We have rarely seen scarier headlines than the ones describing two new studies from Umea University, Sweden, showing that cold sores increase the chance of developing dementia:
“Studies Link Cold Sore Virus to Alzheimer’s Risk” WebMD
“Cold Sores Increase Dementia Risk” Newsmax Health
“Cold Sores may DOUBLE the Risk of Developing Alzheimer’s Disease” Daily Mail
Looking Back at the Research Timeline:
Let’s start with the back story. As long ago as 1974, researchers writing in the British Journal of Psychiatry noted that people with dementia had a greater likelihood of having antibodies to the herpes simplex virus that causes cold sores.
In 1982, Melvyn J. Ball, MD, a pathologist at the Oregon Health and Science University, proposed that herpes simplex virus (HSV) type 1 could be contributing to the brain lesions (plaques and tangles) of Alzheimer dementia (The Canadian Journal of Neurological Sciences). Dr. Ball theorized that the virus “hibernates” in the trigeminal ganglia, a neuronal structure within the brain. In its dormant state, the virus resides within this nerve tissue without seeming to cause mischief. When activated, the virus travels down nerves to the lips and triggers the familiar cold sore lesion.
Dr. Ball suggested that the virus might also travel in another direction, deeper into the brain:
“It is suggested that reactivation of the same dormant viral material travelling centripetally instead might be the cause of the ‘degenerative’ lesions typical both of Alzheimer’s Disease and of the normal aged human brain.”
Dr. Ball Persisted in Studying His Hypothesis:
Most neuroscientists and Alzheimer’s disease researchers ignored Dr. Ball’s hypothesis, but over the last three decades Dr. Ball has tirelessly pursued this idea. In 2006 in the Journal of Alzheimer’s Disease he noted that most research on Alzheimer disease had failed to determine the most important neurological abnormalities of the disease:
“However, during my elusive search, evidence has been slowly gathered that reactivation of latent Herpes simplex virus, traveling from trigeminal ganglia into neighbouring mesial temporal cortex, might best explain the limbic predilection for and earliest site of neurofibrillary tangle formation.”
Other investigators discovered that the herpes virus could be detected within the brain lesions of Alzheimer disease patients (Journal of Pathology, Jan. 2009):
“We discovered a striking localization of herpes simplex virus type 1 DNA within plaques: in Alzheimer’s disease brains, 90% of the plaques contained the viral DNA and 72% of the DNA was associated with plaques…”
The Latest Research on the HSV Type 1 and Alzheimer’s Disease
Although funding agencies and mainstream researchers pretty much dismissed this line of research, some epidemiologists began digging deeper. The Swedes in particular noted that there seemed to be an increased risk of Alzheimer disease after herpes simplex virus reactivation (Alzheimer’s & Dementia, June, 2015). Researchers tracked 3,432 subjects for over 11 years. They found that reactivated herpes infections were linked to a doubling of the risk for Alzheimer disease compared to individuals who were not infected.
The latest headline-making research comes from Umea University in Umea, Sweden (Alzheimer’s & Dementia, June, 2015). These investigators identified 360 individuals with a diagnosis of Alzheimer’s disease and 360 cases of dementia-free controls. All patients had given blood long before (on average 9.6 years earlier), and it had been stored in a medical “Biobank.” The scientists analyzed the blood for antibodies to herpes simplex virus type 1. The presence of the antibodies was associated with a two-fold increased risk for dementia:
“Among persons with a follow-up time of 6.6 years or more, HSV infection was significantly associated with AD [Alzheimer’s disease]. This may indicate a role of HSV in early AD development…”
“It has been hypothesized that immune system weakening in older individuals might contribute to HSV reactivation and spread to the brain, which then may explain the connection seen among persons older than 60 years in this study whereas causes of AD other than HSV might be relatively more common among those younger than 60 years of age…”
“Converging evidence now supports a relationship between HSV and the early development of at least some cases of AD.”
What’s the Bottom Line and What to Do?
First, you will likely read that researchers in the Alzheimer disease mainstream reject this research. I characterize this as the “not invented here” phenomenon. Funding agencies have spent billions of dollars pursuing other avenues, but so far they have proven almost worthless. The idea that they may have overlooked this approach for nearly 40 years will be hard to swallow.
Dr. Hugo Lovheim, the lead author of this research, has been quoted:
“The identification of a treatable cause [herpes simplex] of the most common dementia disorder is a breakthrough…Whether treatment of herpes infection with antiviral drugs may slow the Alzheimer’s progression is not known, but is certainly worth investigating in clinical studies.”
“Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer’s disease.”
Many people may not want to wait years and years for such clinical trials to be funded and for the results to be published. As Dr. Lovheim noted, there are effective prescription antiviral medications against herpes simplex virus type 1. They include acyclovir (Zovirax), famiclovir (Famvir), penciclovir (Denavir) and valacyclovir (Valtrex). Such drugs are surprisingly effective against herpes viruses and reasonably safe. They do require a prescription. And clearly, such drugs have not yet been tested for preventing or treating Alzheimer disease. Consequently, we simply cannot tell whether they will be able to inhibit virus that may already have entered the brain.
What About L-Lysine?
You might want to think about a simple over-the-counter approach. Again, we have no evidence that this will help, but the risks are low. For decades, we have been hearing from readers of our syndicated newspaper column, listeners to our syndicated radio show and visitors to this website that L-lysine works against a number of herpes infections.
One reader wrote about using L-lysine for shingles, a painful rash associate with a different herpes virus, herpes zoster:
“In a recent column you answered a question about L-lysine and shingles. I have been taking L-lysine for various forms of herpes for over 20 years, and it has kept me virtually outbreak-free.
“It is also important to avoid nuts and chocolate. Dietary restraint together with L-lysine have worked better for me than acyclovir, which I took for a year as part of a study at the University of Rochester.
“I have read about both nut avoidance and L-lysine, but often when I speak to physicians about it they are not aware of it. A lot of pain and discomfort could be avoided if they were.”
JS agrees that L-lysine can be helpful:
“I too am a firm believer in L-Lysine. At the very first tingle I will take anywhere from 2 to 5 1000 mg pills. If I know I will have lots of sun exposure, or that I am stressed out or run down, I will take a couple in the morning and a couple before sleep preemptively.
“I keep lysine in my glove box, in my day bag, golf bag, gym bag, and at home. It is so helpful that I literally will not go anywhere without it, so that I can take it immediately if i feel a cold sore coming on, or if I am consciously stressed, tired, sick, etc. I’ve also learned to avoid caffeine, chocolate, most nuts, and other foods that are rich in arginine.
“There are tons of articles explaining how food and diet can assist in preventing and limiting the extent of breakouts. With this current approach, I usually do not get any sores that are visible, and am able to keep them in check.”
Sharon got advice on L-lysine from her dentist:
“My dentist told me many years ago to use Lysine as soon my lip starts to sting. I take three Lysine immediately and the sore will not go on and develop. The second and third days, I take three more. No blisters for me.”
Would you like to read more about controlling recurrent cold sores with L-lysine? Here is a link to some fascinating stories. You’ll find other commentary about whether L-lysine might help protect our brains from Alzheimer disease here.
No one knows whether antiviral drugs or L-lysine will prevent or help Alzheimer disease. But anything that can keep the virus from reactivating is probably worth a try. Since L-lysine seems surprisingly safe, it might be an experiment worth considering. Let us know your thoughts and experience with herpes simplex type 1 in the comment section below.
Could Alzheimer Plaques Be Protecting the Brain?
More recent research demonstrates that two of the beta amyloid compounds that form plaques in the brains of people with Alzheimer disease have antiviral activity (Bourgade et al, Biogerontology, Feb. 2015). In cell cultures, these beta-amyloid peptides inhibit herpes simplex virus growth. The investigators conclude,
“Overproduction of Aβ peptide to protect against latent herpes viruses and eventually against other infections, may contribute to amyloid plaque formation, and partially explain why brain infections play a pathogenic role in the progression of the sporadic form of AD.”
We don’t know if Dr. Ball is still alive, and if so, whether he feels vindicated. But increasingly, other neuroscientists are coming around to his view. One review published last year referred to “a compelling argument for a pathogen-based etiology of AD” [Alzheimer Disease] (McNamara & Murray, Current Alzheimer Research, 2016).
Revised 5/25/17