Context: Cigarette smoke contains many dangerous toxic chemicals, including nicotine, carbon monoxide, cyanide and thiosulfate. Inhaling the chemical mix causes addiction and disease.
Nicotine is the reason for the dependency. Because nicotine is so addictive, smokers, especially those who consume more than one pack per day, have a difficult time quitting. Those who try to quit sometimes use nicotine replacement therapies. The method provides the drug directly through dermal patches, gum or nasal spray in an effort to keep smokers away from cigarettes and ease them off nicotine.
Smokers have a higher risk of developing cancers, such as lung and throat; debilitating respiratory diseases, including emphysema; cardiovascular diseases and other health problems. An estimated 438,000 deaths, or nearly 1 of every 5 deaths, each year in the US is attributed to smoking, according to the Centers for Disease Control and Prevention
During pregnancy, smoking exposes the developing fetus to nicotine and a multitude of chemical contaminants that can affect the health and welfare of the baby. Nicotine from cigarettes or replacement therapies crosses the placenta and concentrates in the amniotic fluid (Jordanov 1990) and fetal blood. It is also found in mother’s milk at levels up to 3 times higher than in her blood.
The habit increases the risk of spontaneous abortion, premature delivery, low birth weight, sudden infant death syndrome and learning and behavioral problems in the children born to smoker mothers. Human studies find strong associations between maternal smoking and obesity, hypertension and type 2 diabetes in their children. Animal studies confirm the human data and find that rats exposed to nicotine during gestation and lactation gained more weight compared to non-exposed animals (Holloway et al. 2005). Exposure to nicotine while in the womb is linked to hormone and metabolic changes similar to type 2 diabetes after birth (Holloway et al. 2005).
Type 2 diabetes is a chronic disease that debilitates the body over time and raises the risk of early death. The disease cripples the body’s ability to use the hormone insulin to convert glucose (the cells’ main source of food) into energy. Normally, beta cells in the pancreas make and release insulin, which causes muscle cells to absorb glucose. In type 2 diabetes, the muscle cells stop responding adequately to insulin. Initially the beta cells produce even more insulin, but ultimately they die.
The malady affects the heart, blood vessels, eyes, kidneys and nerves and is associated with increased heart disease, kidney failure, vision loss, nerve damage (which increases the risk for foot ulcers), impaired healing and death. The chronic ailment imposes an economic burden on the patients and their families, as well as the health care system.
The US and other industrialized nations are facing epidemics of type 2 diabetes. An estimated 4% of the world population had this type of diabetes in 1995 and the disease is likely expand to 5.4% by 2025 (King et al. 1998). In the US, both types of diabetes strike about 7% of the population with higher incidences in American Indians, Hispanic and black populations. Reasons for the prevalence are still a mystery but age, obesity, diet, reduced physical activity and environmental exposures are likely contributors (National Diabetes Information Clearinghouse). |
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Nicotine levels in the mothers and the male pups were checked at birth by measuring the nicotine breakdown product cotinine.
The pancreas was collected from one set of animals on days 1 and 4 and at 26 weeks of age. The researchers weighed the organs and measured proliferation and death of the insulin-producing beta cells.
They tested glucose metabolism in another group of rats. Glucose and insulin levels were measured in the morning after overnight fasting and 30 and 120 minutes after the rats were given 2 grams/kilogram glucose. This test is called oral glucose tolerance test, or OGTT, and it is commonly used to diagnose prediabetes and diabetes.
What did they find? As adults, all of the exposed offspring had similar levels of glucose and insulin in the mornings (called basal levels). However, after being given glucose during the glucose tolerance test, animals with fetal and neonatal nicotine exposure had higher total glucose levels compared to the controls. Those exposed during development and as newborns also could not clear the glucose up to 2 hours after the sugar challenge. The same animals had fewer beta cells in their pancreas because of increased cell death.
At birth, the amount of beta cells was reduced in all animals exposed to nicotine as fetuses (groups B and C) and the effect was still present at 4 weeks of age. However, by the time they reached adulthood at 26 weeks, only those with both fetal and neonatal exposure (group C) continued to have fewer beta cells. Overall, the group had 38% lower beta cell mass than controls due to cell death rather than decreased production.
What does it mean? Continued exposure to medium amounts of nicotine from early development through breastfeeding permanently reduced the number of pancreas cells that produce insulin in male rats. The resulting impaired glucose levels can potentially develop into full-blown diabetes.
The effects were seen after developmental exposure to levels of nicotine commonly experienced by people. The amounts used in this study and measured in mother rats and pups are comparable to those found in women considered moderate smokers and in newborn babies of mothers who smoke.
The results underscore the importance of developmental "windows of susceptibility." Fetal development is a very sensitive and delicate time. There are critical stages when exposure can damage or change cells, and ultimately metabolic body systems. If the insult continues past the recovery window, the changes may become permanent and the system does not return to a normal state. Alterations in the womb can have (a) immediate consequences resulting in spontaneous abortions, (b) mediate consequences such as premature birth or (c) long-lasting consequences that can trigger health problems or conditions many years after birth.
According to the authors, the results suggest that quitting smoking "prior to the completion of pancreatic development may be beneficial in terms of protecting the future metabolic capacity of the offspring." In humans the pancreas develops mostly before birth.
The paper adds much needed information regarding the safety of smoking and nicotine replacement during pregnancy (Oncken and Kranzler 2003). Quitting smoking is not easy. When willingness, counseling, and pharmacological therapies fail, nicotine replacement is used. Many women quit smoking during pregnancy and start nicotine-patch therapy. Nicotine from this smoke-free source still enters the mother’s blood and can affect fetal development. With this in mind, the risk/benefits of nicotine treatment should be evaluated to find a dose that will help the smoker quit without harmful exposure to the unborn baby. |
