The rationale was that warming up with calisthenics, brisk walking, or other activity helps ease the body into a strenuous workout and may reduce injuries. Cooling down is supposed to gradually reduce your heart rate and return your body to a state of rest, thus lowering the risk of soreness and even heart attacks. Or so the exercise physiology textbooks taught for decades.

The problem is, there’s little solid research backing up this advice, and much of what’s out there is conflicting. In terms of stretching, which many people include in their pre-exercise routines (though it’s technically not a warm-up, since it doesn’t raise heart rate much), most studies have found that it does not protect against exercise-induced injuries.

Cool on warm-ups

A review in the journal Sports Medicine tried to make sense of 25 years of research on the effect of warming up on the risk of injuries. The authors concluded that overall the weight of evidence suggests that a “warm-up and stretching protocol should be implemented prior to physical activity.” However, they acknowledged that studies’ conclusions were all over the map, and called for more research.

Most of the studies have been small and focused on certain types of athletes, age groups, and just men or women. What helps a 25-year-old female triathlete, for example, may not help a 75-year-old man who cycles two or three times a week.

Research has also been inconsistent on the effect of warm-ups on performance. An Australian study in the European Journal of Applied Physiology, for instance, found that warm-ups that included some static stretching actually decreased muscle power among young people doing vertical jumps. But an analysis in the Journal of Strength and Conditioning Research found that warm-ups improved performance.

Lukewarm about cool-downs

Good studies on the potential benefits of cooling down are even more scarce. While it feels right and sensible to gradually diminish the intensity of your workout, there hasn’t been much research showing benefits. Still, the American College of Sports Medicine (ACSM) recommends cooling down because it lowers heart and breathing rates and helps prevent pooling of blood in the legs, which can cause light-headedness and fainting. In particular, ACSM advises people taking medication for hypertension to cool down, since some of these drugs can cause blood pressure to drop even lower following an abrupt end to vigorous exercise.
Bottom line: Regular exercise has many proven health benefits; warming up and cooling down do not. Still, if you enjoy doing them and they feel good, there’s little or no downside. In fact, many people find they get a psychological, if not physical, boost from easing into and out of vigorous exercise, and who can argue with that?

The last few weeks — or even days — before starting a diet can be a perilous time for your teeth, thanks to “last chance syndrome.” You know: “Hey, it’s my last chance to indulge before my diet, so why not go for it now?”
3 Smart Steps to Keep Your Teeth
Desserts, such as those brought into the office, can be especially dangerous. There’s recent evidence that the combination of sugar and starch (think pies, cakes, cookies, and breakfast treats) is worse for your teeth than either one alone. The sugar-starch combo kicks a potent mouth bacteria called S. mutans into high gear. It creates a kind of super-plaque that is up to five times harder, stickier, and more acidic than the dental plaque made without much starch.
7 Worst Foods for Your Teeth
Worse, not brushing right after eating these sugary, starchy foods gives those bacteria extra hours to pile up plaque on your teeth. Check out these tips to protect your teeth:
• Wash dessert down with cranberry juice. A molecule in cranberries cuts acid production of certain bacteria by 70% and keeps them from sticking to teeth.
• Avoid soft drinks. Sodas tend to be acidic, which helps erode tooth enamel. That goes for diet soda, too. Carbonated sodas — even diet soft drinks — have been linked to obesity and diabetes, too.
• Chew sugarless gum. Specifically, chew gum sweetened with xylitol. Chewing stimulates saliva, your body’s natural mouth rinse, and xylitol curbs bacteria. Chewing gum can also stifle your cravings.
• Put your toothbrush and floss on your pillow. That way, no matter how tired you are, you’ll remember to safeguard that smile with nightly brushing and flossing.

the article above is an excerpt from RealAge.com

Call our office for more tips to make your smile last a lifetime!
Diamond Dental
contact@MyDiamondDental.com

You probably take steps to prevent cavities by brushing and flossing your teeth. Even so, you’re still at risk for dental erosion.
This growing and underappreciated problem of dental erosion now affects as many as one in five Americans, according to a series of articles in the Journal of the California Dental Association.
Dental erosion is the acidic dissolution of teeth–starting with the softening (demineralization) of the enamel and underlying dentin and subsequent structural tooth loss. It’s caused by acids in food and beverages as well as by regurgitated stomach acid resulting from reflux disease (in contrast, cavities are caused by acid-producing bacteria on the teeth, which feed on sugars). Overbrushing, abrasive toothpaste, tooth grinding, and other excessive mechanical wear and tear can dramatically worsen the damage caused by dental erosion.
Why the rise in dental erosion?
It’s largely because Americans have been drinking more acidic beverages and have become heavier (obesity increases the risk of reflux disease). Older people are also at risk because many take medications that reduce saliva flow, making their teeth more vulnerable to acid. And ironically, in our zeal to clean and polish our teeth, many of us overdo it and thus abrade them.
If your teeth could talk
If you know you have dental erosion, or want to prevent it, take these steps:
• Limit acidic beverages, such as soda (especially cola and citrus flavors, including diet sodas), energy drinks (such as Red Bull), sports drinks (such as Gatorade), citrus juices, and wine. Repeated and prolonged exposures–as in sipping or swirling the liquid in your mouth–are most erosive. Sugary acidic drinks are a double whammy, since they also promote cavities.
• Limit acidic foods such as oranges, lemons, grapefruit, sour candies, raisins, and vinegary items–or at least eat them with other foods, not on their own.
• Rinse with water after consuming acidic foods or beverages. Rinsing with baking soda (sodium bicarbonate) and/or a fluoride mouthwash can further help.
• Eat dairy products. Their calcium helps reduce the damaging effects of acids; their casein enhances remineralization.
• Chew sugarless gum to increase saliva flow, which helps wash away acids.
• Use a less abrasive toothpaste. Whitening pastes are most abrasive. Those containing baking soda, which is alkaline and nonabrasive, tend to be gentlest on teeth.
• Use a toothbrush with soft bristles, but not too forcefully or for more than a couple of minutes. It’s easy to overdo it with an electric toothbrush, since it requires little effort.
Article from BerkeleyWellness Alerts

If you have any questions regarding halitosis, or bad breath, please give us a call or reply online.

Thanks, Diamond Dental

You can find these fats in a variety of sources, including spinach, mustard greens, wheat germ, walnuts, flaxseed (and flaxseed oil), soybean and canola oil, and even pumpkin seeds. But the very best source is fish.

Not all fish are created equal, however. This handy chart will help you choose fish with the highest omega-3 content.
Type of fish

Total omega-3 content per 3.5 ounces (grams)
Mackerel

2.6
Trout, lake

2.0
Herring

1.7
Tuna, bluefin

1.6
Salmon

1.5
Sardines, canned

1.5
Sturgeon, Atlantic

1.5
Tuna, albacore

1.5
Whitefish, lake

1.5
Anchovies

1.4
Bluefish

1.2
Bass, striped

0.8
Trout, brook

0.6
Trout, rainbow

0.6
Halibut, Pacific

0.5
Pollock

0.5
Shark

0.5
Sturgeon

0.4
Bass, fresh water

0.3
Catfish

0.3
Ocean perch

0.3
Flounder

0.2
Haddock

0.2
Snapper, red

0.2
Swordfish

0.2
Sole

0.1

Source: The Health Effects of Polyunsaturated Fatty Acids in Seafoods
©

If you would like further information on preventing gum disease, please contact our office.

February 15, 2012 — In the quest to better understand the causes of periodontal disease, researchers are making big strides on two key fronts: understanding the nature of the bacteria that stimulate gingival inflammation, and the genetic and physiologic foundations that can determine the body’s response to that stimulus.

As a common denominator for a broad range of medical conditions, inflammation has become an especially hot topic in periodontal research. Study after study has set out to try and understand why some people have an inflammatory response to certain bacteria and others don’t, according to Pamela McClain, DDS, president of the American Academy of Periodontology (AAP).

“Our understanding of periodontal disease is veering away from what was considered to be just bacteria causing the disease to the role of inflammation, which is believed to be the most important factor in the progression of the disease,” she explained. “That response can truly vary from one individual to the next. You can have a husband and wife with similar bacteria in their mouths — and studies show they commonly do — yet one gets inflammation and the other doesn’t. We know the bacteria start the process, but it’s the response to those bacteria that ultimately results in the loss of the attachment between the bone and the periodontal ligament.”

Genetic factors

Genetics is one of the most significant factors in that response. Genetic factors ranging from gender — more specifically, being female — to carrying some distinctive single nucleotide polymorphism are believed to play a role in 30% of periodontal disease cases. In two separate studies, Alexandre Vieira, DDS, PhD, and colleagues at the University of Pittsburgh found evidence that genes could, in fact, account for as much as 50% of an individual’s susceptibility to developing caries or periodontitis.

In the first study, Dr. Vieira and colleagues in Pittsburgh and Brazil analyzed 389 individuals in 76 nuclear families and found an association between two variants of the gene FAM5C and periodontal disease (PLoS One, April 7, 2010, Vol. 5:4, p. e10053).

In the second study, published in the Journal of Dental Research (June 2010, Vol. 89:6, pp. 631-636), Dr. Vieira and his co-authors found that people with a variant of the gene DEFB1 (defensin, beta 1) were more than five times more likely to have decayed, missing, or filled teeth compared with those who didn’t carry the variant. Patients with another variant, the rs179946 (G-52A), were only a third as likely to have the dental problems (p = 0.014).

Interestingly, the FAM5C gene has also been associated with another inflammatory condition: heart disease.

“There are a number of common etiological factors modulating these diseases,” said Dr. Vieira, an associate professor and the director of clinical research at the University of Pittsburgh Center for Craniofacial and Dental Genetics. “It appears that the association between these two groups of diseases could be in part related to individual genetic background.”

The same genes modulate inflammation regardless of the process that is happening in the oral cavity or elsewhere, he added.

“Individual responses to specific external factors, since they are modulated by the same genes, can be similar, and this can partly explain associations reported between periodontal diseases and other systemic conditions,” he said.

Other experts agree that the discovery of similarities between the inflammatory process in periodontal disease and that of other chronic inflammatory diseases could represent one of the most promising areas of research.

“It is uncanny how the inflammatory reaction occurs in other chronic inflammatory diseases and periodontitis,” said Samuel Low, DDS, a past president of the AAP and a professor of periodontology at the University of Florida College of Dentistry. “With diabetes, cardiovascular disease, Alzheimer’s disease, and rheumatoid arthritis, for instance, if you review the way the inflammatory process works in those diseases, it is very close to the way it works with periodontal disease.”

One important advantage that periodontal disease has over the other inflammatory conditions, Dr. McClain noted, is a clearly defined stimulus: bacteria.

“With rheumatoid arthritis, the body is attacking the joints with inflammation. Likewise with periodontal disease, the inflammation is in the attachment between the bone and the attachment of the gum tissue,” she said. “But at least with periodontal disease, we know the bacteria are stimulating this whole response. In rheumatoid arthritis or other conditions, we often don’t know.”

New bacteria insights

That being said, more headway is being made in understanding the behavior of the bacteria itself.

Intriguing new research on one of the most notorious of periodontal disease offenders, Porphyromonas gingivalis, implicates the bacterium as a “keystone pathogen” that, in fact, doesn’t directly cause damage, but instead manipulates the oral environment so that otherwise benign bacteria change course and infect the tooth’s supportive structures (Journal of Oral Biosciences, 2011, Vol. 53:3, pp. 233-240).

“In this regard, P. gingivalis’ tactics to undermine innate immunity may promote the survival of other members of the periodontal biofilm community,” wrote the study authors, from the University of Louisville School of Dentistry.

Based on observations on mice, the researchers found that P. gingivalis, in effect, reprograms the front-line immune cells that protect the space in the subgingival crevice, causing them to let down their defenses. Once that’s accomplished, benign bacteria — and not P. gingivalis — then rise in numbers and march in to infect the tooth’s periodontium.

“These subversive strategies of P. gingivalis may explain, at least in part, its ability to persist and establish chronic infections in the periodontium,” the authors wrote.

Interestingly, in a previous study, researchers with the University of Michigan found that people carrying an antibody to a protein of P. gingivalis, called HtpG, have a lower risk of periodontal disease (PLoS One, April, 23, 2008, Vol. 3:4, p. e1984).

The antibody “offers significant potential as an effective diagnostic target and vaccine candidate,” the authors concluded.

Nongenetic causes

Genetics holds plenty of clues to the causes of periodontal inflammation and disease, but it doesn’t paint the whole picture. Other well-known risk factors include everything from smoking to pregnancy (and the state of hormonal flux that it involves), but one key condition is looming ever larger as an important factor in periodontal disease: obesity.

Research demonstrating the role of being overweight and obesity in periodontal disease has mounted in recent years, with one of the more interesting studies coming out of the Case Western Reserve University School of Dental Medicine

(Journal of Periodontology, October 20, 2011). The study authors found significant improvements in periodontal health among gastric bypass patients following their surgeries and weight loss.

The study included 30 obese people with chronic periodontitis. The researchers compared the participants before and after half of the subjects underwent bypass surgery and had fat cells removed from the abdomen. Compared with those who did not have the weight loss surgery, the bypass patients showed greater improvements in periodontal attachment, bleeding, probing depths, and plaque levels.

Importantly, the gastric bypass patients also showed declines in glucose levels following the procedure. The researchers theorized that by making insulin less resistant, weight loss improves diabetic status, which in turn improves response to periodontal treatment. They also speculated that the surgery reduced the production of the appetite hormone leptin, which has been implicated in the regulation of metabolism and may be linked to inflammation due to its role in increasing the production of cytokines and C-reactive protein.

Other studies also have shown evidence of weight loss resulting in reduced periodontal disease, and the combined research supports the suggestion of a relationship between the increased fat cells that occur with obesity and periodontal inflammation, Dr. Low said.

“Belly fat, interestingly enough, becomes an endocrine gland within itself, and with the increase of the fat cells, there is an overstimulation of the inflammatory process,” he said.

Dr. Low noted that diabetes is the second-highest risk factor for periodontal disease, behind smoking.

The relationship between the two diseases is believed to be somewhat reciprocal, with gingival inflammation undermining blood sugar control while diabetes-associated high blood sugar in turn may trigger periodontal inflammation. But the fact that obesity is a leading cause of diabetes would appear to further compound the damage the disease can wage on periodontal tissue.

Prescription drugs

Other known culprits in the development of periodontal disease are medications. Prescription drugs known to potentially cause gingival ulcerations include aantihypertensive drugs, calcium channel blockers, and even some anti-inflammatories.

Some of the newer offenders include certain chemotherapy drugs, antidepressants, and antianxiety medications, which can all cause xerostomia, according to Dr. Low.

“There are probably more than 500 medications out there that create dry mouth,” he said. “Antidepressants and antianxiety medications, for instance, can cause this, and the danger is that saliva is one of the best protectors against inflammation. It contains powerful anti-inflammatory products. So if you don’t have saliva, you lose your natural defense system.”

Certain medications can cause swelling of the gum tissues and result in pseudo or false pockets, making it easier for the disease to progress, Dr. Low added.

Xerostomia resulting from medications can trigger a particularly vicious cycle of erosion on the teeth and gums, Dr. McClain emphasized.

“When you have less saliva being produced, you’re not washing away the bacteria or having the good enzymes that are necessary to fight the bacteria,” she said. “That results in more plaque formation and a bigger challenge in managing periodontal issues.”

Dental practitioners should stay informed of data on new drugs and new drug classes in the marketplace, Dr. McClain added. “We often don’t know the effects of these medications on the teeth or gums until patients have been on them for a long time,” she said.

The issue is tricky, however — some medications may clearly be essential in treating a patient’s medical condition, and Dr. Low warned dentists to use caution in advising patients on their prescription drugs.

“We recommend that dentists tell patients to ask their physician if there is an alternative medication if the current medication they are taking is risking periodontal health,” he said. “If the patient’s doctor says the condition is life-threatening and there is only one drug, then we’ll deal with the dry mouth. But if we find that the dry mouth is contributing to either decay or periodontal disease, then it’s important to see if there is an alternative.”

Fatty acids: Bad and good

Aside from medications, the causes of periodontal disease may also simply lie in the foods patients consume. When it comes to the causes of inflammation, recent research has revolved around fatty acids, both bad and good.

Not surprisingly, many of the same fatty acids implicated in increasing bad cholesterol levels and potentially raising the risk of cardiovascular disease have been linked to periodontal disease.

In one recent study out of Japan, for instance, older nonsmokers who consumed higher levels of saturated fatty acids, including those found in meat fats, milk, butter, lard, and some oils, had a relative risk of periodontal disease that was 1.92 times higher than that of people of the same age with a low saturated fatty acid intake (Journal of Dental Research, July 2011, Vol. 90:7, pp. 861-867).

Conversely, just as polyunsaturated fats, including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are associated with a host of health benefits, ranging from cardiovascular to neurological, so too are the fats emerging as potential key players in the prevention of inflammation and disease.

One recent study involving more than 9,000 adults showed the prevalence of periodontitis to be approximately 20% lower among individuals who reported consuming the highest amount of dietary DHA; reduction, although smaller, was also seen with consumption of EPA (Journal of the Academy of Nutrition and Dietetics, November 2010, Vol. 110:11, pp. 1650-1652).

“We found that omega-3 fatty acid intake, particularly DHA and EPA, are inversely associated with periodontitis in the U.S. population,” stated co-author Asghar Naqvi, MD, MPH, from Beth Israel Deaconess Medical Center, in a press release. “To date, the treatment of periodontitis has primarily involved mechanical cleaning and local antibiotic application. Thus, a dietary therapy, if effective, might be a less expensive and safer method for the prevention and treatment of periodontitis.”

Another line of research on omega-3s adds that the inclusion of low-dose aspirin (81 mg) significantly improves the ability of omega-3 fatty acid supplementation to resolve inflammation.

In one study of 80 human subjects, including 40 who received scaling and root planing and 40 who also received the treatment in addition to supplementation with low-dose aspirin and omega-3 fatty acid (900 mg of EPA and DHA), significant reductions in probing depths and attachment gain were observed after three and six months in the supplementation group, compared with the control group (Journal of Periodontology, November 2010, Vol. 81:11, pp. 1635-1643).

“Omega-3- and omega-6-based polyunsaturated fatty acids play a major role as defense-supporting/catalyzing lipids. The problem is that humans (and many mammals) do not have the means to metabolize these lipids and cannot produce them in sufficient quantities,” said Alpdogan Kantarci, DDS, PhD, of the Forsyth Institute and co-author on several key studies examining the issue. “What we produce is very limited, and their half-lives are very short. Therefore, we need to consume external sources such as fish or plants.”

Aspirin prolongs the half-life of such compounds in blood and dampens the inflammatory reactions by counteracting the mediators and cells that are produced as the first line of defense against pathogens, he added.

“The more we appreciate these mechanisms, the more targeted our treatment would become in inflammatory diseases, including the periodontal diseases,” he said.

In a previous study on mice and rabbits (Journal of Immunology, November 15, 2007, Vol. 179:10, pp. 7021-7029), the researchers even found that omega-3 benefits appeared to extend to the bones, Dr. Kantarci said.

“We have shown that such an approach cannot only reverse the inflammatory process, but also can help in regenerating the lost bone and hard tissues, so there is a lot of exciting potential,” he said.
“Research has demonstrated that supplementation of 900 mg of omega-3 and 81 mg of aspirin can decrease periodontal disease.”
– Samuel Low, DDS

As more becomes known about the mechanism of omega-3 fatty acids, the more valuable they may become as a nonpharmaceutical approach in the prevention or treatment of inflammatory diseases, including periodontal disease.

“This does not mean that the antibiotics will be replaced soon, since many infections will most probably still require elimination or decrease of bacterial load,” Dr. Kantarci said. “But in complex infecto-inflammatory diseases, modulation of the host response can provide novel ways to control and treat the process.”

Dr. Low already recommends that his patients at risk for periodontal disease take omega-3 supplements — and low-dose aspirin.

“We’re very excited about this because research has demonstrated that supplementation of 900 mg of omega-3 and 81 mg of aspirin can decrease periodontal disease,” he said. “The omega-3s basically suppress bad inflammation and express good inflammation. We can also throw in calcium and vitamin D for the bones, but to me the more appropriate approach is anything that is anti-inflammatory.”

Looking ahead

The periodontal community can likely expect to see much more intriguing research as the secrets of chronic inflammatory diseases unfold. Dr. Low recommends dentists simply stay tuned and follow the science.

“What we don’t want to see is dentists falling back on anecdotal data,” he cautioned. “The ‘I’ve seen patients for 25 years and when I’ve seen this, I do that’ approach is just not wise at this point in time. What we want is an approach that respects the scientific relationship between the risk factors, the genetic factors, and the progression of the disease.”