OK as well as diet and exercise, some researchers have discovered another factor, that the medical profession hasn't caught up with yet.
It's the germ responsible for gum disease. Apparently it can invade blood cells, and over time damage lots of important stuff.
The simple answer is to floss your teeth regularly to prevent build up of plaque.
www.newscientist.com/article/mg24332420-900-have-we-found-the-true-cause-of-diabetes-stroke-and-alzheimers/I'm subscribed to this, so in case you can't see all of it, I'll try and post the relevant bits.
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In disease after disease, we are finding that bacteria are covertly involved, invading organs, co-opting our immune systems to boost their own survival and slowly making bits of us break down. The implication is that we may eventually be able to defeat heart attacks or Alzheimer's just by stopping these microbes.
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Until now, bacteria's involvement completely eluded us. That's because they tend to work very slowly, stay dormant for long periods or hide inside cells. That makes them difficult to grow in culture, once the gold standard for linking bacteria to disease. But now DNA sequencing has revealed bacteria in places they were never supposed to be, manipulating inflammation in just the ways observed in these diseases. The findings are so contrary to received wisdom and emerging in so many diseases, each with its own separate research community, that awareness of all this is only starting to hit the mainstream (See "Germ theory"). And predictably, as with any paradigm shift, there is resistance.
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The worst culprits, which seem to play a role in the widest range of ailments, are the bacteria that cause gum disease. This is the most widespread disease of ageing - in fact, "the most prevalent disease of mankind", says Maurizio Tonetti at the University of Hong Kong. In the US, 42 per cent of those aged 30 or above have gum disease, but that rises to 60 per cent in those 65 and older. It has been measured at 88 per cent in Germany.
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Circumstantial evidence is certainly damning. In the US, states that put federal Medicaid funds towards people's dental costs, including those related to preventing or treating gum disease, ultimately pay between 31 and 67 per cent less than states that don't, to help those people later with heart attacks, diabetes, strokes and cancer. Private insurance companies report similar patterns, says David Ojcius at the University of the Pacific in San Francisco.
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When the plaque the bacteria on your teeth live in builds up enough to harden and spread under the gum, it triggers inflammation: immune cells flood in and destroy both microbes and our own infected cells (see Diagram). If this goes on too long, an oxygen-poor pocket develops between gum and tooth. A handful of bacteria take advantage of this and multiply. One of them, Porphyromonas gingivalis, is especially insidious, disrupting the stable bacterial community and prolonging inflammation.
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P. gingivalis may have a hand in it. It actually perpetuates inflammation by producing molecules that block some inflammatory processes, but not all of them, says Caroline Genco of Tufts University in Massachusetts. The resulting weakened inflammation never quite destroys the bacteria, but keeps trying, killing your own cells in the process. The debris is a feast for P. gingivalis, which, unlike most bacteria, needs to eat protein. The destruction also liberates the iron that bacteria need and which the body therefore normally keeps locked up. "These bacteria manipulate their interaction with the host immune response to enhance their own survival," says George Hajishengallis at the University of Pennsylvania.
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But P. gingivalis antibodies seem to be more a mark of its passing than protection. People with these antibodies are actually more likely to die in the next decade than those with none, and more likely to get rheumatoid arthritis or have a heart attack or stroke.
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One explanation for why gum disease makes you more likely to get conditions like diabetes and Alzheimer's disease is that it adds to your general "inflammatory load". But P. gingivalis may act more directly too: the bacteria have been detected in inflamed tissue in the brain, aorta, heart, liver, spleen, kidneys, joints and pancreas in mice and, in many cases, humans.
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The bacteria trigger the molecular changes in artery linings that are typical of atherosclerosis, says Genco. We have also found that P. gingivalis creates the lipoproteins thought to trigger atherosclerosis, causes it in pigs and affects arteries much like high fat diets. Lakshmyya Kesavalu at the University of Florida, who has cultured viable P. gingivalis from the atherosclerotic aortas of mice, calls the bacteria "causal".