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Gum disease–causing bacteria could spur Alzheimer’s (sciencemag.org)
116 points by sohkamyung 26 days ago | hide | past | web | favorite | 48 comments

I don't know what the situation is in the US but, here in the UK, we are bombarded with ads for products that claim to prevent or treat gum disease.

Of course, since I suffered from gum disease in my youth, I know the only way to eradicate it is mechanically, in the dentist's chair. The process removes a layer of gum tissue which will not grow back which then means you are much more susceptible to the problem recurring. Extensive oral hygiene thus becomes a way of life.

Regardless of any link with alzheimer's, I would urge anyone to avoid having to go through this and, if you have bleeding gums, go and see a dental professional as soon as possible - expensive mouthwash may mask the problem for a while but it certainly won't cure it.

A sonic toothbrush will physically kill much of the bacteria in your gums. It also accelerates the sloughing off of skin lining your mouth that those critters live in and feed on. I get infections when I forget mine and revert back to a traditional brush.

I got a Sonicare and was very disappointed. Didn't seem to help me.

Do you have a brand/model recommendation?

Sonicare is fine. Just get the cheapest model. You don't need any of the gimmicky features of the other models.

Sonicare is excellent. I have a base model from ten years ago that I still use and my teeth always get a good review from the dentist.

Flossing is the best preventative solution. Daily flossing with 2x/day brushing with a Sonicare and good mouthwash have made my dental visits much more pleasant.

Make flossing even more painless and easy with a waterpik.

Using the waterpik for the first time, it was like flossing for the first time in a while. I could taste nastiness that has been brewing in between my teeth. The crevasses are now effortlessly cleaned out.

I love my waterpik but I hear it's still important to floss with string to supplement. I guess you get a slightly different type of clean.

be careful about removing the enamel.

You're not going to be removing enamel using water at pressures like these.

Just avoid PFAS in your dental floss to reduce cancer risk: https://www.ajc.com/news/health-med-fit-science/dental-floss...

Ask HN: Preventative, or Preventive?

I remember the hysteria regarding aluminum cookware when higher levels of aluminum were discovered in the brains of those who had had Alzheimer's disease. Then it turned out that the aluminum content may simply have been an effect of the disease, not a cause (and aluminum cookware was once again declared, for the most part, safe). Now, with this new finding, I wonder if part of the Alzheimer's pathogenesis isn't a leaky brain-blood barrier or something similar that allows substances that shouldn't be in the brain through?

Some labs (including the kaufer lab at Berkeley) are investigating the leaky blood brain barrier as a cause of Alzheimer's

Sadly, HN doesn't have a very good way of connecting prior threads together, but potentially of interest, previous discussions of infection-cause theories of Alzheimers:

3mo ago: Some studies show an association between the herpes virus and Alzheimer’s https://news.ycombinator.com/item?id=18265115

6mo ago: Alzheimer's risk 10 times lower with herpes medication https://news.ycombinator.com/item?id=17540094

6mo ago: Link Between Alzheimer’s and Herpes https://news.ycombinator.com/item?id=17521994

7mo ago: Researchers Find Herpes Viruses in Brains Marked by Alzheimer's Disease https://news.ycombinator.com/item?id=17366591

One thing worth noting is that some specialists believe that Alzheimer's has multiple subtypes, eg: https://www.foundmyfitness.com/episodes/dale-bredesen

"1. The inflammatory subtype of Alzheimer’s disease.

A type characterized by systemic inflammation, reflected in such laboratory results as a high hs-CRP (high-sensitivity C-reactive protein), low albumin:globulin ratio, and high cytokine levels such as interleukin-1 and interleukin-6.

2. The atrophic subtype of Alzheimer's disease — a reduction in support for synaptogenesis.

A type characterized by an atrophic profile, with reduced support from molecules such as estradiol, progesterone, brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), testosterone, insulin, and vitamin D, often accompanied by increased homocysteine and insulin resistance, the last feature of which Dr. Bredesen refers to as type 1.5 or glycotoxicity.

3. The cortical subtype of Alzheimer's disease — an environmental toxin-related type associated with chronic Inflammatory response syndrome (CIRS) that presents with more general cerebral atrophy and frontal-temporal-parietal abnormalities, resulting in an emphasis on executive deficits, rather than the more amnestic quality of hippocampal impairment."

There's also plenty linking (and potentially reversing) Alzheimers related to insulin resistance:

Insulin Resistance and Alzheimer’s Disease: Bioenergetic Linkages (2017) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5671587/

Reversal of cognitive decline in Alzheimer's disease (2016) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4931830/

Effects of ketone bodies in Alzheimer's disease in relation to neural hypometabolism, β‐amyloid toxicity, and astrocyte function (2015) https://onlinelibrary.wiley.com/doi/full/10.1111/jnc.13107

Insulin resistance and Alzheimer’s disease (2009) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600067/

Awesome thank you.

Now we have two promising candidates for the cause of Alzheimer's -- gingivalis, and herpes-family viruses.

That doesn't mean one is right and the other wrong. Maybe herpes gets in first and lets gingivalis in, or vice versa, or some other, more interesting interaction.

What's tragic is that effectively none of the present researchers are virologists or bacteriologists. As consequences, (1) progress studying and generating a useful clinical response will be radically slowed by resistance from the old guard to the threat to their livelihood, and (2) they will all need to find something else to do, because you can't pick up those specializations overnight.

The herpes connection was noted twenty years ago, but is only now getting traction. If it's right, then almost everybody who died of AS since then was killed by the structural resistance to the idea.

The best way to accelerate progress, now, would be to find another urgent health problem that seems to need the skillset that had previously been brought to bear on AS, so they jump ship and get the hell out of the way.

Certainly important for people to understand/be aware of the process someone such as Robert Moir (one scientist mentioned in the article) must navigate


How do you explain the rate of Alzheimer’s being higher in developed countries where oral care is statistically better?

Life expectancy. When the life expectancy is 50-70 years, there is less Alzheimer compared to countries where it's above 80.

Also, better diagnostics.

In many developing countries with low exposure to Western-style diet and lifestyle the oral health is way better than in the West. In a sense the advanced oral care indicates that something is wrong with the teeth.

Under diagnosis. When people in developed countries start displaying dementia symptoms they're more likely to visit a doctor and receive a formal diagnosis of Alzheimer's Disease.

More access (frequency and volume) to foods high in sugar.

Time and time again we see epidemiological studies posting findings that are clearly best explained by correlation than causation. For example, think of the people you've met with the worst teeth. They will almost certainly, on average, have worse overall health, lower socioeconomic status, lower intelligence, lower paid jobs, lower educational attainment, worse diet and so on. Surely these are just as likely, if not more, to be on the causal pathway for Alzheimers? And that's completely ignoring the fact that people with early Alzheimers which has not been diagnosed are much less likely to remember to keep up with oral hygiene rules, so the risk for reverse causation is HUGE.

Now I know you're going to argue that the epidemiological studies account for this using multiple regression and so on, but the fact is time and time again it has been demonstrated that this just cannot be done. Indeed, vitamin D in practically every epidemiological study to date has shown to reduce the risk of cancer, cardiovascular mortality, tuberculosis infect. And yet, just this month, someone FINALLY did a randomised trial of vitamin D in TWENTY SIX THOUSAND people (the VITAL trial) and found it made no difference at all (in fact, cardiovascular death was slightly but non-significantly more common in the vitamin D group).

Unfortunately, people's careers and publications rely on this stuff, so it'll keep coming. Please remain skeptical, hacker news.

> the causal pathway

The article very clearly distinguishes between the cause and a cause. "Alzheimer’s is a complex disorder, not a one stop shop" and so on.

> best explained by correlation than causation

They did more than that. They also found gingipains in the brains of patients. Those had to come specifically from P.gingivalis infection, not the other factors you mention. They identified a plausible causal pathway involving tau and amyloid beta, and they induced their production by introducing P.gingivalis in mice. That's a lot more than merely equating correlation with causation.

Skepticism is good. Ignoring what has been presented is not skepticism, and neither is jumping from correlation to non-causation. That's just contrarianism.

Mice don’t get Alzheimer’s. Inducing plaques is not the same thing as giving mice Alzheimer’s.

No, it's not, but it proves that the link between gingipains and plaque is reproducible. That's part of the causative chain, so it still refutes the glib contrarianism to which I was replying.

I agree with some of your comment but I wanted to reply to one part I take issue with.

> Please remain skeptical, hacker news.

Sure, but please don't be the binary-kind of skeptic, the kind that believes that things are either causative or not causative and that everything in between is just "correlated" and that we somehow need to find out what the real causative thing is, and until then, we will not accept anything, until we have the smoking gun. That somehow we have must keep living in denial and ignore growing mountains of evidence because it's "murky" until it finally clicks over into "proven" and we change our minds.

I don't think this article is as bullish on the idea as you might imagine. If anything, such articles should stretch our imagination as to what could be causing and contributing to Alzheimer's and other brain diseases. Like heart disease, it is likely that Alzheimer's as we understand it has a number of symptoms and causative factors that might be affected by thousands of variables. Just discounting whole lines of research this way is binary thinking.

Kudos on those who did the Vitamin D study. But if we're constantly seeking a shocking repudiation or proof of every possible idea, the kind of slam-dunk that goes up in lights and earns everyone backslaps and Nobel prizes, we're already on the wrong mental track, IMHO.

And all of this is not to give license to true believers who catch on an idea based on the thinnest of evidence. IMO skepticism and conspiracy-theory-mindedness are on opposite ends of the same spectrum, and both are close-minded in fairly damaging ways.

This particular article refers to study that claims "evidence for causation" from experiments with mice and initial tests with human volunteers. They were given common antibiotic and it improved cognition. This is of course just exploratory testing with humans, to see if bigger experiments are justified but it's promising.

Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors http://advances.sciencemag.org/content/5/1/eaau3333

> Please remain skeptical, hacker news.

But please, hacker news, don't poison comments with generic "causation is not correlation" tourette. Read the article first and make specific comments.

> > Please remain skeptical, hacker news. > > But please, hacker news, don't poison comments with generic "causation is not correlation" tourette. Read the article first and make specific comments.

Or in a nutshell: Hacker News, please apply scientific principles.

So basically this says don’t get inflamations near your head?

or, perhaps, don't get the thing that causes the inflammation near your head?


The much simpler explanation is they're both caused by carbohydrates and especially sugar.

Already the first paragraph points out the actual bacteria causing gum disease is present in the brain of Alzheimer patients. How strong their evidence is, is another matter, but they appear to be proposing an actual causal chain that involves these bacteria, not just correlation. They're also proposing to treat it with drugs specifically targeting these bacteria.

> proposing to treat it with drugs specifically targeting these bacteria

Which does look initially promising:

> Giving the mice a drug that binds gingipains cleared P. gingivalis from the brain better than a common antibiotic, and it reduced the β-amyloid production and resulting neurodegeneration. [...] In initial tests with human volunteers, a similar drug seemed safe and showed signs of improving cognition in nine participants with Alzheimer’s, the company says.

Would that drug also treat gingavitius?

Simpler, yes, but so is the cosmic-ray theory. Do you have any actual evidence? The causal relationship seems even less established than that in the OP.

Also, did you miss the distinction between a cause and the cause? It's not a zero-sum game.

I have an even simpler explanation : They're both caused by eating.

More seriously, yes, I agree that sugar is nasty, but it's a bit too simple to blame it as the sole factor for all possible diseases that have a mechanism of action that hasn't been clearly identified.

It's not as simplistic a claim as you might be interpreting it as: another somewhat-well-supported theory of Alzheimer's is that it's essentially diabetes of the brain. [1] The GP's comment re: carbs and sugar was presumably referencing that theory.

[1] https://www.alzheimers.net/diabetes-of-the-brain/

Exactly, and put better than I could.

It appears that the simplicity of the explanation is itself a problem. Surely - all these chronic diseases can't be that simply explained? Dr. Wahls essentially claims carbs are the root cause of MS, which she cured in herself (with the corollary that carbs eliminate other nutrition). Dr. Fung claims it's the root cause of diabetes. Prof Seyfried claims it's the root cause of cancer. It surely can't be that simple?

Reading all their work, and others, I'm struck that it's very much a five-whys scenario[1].

Also there are two points wrapped up in the original response. One is about the cause, but there's a bigger issue about the avoidance of the problem in a first place. If someone never eats refined carbs and therefor avoids the root cause, why would they care about the details of the cause? We care about the details insomuch as we would like to treat the disease, but today we can't do that. On the other hand we do know with a lot of certainty that eating well, fasting and exercising are good for us and avoid the problems in the first place. For some reason, that doesn't matter as much.

The downside with treating the disease is that you also enable it, like how we "treat" T2 diabetes by essentially just giving you more diabetes via insulin shots.

[1] - https://stevecoast.com/2015/03/27/the-world-will-only-get-we...

Occam's razor

Interesting side note, when I did a 4-day water fast, I noticed around day 2 that my morning breath was virtually gone.

I figured there's always enough bacteria in the mouth to cause morning breath, food consumption or not, but there is definitely an exacerbation of mouth bacteria from food consumption.

When did your ketosis breath disappear?

IIRC, within hours of breaking fast. At most a day. Unless one still stays at significant enough caloric deficit.

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