Right on the heals of the recent publication that shows that beta-amyloid in the brain specifically wraps around HerpesViral particles in order to prevent them from spreading!
Turns out, a great many viruses use low-density-lipoproteins (LDLs, of heart disease fame) to travel around the body, and some even enter our cells by binding to LDL receptors. The APOE gene, associated with alzheimers, binds and transports herpes in the brain and hepatitis viruses in the liver!
If I understand correctly, APOE helps viruses enter neurons. How does APOE4 behave differently than other isoforms in this regard? APOE itself isn't implicated in AD risk, just the APOE4 isoform. And I couldn't tell from your post or a brief lit search, what's the current thinking on the relationship btw APOE and amyloid beta?
I think APOE4 is associated with higher levels of beta amyloid but I don't know why. You mention a study showing beta amyloid traps herpes simplex? Is there a mechanism by which APOE4 drives more beta amyloid aggregation to fight viral infections, but as an unintended result leads to AD?
I've briefly followed some of the recent papers on a viral link to AD but haven't spent much time on it, your post has inspired me to do some more research!
* APO-E isoform, that predicts alzheimers risk, correlates with how much beta amyloid is present in the brain
* It also correlates with how much Herpes Virus is present : https://www.theatlantic.com/science/archive/2018/07/herpes-v...
"Readhead and his colleagues have shown that the more E4 copies someone has, the more HHV–6A and HHV–6B viruses they are likely to have in their brains."
* We also know that if you knock APOE out in a mouse, and then infect it, there is WAY less HSV penetration in the brain (see figure 1, and note that the Y-axis is logarithmic!) : http://jvi.asm.org/content/76/23/12394.full
* Also, APOE isoforms predict whether or not Hepatitis B virus will give you liver cancer. Note that its the E3 genotype that is risky for this, yet its the E4 genotype thats bad for Alzheimers. I take this to be evidence that hepatitis viruses and herpes viruses likely have different binding affinities to these two isoforms.
https://www.ncbi.nlm.nih.gov/pubmed/26823800
* Someone should do some drug screening to eliminate binding between known viral capsids and APOE variants. cough YC Bio
Seems like there is still a lot to learn about the underlying biology, though very provocative findings thus far. I may be misunderstanding but I'd think that if beta amyloid traps herpes, then higher levels of beta amyloid would correlate with lower levels of virus, but it seems that isn't the case?
Would antiviral therapy be more effective that blocking capsid-APOE interaction? It's my understanding that blocking protein protein interactions is challenging, although inhibiting that interaction would be a nice specific way to block the mechanism
It's a fair point, for sure. I'm not so sure how antivirals work but that is probably a more direct pathway to target.
Alternatively, maybe we could train our immune systems to detect when a lipoprotein is transporting malicious cargo. Ideally, if we could realiably distinguish between healthy LDL particles and lipoviral particles, maybe we can find surface epitopes!
I wonder if the reason foam cells are forming in atherosclerosis is because the immune system suspects that they may be infected and carrying payloads.
Certainly seems like an interesting avenue, though I don't know enough to speculate as to whether there are surface epitopes (i dont even know how / where on the LDL the virus binds haha)
The relationship btw HSV, APOE, amyloid beta and AD is certainly intriguing but it seems quite messy at this point. Would imagine there's a lot of work to do to unravel the mechanism before we get to the point where we can think about how best to drug whatever target emerges. Unfortunately mouse models in AD are terrible, so studying the biology may be very tough, although it seems iPSC derived neurons are proving to be decent models.
One thing I like about a lot of HN discussions, as opposed to those on many other sites on the web, is that the people involved have a clear sense of what they do and don't know.
> the people involved have a clear sense of what they do and don't know.
As someone who has, on more than one occasion, called out top-posts that were flat-out wrong, but conformed to HN's biases (I was 100% certain of this because the posts concerned either my area of expertise or my first-hand experiences) - I will disagree with you. The occasions made me wonder about the other HN posts where I'm not an expert.
HN isn't anywhere near as free of the usual human love of gossip, valuing social pecking order over objective facts, etc as it imagines itself to be.
But it's a little like that saying about democracy being "the worst thing ever -- except for everything else". In spite of HNs serious delusions about how objective etc it is, it still remains vastly more objective, rational etc than anything else I've found.
Perhaps the presence of the virus causes the beta amyloid to be produced, or to not be cleared (because it's being used to trap the virus)? I'm no biologist but spitballing on why you might see a direct relationship vs an inverse one.
your question: higher levels of beta amyloid would correlate with lower levels of virus. A metaphor for answering it: if the protection arrives late and the harm is done then the number of protectors can't be used to predict the harm. So to anaylize the correlation one has to know if the effect of the protection happen before it makes the harm or not. That is the speed here is an essential ingredient.
Emperator caveat: I applied abstract reasoning and a metaphor, don't know about the specific details of how beta amyloid is generated.
Hah! I've spent the last several years studying dementia at UCSF actually, and I'm well known in the building for compulsively making puns CONSTANTLY...
I once told my boss, who studies sociopaths, that I have "sociopuny" ... and she facepalmed harder than you can imagine .... This one wasn't intentional. I have a problem.
No. The beta amyloid protein is the primary 'cause' of Alzheimer's. It builds up in the brain and kills neurons and synapses. Tens of billions of dollars have been spent developing drugs to reduce the amount of amyloid in the brain to try and combat Alzheimer's, none of which has led to an effective treatment.
This newer theory is that the cause of the amyloid build-up is an immune response to the herpes virus increasingly infiltrating the brain (as you get older the blood/brain barrier that protects your brain from infections weakens) so a possible treatment is to try and reduce the levels of herpes infection rather than attacking the amyloid protein which is your body's immune response to the herpes infection.
The APOE4 gene is infamous for increasing amyloid production and being a major risk factor for early-onset Alzheimers and so carriers of the gene are often used in studies to see the effect of treatments. (@subcosmos below has a good explanation of what this gene actually does)
The thing about viral infections of the nervous system is that you don't even need to consider the blood brain barrier. Viruses travel backwards through neurons by hijacking microtubule transport networks, and many groups have hypothesized in the literature that it could be getting into the brain by simply infecting a peripheral nerve and traveling up the spinal chord.
Check out Figure 1 in this paper. The model effectively is that HSV infects a great many people in early life, and becomes latent in neurons until old age. Then it suddenly wakes up again and travels to the brain. All it takes is an infected muscle or other tissue, allowing the virus to get into the nerve.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546524/
Some VERY notable statistics mentioned in the paper : "Such studies have revealed endemic infection rates of 31% in children aged 6–14, rising to 49% in adults aged 14–49, and to a high of 80–90% in the population over 65. In one study of 40 autopsied TGs, HSV-1 sequences were amplified from DNA or RNA extracted from 81% of TGs from demented subjects, and 74% of controls"
I blogged about these connections here, for I think that this retrograde transport phenomenon might explain Tau phosphorylation, which is a secondary hallmark of Alzheimer's and other dementias : https://medium.com/@InfinoMe/cholesterol-have-we-shot-the-me...
As its name implies, the blood brain barrier protects the brain from whatever happens to flow in the blood stream. The herpes virus enters the brain by another channel : the peripheral, somatosensory nerve cells whose axon has a T shape. One prong of the top bar goes to the peripheral tissue, and the other prong goes up to the brainstem.
Expanding further: the blood brain barrier is made of cytoplasmic expansions of astrocytes in the central nervous system. The T-shape sensory cells are part of the peripheral nervous system, their axon ends up in the encephalon.
After reading a bit about it, I think the hypothesis is more that Alzheimer’s is the side effect of the body’s own anti-viral systems acting to contain viruses in the brain.
Most of the latest studies are showing a reduction in Alzheimer’s risk after treating patients who have some form of herpes with anti-viral medication.
Correct, as humans evolved, parasitic infections increased. The APOE gene was a method of slowing down or stopping parastic infection to the brain.
"Among the Tsimane as a whole, adults with APOE4 got poorer scores in these tests. But when the team focused on the people with high parasite levels, they saw that the APOE4 carriers had better mental skills, even outperforming APOE3 carriers who were parasite-free."
No.... APOE is a lipoprotein that transports cholesterol, and viruses jump onto it to get into cells. Amyloid-Beta is what seems to be wrapping around the virus particles to block their transit.
Clickbait. The actual finding appears to be this: if you are diagnosed with HSV (herpes simplex virus), your risk of dementia is 2.5 times higher. If however, you get an aggressive antiviral treatment, then the risk is reduced by a factor of 10. I take this to mean that overall, the risk do develop dementia is 2.5/10 = 0.25 times the base risk, so overall, the Alzheimer's risk is only 4 times lower with herpes medication, when compared with the general population.
The relevant quotes from the article:
"The two groups were followed for almost a decade, between 2001 and 2010. In the herpes group, the risk of dementia was over 2.5 times higher than in the control group.
Significantly, the study also revealed that aggressive antiviral treatment reduced the relative risk of dementia by 10 times."
>I take this to mean that overall, the risk do develop dementia is 2.5/10 = 0.25 times the base risk, so overall, the Alzheimer's risk is only 4 times lower with herpes medication, when compared with the general population.
Looking at Wikipedia "According to the World Health Organization 67% of the world population under the age of 50 have HSV-1." and according to the source there 11% have HSV-2. There's probably some good amount of overlap between the two, but we have somewhere between 67 and 78% of the population with some form of herpes. In any case the "general population" is closer to having herpes than not having herpes, so we'd probably arrive at a factor somewhere closer to the 10x.
In most cases that HSV-1 or HSV-2 is dormant, and the person is considered healthy. In this study, the people diagnosed with HSV were considered sick, and in some cases there was a need for the so-called "aggressive antiviral therapy". Now, the study seems quite well conducted, there was a large enough group of people diagnosed with HSV (about 8k people) and a control group of about 25k people who were aged-matched with the first group, but healthy. The two group were followed for 9 years. The main conclusion of the group, that the people with HSV were 2.5 times more likely to develop dementia appears sound, and the power of the experiment probably many times higher than the one necessary to determine statistical significance. The secondary conclusion, that the people "aggressively treated with antivirals" is not as strong, in my opinion. First of all, it's not clear how many in the primary group were subject to that treatment. In an extreme scenario, maybe we are talking only about 50-100, in which case, we may end up with an intended or unintended case of p-hacking. Second, the researchers may have looked for hundreds of things, like how more prone to Alzheimer people who drank more alcohol were, or people who watched too much TV, or other hypotheses. And we may end up again with p-hacking (like in the acne-causing-green-jelly-beans xkcd [1]).
It's clickbait because it only reduces the risk 10x for people with HSV? You really need to evaluate whether your dismissal of this article is helpful in any way.
According to the CDC "54% of persons aged 14 to 49 had HSV-1 infection" 10X for 54% is a big thing.
I was a bit harsh, I admit. That being said, the claim of 10x reduction is definitely a misrepresentation of the research findings. The 10x reduction was not for people who have had HSV-1 infection at some point in their life, it was for people who were diagnosed with an HSV infection at the beginning of the study. Most people who get cold sores don't seek medical attention for that, they just either ride it out, or apply some Abreva that they buy at their local pharmacy. The population that was subject to the study in no way represents 54% of the total population. And then, the population for which the 10x reduction of dementia risk was only a small subpopulation, namely those where an "aggressive antiviral treatment was applied". The actual article quoted ([1]) even stressed that:
"It should be stressed that [...] those treated were the few rare cases severely affected by HSV."
Yes, it's definitely a clickbait article. Nearly all the links within the article go to other pages on the site and the antiviral drug is never specifically named.
I'm guessing it's acyclovir since there's a link to another page on the site in the "Related Coverage" section.
Interesting. Afaik Indians have a very low Alzheimer risk supposely because of curcurma. My friend claimed curcuma also mildens Alzheimer syndromes. This made me Google if curcuma helps against herpes. It does!
Curcumin is one of those compounds that does everything, that's not necessarily a good thing, it is a hit in every assay. When you google compounds and they are antifungal, antidiabetic, antibacterial, anticancer, etc., it isn't a reason to get excited, they have no specificity.
I also hate the term anticancer which gets tossed around a lot. Everything that is toxic to human cells is anticancer which is what chemotherapy does. If we found a substance that wasn't toxic to normal cells and killed cancer cells, we'd have a safe cure for cancer.
Interesting, I wonder if it's linked with thyroid hormones. In culture, that would seem odd, unless it's binding to receptors in a manner that hormones would, or competing with hormones in the growth serum?
I'm beginning to think the thyroid hormones are just a storage mechanism for iodine. The hormones T1, T2, T3, and T4 are actually named for the number of Iodine atoms in the molecule.
Normal curcuma (aka tumeric) only contains about 2.5% of the actual beneficial compound curcumin. But curcumin is indeed amazing, not only does it help with Alzheimer’s, it also has anti-tumor, blood sugar regulating and fat controlling properties.
I saw a rando blog article out there about an old paper studying the components of tumeric. They found it had lots of components each with separate benefits. Unfortunately, the conclusion of the paper was “We should separate all the components so that we can market and sell the same tumeric 10 times!”
Obligatory mention of how piperine (black pepper extract) is necessary for bioavailability.
Black pepper is not necessary. There are extracted forms with patented formulas that have studies showing possibly increased effectiveness compared to black pepper. Theracurmin and Longvida
I'm a mathematical illiterate (no really, and I'm not proud). The headline hurts my head - does "risk 10 times lower" mean that there is one 10th of the risk? so a 1 in 10 chance becomes 1 in 100?
> does "risk 10 times lower" mean that there is one 10th of the risk? so a 1 in 10 chance becomes 1 in 100?
There’s no way to tell from reading the article, you’d need to read the paper. From the article it’s not clear whether it’s the 2.5x increased risk that’s decreased to 1.25x, or whether people on antiviral meds had a lower risk than the control group (0.25x).
From the abstract:
"These authors report that infection with a different herpes virus, herpes simplex virus type 1 (HSV1), leads to a similarly increased risk of later developing SD [Senile Dementia]. Further, when the authors looked at patients treated aggressively with antiherpetic medications at the time, the relative risk of SD was reduced by a factor of 10. [...] antiherpetic medication prevented later SD development in 90% of their study group"
Yes, this is exactly the kind of question I wanted to ask, but was to embarrassed to ask. Thank you! (also suffering from functional maths illiteracy, although I suspect mathematicians would say functional arithmetic illiteracy)
The way I understand it - let's say in a control group 1 in 100 got the disease in a predetermined period of time, 10 times lower risk means that in the group that got the treatment 1 out of 1000 people contracted the disease...
I think it's worth noting that the herpes simplex patients were seeking treatment for severe symptoms and were diagnosed using an antibody test. That seems very unusual.
It wouldn't occur to me to see a doctor over a cold sore and if I did my GP would probably laugh me out of the office.
So maybe (here's me grasping at straws) these people had herpes of a severity completely unlike the millions that buy cold sore cream at the supermarket. Or they had symptoms for the very first time, which would be extremely unsual as well considering they were all over 50.
None of that takes away from the surprising effect of the anti-viral treatment on Alzheimer's, but I think the size of the effect may be related to the unusual severity of these particular herpes outbreaks.
You're being silly. I doubt your doctor would laugh you of the office for requesting an HSV test. Now a days HSV testing combines type 1 & 2 into a single test, so if you ever go in for STD testing you would get tested for both. You don't have to have symptoms to go in for STD testing. You keep everyone safer by being tested regularly despite the lack of symptoms. It's not usual not to have HSV at that age, I'm 30 years old without HSV, and my father who was in his 70s when he died had never contracted the virus either.
Most STD panels do not include HSV tests though, you have to specifically ask for those. Which is IMO a big part why 90% of people contracting HSV have no idea they have it, in addition to simply being asymptomatic.
The typical set doctors look for are HIV, Syphilis, Gonorrhea and something else that escapes me right now.
I didn't mean it quite so literally. The point is that those who do get cold sores regularly would know what it is and wouldn't normally seek treatment or get tested.
So that's why I think the people included in that study must be somewhat atypical.
Antibody tests aren't unusual at all. In terms of why they were tested, some of the articles in the press lately seem to indicate that its in response to a shingles infection. Thats when the chickenpox virus (a herpesvirus) becomes reactivated later in life and specifically infects a nerve.
We all get exposed to chickenpox and most of us are latently harboring it.
I wish I understood all of the herpes isoforms better.
I'm talking about the third study included in the meta study mentioned in the article. That study only includes HSV1 cases, i.e cold sores on the lips. I don't think many of those are ever tested.
Background: HSV1 is commonly known as cold sores. Some people get them in their mouth, or on their lips. Most of the population don't develop any symptoms.
This link between HSV1 and Alzheimer's could be big business. The numbers are wildly divergent, but it sounds like a sizable chunk of the US population has HSV1. I've seen estimates from 20% to 80%. Even if it's the very conservative 20% number, that's still a big market.
The skeptic in me (his name is David) is suspicious of this article precisely because it has the potential to be such a big market. Case in point, there's a link to some HSV1 medicine at the bottom of the article. I wonder if they have an affiliate marketing arrangement with the makers of acyclovir. Tangentially related, I think that this article is on the front page of HN precisely because HSV1 is so widespread. For example, if another article discussed a cure for Alzheimer's, but that article involved some rare condition that does not affect the general population, would that article hit page #1?
With that said, I think our society's lax approach to HSV1 is bizarre. In Sex Ed, I didn't get any education around the fact that kissing people and sharing drinks can spread a virus. After reading quite a few articles on the virus, I got the impression that STD researchers don't really know much about it. I could be wildly incorrect about that last point, I'm not a medical expert. It's just the general impression I got when trying to understand HSV1 from an STD perspective. For example, it's been common wisdom for a long time that, if you have HSV1 (cold sores), then you can't get HSV2 (genital herpes). But the reality seems to be more ambiguous than that. Apparently there was a fairly recent study mentioning that college students who have HSV1 performed oral sex on their partners and transferred HSV1 to the partner's genitals. Or something like that.
Long story short, although I'm skeptical of the business incentives around associating HSV1 with something as scary as Alzheimer's, I welcome more research around understanding HSV1.
>> Long story short, although I'm skeptical of the business incentives around associating HSV1 with something as scary as Alzheimer's, I welcome more research around understanding HSV1.
If this is proven, I imagine almost all the funding for Alzheimers getting diverted to curing HSV1. That would suck for one group of researchers while being a boon to another - as well as half the world population with HSV1. Shingles (adult chickenpox) is also in the herpes family.
I wonder why that hasn't been possible so far. HSV has a huge impact on people's lifestyles in the US. You'd think just about everything would have been attempted by now to address it.
Both types of HSVs supposedly have been with humanity for thousands of years and are mostly asymptomatic or "occasionally unpleasant" as a condition, hence the liberal attitude. When doing an STD screening, in the US at least, your doctor will almost never bother with checking for HSV because 1. it's super prevalent 2. it's not harmful with the exception of people with deeply compromised immune systems
If you read about the history of the virus, supposedly in the past most people figured they'd get it (both variations) sooner or later and didn't particularly care. The stigma, especially of HSV2, allegedly started mid 20th century when acyclovir / zovirax came on the market and the company who created it needed a reason to push people to start using the medication. Nobody wanted to at the time, as HSV wasn't a big deal. However once you call people who have it "dirty" and make it shameful, the sales go up. Now you want to suppress outbreaks and potential spreading at all costs. Similar to AIDS in the 80s, in the US people won't even hug you if news leaks that you have HSV2.
Also amusing that, in the state of CA, receiving HSV (1 or 2) to the genitals from someone of wealth is a great source of compensation. Most of the money you'll receive from the civil case will not be for the medical treatment, it will be because of the "psychological damages and impact to lifestyle" from suddenly becoming a social pariah. Like you said, why this would be suable is not obvious. If 80% of the population has HSV1 and you transmit it to the genitals through oral sex, you're now a 2 year-long (statute of limitations) juicy target for a lawsuit. People of means have lost millions of dollars to this. Everybody having sex becomes a ticking timebomb of legal extortion. Better have your partners sign a consent form.
Perhaps. Or perhaps something you can get a lip balm for at the Walgreens checkout shouldn't cost you millions of dollars.
Also, if you do disclose, you better have in it writing. If there's no evidence of STD disclosure, you can still be sued, and then it's he said vs she said (or pick your permutation of genders) and it's your two reputations competing for who's more trustworthy in court and can have the upper hand. That disclosure can still cost you.
Lawyers will always advise you to have disclosure confirmation in writing (email or paper is best, text might be still ok).
Lip balms do nothing to stop the spread of herpes, nor do they treat the infection. At best they soothe the symptoms. The only OTC medication currently available for cold sores, docosanol, seems to reduce the time it takes an outbreak to heal, but there are questions about both its effectiveness and the biological mechanism by which it works. The anti-viral acyclovir is also used to treat cold sores as well as other forms of HSV, chickenpox, and shingles, but it isn't available OTC.
I'm the poster. I posted it because I wanted to get some of my dot-connecting noticed more (https://medium.com/@InfinoMe/cholesterol-have-we-shot-the-me...), but links to "viral" news content is more click-worthy than the "Show HN" section. As a scientist I've slowly learned hard lessons about how to hook people, and I'm terrible at it.
I don't profit from spreading these ideas. I'm just one of the head data scientists at one of the top dementia labs and I'm tired of longevity-based research taking so friggin long. I also have zero desire to spend a year writing this up only to pay some scientific journal top-dollar so they can paywall it. Putting it up on Medium hopefully saves more lives faster.
I guess I took inspiration from the viruses and snuck my medium post on an innocuous buzz article that is exploding on social media now. Sorry not sorry :p
I'm sorry. I didn't mean to insinuate that you had any shady objectives. From my casual research, I do think that it's important that we develop more understanding around HSV1, especially if there's a link to something as devastating as Alzheimer's.
My only goal was to inject some skepticism and awareness around why this particular article might receive more attention.
Ruth Itzhaki from the University of Manchester notes that “hostility or derision occurred with most of my papers on this topic, and many people simply ignored them.”
It's probably because it's fairly easy to get when your a small child. It's like trying to prevent 6 year olds or 2 year olds from getting a cold from other kids, pretty much neigh impossible.
As someone at hopefully an early enough age who hasn't had any (known? -- since there's never any certainty with it) outbreaks, I'm wondering whether getting such a prescription based on family history at this point would be well advised. It'd also be neat exploring the side effects and seeing if that's a worthy trade, but it sounds like it probably is.
> It'd also be neat exploring the side effects and seeing if that's a worthy trade, but it sounds like it probably is.
If the parent means, 'it sounds like herpes treatment will probably reduce my risk of Alzheimers', it is almost certainly wrong. That is a dangerous conclusion of amateur medical research.
The existence of a couple studies or analyses correlates very poorly with an effective treatment. Look at all the problems of the drug industry and scientists, with all their knowledge and resources, when trying to convert far more proven research into effective treatments. Even when there are effective treatments, they often need to be carefully implemented in terms of drug design, delivery, dosage, etc.
> Biohacking is fun.
That's a sci-fi fantasy. If someone reading this thinks it's "fun", they have no idea what they are talking about and should stop immediately.
23andMe says my risk of being diagnosed with Alzheimer's Disease during my lifetime is 5.59x the average. There are few side effects that would make me hesitate to try something like this to essentially reduce my risk back to average.
The less frequent side effects of aciclovir raw are interesting. Likewise for the prodrug valaciclovir (Valtrex). Some of these sound like they're a result of some level of impact on brain function. I can't help but wonder if there's any relation.
But you're right. The adverse effects here don't seem like much of a deterrent in the face of elevated risk.
> 23andMe says my risk of being diagnosed with Alzheimer's Disease during my lifetime is 5.59x the average.
Be careful with those numbers. I would neither fully trust it nor dismiss it. But these genetic heritage companies have been known to get it wrong, a lot (and very wrong in some cases).
From what I heard those genetic tests are about as accurate as saying "You kinda look European and Europeans have a higher risk of Alzheimer's". Not wrong, but also not a guarantee.
That's not true, 23andme tests the APOE gene (and possibly some others too) which does indeed have a large affect on the risk of developing Alzheimer's.
Although having the good version of APOE doesn't mean you'll never get it, and having the bad version doesn't mean you're guaranteed to get it. The odds do shift quite a bit, though.
>Although having the good version of APOE doesn't mean you'll never get it, and having the bad version doesn't mean you're guaranteed to get it.
Well, having the bad version of the genes certainly doesn't guarantee anything if you don't live long enough too. Only 5% of all people who have the disease have developed symptoms before the age of 65 after all, while average life expectancy of men in the US is at 76. It's very well likely to be predisposed to diseases like these and not develop symptoms because something else killed you before it could show up.
Couple things: First, 23andMe is not medical advice and I don't know how they get away with supplying such advice. Second, all medications incur risk to your body, so taking something like a Herpes medication for years in the hope that it might prevent Alzheimer's is a bit insane. A doctor needs to prescribe it (in the US, anyways) so you would have to have their approval anyways.
My mother has dementia, so this issue hits home for me, btw. But I don't see myself taking some medication in order to try and prevent something I may never end up getting. Herpes medications are not vitamins, if you get what I mean.
Is there any link between high heat and herpes? There was some sauna study showing that people often doing sauna had significantly lower risk of Alzheimer. Maybe herpes is flushed out by excessive heat and sweating or rendered inefficient, even beyond blood-brain barrier?
Just a random guess, but I would hazard that it's not the heat. Going in a properly hot sauna and 'soaking' for 15min or more gets you really sweating, and increases your heart rate. Basically it 'gets your blood pumping', and _probably_ produces an activity profile not too different from mild exercise; and regular exercise has also been shown to consistently lower risk.
Could be, but I'd guess this works at the molecular level, with a set of genes that is turned on/off in hot environments and producing some kind of desired mechanism.
These developments are seriously exciting, and I can't wait for there to be more studies done! If viral links turn out to be causal, then perhaps we have a path towards a cure.
I wonder if there could be a link between HSV and the development of ADHD in early childhood. Or perhaps other mental dysfunction?
Furthermore, I wanted to add that there are a lot of studies that indicate lack of sleep as a risk factor for Alzheimer's. Lack of sleep is also one of the biggest causes of HSV reactivation and outbreak.
I'd be interested in knowing if Lysine supplements have similar effect to acyclovir. The amino acid has a well studied suppressive effect [1, 2].
I'm going to email some of these authors to inquire.
I tried to visit the website and a pop-up appeared trying to get my consent re. tracking. Since I didn't agree, the website denied access displaying this page:
https://anon.healthline.com/
I believe NPR also uses the same tactics. How is this legal under GDPR?
In any case, I just disabled JS and read the article as usual. Moreover, I realized the web (the document part, not the apps part) is actually so much better without JS. Honestly, whenever JS is being used, it's almost exclusively against the user, not to help them. This is from someone who is coding in JS for a living.
I've been using Cookie AutoDelete[1] (Chrome Extension). This way I can happily 'agree' to all of these popups that are the new scourge of the internet, knowing that any Cookies they do set get auto deleted from my browser 15 seconds after I close the offending tab. You have to train it by white-listing the domains you want to keep cookies for (like *.ycombinator.com) but once that's done it just does its job, and I can surf knowing that I'm not being tracked (well, not as heavily as I would be NOT using it).
The argument is that they need to do this particular tracking in order to make their website work.
I believe this is against the GDPR, but need to make a complaint against them.
Arguments why it is against the GDPR, if you can display the text to a googlebot and you will do no change to the structure of the document that is the main purpose of coming to the site then it is not GDPR compliant to deny someone access to the resource based on the argument that they need to do tracking to make the particular resource work.
In other words they are quite clearly lying and should be fined.
There should be some general make GDPR complaint tool where people can go, say where they are from, write what site complaining about, and it shows you similar complaints for you to add yourself to, or to send a new complaint. Then it packs them off to the relevant organizations to handle the complaint. Probably someone has already made this tool but I don't know about it.
It's not compliant at all, but we'll have to wait for these practices to actually get punished (severely, one can only hope) before people will actually get it through their skulls that it's important to respect your users.
Regarding the JS, I have come to the same conclusion. On a large amount of news websites, I have everything blocked (CSS too) with some element hiding rules to remove the strange menus and whatnot. The content you care about on such a site is the text, with maybe one picture. Almost nothing is lost by refusing everything else.
Did the people with the anti-virals take them immediately and upon getting infected? Or did they just have to take them at some point post-infection? Couldn't really tell from the article/not sure how the biology works.
It’s not clear to me, either. Here’s my interpretation, based off the abstract:
> These authors report that infection with a different herpes virus, herpes simplex virus type 1 (HSV1), leads to a similarly increased risk of later developing SD. Further, when the authors looked at patients treated aggressively with antiherpetic medications at the time, the relative risk of SD was reduced by a factor of 10. It should be stressed that no investigations were made on subjects already suffering from SD, and that those treated were the few rare cases severely affected by HSV. Nonetheless, antiherpetic medication prevented later SD development in 90% of their study group.
> The latter study — deemed "most important" by Profs. Itzhaki and Lathe — examined 8,362 people aged 50 and above who received a diagnosis of herpes simplex virus (HSV) infection, as well as a control group of 25,086 age-matched healthy people.
Within the HSV1 population, a small amount happened to get aggressive treatment at some point. It’s not clear whether they got treatment at any point in their life, or if they got treatment after the study began (meaning they got treatment at age 50 or later). This minority happened to have much less chance of Alzheimer’s later on in life.
In regards to the timing of the treatment, my guess is that they got treated upon outbreak, since it said that they were severely affected. They would get treatment when they were in the most pain or discomfort.
It sounds like only a small minority of the 8K people in the HSV group got treatment.
Apparently the virus in question is very common, most kids have it. So it could be that Alzheimers indicates some immunodeficiency and that herpes medication compensates for it.
Edit: I must have gotten confused. I was thinking they talked about HHV6/7 as I saw another discussion about that recently https://news.ycombinator.com/item?id=17366591 From another source: "Nearly 100% of humans are exposed to HHV-6 by the age of three"
Edit 2: Although HSV 1 is also apparently very common in adults. 2 out of 3 have it.
There is this other theory, from what I understand, that Altzheimers is due to the tau protein. I am wondering if that is true in some cases, and is due to some sort of similar mechanism to the one the article is talking about. Or maybe tau is getting dragged along when amyloid wraps around HSV particles.
But what this article seems to be indicating is that the drugs need to target the HSV that the amyloid beta is wrapped around, not the amyloid beta itself.
https://www.cell.com/neuron/fulltext/S0896-6273(18)30526-9
Turns out, a great many viruses use low-density-lipoproteins (LDLs, of heart disease fame) to travel around the body, and some even enter our cells by binding to LDL receptors. The APOE gene, associated with alzheimers, binds and transports herpes in the brain and hepatitis viruses in the liver!
https://medium.com/@InfinoMe/cholesterol-have-we-shot-the-me...