer and 340 healthy patients as controls. The researchers administered questionnaires to obtain demographic characteristics, cigarette smoking habits, green tea consumption, dietary intake of fruits and vegetables, cooking practices and family history of lung cancer. They also performed genotyping on insulin-like growth factors as polymorphisms on the following insulin-like growth factors: IGF1, IGF2 and IGFBP3, which have all been reported to be associated with cancer risk.
Among smokers and non-smokers, those who did not drink green tea had a 5.16-fold increased risk of lung cancer compared with those who drank at least one cup of green tea per day. Among smokers, those who did not drink green tea at all had a 12.71-fold increased risk of lung cancer compared with those who drank at least one cup of green tea per day.
Lin and colleagues suspect genetics may play a role in this risk differential. Green tea drinkers with non-susceptible IGF1 (CA)19/(CA)19 and (CA)19/X genotypes reported a 66 percent reduction in lung cancer risk as compared with green tea drinkers carrying the IGF1 X/X genotype.
Heavy smokers carrying susceptible IGF1, IGF2 and IGFBP3 genotypes also had a higher risk of lung cancer compared with nonsmokers carrying non-susceptible IGF1, IGF2 and IGFBP3 genotypes.
"Our study may represent a clue that in the case of lung cancer, smoking-induced carcinogenesis could be modulated by green tea consumption and the growth factor environment," said Lin.
Source : Science Daily
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Secondhand Smoke Impairs Vital Cough Reflex in Kids
New research from the Monell Center reveals that exposure to secondhand smoke decreases sensitivity to cough-eliciting respiratory irritants in otherwise healthy children and adolescents. The findings may help to explain why children of smokers are more likely to develop pneumonia, bronchitis and other diseases and also are more likely to experiment with smoking during adolescence.“Cough protects our lungs from potentially damaging environmental threats, such as chemicals and dust. Living with a parent who smokes weakens this reflex, one of the most vital of the human body,” said Julie Mennella, Ph.D., a developmental biologist at Monell who co-directed the study with Monell sensory scientist Paul Wise, Ph.D.
Children are exposed to more secondhand smoke than nonsmoking adults, with 60 percent of U.S. children aged 3-11 years and 18 million youth aged 12-19 years exposed to tobacco smoke on a regular basis.
Adult smokers are known to have a less sensitive cough reflex relative to non-smokers, meaning that it takes more irritation to elicit a cough in the smokers. The Monell research team conducted the current study to ask if the cough reflex of children and adolescents who are regularly exposed to secondhand smoke is affected in a similar fashion.
In the study, which appears in Tobacco and Nicotine Research, 38 healthy children aged 10-17 years old inhaled increasing concentrations of capsaicin from a nebulizer. Capsaicin is the burning ingredient in chili peppers and a potent chemical stimulus for cough. Seventeen of the youth were regularly exposed to smoke in the home, while 21 were never exposed to smoke at home. Parents also were tested.
The amount of capsaicin in the nebulizer was increased after each inhalation until the subject coughed twice. The capsaicin concentration that induced the two coughs was labeled as the individual’s cough threshold.
Youth regularly exposed to secondhand smoke required twice as much capsaicin to trigger cough as did non-exposed children, meaning that the exposed children were less sensitive to the irritating environmental stimulus. A similar finding was true for the parents, confirming earlier findings.
The findings highlight a previously unrecognized public health risk from exposure to secondhand smoke. An insensitive cough reflex could make exposed children less able to cope with environmental threats, which could in turn play a role in their increased risk for developing respiratory illness.
"This study suggests that even if an exposed child is not coughing, his or her respiratory health may still be affected by secondhand smoke," said Wise.
It is also possible that an insensitive cough reflex could increase the risk of adolescents acquiring a smoking habit by making experimentation with smoking less unpleasant.
Future research will explore the relationships among secondhand smoke exposure, cough reflex and the sensory response to cigarettes to ask if exposure-related decreased sensitivity to irritants makes smoking more pleasurable to teens. The researchers will also seek funding to determine whether impairment of the cough reflex is reversible and how this may relate to the age when secondhand smoke exposure ceases.
Source : Newswise
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Vitamin D May Protect Lung Function in Smokers
Vitamin D deficiency is associated with worse lung function and more rapid decline in lung function over time in smokers, suggesting that vitamin D may have a protective effect against the effects of smoking on lung function, according to a new study from researchers in Boston. “We examined the relationship between vitamin D deficiency, smoking, lung function, and the rate of lung function decline over a 20 year period in a cohort of 626 adult white men from the Normative Aging Study,” said lead author Nancy E. Lange, MD, MPH, of the Channing Laboratory, Brigham and Women’s Hospital. “We found that vitamin D sufficiency (defined as serum vitamin D levels of >20 ng/ml) had a protective effect on lung function and the rate of lung function decline in smokers.”
The findings were published online ahead of print publication in the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine.
In the study, vitamin D levels were assessed at three different time points between 1984 and 2003, and lung function was assessed concurrently with spirometry.
In vitamin D deficient subjects, for each one unit increase in pack-years of smoking, mean forced expiratory volume in one second (FEV1) was 12 ml lower, compared with a mean reduction of 6.5 ml among subjects who were not vitamin D deficient. In longitudinal models, vitamin D deficiency exacerbated the effect of pack years of smoking on the decline in FEV1 over time.
No significant effect of vitamin D levels on lung function or lung function decline were observed in the overall study cohort, which included both smokers and non-smokers.
“Our results suggest that vitamin D might modify the damaging effects of smoking on lung function,” said Dr. Lange. “These effects might be due to vitamin D’s anti-inflammatory and anti-oxidant properties.”
The study has some limitations, including that the data is observational only and not a trial, that vitamin D levels fluctuate over time, and that the study has limited generalizability due to the cohort being all elderly men.
“If these results can be replicated in other studies, they could be of great public health importance,” said Dr. Lange. “Future research should also examine whether vitamin D protects against lung damage from other sources, such as air pollution.”
“While these results are intriguing, the health hazards associated with smoking far outweigh any protective effect that vitamin D may have on lung function ,” said Alexander C. White MS, MD, chair of the American Thoracic Society’s Tobacco Action Committee. “First and foremost, patients who smoke should be fully informed about the health consequences of smoking and in addition be given all possible assistance to help them quit smoking.”
Source : Newswise
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Secondhand Smoke is Linked to Type 2 Diabetes and Obesity
Adults who are exposed to secondhand smoke have higher rates of obesity and Type 2 diabetes than do nonsmokers without environmental exposure to tobacco smoke, a new study shows. The results will be presented Sunday at The Endocrine Society’s 94th Annual Meeting in Houston.“More effort needs to be made to reduce exposure of individuals to secondhand smoke,” said study co-author Theodore C. Friedman, MD, PhD, chairman of the Department of Internal Medicine at Charles R. Drew University, Los Angeles.
Studies have shown an association between cigarette smoking and an increased rate of Type 2 diabetes despite the fact that most smokers are leaner than nonsmokers and obesity is a risk factor for Type 2 diabetes. Although some studies have suggested a relationship between Type 2 diabetes and passive, or secondhand, smoking, Friedman said these studies have not verified exposure to secondhand smoke through serum (blood) levels of cotinine. Cotinine is a metabolite of nicotine, and serum cotinine measures a person’s exposure to tobacco smoke.
In their current study, Friedman and his fellow researchers used serum cotinine levels to verify passive smoking. They examined data from more than 6,300 adults who participated from 2001 to 2006 in the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the U.S. population.
The investigators defined current smokers, which made up 25 percent of the sample, as survey participants who reported that they smoke cigarettes and who had a measured serum cotinine level greater than 3 nanograms per milliliter (ng/mL). Nonsmokers (41 percent of the sample) were those who answered “no” to the question “Do you smoke cigarettes?” and who had a cotinine level below 0.05 ng/mL. Participants who answered “no” to this question but whose cotinine level was above 0.05 ng/mL were defined as secondhand “smokers” (34 percent).
In analyzing these groups, the researchers controlled for age, sex, race, alcohol consumption and physical activity. They found that, compared with nonsmokers, secondhand smokers had a higher measure of insulin resistance, a condition that can lead to Type 2 diabetes; higher levels of fasting blood glucose, or blood sugar; and a higher hemoglobin A1c, a measure of blood sugar control over the past three months.
Secondhand smokers also had a higher rate of Type 2 diabetes, as defined by a hemoglobin A1c greater than 6.5 percent. Secondhand smokers had a similar rate of diabetes to that of current smokers, according to Friedman.
Secondhand smokers also had a higher body mass index (BMI), a measure of body fat, compared with nonsmokers, Friedman reported. Current smokers had a lower BMI than nonsmokers but a higher hemoglobin A1c. When the researchers controlled for BMI, they found that secondhand smokers and current smokers still had a higher hemoglobin A1c than did nonsmokers.
“This finding shows that the association between secondhand smoke and Type 2 diabetes was not due to obesity,” Friedman said. “More studies are needed to show whether secondhand smoke is a cause of diabetes.”
Source : Newswise
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Second-Hand Smoke Affects Bladder Function in Children, Study Suggests
According to the Environmental Protection Agency, parents are responsible for 90 percent of children's exposure to environmental (second-hand) tobacco smoke. Children with mothers who smoke are at even higher-risk for developing health disorders. In a presentation at the American Urological Association Annual Meeting, physicians at the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School and Robert Wood Johnson University Hospital showed that second-hand cigarette smoke was associated with moderate to severe irritative bladder symptoms in children.
"Our research shows that exposure to second-hand cigarette smoke increases the risk of severe urinary disorders in children, that may otherwise be reduced or even prevented," said Joseph G. Barone, MD, an expert pediatric urologist, associate professor of surgery at UMDNJ-Robert Wood Johnson Medical School and surgeon-in-chief of Bristol-Myers Squibb Children's Hospital at Robert Wood Johnson University Hospital. "Our results emphasize the importance of smoking cessation for parents. Pediatricians and family physicians are urged to discuss with parents opportunities that are available to quit smoking."
The study included children aged 4 through 17 who sought care of a pediatric urologist for irritative bladder storage symptoms including urinary urgency, increased urinary frequency and incontinence. 28 percent of children in the study were exposed to environmental tobacco smoke. More than half of the children in the study had moderate to severe symptoms, 50 percent of which were exposed to cigarette smoke within a car and 23 percent of which had mothers who smoked. The presentation noted that symptom severity increased with greater exposure to second-hand smoke; in children aged 4 through 10, the increase in severe urinary symptoms was significant.
"Cigarette smoke is an environmental toxin and dangerous to children's health -- particularly hazardous to very young and pre-pubescent children," said Dr. Barone. "Parents should make a concerted effort to reduce their child's exposure to smoke in confined places, especially in the home and in cars. Quitting smoking is the healthiest option for children."
Source : Science Daily
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