“Pot Belly” Can Be Due to Smoking: How True?
Observational study: Cigarette smoking increases abdominal and visceral obesity but not overall fatness.
An observational study found cigarette smoking to increase abdominal and visceral obesity but not overall obesity.
Cigarette smoking and obesity are the most severe hazards to the general population’s health. Cardiovascular disease, cancer, and metabolic problems are more likely when one has either of these two risk factors. The goal of this study was to find out how much smoking cigarettes contributes to obesity-related health problems.
How to Determine the Connection Between Pot-Belly and Smoking
Participants in the study included 283 patients who had treatment at university hospitals in South Korea. Only current/past smokers or those who never smoked were included in this study to define each participant’s quartile. Experts tallied our BMI, waist circumference, total body fat percentage, visceral fat area, and abdominal subcutaneous fat area. Each group’s findings were analyzed and contrasted.
According to the results, cigarette smoking has a J- or U-shaped relationship with waist circumference and visceral fat distribution throughout a lifetime. After focusing on former and current smokers, we observed significant, dose-dependent links between smoking pack-years and abdominal and visceral obesity. Dose-dependent correlations were found.
These connections were not found according to body mass index (BMI) and total body fat percentage (TBF%). Former smokers could not show any meaningful associations, even though current smokers did. Possibly because of the tiny sample size we had.
Smoking enhanced smokers’ physiologically undesirable fat distribution, although there was no statistically significant difference in body mass index between smokers and nonsmokers.
The results of this study support the idea that smoking does not help people lose weight more effectively. Smoking cessation is a significant public health issue in reducing obesity and its negative repercussions and should be handled as such.
Cigarette smoking and obesity are the most severe risks to public health in today’s society. They both harm cardiovascular, cancer, and metabolic health, even though they appear to have different mechanisms.
Cigarette smokers tend to have a lower BMI than nonsmokers, and quitting smoking is commonly associated with increased overall body weight. One of the most challenging aspects of quitting smoking is the fear of gaining weight, one of the most significant.
However, a growing body of evidence suggests that smoking cigarettes are linked to an increased risk of abdominal obesity. Since abdominal obesity is a more important risk factor for obesity-related comorbidities and death, this study highlights an urgent therapeutic need to prevent smoking as a method of weight control.
Most previous research on abdominal obesity has focused on the measurement of waist circumference (WC) and the waist-to-hip ratio (WHR) (WHR). This begs whether smoking contributes to abdominal obesity by increasing visceral or subcutaneous adiposity or if both are exacerbated by smoking.
This is a critical issue that one must address. One of the questions that have to be answered is whether the association between smoking and abdominal obesity is only a reflection of lifestyle variables like physical activity and alcohol usage.
When we realized how much time it takes for smoking to impact, we undertook research that looked at long-term implications (pack-years). Researchers employed computed tomography (CT) data and other technologies to help us better understand the link between smoking and abdominal fat.
Statement on the Ethics of Methods
The Ilsan-Paik Hospital Institutional Review Board (IRB) has approved this study. Every participant signed an informed consent form before participating in the study.
Between September 1 and December 31, 2004, data on 283 male patients who visited university hospitals in the four most populated provinces of Korea were compiled for this research project. Nurses or physicians examined the subjects ‘ medical histories to get a complete picture of the subjects’ medical records.
They asked them a wide range of questions about their age, level of educational attainment and employment, marital status, and the status of their health, and questions about their family history of the disease.
Subjects who engaged in regular moderate-intensity exercise were asked about the frequency of their workouts and the amount of time they spent doing so. Researchers asked questions about their drinking habits during the previous month to accurately read the respondents’ alcohol use before the medical exam.
They used two methods to measure obesity: the body mass index (BMI) and waist circumference (WC). To get an accurate reading of their height and weight, the patient had to stand on a digital scale while wearing a light gown.
The waist circumference was measured with a tape measure to the nearest 0.1 cm at the point where the lower costal border and the iliac crest meet. BF % was determined using an eight-polar tactile-electrode impedance meter with eight electrodes (Inbody 3.0, Biospace, Seoul, Korea).
Two hours before the physical examination began, participants were instructed to abstain from food and drink. The abdominal fat quantity was measured using CT images taken at the L4–L5 level. Abdominal fat was represented by an area corresponding to the pixel range between -190 and -30 Hounsfield units.
They mapped out the visceral and subcutaneous layers of the abdominal cavity’s fatty tissue. Fatty tissue in the peritoneum was called visceral adipose tissue; subcutaneous adipose tissue was found between the dermis and muscle fascia.
A BMI of more than 25 kg/m2 was defined as obese by the World Health Organization (WHO) for the western pacific regions and elsewhere. They described men’s overall fatness as having more than 25% body fat percentage.
Abdominal obesity was previously defined as having a waist circumference of more than 90 cm. Viscose obesity was defined using previously suggested cut-off values without established cut-off points. Visceral obesity can be accurately diagnosed based on blood pressure, waist circumference, and hip-to-hip ratio.
Tobacco use has been categorized into three distinct periods: the past, the present, and the future. People who had not used tobacco products for at least three months before the study’s evaluation were labeled “past smokers.” Multiplying years smoked with the average number of packs per day, we came up with the total number of “pack-years.”
However, many could not establish a precise classification of entire pack years accrued throughout a lifetime. Thus, the total number of years smoked by all former and present smokers was divided into quartiles, which allowed for more in-depth analyses, such as dose-dependent connections.
Correlation of Smoking and Fats
Current smokers, former smokers, and never smokers all made up the study’s participant pool. To perform further analysis, the total pack years were divided into quartiles. A one-way analysis of variance (ANOVA) and Duncan’s posthoc test were used to determine if the differences in the mean values of these groups are statistically significant.
They used polynomial contrasts to establish whether there was a linear or quadratic trend. Multiple logistic regression analysis was used to establish the odds ratios for all three types of obesity: body mass index (BMI), abdominal obesity, and visceral obesity.
The number of times per week people exercises (none, 1–2, 3–4, and 5 times per week with a duration of 30 minutes for each session) and continuous alcohol intake were all taken into account in developing a model. The linear trend in the odds ratio was examined using a trend test.
Many also did separate investigations based on whether a person was a current or ex-smoker to find any possible relationships. They chose the significance level of P0.05 in all of the studies, and they used two branches. The statistical analyses were carried out using the SPSS program for Windows, version 11.0.1. (SPSS Inc., Chicago, IL, USA).
Results of Smoking
A BMI of 26.4 4.8 kg/m2 and a waist circumference of 89.0 12.4 cm were the averages of the individuals in the study. There were 118.7 62.9 cm2 of visceral fat, while 187.8 10.7 cm2 of abdominal subcutaneous fat. However, most anatomical tests failed to detect any statistically significant differences between never and former or current smoker groups. Only the daily average amount of alcohol drank shows a substantial difference between the groups.
At no point in time did any anthropometric measurements show a linear trend. There were quadratic tendencies (U- or J-shaped correlations) in anthropometric parameters such as BMI, waist circumference, and visceral fat area with increasing cumulative smoking quantities. Subcutaneous fat in the abdomen did not significantly correlate with body fat percentage.
There was no evidence of a correlation between the variables in the logistic regression study. There were significant dose-dependent associations with abdominal obesity, which was defined as having a waist circumference greater than 90 centimeters (P = 0.004), and visceral fatness, which was defined as having visceral fat area greater than 100 cm2 (P = 0.012) or 130 cm2 (P = 0.016), when the analyses were restricted to only include former and current smokers.
As a result of this study, we were unable to show an association between overall obesity (defined as a BMI of > 25 kg/m2) and overall body fatness (defined as a BF percent of over 25).
The relationships between abdominal obesity (P = 0.006) and visceral fatness (P = 0.019 and 0.020) were also significant when the analysis was restricted to current smokers (n = 118). A correlation between abdominal obesity and smoking (P = 0.024) was seen when the analysis was restricted to those who had previously smoked (n = 60).
How Smoking Affects Visceral and Abdominal Fat
The current research demonstrated that smoking is connected with increased visceral and abdominal fat in smokers. A rise in visceral fat is the leading cause of the link between smoking and abdominal obesity.
Unavoidable problems marred this study. Because this study was cross-sectional, we couldn’t establish conclusive temporal connections to uncover causal links.
We relied on self-reported smoking habits and didn’t examine passive smoke exposure in never-smokers. We found weak to moderate links between smoking and obesity because women were smokeless (only 3.6 percent of 363 women participated in the study).
We couldn’t prove smoking causes fat. The study’s subjects weren’t representative of the overall population. Our study’s strengths were the patients’ relatively comprehensive smoking histories and the CT-measured visceral and subcutaneous fat. Both factors aided our investigation.
Regional adipose depots have diverse relationships with physiological and pathological processes. Visceral fat is a more accurate measure of obesity than other anthropometric measures. Visceral adipose tissue has a faster flow rate of adipose-driven free fatty acid to the liver through the portal vein than subcutaneous adipose tissue.
Subcutaneous fat has a lower flow rate. They cause insulin resistance in the liver, which increases glucose and LDL synthesis. Smoking correlated positively with visceral adiposity but not subcutaneous fat. This study shows our findings.
Smoking may increase the risk of obesity-related comorbidities, especially those linked to visceral adiposity. In another study, smokers had greater triglycerides and lower HDL cholesterol than nonsmokers. Both contribute to metabolic syndrome. Our data demonstrated a link between smoking and abdominal obesity among former and current smokers.
Smoking is linked to obesity-related comorbidities like type 2 diabetes, hypertension, and insulin resistance. Our data suggest that smoking may be linked to metabolic problems through visceral adiposity. Our data indicate that this may be the case, even though the underlying mechanism isn’t fully known.
Earlier studies found a link between smoking and obesity. Active smokers had a lower BMI or smaller waist circumference. BMI, waist circumference, and visceral fat area are all quadratic with smoking. Even if smokers never had high BMI, waist circumference, and visceral fat, these characteristics would rise with smoking.
Although smoking’s effects are cumulative, the previous study has focused on daily cigarette counts, despite smoking’s cumulative consequences. The current study examined the influence of total pack-years smoked over a lifetime by combining cigarettes smoked and time spent smoking.
Visceral fat and waist circumference measures show that smoking increases body fat. In former smokers, we found no link between smoking and visceral adiposity. How long a former smoker hasn’t smoked affects whether they have abdominal obesity.
Some research suggests that quitting smoking for a long time reduces abdominal obesity to a level comparable to those who have never smoked. People who have smoked for more extended periods of time or more heavily require longer periods without smoking to achieve the same result as those who have never smoked.
This led us to conclude that we should consider how long we’ve stopped smoking. Long-term smoking cessation was not beneficial. The researchers could not detect a link between visceral fat and the amount of smoking done by former smokers.
This may be attributed to a limited sample size of former smokers or mistakes in getting specific information on smoking cessation periods. More research is needed to discover how long a person has been smoke-free affects the link between visceral fat and past cigarette use.
According to prior studies, visceral adiposity develops with age, physical activity decreases it, and alcohol increases abdominal fat. Despite these other characteristics, we still found that smoking increases body fat.
The particular biological mechanisms underlying these links are difficult to establish because cigarettes contain dozens of chemicals, and body fat control is a complex physiological process. Due to women’s low smoking rates, we limited our study to men.
In terms of obesity and metabolic indicators, smoking affects men and women differently. Smoking’s anti-estrogenic effects and an imbalance in androgenic and estrogenic activity have been postulated as probable causes, but more research is needed.
Because of their higher abdominal and visceral fat levels, heavier smokers have a more metabolically detrimental fat distribution profile than lighter smokers while having a lower mean BMI than nonsmokers do.
Those who smoke a lot are more likely to have a lot of fat in their abdomens and viscera. Here, the metabolic impacts of smoking can be seen.
As evidenced by the association between smoking and visceral fatness, stopping smoking and avoiding smoking should be emphasized as crucial components in the prevention of obesity and the issues that come along with it.