I have lost a lot of teeth, and the dental implants I got to replace some of them are causing me a lot of trouble.
If I had known in my thirties and forties what I know now, I would still have all my own teeth, I'm sure of it!
Before I say more, however, keep in mind that nothing is the same for everyone. For example, when new drugs are tested only a percentage of the subjects benefit. Some have no benefit and some experience negative outcomes. It is when there are more good outcomes by a "significant" percentage that a new drug is given the okay. Though clearly in the case of some drugs that are approved by the FDA some people who take them may have very serious health episodes, and even die as a result, as for instance the over 27,000 who took Vioxx and died or were seriously harmed.
Therefore, one of the most important things in dealing with our health is to pay attention to our own individual health, and keep notes so that it's possible to see clearly what happened, specifically, as opposed to what we may remember inaccurately. And, that's true when it comes to our teeth, too.
In my case I had a lot of "tartar" ever since I was a child. In the last few decades it has been referred to as plaque, but it is the same thing. Dental plaque is composed of about 80% water and 20% protein accumulated from the protein in our saliva.
Dentists exclaimed at me over the large amount of tartar/plaque I had and how quickly it built up. I used to need to have my teeth cleaned every three months, sometimes more often than that.
The extensive and quick building plaque is what eventually led to my teeth loss, but in between there were times when I was under extreme stress when my gums bled without even having to brush my teeth to cause the bleeding.
There were two times in my life when the plaque fell off in chunks all on its own: once was after a party in London where everyone had been extremely nice and I felt that people had genuinely liked me and I wasn't alone (I was living in a rather isolated situation at the time); and the other was the day after nearly a dozen people went to court with me to support me. These two experiences led me to believe that if we had a lot of support most of the time, and little stress, that our teeth and gums would benefit.
The trouble is that a lot of us suffer abuse at home rather than receiving love and support. So, the most important thing that I have observed is very different from relying on those around me, and, it's not immediately easy to observe. In fact, it's related in a rather hidden, underlying way.
What I mean is, after I had B12 replacement therapy with regular shots every month for several months I was surprised to discover that plaque was no longer building up as it had always done in the past, I no longer had to have my teeth cleaned more than once or possibly twice a year.
So, I think there is a relationship between feeling supported and loved and higher B12 levels. My feeling is that just as stress lowers B12 levels, love and appreciation raise them.
I have huge amounts of stress in my life so I continue with B12 replacement and now use methylcobalamin lozenges which are much nicer than shots.
When I recently told a friend about methylcobalamin benefiting teeth and gums, she was skeptical, "I just don't see how there can be a connection."
While I can't say for sure, what I think may be involved is the effect B12 has on our blood: when we are low on B12 our blood cells become larger and larger because they can't divide the way that they are supposed to, which is why when we have low B12 we tend to feel tired and our feet and hands tend to fall asleep and feel numb.
I suspect that when our B12 levels are healthy and our blood is healthy that it cleans our systems for us, getting rid of the makings of plaque before they can materialize into a damaging coating on our teeth or inside our veins and brains.
Plaque in the brain is a know factor in Alzheimer's Disease as well as Parkinson's Disease.
Amyloid Plaques
A characteristic of Alzheimer's disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Amyloid is a general term for protein fragments that the body produces normally. In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's the fragments accumulate to form hard, insoluble plaques.
It is also known, as a result of studies, that people with Alzheimer's and Parkinson's have a tendency to low levels of vitamin B12. (See the research excerpts below.)
So, if your fingernails have lines/ridges or you are losing your moons on your fingernails or have other symptoms of low vitamin B12, then you may be like me with excessive plaque that can lead to tooth loss.
But, I think you have a choice. I think you don't have to let it happen. I think that if you begin to use methylcobalamin lozenges you will begin to enhance the health of your blood and nerves and you will see a difference in the health of your gums and teeth.
Try it! But be sure to keep notes. See if it makes a difference for you.
Note: If you are sick and have trouble standing long enough to regularly brush your teeth, try taking a mouthful of hydrogen peroxide, you can dilute it a bit if you like, and swish it around your mouth for a minute or so, then spit it out. I discovered that it helps clean at the gum line. I just wish I'd discovered it earlier than I did while I had tetanus.
1/6/09 - Several of my teeth that were loose are now tight in my jaw bones. I had no idea that loose teeth could become strong and tight again. But, they can and they did for me.
I attribute the change to no longer taking Ibuprofen except when I'm having extreme pain (Ibuprofen weakens the jaw bones, as in fact does Fosamax) and to taking a lot more magnesium. I try to take a magnesium table or capsule every time I have vitamin C, partially because the vitamin C helps my body make use of the magnesium and partially because I take a lot of C and I want to be sure to take a lot of magnesium.
Just to clarify, my teeth were just this side of wobbly in my jaw in the same way the ones were which the dentists insisted had to come out. And, my teeth did not regain their firm anchoring in a day or week or month, it took about two years.
Research - The following research deals with Alzheimer's Disease and low vitamin B12 levels. I am showing this research because in my experience plaque around my teeth was significantly reduced by vitamin B12 replacement. BBC News report September 9, 2008 Vitamin 'may prevent memory loss' A vitamin found in meat, fish and milk may help stave off memory loss in old age, a study has suggested.
Older people with lower than average vitamin B12 levels were more than six times more likely to experience brain shrinkage, researchers concluded.
The University of Oxford study, published in the journal Neurology, tested the 107 apparently healthy volunteers over a five-year period looking at a group of people between 61 and 87, and splitting the group into thirds depending on the participants' vitamin B12 levels.
Even the third with the lowest levels were still above a threshold used by some scientists to define vitamin B12 deficiency. However, they were still much more likely to show signs of brain shrinkage over the five-year period.
Professor David Smith, who directs the Oxford Project to Investigate Memory and Ageing, said: "This study adds another dimension to our understanding of the effects of B vitamins on the brain - the rate of shrinkage of the brain as we age may be partly influenced by what we eat."
Shrinkage has been strongly linked with a higher risk of developing dementia at a later stage and Rebecca Wood, the chief executive of the Alzheimer's Research Trust, said: "This study suggests that consuming more vitamin B12 through eating meat, fish, fortified cereals or milk as part of a balanced diet might help protect the brain. Liver and shellfish are particularly rich sources of B12."
"Vitamin B12 deficiency is a common problem among elderly people in the UK and has been linked to declining memory and dementia," Dr Susanne Sorensen, from the Alzheimer's Society said, "Shrinkage is usually associated with the development of dementia."
Homocysteine, vitamin B12 relationship linked to Alzheimer's; 23-Jul-2002
A combination of high levels of homocysteine and low levels of vitamin B12 is a significant risk factor for Alzheimer's disease among African Americans, according to a paper presented today at the International Conference on Alzheimer's Disease and Related Disorders in Stockholm, Sweden.
Floyd Willis and colleagues at the Mayo Clinic in Florida conducted a study to evaluate the association between homocysteine, B12 and folic acid levels in African Americans with Alzheimer's disease.
The researchers collected blood samples from 256 African Americans who showed no signs of cognitive impairment and 58 African Americans who had a clinical diagnosis of Alzheimer's disease. All study participants were over the age of 50.
When comparing the two groups, the researchers found homocysteine levels were significantly higher in the individuals with Alzheimer's disease and levels of B12 were significantly lower.
High-dose vitamin B12 for at-home prevention and reversal of Alzheimer's disease and other diseases Townsend Letter for Doctors and Patients -- May, 2006 by Joseph G. Hattersley
It is interesting to consider what proportion of Alzheimer's dementia (AD) may result from under-nutrition, (1) especially when it seems that there may be an easy, low-cost, perfectly safe, nutritional way that may allow people to avoid a miserable illness that many people consider worse than death. Some people might say, "That's too good to be true!" In fact, an at-home nutritional program, using a lot of vitamin B12 may indeed prevent and virtually eliminate AD. An early launch of the treatment soon after first warning symptoms start could even turn off the process.
Confusion, difficulty concentrating, loss of memory, marked changes in personality that can lead to outbursts of violence, hallucinations, wandering away, and early death all characterize Alzheimer's dementia. An estimated 2.3 million Americans now have AD. Prevalence doubles every five years after the age of 60, increasing from one percent among those 60 to 64 up to 40% among those aged 85 years and older.
Let's start with a little background. Mammals, including humans, are born with serum levels of vitamin B12 at about 2,000 pg/ml. The level declines throughout human life owing to practices common in Western societies. Below 550 to 600 pg/ml, deficiencies start to appear in the cerebrospinal fluid. US clinical laboratories regard 200 pg/ml as the lower range of normal.
"Most cases of Alzheimer's dementia are actually missed B12 deficiency cases, because of the too-low normal range for B12," wrote John V. Dommisse, MD in 1991 in Medical Hypotheses. Dommisse, who practices medicine in Tucson, Arizona, has confirmed that Alzheimer's disease appears to result from too-low serum vitamin B12, and repletion of the vitamin succeeds despite other risk factors. Repleting B12, according to Dommisse, can reverse 75% of B12 deficiency dementias when the condition is discovered early enough.
Other aspects of the therapy should be noted: The neurological and cerebral manifestations of B12 deficiency require dosages larger, and extending over a longer time, than to those needed to reverse hematologic effects. B12 therapy appears to be perfectly safe; in other words, the risk of overdose is virtually nil. Patients of Dr. H.L. Newbold in New York City injected themselves three times daily with triple-strength doses of B12 (9,000 ug/micrograms/per day) indefinitely. Their serum B12 levels reached 200,000 pg/ml (100 times the normal level found in newborn babies and higher), but none had any significant side effects.
Functional vitamin B12 deficiency and Alzheimer disease A. McCaddon, MRCGP, B. Regland, MD PhD, P. Hudson, MSc and G. Davies, MSc -- From the University of Wales College of Medicine
Moderately elevated total serum homocysteine is associated with an increased risk of atherothrombotic vascular events. Accordingly, serum homocysteine is increased in patients with vascular dementia but is also increased in clinically diagnosed and histologically confirmed AD.
It is generally considered that homocysteine potentiates endothelial and neuronal oxidative injury in these diseases.
A complementary model of oxidative stress induced hyperhomocystinemia is proposed by the authors. The hypothesis accounts for several unusual features relating to single-carbon metabolism and AD, including the absence of macrocytic anemia in these patients. It is suggested that cerebral oxidative stress augments the oxidation of an intermediate form of vitamin B12 generated in the methionine synthase reaction, thereby impairing the metabolism of homocysteine. Oxidative stress also compromises the intraneuronal reduction of the vitamin to its metabolically active state.
Neurology, 2002
Low Vitamin B12 Is Associated With Poorer Memory In Older People With High Risk For Alzheimer's David Bunce, PhD, a psychologist at Goldsmith's College, University of London, Miia Kivipelto, PhD, MD, of the Aging Research Center at the Karolinska Institute in Stockholm and the Stockholm Gerontology Research Center, and Wahlin, PhD, a psychologist at University of Stockholm
Among healthy people over the age of 75 who have the genotype associated with higher risk for Alzheimer's, low levels of vitamin B12 are associated with significantly worse performance on memory tests.
Scientists already knew of a genetic predisposition for Alzheimer's disease, and that low levels of two B vitamins -- B12 and folate -- were also linked to problems.
The apolipoprotein E gene, which moves cholesterol in the body, has a version called the 4 allele. Carried by perhaps 15 percent of the population, it is a risk factor for dementia. Current data collected over a six-year period suggests that nearly one out of four carriers with one copy of this allele and nearly half carrying two copies will develop Alzheimer's disease. Non-carriers also can get Alzheimer's.
Carriers of the 4 allele have smaller hippocampi, brain areas associated with memory, so the researchers wanted to measure how an additional physiological shortfall such as low Vitamin B, affected this particular group -- given that reduced B12 and folate have been linked generally with diminished memory and increased risk for Alzheimer's.
Bunce, Kivipelto and Wahlin studied 167 healthy older people, averaging nearly 83 years old. Among carriers of the 4 ApoE allele, people with normal B12 levels recalled a greater number of words.
A significant difference showed up in the experiment's most demanding condition, when participants had just two seconds to encode words. In that situation, the high-risk genotype plus low B12 levels was significantly associated with poorer memory.
The findings endorse a complex model of vulnerability in which genetic and non-genetic factors interact. According to the authors, "4 ApoE carriers may derive relatively greater cognitive benefits from B12 and folate supplements. Supplement treatment is relatively inexpensive and may be required as part of preventive health regimes for older persons."
Individuals with Alzheimer's disease often have low blood levels of vitamin B12. Lower vitamin B12 levels are found in the cerebrospinal fluid of patients with Alzheimer's disease than in patients with other types of dementia, though blood levels of vitamin B12 did not differ.
Am J Clin Nutr. 2000
Low vitamin B-12 status in confirmed Alzheimer's disease as revealed by serum holotranscobalamin H Refsum, A D Smith -- Department of Pharmacology, University of Oxford, Oxford, UK
51 patients with pathologically confirmed Alzheimer's disease and 65 cognitively screened elderly controls were studied. Serum holotranscobalamin was measured by a new solid phase radioimmunoassay.
Geometric mean levels showed no significant differences for serum total cobalamin, but lower levels of holotranscobalamin in Alzheimer's disease (41.1 pmol/l) than in controls (57.1 pmol/l) (p < 0.001). The odds ratio of Alzheimr's disease was significant for low holotranscobalamin but not for low total cobalamin.
Conclusion: Disturbed cobalamin status is common in Alzheimer's disease and accordingly measurement of holotranscobalamin should be considered in the assessment of cognitively impaired patients.
Journal of Neurology Neurosurgery and Psychiatry; 2003
Alzheimer's linked to vitamins
People with low levels of the vitamins B12 or folate may have a higher risk of developing Alzheimer's disease; scientists found that 46 out of 78 Alzheimer's patients they examined had low levels of both vitamins and they believe a lack of the two vitamins may influence levels of chemicals that play a vital role in transmitting signals around the brain.
Researcher Dr Hui-Xin Wang said, "In our study, we found that low levels of either of these two vitamins were related to an increased Alzheimer's disease risk."
Monitoring B12 and folate levels is important in order to avoid unfavourable conditions, even for those elderly people who are quite healthy in terms of cognition.
Dr Wang said that researchers had recorded low vitamin levels in elderly people for more than 30 years.
Previous research has linked low leverls of B12 and folate to neurological or psychiatric disorders - but never to Alzheimer's disease.
Professor David Smith, of the Alzheimer's Research Trust, said the research confirmed previous studies which suggested a similar link. He also said that the deficiencies may increase levels of a chemical called homocysteine that is known to poison nerve cells.
Vitamin B12 is naturally found in animal foods including fish, milk and milk products, eggs, meat, and poultry.
Leafy greens such as spinach and turnip greens, dry beans and peas, fortified cereals and grain products, and some fruits and vegetables are rich food sources of folate - a form of water- soluble vitamin B.
Neurology, the scientific journal of the American Academy of Neurology. 2001
Ageing and aberrant assimilation of vitamin B12 in Alzheimer's disease. McCaddon, A; Hudson, P.; Abrahamsson, L.; Olofsson, H.; Regland, B.
Vitamin B12 assimilation might be disrupted in patients with Alzheimer's disease. Twenty-three patients, aged 60 or over, with features compatible with degenerative dementia of the Alzheimer type were recruited together with 18 cognitively intact age- matched control subjects. Total vitamin B12 was measured in serum. Alzheimer patients had significantly lower active corrinoid and the analogue/corrinoid ratio was significantly higher in the Alzheimer group. Two disparate mechanisms might exist for the development of cerebral B12 deficiency in Alzheimer's disease, although both imply a disruption of selective B12 assimilation and analogue elimination in such patients.