Category: Diabetes 101

A team of United States-based scientists are hopeful that new research on a natural chemical found in body cells could set the stage for the development of a vitamin-like pill that could prevent diabetes or perhaps even reverse the disease completely.

The chemical is called nicotinamide mononucleotide (also known as NMN) and it serves an important purpose in the way body cells utilize energy. The U.S.-based researchers tested the compound by injecting diabetic mice with it. After the injections, the mice showed normalized blood glucose levels in addition to lowered triglyceride blood fat and cholesterol levels.

The next step for the research team is to develop a method of administering the NMN compound to mice directly through their drinking water instead of through injections. In the future, the team’s long-term goal is to develop a “nutriceutical” pill, similar to a normal daily vitamin, that can be taken to reverse or prevent Type 2 diabetes.

“Once we can get a grade of NMN that humans can take, we would really like to launch a pilot human study,” said Dr. Shin-ichiro Imai, M.D., Ph.D., from the Washington University School of Medicine in St. Louis; Dr. Imai also headed the study. Since mice share a similar genetic code with humans, medications meant for human use are often tested on mice first. However, even when a medication appears safe when used on mice, it must be extensively tested on humans as well before being approved for prescription and sale. According to Dr. Imai, the effect of NMN was “remarkable,” and it was more pronounced in female mice: “After giving NMN, glucose tolerance goes completely back to normal in female diabetic mice,” said Dr. Imai.

The researchers triggered the onset of Type 2 diabetes in the mice by feeding a high-fat diet to young, otherwise healthy mice. All of the mice displayed decreased levels of a molecule called NAD, which is responsible for extracting energy from nutrients in food and turning it into a form that cells can use to operate. In mice as well as humans, NAD is derived from NMN and is created by cells through a series of metabolic reactions.

One important effect of NAD is the activation of SIRT1, a protein that has been the subject of much study and which has been demonstrated to encourage well-functioning metabolism throughout the body and to increase insulin sensitivity. SIRT1 — or NAD-dependent deacetylase sirtuin-1 — is encoded by a gene also called SIRT1. Since NAD is toxic when administered directly to organisms such as mice and humans, researchers injected mice with NMN instead, which leads to an increase in NAD levels. After they were treated with the compound, the mice displayed significantly improved glucose response. NMN is produced naturally by the body but its levels decrease as the individual ages. High-fat diets also discourage the production of NMN.

According to Dr. Imai, NMN exhibits very similar behavior in mice and humans. However, the further testing will be required before it can be determined whether a lack of the compound is equally responsible for Type 2 diabetes in humans. “Whether this mechanism is equally compromised in human patients with Type 2 diabetes is something we have to check,” said Dr. Imai. “We have plans to do this in the very near future.”

A study published in the October issue of the journal “Diabetes Care” has demonstrated that, in patients with Type 1 diabetes who receive intensive insulin therapy through the use of a pump, a new algorithm based on the food insulin index is more effective at improving acute postprandial glycemia — or blood sugar levels after a meal — than a carbohydrate counting plan.

The study was headed by Jiansong Bao of the University of Sydney in Australia. Bao’s research team compared the effectiveness of a new food insulin index (FII) algorithm, which is used to estimate the dose of insulin that should be given at mealtimes, with counting carbs. The study consisted of 28 adult participants who had been diagnosed with Type 1 diabetes and were users of insulin pumps.

Study participants randomly ate two breakfast meals over the course of three consecutive days. The two separate meals were similar in factors such as total energy, fiber, glycemic index, and calculated insulin demand, but one meal had approximately twice the carbohydrate content of the other meal. For the meal with higher carbohydrate content, the proper insulin dose for the participants was determined by counting the amount of carbohydrates in the meal — 75g. On the other two mornings, participants received the less carb-heavy meal (41g carbohydrate) and used the new FII algorithm to determine proper insulin dosage. Researchers used continuous glucose monitors to determine postprandial blood sugar levels in the participants for the three hours following the meals.

Upon analyzing the results, the researchers discovered that the new FII algorithm had a significant effect in decreasing peak glucose excursion and glucose incremental area under the curve for the three hours after a meal. Participants spent significantly more time after a meal in normal blood glucose ranges when using the FII algorithm, although hypoglycemia was not significantly different between the two groups.

“An insulin algorithm based on physiological insulin demand evoked by foods in healthy subjects may be a useful tool for estimating mealtime insulin dose in patients with type 1 diabetes,” wrote the authors of the study.

Carbohydrate counting is a popular method of ensuring that insulin levels remain under control in both Type 1 and Type 2 diabetics, who must plan their meals to avoid excessive intake of carbohydrate in a single meal. Foods containing carbohydrates increase blood glucose levels, which can prove dangerous for diabetics. By planning their meals carefully and setting a maximum amount of carbohydrate in a single meal, diabetics can ensure that their blood sugar levels will remain well-managed. Most diabetics are advised to start at about 45-50 grams of carbohydrate per meal, though the number varies according to the plan of treatment and the severity of the disease. Doctors can help diabetics establish guidelines for the amount of carbohydrate they should be consuming at every meal.

Not only are diabetics advised to count carbohydrates to better manage blood glucose levels, but they can also use food nutrition labels to determine the total number of calories in the food and to avoid undesirable ingredients such as trans fats and saturated fats. Such fats are especially harmful to patients with heart disease or who are at risk for heart disease; doctors also advise against the consumption of excessive sodium, especially in those who are already hypertensive.

A recent randomized trial showed that increasing the intensity of weight loss interventions only in patients who do not succeed in reaching their goals may be an effective alternative to typical approaches.

According to John Jakicic, Ph.D., with the University of Pittsburgh, the findings did not demonstrate a significant difference in the number of patients who achieved a 10 percent reduction in weight after 18 months between a group that received stepped care and a group that received normal treatment (26 percent versus 32 percent). The two groups also reported similar average weight loss — 5.8 percent loss for the stepped care group versus 6.8% for the normal care group. “So the stepped-care approach may present an effective alternative to standard behavioral weight loss interventions,” said Jakicic.

Jakicic continued to note that 30 to 40 percent of the patients who received stepped care stayed at the first two steps, involving monthly group meetings, lessons mailed to the patients weekly, feedback from doctors on a weight loss diary that the patients completed, and one phone call every month.

Behavioral interventions that promote lifestyle changes have been previously shown to be effective in helping patients lose weight. However, the intensity of the intervention generally remains the same whether or not the patients are responding to the treatment.

Stepped approaches use feedback from the patient’s success with the program to determine its intensity. When a patient does not respond to the intervention, the intensity of the approach is increased. These types of intervention had not been previously compared to standard behavioral interventions for weight loss through the use of a randomized trial.

Jakicic and his team designed the Step Up study, an investigation of 364 overweight and obese men and women that randomly assigned stepped care or standard intervention to each participant. The participants’ mean age was 42.2 and mean body mass index was 33kg/m2. A significant majority of the participants were female (82.7 percent).

Both the standard and stepped care groups were given dietary goals intended to reduce total calorie intake as well as fat intake. Participants were also given targets for engaging in physical activity, increasing in duration to 300 minutes of moderate-to-vigorous exercise each week.

The stepped care group also attended a group session every month throughout the duration of the study and received weekly mailed lessons. They also kept diaries on their progress and received feedback from doctors on those diaries. Participants who failed to achieve their goals — 5 percent of the participants at three months, 7 percent at six months, and 10 percent at nine months — were contacted more frequently by researchers and saw the intensity of their interventions increased. The more high-intensity measures included two phone calls per month instead of one, two individual sessions per month to discuss weight loss, and meal replacements provided to the participants.

Participants in both the standard and stepped care groups lost weight. However, absolute weight loss was significantly higher in the standard care group for the first six months (22 pounds versus 17.6 pounds). For each follow-up beginning at six months from baseline, however, participants did not exhibit a significant difference in weight loss between the two groups.

According to Jakicic, more research is needed to determine the effectiveness of stepped care interventions. Factors that need to be addressed include: the effectiveness of each of the steps as compared to other steps; who responded to the stepped care approach; the possible effect of diet and physical activity; and different approaches that may be more useful in stepped care.

A new study warns that eating food too quickly more than doubles an individual’s chance of developing impaired glucose tolerance, also known as pre-diabetes and the precursor to Type 2 diabetes. It appears that eating quickly is the only mechanical eating practice that can promote the onset of pre-diabetes; people who engaged in snacking and eating late at night were not an increased risk of developing the disease. The study appeared in the journal “Diabetes Research and Clinical Practice” and was conducted at the Institute of Clinical Medicine at the University of Tsukuba.

The Japanese study found that eating food quickly was the only eating pattern that caused a significant increase in risk of developing pre-diabetes. The results were adjusted for factors that may have skewed the results, including age, sex, weight, smoking, alcohol, blood pressure, cholesterol, and whether the individual had a family history of diabetes.

The investigation followed 172 Japanese men and women who were diagnosed as healthy at the beginning of the study for three years. They were asked to self-report various aspects of their eating habits, such as whether they were fast eaters, ate late at night, snacked frequently, skipped meals, or ate out frequently. Throughout the three-year period of the study, 39 participants developed impaired glucose tolerance and two of those went on to develop Type 2 diabetes.

Scientists aren’t sure exactly why eating faster makes an individual more likely to develop pre-diabetes and Type 2 diabetes, but one hypothesis states that eating rapidly results in higher postprandial blood glucose levels — the level of sugar in the blood after a meal. Some doctors also speculate that eating too quickly results in an overall increase in the amount of calories eaten since it takes about 20 minutes for the brain to receive the signal that the stomach is full; thus, those who eat quickly will consume more calories before realizing that they’re finished eating.

Previous research has also confirmed that eating quickly results in increased weight gain, which is associated with pre-diabetes and Type 2 diabetes. One study presented to the North American Association for the Study of Obesity found that overweight men and women consumed fewer calories overall when they slowed their eating pace. Another study conducted in Japan found that among 1,700 young women, eating slowly resulted in feelings of fullness occurring sooner, which meant that the women consumed fewer calories throughout the meal. Additionally, a recent study conducted in New Zealand found that women who were fast eaters were at an increased risk of obesity.

It is thought that there are 2.8 million people throughout the United Kingdom with undiagnosed Type 2 diabetes. The disease reduces or eliminates the body’s ability to produce insulin, which helps shuttle sugar in the bloodstream into cells to be used as energy. Since a Type 2 diabetic’s body does not produce enough insulin on its own, diabetics require insulin supplements in the form of injections or other delivery methods.

Impaired glucose tolerance (IGT), or pre-diabetes, is a sign that the individual will soon develop diabetes if blood sugar levels are not more tightly controlled. In pre-diabetes, those blood glucose levels are elevated, but not high enough to cause diabetes.

Preventative measures such as a healthy diet and regular exercise can help those with pre-diabetes keep their glucose levels under control so that they do not develop Type 2 diabetes. However, 40 to 50 percent of individuals with pre-diabetes will be diagnosed with Type 2 diabetes within ten years.

A study recently published in the journal “Cancer” has discovered that therapy with the drug tamoxifen — an oral medication used in women with breast cancer — is linked to a significant increase in development of diabetes in older survivors of breast cancer.

The study was headed by Lorraine L. Lipscombe, M.D., with the Women’s College Hospital in Toronto. Dr. Lipscombe’s team studied 14,360 women over the age of 65 who had been diagnosed with early-stage breast cancer and had survived. The women had received treatment for breast cancer with tamoxifen therapy. The study used data collected from 1996 to 2006; the patients who were diagnosed with diabetes through March 31, 2008 were matched with control subjects who had not developed diabetes. The research team adjusted for other risk factors and compared the risk of developing diabetes in participants who received tamoxifen and aromatase inhibitor therapy compared to women who were not treated with those drugs.

According to the study’s findings, 10 percent of the patients received a diagnosis of diabetes over a mean follow-up of 5.2 years. Women who were currently receiving tamoxifen therapy had a significantly higher chance of developing diabetes (1.24 adjusted odds ratio) over women who were not being treated with tamoxifen. Treatment with aromatase inhibitors, on the other hand, was found not to be linked to an increased risk of developing diabetes.

“Current tamoxifen therapy is associated with an increased incidence of diabetes in older breast cancer survivors. These findings suggest that tamoxifen treatment may exacerbate an underlying risk of diabetes in susceptible women,” wrote the authors of the study.

Tamoxifen, marketedd as Nolvadex, Istubal, and Valodex in the U.S., is an orally-administered tablet that disrupts the female body’s production of estrogen, which is known to promote breast cancer in women. Tamoxifen binds to the estrogen receptor proteins, effectively blocking additional binding at the site that would cause cancerous growth. Tamoxifen is approved by the FDA for the treatment of breast cancer and other types of cancer and has been used for over 30 years in the treatment of early-stage breast cancer.

The drug has also been used to reduce the risk of breast cancer in women who are at increased risk of developing the disease. It works by blocking the effects of estrogen on breast cancer cells with estrogen receptor-positive proteins, preventing the growth of the cancerous cells. However, the medication is only useful in treating cancer cells that are specifically estrogen receptor-positive. Doctors must determine whether the tumor will respond to tamoxifen treatment before prescribing the drug.

Tamoxifen therapy is known to be associated with several serious side effects, including stroke, blood clots, uterine cancer, and cataracts. It may also cause symptoms similar to menopause such as hot flashes, irregular menstrual periods, headaches, nausea, and fatigue. Though tamoxifen therapy does cause blood clots or stroke in a small number of women, the chances of developing such complications are similar to those associated with estrogen replacement therapy.

Additional adverse side effects associated with tamoxifen therapy include an increased risk of thromboembolism and fatty liver as well as mental effects such as reduced cognition and degraded memory, though memory loss with tamoxifen therapy is not as severe as with aromatase inhibitor therapy. Tamoxifen has also been associated with reduced libido.

However, not all the side effects of tamoxifen therapy are negative; it is known to improve bone health, especially in women, by inhibiting osteoclasts and preventing osteoporosis.

Doctors and scientists have long known that people with Type 2 diabetes are at an increased risk of developing certain types of cancer. Until recently, the mechanisms behind the link between the two diseases have been unclear to medical professionals.

However, the mystery may finally be solved: researchers with the Harvard Medical School have reported that variations in levels of two different proteins are present in both diabetics and cancer patients. The findings were reported in the journal “Cell.”

The study demonstrated that mice who were engineered to have increased levels of the proteins Lin28a and Lin28b had a lower chance of developing diabetes when they were fed a high-fat diet. In contract, mice who are fed the same diet with those proteins functioning at normal levels are apt to become obese and develop Type 2 diabetes. The two proteins have also been proven to be related to an individual’s risk of developing some types of cancer, underscoring a relationship between cancer and diabetes in the activity of these two proteins.

“This highlights the overlap in the biology of these disorders,” says George Daley, M.D., Ph.D., a researcher who was involved with the study. Daley is also director of Stem Cell Transplantation and head of the Stem Cell Research Program at Children’s Hospital Boston. “It may be the same kinds of metabolic shifts that allow cancer cells to grow are also related to [whole-body] glucose metabolism.” Cancer and diabetes appear to both be caused by certain metabolic processes that may be signified by elevated levels of the two proteins.

“The results were startling,” says Daley. “Previously we had considered these molecules only as regulators of cell growth and cancer. But in these mice we discovered remarkable effects on sugar processing and diabetes.”

Daley commented that these findings have provided scientists with a molecular pathway related to diabetes and cancer that could be used in reducing the risk of those diseases. With new knowledge of the pathway in hand, scientists may be able to develop medications that target the processes and lower the risk of developing diabetes and cancer.

In addition, the findings of the study demonstrate that elevated blood sugar levels associated with diabetes are not the cause of higher rates of cancer, as was once hypothesized. This knowledge allows scientists to focus their research in other directions that may prove more fruitful. Researchers have already conducted many investigations on the link between high blood sugar levels and complications related to diabetes.

While diabetes is associated with an elevated risk of various types of cancer, it’s likely that the link between diabetes and pancreatic cancer is the most-researched one. Since the two diseases affect the same organ, it can be difficult to understand the causes and effects of one disease independently of the other. Other types of cancer that commonly follow diabetes include colorectal, prostate, endometrial, breast, liver, renal cell, and non-Hodgkin’s lymphoma. Previous research commonly stated that the strongest link between diabetes and cancer was probably elevated insulin levels, which cause Type 2 diabetes and which are believed to also promote growth of tumors.

While further research is required before scientists can fully understand the link between the two diseases, previous research has made it clear that diabetes typically precedes cancer, not the other way around.

A large meta-analysis of genetic data has discovered previously unknown genes related to Type 1 diabetes. The new information supplements existing knowledge about the genetic networks responsible for the complex range of processes that cause the disease. Type 1 diabetes affects 200 million people around the world; those diagnosed with the disease must use insulin injections to ensure that their blood sugar levels remain under control. The study was published in the journal “Public Library of Science Genetics,” also known as “PLoS Genetics.”

“Genome-wide association studies, as we used here, have been extremely powerful in identifying gene locations involved in the pathogenesis of complex, common diseases,” said Hakon Hakonarson, M.D., Ph.D., head of the study and director of the Center for Applied Genomics at The Children’s Hospital in Philadelphia, Pennsylvania. Dr. Hakonarson noted that the size of the study provided a large pool of data from which the team could draw conclusions. “The larger the cohort used, the more discoveries we can make, and the more we find intriguing biological pathways offering insight into causes of disease.” said Dr. Hakonarson, who collaborated with Constantine Polychronakos, M.D., the director of Pediatric Endocrinology at McGill University.

Called a “genome-wide association study” (GWAS), the study was a meta-analysis that pooled data from six large, existing databases of information about Type 1 diabetes patients. The six studies together comprised information on about 10,000 individuals with Type 1 diabetes in addition to 17,000 control subjects. Information in the databases included single nucleotide polymorphisms (SNPs — pronounced “snips”), single-base alterations in our genetic code that can tip off scientists to the mutations with which they are associated.

The SNPs themselves do not actually cause mutations; they simply appear in regions of the genetic code associated with mutations and allow for more in-depth DNA sequencing studies that can uncover the genes that do actually cause mutations. Hakonarson and his team have conducted studies over the past four years that found SNPs believed to be related to Type 1 diabetes.

Not only did the meta-analysis reinforce previous findings, but it also identified three new SNPs that are located in regions of the genetic code known to have influence on interactions between proteins, cell signaling activity, and inflammation. “Our study found SNPs that we had not expected to have any connection to type 1 diabetes,” says Hakonarson. “The strongest association among the three SNPs was in the region of the LMO7 gene on chromosome 13. We previously associated another member of the LMO gene family with the childhood cancer neuroblastoma. This gene family plays an important role in protein-protein interactions, but it would not have occurred to anyone that it may be active in type 1 diabetes. GWAS continues to turn up surprising biological associations.”

Hakonarson commented that the team would be conducted future studies intended to sequence entire regions of the genetic code which are related to the SNPs. Such a thorough sequencing would provide a better picture of specific mutations which are responsible for the processes that result in Type 1 diabetes.

SNPs have been used for a variety of functions, from predicting an individual person’s response to certain medications to risk of developing certain diseases to breeding livestock. SNPs are single-nucleotide modifications, meaning that they change a single nucleotide; for example, changing a thymine (T) nucleotide to a cytosine (C) nucleotide. Scientists hope that further research will allow SNPs to be used to discover the exact genes responsible for diseases such as diabetes and cancer.

A study recently conducted by researchers at Glasgow University in Scotland found that men develop Type 2 diabetes faster than women do in terms of weight gain. The study’s findings showed that Type 2 diabetes occurred in men at a lower body mass index (BMI) than it did in women. The research could provide the reasoning behind higher rates of diabetes among men throughout many areas of the world.

The study was headed by Professor Naveed Sattar with the Institute of Cardiovascular and Medical Sciences. According to Dr. Sattar, being obese or overweight is a significant risk factor that makes Type 2 diabetes much more likely. Additional risk factors for the disease include older age, ethnicity, and a genetic predisposition toward diabetes.

Researchers used data from 51,920 men and 43,1367 women from Scotland who had been diagnosed with diabetes. Their findings demonstrated that the mean BMI for males at the time of their diabetes diagnosis was 31.83; meanwhile, the same statistic for females was only 33.69. The difference in mean diagnosis age was more significant at younger ages.

“Previous research has indicated that middle-aged men are at a higher risk of developing diabetes than women and one possible explanation is that men have to gain less weight than women to develop the condition,” said Dr. Sattar. “In other words, men appear to be at higher risk for diabetes,” he continued.

According to Dr. Sattar, human physiology could be partly to blame for the younger age at which men are diagnosed with diabetes. A man carries body fat around the stomach and liver; this distribution could be responsible for men developing diabetes earlier in life than women.

Chronically elevated blood glucose levels, which disrupt the body’s ability to regulate sugar in various parts of the body, cause the development of Type 2 diabetes. The disease is associated with excess stores of fat in certain organs, such as the liver and muscles.

According to the Centers for Disease Control and Prevention, 16 million Americans have diabetes; 55 percent of them are women. Women comprise 58.4 percent of Type 1 diabetics. However, they only comprise 47 percent of individuals with Type 2 diabetes. While more women have Type 1 diabetes, slightly more men have Type 2 diabetes.

Both forms of diabetes still have a significant impact on women’s health. Gestational diabetes — a glucose intolerance first diagnosed during pregnancy — affects about 2-5 percent of all pregnancies. Nearly twice as many women receive a diagnosis of nonketotic hyperosmolar coma than men, and women are diagnosed with hypoglycemia about 1.5 times more than men are. Women are also diagnosed with vision loss due to diabetes more than men in the 40-59 age range, the 60-69 range, the 70-79 range, and the 80 and above range. Doctors hypothesize that women may be diagnosed with vision loss more frequently because their diabetes has a long duration, there may be a smaller percentage of blind men registering as such, and because men’s shorter life spans could result in death before severe vision loss.

Dr. Sattar works in the metabolic medicine group at the BHF Glasgow Cardiovascular Centre, which works to uncover new information about the causes of diabetes and vascular disease as well as the complications associated with those illnesses. The group has conducted physiological studies to determine the cause of diabetes and aims to discover new treatments for the disease.

A recent study suggests that significant accumulation of calcium buildup in coronary arteries could be a signal of an impending heart attack in individuals who have metabolic syndrome and diabetes.

The study analyzed data from 6,600 people age 25 to 84; it was conducted by the UC Irvine Heart Disease Prevention Program.

The findings of the study showed that while 16% of the participants had been diagnosed with diabetes — mostly Type 2 diabetes — an additional 25% of the patients had metabolic syndrome, a series of disorders that is often a precursor to diabetes and heart disease.

“Our study points out that there’s a wide range in risk for cardiovascular consequences seen in persons with metabolic syndrome and diabetes and that screening of coronary calcium by heart scans – and, to a lesser extent, carotid arteries by ultrasound – may be helpful in picking out those most vulnerable,” says Nathan Wong, a professor of medicine at UC Irvine and director of the Heart Disease Prevention Program. Dr. Wong was also senior author on the study.

“Our findings also suggest that individuals with significantly high levels of coronary calcium or carotid wall thickness should receive more aggressive monitoring and treatment for any associated risk factors,” said Dr. Shaista Malik, co-author on the study and a cardiologist at UC Irvine.

The buildup up plaque in the arteries is called atherosclerosis. Such arterial plaque is composed of a variety of substances, including calcium, cholesterol, fat, and other materials found in the bloodstream. In patients with atherosclerosis, plaque hardens over time and causes a narrowing of the arteries that restricts the flow of blood to the organs and elsewhere throughout the body. As plaque buildup can develop in any artery in the human body, it can cause different negative effects depending on which artery is restricted.

The most common effect of calcium buildup in the arteries is coronary heart disease (CHD), the number one killer of adults in the United States. The buildup of plaque in the coronary arteries causes CHD; the narrowing of the arteries means that the heart receives less blood, and increases the likelihood of blood clots forming in the arteries, which can completely block blood flow through an artery. Such blockage of blood flow in the coronary arteries can cause angina — pain in the chest — or even heart attacks.

Some other complications that can arise from the buildup of arterial calcium include carotid artery disease, peripheral arterial disease, and chronic kidney disease.

Atherosclerosis is known to cause heart attacks, strokes, and death. While the exact cause of the buildup is unknown, risk factors such as a lack of exercise, smoking, poor diet, and a family history of heart disease can contribute to the development of atherosclerosis.

Arterial calcium buildup has been previously studied in the Multi-Ethnic Study of Atherosclerosis (MESA), which was funded by the National Heart, Lung, and Blood Institute division of the National Institutes of Health. Previous studies had shown that buildup of arterial calcium was associated with a greater risk of heart disease in Caucasians, but the MESA study conducted in 2007 showed that the same was true of other ethnic groups, including African Americans, Hispanics, and Chinese.

The MESA study analyzed data from 6,814 individuals, both men and women, who had no history of heart disease from coronary calcium. The study followed those individuals for 3.5 years on average.

A recent review of past research has confirmed that individuals with diabetes are at an increased risk of developing colon cancer. However, scientists aren’t sure why the connection exists or what can be done to lower the risk. The findings were reported in the American Journal of Gastroenterology.

Researchers analyzed the results from 14 international studies, finding that on average, individuals with diabetes were 38% more likely to develop colon cancer than those who did not have diabetes.

In addition, diabetic men involved in the study showed a 20% increase in risk of colon cancer over non-diabetic men. However, the results of the study did not prove that diabetes is directly related to the development of colon cancer.

The findings were produced through observational studies, which demonstrated that diabetics were more likely to be diagnosed with colon cancer than non-diabetics. Researchers adjusted for confounding factors such as age, obesity, and smoking in most of the studies, yet the connection between diabetes and cancer remained.

“I think we can make the statement that diabetes is consistently associated with colorectal cancer,” said Dr. Edward Giovannucci, with the Harvard School of Public Health. Dr. Giovannucci was not one of the researchers involved with the study.

“The cause-and-effect aspect is a bit difficult to consider since diabetes is such a complex disease,” continued Dr. Giovannucci. While he believes that the results do likely show a direct connection between diabetes and colon cancer, it’s still uncertain what factor connects the two diseases.

One theory hypothesizes that hormonal imbalances caused by diabetes could be responsible for the growth of cancer cells. Diabetics have elevated levels of the hormone insulin as well as insulin-like growth factors, which are both responsible for the growth of cells. This growth may include cancer cells.

According to Dr. Hiroki Yuhara, head of the study conducted at the University of California Berkeley, patients with diabetes are not currently advised to receive colon cancer screening more often than patients without diabetes. Yuhara says that it’s unclear whether doctors will begin recommending more frequent colon cancer screenings for diabetics.

Most individuals are advised to begin colon cancer tests at the age of 50. Such tests may include sigmoidoscopies, colonoscopies, or tests that check for the presence of blood in the stool. Individuals with risk factors for colon cancer, such as inflammatory bowel disease or family history of the disease, are advised to begin screening earlier in life. Currently, diabetes is not considered cause for recommendation of earlier screenings.

There is also evidence that the link between diabetes and colon cancer may not be as strong as once thought. Last year, researchers at the American Cancer Society published a study which found that among 184,000 older American men, diabetes was associated with a 25% increase in the risk of colon cancer. However, according to the researchers on the study, the risk was modest and was not as severe as previous studies had suggested.

It was also discovered that the link between the two diseases did not exist in women. The ACS researchers thought that the findings of the study could point to improved diabetes control, among women in particular. Better control of blood sugar would lead to reduced insulin levels, which would limit the factor that may be the link between diabetes and colon cancer.