- Clinician insulin resistance is still an issue despite many advances, and sharing these advances with providers might be a first step;
- Get someone in your office who can help you so that it is not on the clinician alone to have to do this; and
- Trust some of these tools and get some positive experiences.
April 15, 2017
At least Dr. Stephen A. Brunton, executive director of the Primary Care Metabolic Group, concedes that doctors may be the cause. Dr. Jay Shubrook, family physician and diabetologist at Touro University in California, is the doctor interviewing Dr. Brunton
Dr. Brunton says that doctors have always talked about insulin resistance being something that is the result of patient resistance. However, a lot of insulin resistance comes from practitioners. We resist using insulin for many reasons, and that has an impact on getting our patients to target.
Dr. Shubrook asks, what is clinician insulin resistance?
Then to quote Dr. Brunton, “Traditionally, we have been reticent to use insulin because of the impact it would have on slowing the flow in the office, and even in terms of our feelings of expertise. When the basal insulins came out, it made things so much easier—insulin could be initiated with 10 units daily. At that dose, there is a very low risk for hypoglycemia or any other problems. With the insulin pens, it became so much easier.
Part of it, however, is that we assume that our patients do not want to start insulin. Perhaps, in the past, we used insulin as a threat: "If you do not behave, you are going to get insulin." Now we have realized that it is the most effective regimen for getting patients under control. Part of the problem is that the patients may still have some of those other considerations that we may have originally laid upon them. It is our resistance to start patients on a very therapeutic regimen.
Part of the issue of complexity is that when patients come for the management of diabetes, many don't have only diabetes. They may have eight to 10 different comorbidities. We are so busy trying to manage all of that that we tend to put off starting insulin. We may have them on three or four oral antidiabetic drugs. So, we need to look at where our patients are and how we can get them to target.
Many studies show how long it takes us to make a change. It's therapeutic inertia. It has been shown that sometimes for years, the patient is out of control, and we will give them one more chance. We will add another oral agent, but it is not going to have a benefit, particularly when these patients have glucotoxicity.
We need to recognize that we have a broad base of different therapeutic options and that today's insulin is not your grandparents' insulin. We have better analog insulins. We have pens. We have very small needles, so patients are much more likely to accept insulin than we think. Insulin resistance is really our problem. Patients are not as frightened of needles as we think.
Patients may have misconceptions about what insulin means; for example, they might have heard, "I started insulin and my leg dropped off." That, as you and other clinicians know, is not why that person lost their leg, but the patient still holds onto that, and insulin becomes a big fear. It is up to us to help them overcome that.
Dr Shubrook says: You mentioned many things that make it easier for us to overcome our resistance—insulin pens, easy-to-titrate insulins, and algorithms for treatment. How do we address the clinician resistance to using insulin that remains?
Dr Brunton answers: The issue is to try to develop a system in the office so that you do not have to do everything yourself. Educate the staff to overcome some of the barriers to implementation in the office. Introduce insulin early on in the diagnosis. With people who have type 2 diabetes, insulin seems to be far in the future, and the thinking is, "Oh my God, I hope not." I say, "I have a natural therapy that eventually you might use." We recognize that diabetes is a progressive disease and eventually a significant proportion of patients are going to need insulin. I view this as a positive and say, "This natural therapy is insulin, and we will talk about that as it gets a little closer, but let me tell you a little bit about it." I explain the pathophysiology of diabetes and where insulin fits in. Then, I also have staff who can go over injection techniques and some of the algorithms, so that it is not all laying on my shoulders.
Dr Shubrook says: Those are important points, but I can still see some of my partners being resistant to the use of insulin. Maybe it's based on a bad experience they have had in the past, maybe it's just a lack of experience, or maybe it's the math. If I wanted to talk to one of my colleagues about starting insulin more frequently, what are some steps that they can follow?
Dr Brunton answers: First, try to understand the concerns. Sometimes it relates to misconceptions. Not only do we have an easier process now with basal insulin, but show them how to titrate it. A lot of patients will start on 10 units and if they stay on that, they are not going to get the benefits. The benefit of basal insulin comes with titration. One does not have to go from a basal all the way to a basal bolus with four injections a day. We can use the basal-plus approach where you provide some short-acting insulin for the main meal. That makes things a little easier. Now we also have GLP-1 agonists that we can use in concert with insulin. There are many ways that we can use insulin to help get our patients to goal.
Dr Shubrook commented: This is really still a very important topic because we know that most of our patients with type 2 diabetes and all of our patients with type 1 are going to need insulin. If clinicians are not comfortable, these patients are certainly not going to get the treatment they need.
What I have heard you say today is:
Dr Brunton: Yes. We have come a long way, Jay, and that is one of the exciting things about managing diabetes today. We have so many tools at our fingertips that can help our patients get to goal. We have been at a plateau—about 55% of patients are getting to goal and 45% are not. Now that clinicians have these tools, if they feel more comfortable with them, we can help our patients.
This discussion points out the problems many people new to diabetes have with doctors. This reinforces earlier blogs by David Mendosa and myself on February 24, 2017 about starting insulin at diagnosis. Please take time to read both.
April 14, 2017
It’s common knowledge that sugar is bad for your teeth. As science has progressed, one thing is certain — sugar causes tooth decay. Sugar on its own is not the culprit. Rather, the chain of events that takes place afterward is to blame.
Many different types of bacteria live in your mouth. Some are beneficial to your dental health, but others are harmful. Yes, it is a battleground. Studies have shown that a select group of harmful bacteria produces acid in your mouth whenever they encounter and digest sugar. These acids remove minerals from the tooth enamel, which is the shiny, protective, outer layer of your tooth. This process is called demineralization.
The good news is that your saliva helps to constantly reverse this damage in a natural process called remineralization. The minerals in your saliva, such as calcium and phosphate and water, help the enamel repair itself by replacing minerals lost during an “acid attack.” This helps strengthen your teeth. However, the repeated cycle of acid attacks causes mineral loss in the enamel. Over time, this weakens and destroys the enamel, forming a cavity.
Simply put, a cavity is a hole in the tooth caused by tooth decay. It’s the result of harmful bacteria digesting the sugar in foods and producing acids. If left untreated, the cavity can spread into the deeper layers of the tooth, causing pain and possible tooth loss. The signs of tooth decay include a toothache, pain when chewing and sensitivity to sweet, hot or cold foods and drinks.
Sugar is like a magnet for bad bacteria. The two destructive bacteria found in the mouth are Streptococcus mutans and Streptococcus sorbrinus. Both of them feed on the sugar you eat and form dental plaque, which is a sticky, colorless film that forms on the surface of the teeth. If the plaque is not washed away by saliva or brushing, the bacteria convert it to acid. This creates an acidic environment inside the mouth. The pH scale measures how acidic or basic a solution is, with 7 being neutral. When the pH of plaque drops below normal, or less than 5.5, these acids start to dissolve minerals and destroy the tooth’s enamel. In the process, small holes or erosions will form. Over time, they will become larger, until one large hole or cavity appears.
A word to the wise - think before you reach for that sugary snack. Many studies have found that the frequent consumption of sweets and sugary drinks leads to cavities. Frequent snacking on foods high in sugar increases the amount of time your teeth are exposed to the dissolving effects of various acids, causing tooth decay.
One recent study among school children found that those who snacked on cookies and potato chips were four times more likely to develop cavities than children who did not.
The most common source of liquid sugar is sugary soft drinks, sports drinks, energy drinks and juices. In addition to sugar, these drinks have high levels of acids that can cause tooth decay.
In a large study in Finland, drinking 1–2 sugar-sweetened beverages a day was linked to a 31% higher risk of cavities. Also, an Australian study in children aged 5–16 found that the number of sugar-sweetened drinks consumed was directly correlated to the number of cavities found.
One study involving more than 20,000 adults showed that just one occasional sugary drink resulted in a 44% increase in the risk of losing 1–5 teeth, compared to those who did not drink any sugary drinks. This means that drinking a sugary drink more than twice daily nearly triples your risk of losing more than six teeth.
Fortunately, one study found that reducing your sugar intake to less than 10% of daily calories decreases your risk of tooth decay.
Just as you learn for diabetes, if you constantly sip sugary drinks throughout the day, it’s time to rethink that habit. Research has shown that the way you drink your beverages affects your risk of developing cavities. One study showed that holding sugar-sweetened beverages in your mouth for a prolonged time or constantly sipping on them increased the risk of cavities. The reason is because this exposes your teeth to sugar for a longer time, giving the harmful bacteria more opportunity to do their damage.
Research has found that these factors can hasten or slow the development of cavities. These include saliva, eating habits, oral hygiene, and overall diet.
Below are some ways you can fight tooth decay.
Make sure to eat a balanced diet of fresh fruits, vegetables and dairy products.
If you do eat sugary foods and sweetened or acidic beverages, have them with your meals, instead of between them.
Also, consider using a straw when drinking sugary and acidic beverages. This will give your teeth less exposure to the sugar and acid in the drinks. Add raw fruit or vegetables to your meals to increase the flow of saliva in your mouth.
Finally, do not allow infants to sleep with bottles containing sweetened liquids, fruit juices or formula milk.
Sugary and sticky foods should only be eaten occasionally.
If you do indulge in sweet treats, drink some water, preferably tap water that contains fluoride, to help rinse out your mouth and dilute the sugar that sticks to the tooth surface. Moreover, only drink soft drinks in moderation, if at all. If you do drink them, don’t sip them slowly over a long period of time. This exposes your teeth to sugar and acid attacks for longer. Instead, drink water. It contains no acid, sugar or calories.
Practicing good oral hygiene is one way to fight bad habits and the wrong food.
Brushing at least twice per day is an important step in preventing cavities and tooth decay. It is recommended to brush after each meal whenever possible and then again before you go to bed.
Additionally, stimulating saliva flow helps bathe the teeth in beneficial minerals.
Chewing sugar-free gum may also prevent plaque build-up by stimulating saliva production and remineralization.
Lastly, nothing ensures keeping your teeth and gums healthy like visiting your dentist every six months.
Just remember that whenever you eat or drink anything sugary, the bacteria inside your mouth work to break it down. They produce acid in the process. Acid destroys the tooth enamel, which results in tooth decay over time.
To fight this, keep your intake of high-sugar foods and beverages to a minimum, especially between meals and right before bedtime. Taking good care of your teeth and practicing a healthy lifestyle are the best ways to win the battle against tooth decay.
April 13, 2017
Yes, better outcomes happen when doctors work with patients to intensify oral antidiabetic drugs (OADs). Again, another article claiming that type 2 diabetes is a progressive disease. The only time it is progressive is when the patients with their doctors', refuse to aggressively treat type 2 diabetes and let it get out of control. Treated aggressively, type 2 diabetes can be managed and prevented from becoming progressive.
According to guidelines, antidiabetic drugs (OADs) must be added three months after the failure of initial therapy with metformin monotherapy and lifestyle modifications in order to achieve glycemic goals. Many patients with T2D on OADs are deprived of timely treatment intensification, regardless of hemoglobin A1c (HbA1c) being above target range. The failure to intensify treatment in a timely manner has been termed ‘Clinical Inertia.’ According to Dr. H.J. Folse and colleagues, this delay is associated with an inability to achieve target HbA1c in a timely manner, increased risks of cardiovascular events, and amputations.
Previous studies have shown that poor glycemic control due to clinical inertia can be improved by earlier intensification with OADs. In a retrospective cohort, ‘the Inertia study,’ a large United States claims database was used to estimate time to intensification (TTI) with an additional OAD or injectable medication for adults with type 2 diabetes and poor glycemic control (HbA1c greater than or equal to 8%) after three or more months of therapy that included metformin (index date), and no history of injectable antidiabetic medications. The results showed that less than 48% of subjects had received treatment intensification within 12 months after the index date. However, not much is known about long-term consequences of clinical inertia. The primary outcome was the time from index date to treatment intensification, defined as patients filling a prescription for injectable or additional OADs. The purpose of the study was to use the Archimedes Model in a cohort of hypothetical patients with HbA1c greater than or equal to 48% on metformin with no history of insulin use to examine the consequences of delayed OAD treatment intensification on glycemic control and long-term outcomes at 5 and 20 years in patients with T2D.
Using real world data, the study used a cohort of hypothetical T2D patients with HbA1c greater than or equal to 8%, and greater than or equal to 18 years old, on metformin, with no history of insulin use. The cohort included three strata based on the number of OADs taken at baseline. Treatment intensification sequence included addition of a sulfonylurea, followed by a dipeptidyl peptidase-4 inhibitor, and a thiazolidinedione. Based on observed and extrapolated times to intensify the treatment, the result included either ‘No Delay’ or ‘Delay.’ Treatment failure was defined as HbA1c greater than or equal to 8% and patients were followed for one year following the index date and when patients filled a prescription for injectable or additional OADs. Subgroup analyses were based on metformin monotherapy, metformin with one other OAD, and metformin with two or more other OADs. Time to treatment intensification was grouped as early intensified (within 6 months), late intensified (6 to 12 months), or never intensified within 12 months.
The mean HbA1c at one year for patients intensifying without delay vs. with delay was 6.8% and 8.2%, respectively with an absolute reduction of 1.4%. Also, at five years for no Delay vs. Delay, reductions in the risks of major adverse cardiac events, myocardial infarction, heart failure, and amputations were seen at 18.0%, 25.0%, 13.7%, and 20.4%, respectively. The timing of intensification of OAD therapy per guideline recommendations steered greater reductions in HbA1c and lower risks of complications, but severe risk of hypoglycemia increased to 19% for the no Delay group in comparison to 12.5% for the Delay group. In general, the relative risk reduction (RRR) trend at five years was similar to the results at 20 years. At five years, the incidence of hypoglycemia was 51.7% higher and at 20 years, it was 18.0% higher in the No Delay groups versus the Delay group.
Some of the limitations in this study included lack of other adverse effects besides hypoglycemia, the effects of hypoglycemia on costs, quality of life, and cardiovascular risk. Also, the OAD add-ons selected were based on the U.S. OADs prescribing patterns observed in the retrospective Inertia study from 2009-2013. However, the addition of following medications in the treatment sequence was universally applied to everyone at an average dose for each treatment. Future studies should expand the treatment sequence with the addition of other classes of OADs.
In conclusion, this study supports the timing of intensification of OAD therapy per guideline recommendations, which leads to greater reductions in HbA1c and lower risks of complications, but increases the risks of hypoglycemia instead of delaying intensification. The differences in HbA1c between patients delaying and not delaying have important long-term consequences with substantial risk of complications of diabetes. HbA1c has been found to be a relatively important risk factor for the progression of diabetic retinopathy, but not so much for stroke and ESRD. Overall, the results emphasized the potential impact of timely treatment intensification on long-term outcomes.
- Intensifying OAD therapy at guideline-recommended time intervals results in greater reduction in HbA1c.
- Failure to intensify treatment in a timely manner results in a higher risk of complications, including adverse cardiac events, myocardial infarction, heart failure, and amputations.
- This study proves that intensifying OAD therapy results in a higher risk of hypoglycemia than delaying intensification.
April 12, 2017
Regular physical activity is considered key for the prevention of obesity and associated health conditions, but some people reap greater rewards from exercise than others do. A new study may have shed light on why this is.
In a study of both mice and human subjects, researchers found that higher levels of selenoprotein P - a protein secreted by the liver - was associated with reduced exercise capacity and fewer exercise-related benefits.
Study co-author Hirofumi Misu, of the Kanazawa University Graduate School of Medical Sciences in Japan, and colleagues say that their findings indicate that selenoprotein P may be a driver of exercise resistance.
The researchers recently published their findings in the journal Nature Medicine.
According to current guidelines, adults should engage in around 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous-intensity aerobic activity each week in order to maintain good health.
However, responsiveness to exercise - in terms of both endurance and metabolic health - can vary widely from person to person. "In particular, some people show complete non-responsiveness to exercise training in terms of aerobic improvement. Similarly, 15-20 percent of patients with type 2 diabetes show a poor hypoglycemic effect to regular exercise therapy," the authors note.
"These findings indicate that some people suffer from exercise resistance and derive limited benefits from the health-promoting effects of physical exercise."
The precise mechanisms behind exercise resistance, however, have been unclear. Previous research has indicated that selenoprotein P might play a role, so Misu and colleagues set out to investigate this association further.
Firstly, the team assessed the effects of exercise training on two groups of mice: one that was deficient in selenoprotein P, and one group of wild-type mice (the controls).
Both groups ran on a treadmill for 30 minutes per day for 1 month. The researchers found that the selenoprotein P-deficient mice had double the exercise capacity of the wild-type mice.
Furthermore, at the end of the 1-month exercise training, the selenoprotein P-deficient mice demonstrated a larger reduction in blood glucose levels following an injection with the hormone insulin.
The researchers also administered selenoprotein P to wild-type mice prior to 1 month of exercise training. These mice showed a reduction in phosphorylation of the enzyme AMPK in their muscles. The researchers explain that AMPK phosphorylation is associated with a number of exercise benefits.
Additionally, the researchers found that mice lacking LRP1 - a selenoprotein P receptor in muscles - were unable to absorb selenoprotein P into their muscles. Furthermore, AMPK phosphorylation was not impacted by exercise training.
Next, Misu and team sought to determine the effects of selenoprotein P on exercise in humans. The researchers enrolled 31 women who were healthy but who did not engage in regular exercise. All women took part in 8 weeks of aerobic training, and their maximal oxygen intake was monitored throughout as a measure of exercise endurance.
The team found that women who had high levels of selenoprotein P in their blood prior to the 8-week exercise program demonstrated a lower maximal oxygen intake than those with lower levels of selenoprotein P.
Taken together, the researchers believe that their results indicate that selenoprotein P contributes to exercise resistance by targeting the LRP1 receptor in muscles.
Further research is needed in order to gain a more detailed understating of how selenoprotein P impacts physical activity, but the team believes that this current study may pave the way for drugs that reduce selenoprotein P production to improve exercise endurance.
Misu and colleagues write: "The current findings suggest that future screening for inhibitors of the [selenoprotein P]-LRP1 axis could identify exercise-enhancing drugs to treat physical-inactivity-associated diseases such as type 2 diabetes."
April 11, 2017
I have wondered about some of the low-calorie sweeteners and now there is a study raising even more questions. There is some questions about the study and if they can't confirm this in other studies, it may go away.
Many people opt for low-calorie sweeteners as a "healthful" alternative to sugar, but a new study suggests that they may not be so beneficial after all. Researchers have found that consuming high amounts of low-calorie sweeteners may promote fat formation, particularly for individuals who are already obese.
Principal study investigator Dr. Sabyasachi Sen, of George Washington University in Washington, D.C., and colleagues reached their findings by analyzing the effects of sucralose on stem cells derived from human fat tissue, as well as on abdominal fat samples.
The researchers recently presented their findings at ENDO 2017 - the 99th annual meeting of the Endocrine Society, held in Orlando, FL.
Sucralose is a zero-calorie, artificial sweetener that is up to 650 times sweeter than sugar. It is used as a sugar substitute in a wide variety of products, including diet sodas, table-top sweeteners (such as Splenda), baking mixes, gum, breakfast cereals, and even salad dressings.
Given the widely documented health implications of sugar consumption, an increasing number of people are turning to products containing sucralose and other artificial sweeteners, with the view that they are better for health.
"However, there is increasing scientific evidence that these sweeteners promote metabolic dysfunction," notes Dr. Sen.
For their study, the researchers sought to gain a better understanding of how low-calorie sweeteners affect the body's metabolism at a cellular level.
Sucralose led to buildup of fat droplets in fat-derived stem cells.
Firstly, Dr. Sen and team applied sucralose to stem cells derived from human fat tissue.
The stem cells were exposed to the artificial sweetener for a total of 12 days at a dose of 0.2 millimolars - a dose comparable to the blood concentration of people who drink around four cans of diet soda daily.
The researchers found that the stem cells showed an increase in the expression of genes that are indicators of fat production and inflammation. Additionally, the stem cells demonstrated an increase in the accumulation of fat droplets, especially when exposed to a higher sucralose dose of 1 millimolar.
Next, the researchers took biopsies of abdominal fat from eight adults, of whom four were obese and four were a healthy weight. All adults reported consuming low-calorie sweeteners, primarily sucralose and aspartame.
Abdominal fat samples were then compared with samples taken from adults who did not consume low-calorie sweeteners.
The team found that adults who consumed low-calorie sweeteners not only showed an increase in the transportation of glucose into cells, but they also demonstrated an over expression of genes associated with fat production.
Furthermore, the researchers identified an over expression of sweet taste receptors that was up to 2.5 times higher among the fat samples of adults who consumed low-calorie sweeteners. Such over expression may play a part in the transportation of glucose into cells. From there, glucose is absorbed into the bloodstream.
The effects of low-calorie sweeteners were strongest among adults who were obese, the team notes.
Findings a concern for people with pre-existing high blood glucose.
Taken together, Dr. Sen and colleagues say that their findings indicate that low-calorie sweeteners may dysregulate the metabolism in a way that boosts the formation of fat.
The increase in transportation of glucose into cells may be of particular concern for adults who have prediabetes or diabetes, the researchers note, as these individuals already have higher levels of blood glucose.
Still, the researchers caution that further studies are required in larger samples of people before any concrete conclusions can be made about the effects of low-calorie sweeteners on metabolism.
"However, from our study, we believe that low-calorie sweeteners promote additional fat formation by allowing more glucose to enter the cells, and promotes inflammation, which may be more detrimental in obese individuals."
Dr. Sabyasachi Sen
April 10, 2017
Are you new to diabetes? Are you wondering what to eat? Hopefully the following will give you some encouragement and ideas.
Who says that having diabetes means you can’t still whip up delicious, homemade food? When you know the basics of meal planning, you can make almost any recipe work.
So, don’t throw out your cookbooks or toss your favorite recipes. Instead, learn some tips about how to cook wisely.
1. Cook with liquid fats in place of solid fats – no definitely not. You may use both and the solid fats are excellent. Just avoid any trans fats.
Solid fats often include saturated fats, which you should limit, or trans fats, which you should avoid totally.
If a recipe calls for solid fat like butter, lard, or hydrogenated shortening, try trans-fat free margarine (never use margarine), spreads, or shortening instead. Check the label to see whether the product will work for cooking or baking.
Many liquid fats -- oils such as canola, corn, olive, and grape seed -- can be healthy when used in moderate amounts (and these fats have added to the epidemic of obesity. Some oils have stronger flavors that may affect the taste. Experiment to find which oils work best with which recipes.
Many dairy products used in cooking and baking are high in fat. You can lower the fat content without compromising taste (do be careful of complete low fat).
Or, if you’re whipping up a treat that calls for chocolate or chocolate chips, try cocoa powder, or use mini-chocolate chips and use fewer of them.
When cooking up a soup or stew, skim off the fat that floats to the surface while it’s on the stove. Or, place the pot in the refrigerator. When the fat has hardened at the top, it's easy to skim off. (I do not agree with removing all fat, as you body needs some fat for the intestines to be healthy).
Choose those that give you energy that lasts and fiber.
When a recipe calls for "white" flour, "white" rice, or other refined grains, try substituting whole-wheat flour, brown rice, or other whole-grain flours or grain products. You can also use ground nuts such as almond or hazelnut (filbert) meal. Or you can mix several of these whole-grain ingredients together in the same recipe. (Be cautious with whole-grain flours as they do spike your blood glucose levels).
Sugar can quickly raise your blood sugar, unlike the carbs from vegetables or starches, which are absorbed more slowly.
Many times, you can cut the amount of sugar without seriously affecting taste or texture, though you may need to add more flour. An exception: You can’t cut corners if something you're baking needs yeast, because the yeast needs the sugar in order to do its job. If you’re using a sugar substitute, check the product label to be sure it’s designed for baking.
Reach for ingredients other than sugar, salt, and fat to satisfy your taste buds. Try out different herbs, spices (cinnamon, cardamom, nutmeg), mustards, and vinegars (balsamic, sherry).
Some spices may even have health benefits of their own. Cinnamon, for example, may help lower blood sugar levels.
You can also cut the amount of salt in a recipe, unless the recipe includes yeast, which needs the salt for rising. Or skip the salt entirely when you’re cooking, and then sprinkle a little on at the table when it’s time to eat.
Another way to reduce how much sodium you get is to choose fresh over canned and frozen foods, which tend to be higher in salt. If you’re cooking with nuts, check that they aren't salted.
If you have favorite recipes that you’d like to make diabetes-friendly, ask your doctor for a referral to a nutritionist. They’re experts at helping plan meals that are appropriate for people with diabetes or other health issues.
If you don't agree, please read the full article here. I say that people are still promoting low fat and high carbohydrate, which over the years since 1977 has been shown not to be healthy for us.
April 9, 2017
Overactive bladder (OAB) is a condition that about 16 percent of the American adult population has; however, the actual percent is unknown. OAB is a condition defined by a group of urinary symptoms related to the control and frequency of urination. Overactivity of a muscle in the bladder wall is considered to be the main cause of OAB. Stimulants like caffeine and alcohol can also cause symptoms.
Causes - A variety of physical conditions and lifestyle habits can influence the chances of developing OAB. It is often the result of a combination of factors where no single cause may be determined. Within the body, OAB is often the result of spasms in the detrusor muscle, the main muscle of the urinary bladder wall.
When the brain senses the bladder is about half full, it usually sends out nerve signals. These cause the pelvic floor and sphincter muscles to relax while the detrusor contracts, squeezing out urine.
In people with OAB, detrusor muscle contractions occur at random. This leads to a sudden urge to urinate, even when there's very little urine in the bladder. Depending on how the urinary sphincter muscles reacts, urine leakage can occur.
Nerve damage and neurocognitive disorders have long been known to cause OAB symptoms by interfering with nerve signaling. Some definitions of OAB include neurological causes. Others refer to the symptoms as the result of nervous system conditions affecting the bladder. Research is still being conducted to better understand the role of the nervous system in OAB.
One 2015 study found that the brain of one person might react to the sensation of the bladder filling differently to another person. This could mean that treatment options need to be tailored individually to be effective.
Common OAB causes include: pelvic organ prolapse, catheter use, stretched or weakened pelvic muscles, low estrogen levels, especially after menopause, enlarged prostate, giving birth via the vagina, bladder abnormalities such as bladder stones or tumors, nerve damage, Parkinson's disease, stroke, and multiple sclerosis, decreased thinking ability or related diseases, including Alzheimer's disease, hip surgery or hip problems, stretched or weakened bladder muscles, incomplete bladder emptying, and structural problems with the bladder.
While OAB can impact anyone at any age, the likelihood of developing the condition increases greatly with age. Despite being so common among older adults, OAB is not simply a part of aging. If someone's OAB symptoms become severe or disrupt everyday life, they should see a doctor. Anything that puts excess weight on or restricts the bladder can increase the risk of developing OAB.
Activities may also increase the risk of OAB if they weaken or damage the pelvic floor, urinary, or sphincter muscles. Conditions that limit the use of pelvic and abdominal muscles may have the same effect.
The relationship between race and ethnicity is still unclear. However, one study found higher prevalence rates of OAB among African American and Hispanic adults compared with other groups.
Common OAB risk factors include: age, smoking, being overweight or excess belly fat, gestational diabetes, pregnancy, frequent or chronic urinary tract infections, long-term constipation, long-term dehydration or overhydration, chronic coughing, and medications that cause a clear increase in urination or fluid intake.
Symptoms - Though many OAB cases aren't reported, available data indicates the condition affects a large portion of adults globally. An estimated 40 percent of American women and 30 percent of American men are thought to experience OAB symptoms.
At least 30 million American adults consider their OAB symptoms bothersome to everyday activity. The direct costs of OAB in the United States are similar to those of breast cancer and osteoporosis, totaling more than $12 billion annually.
Most OAB cases are marked by three main symptoms: urinary urgency, urinary frequency, and urge urinary incontinence (UUI). Urinary urgency describes a sudden and uncontrollable desire to urinate even when the bladder isn't full. In some cases, this urgency can make it difficult to reach a bathroom in time, leading to UUI.
Urinary frequency describes the need to urinate an abnormally high amount of times throughout the day and night. Urinating eight or more times daily without excessive fluid intake may be a sign of urinary frequency and OAB.
Around half of those with OAB also experience UUI, or urine leakage. Other common OAB symptoms include bed-wetting and the need to urinate several times during the night. OAB tends to affect men and women equally but differences in anatomy influence aspects of the condition.
A similar proportion of American women with OAB are estimated to have UUI alongside urgency and frequency. However, less than 3 percent of American men with OAB report this combination. Men with OAB may experience higher rates of nocturia than women.
The physical symptoms of OAB can also lead to emotional and mental symptoms including depression. Similarly, fear of an accident, or being far from a bathroom, can cause social anxiety in those with OAB. In more severe cases, people with OAB may avoid social situations or change their daily routine altogether.
Many people with OAB also suffer a loss of self-esteem and the desire for intimacy. Sleep loss, due to frequent nighttime urination, is another common symptom of OAB.
Prevention - Medication and minimally invasive surgery options exist to treat OAB although the first line of treatment can often be lifestyle changes.
Many factors like smoking, diet, and being overweight increase the likelihood of developing OAB and the severity of symptoms. The lifestyle changes that are recommended for preventing and managing OAB are essentially the same.
OAB prevention and management options include: staying hydrated but not overhydrated, losing weight, treating chronic constipation through medication or diet, pelvic floor muscle exercises, including Kegels, treating urinary and bladder infections, quitting smoking to reduce coughing, and regular exercise.
Many foods and drinks worsen OAB symptoms. Making a few dietary changes will often reduce symptoms greatly. Caffeine, alcohol, and salty foods can act as a diuretic, increasing urine output and trips to the bathroom.
Spicy and acidic foods irritate the bladder lining, causing discomfort and typically increasing the need for more bathroom visits. Dehydration also allows bladder irritants closer contact with the bladder lining, making their effect more intense.
Foods and drinks to avoid include: spicy foods, salty foods, caffeinated foods, and drinks such as coffee, tea, and chocolate, alcohol, items with artificial sweeteners, acidic foods and drinks, citrus fruits and juices, tomatoes including juice, whole fruit, and sauces, cranberry juice and whole fruit, vinegar based products, soda and carbonated drinks, and MSG.
Onions can also irritate the bladder. These can be cooked or replaced with shallots to lessen the effect. Condiments like soy sauce, ketchup, and mustard, are high in salt, sugar, and acidity. Preservatives in processed foods like takeout meals and deli meats are also known bladder irritants.
People with severe cases of OAB or symptoms of the condition may need to treat these suggestions as rules that they want to adhere to.
To avoid complications, people with severe OAB are often advised to cook meals at home as much as possible.