Oral Hygiene’s Sweet Disaster11 Oct 2019
It was a long time coming but finally, in 2014, a prominent medical journal published the definitive scientific study telling consumers what many of us had already had intuitively known: eating sugar triggers not just tooth decay, but initiates the more serious condition called periodontal disease, a gum impairment which leads to even more devastating ailments.
Writing in the American Journal of Clinical Nutrition, a team of five scientists described how they studied data from 2,437 young adults, ages 18 to 25, and estimated their sugar intake using food-frequency questionnaires. Periodontal disease in the study participants was considered to be present based on gum bleeding on probing to a depth of about 3 mm at one or more gum sites. In both the upper and middle levels of sugar consumption among the young adults, periodontal disease was found. The sugar connection was clear.
It’s known that the type of bacteria producing periodontal disease thrive when the human mouth is an acidic environment, which is what dietary sugars are expert at creating. When those bacteria and resultant plaque produce inflammation of the gums around the teeth, gingivitis starts and if left untreated, evolves into pyorrhea, a chronic degenerative gum condition resulting in tooth loss.
Periodontal disease is accelerated even more as a result of nutritional deficiencies, such as Vitamin C and Vitamin D deficits. These deficiencies also destroy bone around the teeth and the periodontal ligaments anchoring your teeth to your jawbone.
It’s estimated that up to 75% of all American adults, and most likely the same in most developed countries, currently have some degree of gum disease, mostly as a result of high sweetener usage.
In postmenopausal women, it’s well established that the loss of bone density, the disease commonly called osteoporosis, can be traced in part to the occurrence of periodontal disease. One reason is that periodontal conditions can combine with postmenopausal estrogen deficiencies to dramatically reduce bone mineral density. Whole Food Vitamin and mineral supplements are important for these women to take in order to help correct the risk factors.
Among other findings in the sugar consumption=periodontal disease=other ailments scenario is the connection to Rheumatoid arthritis.
Still another connection exists between sugar consumption, periodontal disease, and the onset and severity of diabetes. After reviewing research on the common links between sugar, periodontal disease, and diabetes, Dr. Steven W. Seibert, an Illinois specialist in the field of Periodontology, noted how the sugar link swings both ways: “Research has emerged that suggests that the relationship between periodontal disease and diabetes goes both ways. Periodontal disease may make it more difficult for people who have diabetes to control their blood sugar, and people who have uncontrolled diabetes and uncontrolled blood sugar level may be more prone to having periodontal disease.”
We’ve come a long way in our understanding of sugar’s toxic effects on the human mouth since 1983, when a report in the British medical journal, The Lancet, observed: “Sugar is the principal cause of the most common disease in industrialized countries, dental caries (decay).”
Now with confirmation that sweeteners are directly linked to periodontal disease and not just tooth decay, medical science can finally begin to explore all of the many possible ways that migration of toxic bacteria from the mouth, caused by sugar consumption, can wreak havoc on the human body and its health.
“Sugar is the principal cause of the most common disease in industrialized countries, dental caries. The sugars implicated in dental caries, in decreasing order of cariogenicity, are sucrose, glucose, and fructose; brown sugars are as cariogenic as white. The level of sugar consumption at which most of the population will not get dental caries is 15 kg/person a year. The goal should therefore be to reduce consumption to this level and below.” Sugars and Dental Decay. Sheiham A. The Lancet. 1983 February;321(8319):282–284.