How binge drinking, smoking drive heart disease, cancers
THE holidays are here again! It comes with the lure to over indulge in drinking or/and smoking. But more reasons are emerging on why fun seekers should quit heavy drinking and smoking. CHUKWUMA MUANYA reports.
AS preparations for the Yuletide reaches top gear, more reasons are emerging on why people should quit heavy drinking, smoking and even being passive smokers. Passive smoking is the involuntary inhalation of smoke from tobacco products.
Although moderate drinking, especially, of red wine, has been shown to be beneficial to the heart, researchers have identified how binge drinking may drive heart disease.
Heavy drinking and smoking have also been linked to low sperm count, obesity, and infertility. Some other studies have shown that drinking during pregnancy increases the risk of birth defects such as cleft palate.
According to a study published last week in the journal Atherosclerosis, a group of researchers has identified the precise mechanisms by which binge drinking (consuming large amounts of alcohol infrequently, such as on weekends) contributes to clogs in arteries that lead to heart attack and stroke.
The works adds to a growing body of evidence that drinking patterns matter as much, if not more, to risk for cardiovascular disease than the total amount consumed.
It has also been shown that cigarette smokers have a higher risk of developing several chronic disorders. These include fatty buildups in arteries, several types of cancer and chronic obstructive pulmonary disease (lung problems).
Atherosclerosis (buildup of fatty substances in the arteries) is a chief contributor to the high number of deaths from smoking. Many studies detail the evidence that cigarette smoking is a major cause of coronary heart disease, which leads to heart attack.
A new study has found that women with a particular gene mutation linked to breast cancer may further raise their risk of the disease if they smoke.
The gene in question is known as the ataxia-telangiectasia, or A-T, gene. At least one percent of the population carries a mutation in the gene, and women, who carry mutated A-T have a higher-than-average risk of developing breast cancer.
But until now it had not been known whether smoking increases this risk even more. Studies on smoking and breast cancer in the population as a whole have generally found little or no evidence that the habit contributes to the disease.
These latest findings published in Cancer Epidemiology, Biomarkers and Prevention, however, should give women yet another reason not to smoke.
According to lead researcher, Dr. Michael Swift, of the Disease Insight Research Foundation in Ardsley, New York, United States, while the study focused only on women with an A-T mutation, most women, who carry such a mutation do not know it. So it is wise -- for a whole range of health reasons -- for all female smokers to give up the habit.
Most people do not know whether they have an A-T mutation because the defect causes no symptoms when a person carries only one copy of the mutated gene. In the uncommon case where a child inherits two copies of a mutated A-T gene -- one copy from each parent -- it causes ataxia- telangiectasia, a disorder that attacks the nervous system.
So while parents of children with ataxia-telangiectasia know they are carriers, most carriers remain unaware.
Previous studies have shown that babies exposed to tobacco in uterus are more likely to have a low birth weight and are at increased risk for sudden infant death syndrome.
Now new research by The Miriam Hospital, United States, reveals that these babies are also less likely to self-soothe and are more aroused and excitable than newborns whose mothers did not smoke during pregnancy.
Researchers from The Miriam Hospital's Centres for Behavioral and Preventive Medicine say early identification and targeted intervention efforts aimed at both infants and parents may help prevent possible disruption in early maternal-infant bonding and, ultimately, long-term adverse outcomes. The study is published online by the Journal of Pediatrics.
According to new research, while smoking poses a health threat to both men and women, women require less tobacco exposure than men to have a significant increased risk for colorectal cancer.
In a separate analysis, researchers found smoking may increase the risk of pancreatic cancer precursor lesions, particularly in patients with a strong family history of the disease.
While research has demonstrated that smoking is associated with a two-fold risk for colorectal neoplasia, less is known about the exposure quantity needed.
President of African Heart Network (AHN), Dr. Kingsley Akinroye, told The Guardian: "Heavy drinking puts more fat into the circulation in the body, raising the triglygeride level. That is why doctors will tell you 'if you do not drink, do not start.' There are other, healthier ways to reduce the risk of heart disease like eating right, getting regular exercise and maintaining a healthy weight.
"What is 'moderate drinking' for one may be legally drunk for another. By nature's design, a woman's body metabolises alcohol differently so that one alcoholic beverage in a woman is equal to two in a man. Alcohol remains in a woman's body longer than in a man's. Also, the older you are, the less efficient the body can metabolize alcohol. Women, especially women of small stature, must be alert to the metabolic differences when drinking, and limit their alcohol intake accordingly."
Akinroye said cigarette and tobacco smoke, high blood cholesterol, high blood pressure, physical inactivity, obesity and diabetes are the six major independent risk factors for coronary heart disease that one can modify or control.
Akinroye said, "cigarette smoking increases the risk of coronary heart disease by itself. When it acts with other factors, it greatly increases risk. Smoking increases blood pressure, decreases exercise tolerance and increases the tendency for blood to clot. Smoking also increases the risk of recurrent coronary heart disease after bypass surgery.
"Cigarette smoking is the most important risk factor for young men and women. It produces a greater relative risk in persons under age 50 than in those over 50.
"Women, who smoke and use oral contraceptives greatly increase their risk of coronary heart disease and stroke compared with nonsmoking women, who use oral contraceptives. Smoking decreases HDL (good) cholesterol. Cigarette smoking combined with a family history of heart disease also seems to greatly increase the risk."
Consultant Obstetrician and Gynaecologist at Optimal Specialist Hospital, Surulere, Lagos, said men and women, who indulge in heavy drinking and smoking have lower fertility. "I have seen couples who conceived after the man stopped drinking alcohol. Alcohol induces obesity, clogs the arteries and reduces sperm quality," he told The Guardian.
Joint Medical Director of EKO Hospitals, Dr. Sunny Kuku had recommended a bottle of beer daily for men over 40 years.
Passive smoking occurs when tobacco smoke permeates any environment, causing its inhalation by all people within that environment. Such smoke is called secondhand smoke (SHS) or environmental tobacco smoke (ETS).
Scientific evidence shows that exposure to secondhand tobacco smoke causes disease, disability, and death. The risks associated with passive smoking are one of the main reasons for smoking bans in workplaces and indoor public places, including restaurants, bars and night clubs.
Research has generated scientific evidence that secondhand smoke (that is, in the case of cigarettes, a mixture of smoke released from the smoldering end of the cigarette and smoke exhaled by the smoker) causes the same problems as direct smoking, including heart disease, cardiovascular disease, lung cancer, and lung ailments such as COPD, bronchitis and asthma.
Specifically, meta-analyses have shown lifelong non-smokers with partners, who smoke in the home have a 20-30 per cent greater risk of lung cancer, and those exposed to cigarette smoke in the workplace have an increased risk of 16-19 per cent.
A wide array of negative effects are attributed, in whole or in part, to frequent, long term exposure to second hand smoke. Reviewing the evidence accumulated on a worldwide basis, the International Agency for Research on Cancer concluded in 2002 that "involuntary smoking (exposure to secondhand or 'environmental' tobacco smoke) is carcinogenic to humans.
The effect of passive smoking on lung cancer has been extensively studied. A series of studies from the United States from 1986-2003, the United Kingdom in 1998, Australia in 1997 and internationally in 2004 have consistently shown a significant increase in relative risk among those exposed to passive smoke.
Breast cancer risk is increased by 70 per cent in younger, primarily premenopausal women. The California Environmental Protection Agency has concluded that passive smoking causes breast cancer and the U.S. Surgeon General has concluded that the evidence is "suggestive," one step below causal.
Until now, numerous studies suggest that moderate alcohol consumption helps protect against heart disease by raising good cholesterol, that is High Density Lipo-protein (HDL), and reducing plaque accumulations in the arteries. Alcohol also has a mild anti-coagulating effect, keeping platelets from clumping together to form clots. Both actions can reduce risk of heart attack but exactly how alcohol influences either one still remains unclear.
On the other hand, drinking more than three drinks a day has a direct toxic effect on the heart. Heavy drinking, particularly over time, can damage the heart and lead to high blood pressure, alcoholic cardiomyopathy, (enlarged and weakened heart), congestive heart failure, and stroke.
Studies show that alcoholics have a worse outcome after undergoing surgical procedures. The reasons for this are not entirely clear. Poorer outcomes may be attributed to a poorer general state of health with malnutrition and the depressant effects of alcohol. Binge drinking places one at risk for atrial fibrillation, which may also be a factor in surviving surgery. Still another factor is that heavy drinking affects the body's ability to stop bleeding. A liver damaged by alcohol has trouble making clotting proteins.
Alcohol interacts with many drugs - both prescription and non-prescription. Mixing alcohol with your medicine can lead to serious untoward effects. Alcoholism increases risk of cancers, including breast cancer, lung cancer and cancer of the liver.
Long-term heavy use of alcohol destroys the cerebellum of the brain, causing irreversible brain damage and resulting in slowed thinking, an unsteady walk and slurred speech.
Alcoholism contributes to many diseases, including hepatitis, cirrhosis, malnutrition, pancreatitis, stomach ulcer, fetal alcohol syndrome and heart disease, just to name a few.
According to the United States National Institute on Alcohol Abuse and Alcoholism (NIAAA), going on a 'binge' means having five or more drinks for men, and four or more drinks for women, in two hours.
Many studies suggest that an irregular pattern of heavy drinking brings about a two-fold increase in risk for a fatal heart attack, even as moderate drinking has been shown to reduce risk (the red wine effect).
Alcoholic beverages contain ethanol, which is mostly converted into acetaldehyde once in the human system at 'binge' levels, with the levels of acetaldehyde remaining high for many hours after the binge has ended.
The Atherosclerosis study clarified for the first time that binge levels of acetaldehyde cause an important type of immune cell, the monocyte, to become better able to stick to blood vessel walls, an important step in initiating atherosclerotic disease.
Clarifying these mechanisms promises to empower the design of new treatments to counter the effects when combined with lifestyle change, researchers said.
In the past, experts believed that atherosclerosis developed when too much cholesterol clogged arteries with fatty deposits called plaques. When blood vessels became completely blocked, heart attacks occurred.
Now most believe that the reaction of the body's immune system, more than the build-up itself, creates heart attack risk. Vessel walls mistake fatty deposits for intruders, akin to bacteria, and call for help from the immune system. Among other cell types, monocytes arrive with the goal of preventing infection, but end up causing inflammation that drives blood vessel blockage.
The leader of the team of researchers and assistant professor in the Department of Surgery at the University of Rochester Medical Centre, United States, Dr. John Cullen, said, "factors like binge-drinking have been linked to increased risk for heart disease, and the newer inflammatory model is beginning to explain how. One of our experiments found that acetaldehyde, at levels found in the blood after binge drinking, increased the number of monocytes that can adhere to cells lining blood vessels by 700 per cent."
Health psychologists argue that motivating people to stop binging depends upon their belief that it is harming them. Thus, the authors of the current study hope the results empower public health campaigns that discourage binge drinking.
According to the study, "in between infections and injuries, dormant monocytes ride along with the bloodstream until they "realise" they are passing by part of a blood vessel wall close to the site of an injury or infection, or in the case of atherosclerosis, the site of cholesterol buildup. At this point, adhesion molecules on the monocyte surfaces unfold and grab onto key proteins on the surface of blood vessel wall cells, resisting the surrounding blood flow.
"Whey they arrive on the scene, monocytes send out tethers, like anchors that snag the vessel wall. Once the monocyte swings close to the wall on its tether, it can then roll along the wall, getting stickier and sticker until it sticks in place permanently. Without this step, a major part of the immune component of atherosclerosis could not get underway."
In the current study, the team examined the effects of acetaldehyde on the ability of monocytes to home in on, tether to and roll along cells lining blood vessel walls. Researchers made cultures of the cells lining blood vessels (example human umbilical venous endothelial cells (HUVEC)), and of two types of monocytes that stick to those vessel-lining cells when activated (example primary blood monocytes (PBM) and THP-1 monocytes). The team then treated all cell cultures with acetaldehyde at varying doses (0.1µM) known to correlate with binge drinking for six hours.
Specifically, the current study found that acetaldehyde stimulated monocyte adhesion through its effect on three important proteins, CCR2, P-selectin, and tumor necrosis factor alpha (TNF).
Several studies provide compelling evidence for a direct role of the monocyte chemoattractant protein-1 (MCP-1) receptor called chemokine (C-C motif) receptor 2 (CCR2) in the rush of monocytes to blood vessel walls as part of atherosclerosis. CCR2 is a receptor, a protein that occurs on the surfaces of monocytes that links up with MCP-1 as part of the signal that brings monocytes homing in on diseased blood vessel walls.
The current study found that the addition of acetaldehyde to monocytes increased by more that twofold the number of cells with CCR2 expressed on their surfaces.
P-selectin is a cell adhesion molecule (CAM) that, upon receiving the right signal, quickly rises to the surface of the cells lining blood vessels (endothelial cells) to help monocytes grab them. The team found a 40 per cent increase in endothelial cells showing P-selectin on their surfaces when exposed to acetaldehyde, and a 50 per cent increase in the density of P-selectins expressed on the surface of each cell.
The study also found that the genetic expression of TNF, an important driver of several aspects of inflammation in blood vessels, in endothelial cells increased by about 2.5 fold in the presence of acetaldehyde (10µM). Given the above results, it is not surprising that the addition of acetaldehyde increased the overall adhesion of primary blood monocyte to endothelial cells by approximately 250 per cent for 0.1µM acetaldehyde, and 700 per cent for 25µM acetaldehyde, when compared to controls.
When endothelial cells were subjected to a technique that shut down the genes that code for both P-selectin and TNF_ prior to the addition of acetaldehyde, the ability of acetaldehyde to cause increased monocyte adhesion was reduced by 90 per cent. These results argue strongly that acetaldehyde has its effects on monocytes primarily through these proteins.
Cullen said, "our study demonstrates for the first time that physiologically relevant concentrations of acetaldehyde can initiate several key steps involved in the monocyte recruitment cascade, specifically through P-selectin, CCR2 and TNF. We hypothesise that, following alcohol consumption, there is a delicate equilibrium between the effects of alcohol and its metabolite, acetaldehyde, on blood vessel walls. Further studies are underway to confirm that these actions of acetaldehyde underlie, in part, the detrimental effects of binge drinking on cardiovascular disease."
Meanwhile, Dr. Joseph C. Anderson of the University of Connecticut in Farmington, United States, and Dr. Zvi A. Alpern of Stony Brook University in New York, United States, compared the quantity of tobacco exposure to increased colorectal cancer risk in men and women. The levels of tobacco exposure were measured by multiplying the packs of cigarettes smoked per day by the number of years smoked ("pack years.")
In a large cross-sectional study, Anderson and Alpern analysed data of 2,707 patients (average age 57.3), who underwent colonoscopy between 1999 and 2006. Data collected included age, height, weight, family history of colon cancer, medication use, surgery, exercise, diet and smoking history.
Patients were divided into three smoking groups: heavy exposure, low exposure, and no exposure. The heavy exposure group was placed into two different groups: those who smoked 30 pack years or less and those, who smoked more than 30 pack years.
Women's Risk Higher for CRC with Fewer "Pack Years" After adjusting for potentially confounding factors such as age, body mass index, and family history, researchers found women, who smoked less than 30 pack years were almost twice as likely to develop significant colorectal neoplasia compared to women, who were not exposed to cigarette smoke.
"While men and women shared a similar two-fold risk for developing significant colorectal neoplasia, women required less tobacco exposure in pack years than men to have an increase in colorectal cancer risk," said Anderson.
In a separate study conducted at Memorial Sloan-Kettering Cancer Centre in New York, United States, Dr. Emmy Ludwig and her colleagues examined tobacco exposure and the risk of pancreatic cancer precursor lesions in patients enrolled in a familial pancreatic cancer registry and screening programme.
In this analysis, at-risk relatives of familial pancreatic cancer patients were screened using MRCP (magnetic resonance cholangiopancreatography) or CT scan with an endoscopic ultrasound performed if imaging showed any pancreatic abnormality. Patients underwent surgery if suspicious lesions were found.
Of the 113 relatives, who completed at least one screening study, 8.9 per cent had a significant pancreatic lesion, 6 of whom underwent surgery. In a key finding, researchers found 70 percent of relatives with pancreatic abnormalities had a history of smoking compared to 40 per cent of participants, who did not smoke.
According to lead investigator Ludwig, "because more of the relatives with positive findings smoked than did relatives without positive findings, our study suggests that smoking may have been responsible for the development of the precursor lesions, especially in light of the fact that smoking is a known risk factor for pancreatic carcinoma."
For the study reported in the journal Cancer Epidemiology, Biomarkers and Prevention, Swift's team used data on 859 women, who'd been recruited into a long-term A-T gene study between 1971 and 1999.
All had a family member affected by ataxia-telangiectasia, and blood and tissue tests had confirmed that 539 carried an A-T mutation.
Among the gene carriers who did not smoke, 21 per cent developed breast cancer by the age of 80. In contrast, a full 80 per cent of carriers, who smoked developed the disease.
Of women who did not carry an A-T mutation, 16 percent of non-smokers and 20 per cent of smokers developed breast cancer before the age of 80 -- an insignificant difference in statistical terms.
"Women, who know they carry an A-T mutation and are still smoking should certainly get off of it," Swift said.
But the same advice, he added, goes for all smokers. As yet, there is no test for A-T mutations available for the general public.
It's not clear why the combination of smoking and a mutated A-T gene carries such a high long-term risk of breast cancer. Smoking damages the DNA within body cells, and the A-T gene is involved in repairing such damage; so it's possible that people with an A-T mutation are unable to overcome the gene-level harm that smoking causes.
