A new hypothesis is proposed in this entry, namely: that sporadic Alzheimer's Disease (AD) and Mild Cognitive Impairment (MCI) are caused by a toxin acquired through unprotected oral sex. The most likely source of toxin is urea in urine - the most likely toxin is ammonia.
Carried very slowly by oral bacteria to and throughout the brain, the toxin triggers a brain "infection" which results in AD. Hence, according to this hypothesis, AD is not a "true" dementia, caused by growing old, but a form of STI. If AD was caused by ageing alone, the Japanese should have just about the highest prevalence in the world. Currently, Japan has only about half the prevalence of AD seen in the US and Europe.
Key evidence supporting this claim:
1. Oral bacteria, specifically treponemes, have been found post-mortem in brain samples and trigeminal nerves from 90%+ of AD patients.
2. Cultures and societies, around the world, where AD has low prevalence such as: Inuit in Canada, Amish in the US, all of Sub-Saharan Africa, rural villages of India, Filipinos in California and (possibly) Rastafarians in Jamaica - have all, until quite recently, largely abstained from oral sex.
3. In cultures and societies where AD prevalence is high, oral sex increasingly became "the norm" during the second half of the twentieth century - notably, in the U.S. and Europe.
*NB In places where AD prevalence lies between these extremes, such as Japan, the prevalence of oral sex also appears to lie mid-way between the extremes.
Any epidemiologist will confirm that unprotected oral sex is not safe. The claim that unprotected oral sex causes sporadic AD is therefore not unrealistic, indeed, it explains many features of the disease. It also suggests a possible cure, through the use of special antibiotics designed to kill treponemes.
Potentially important new thinking about AD is suggested by two questions:
1. Does unprotected oral sex transfer a toxin, in urine, to oral bacteria (spirochetes such as Treponema Denticola) that migrate very slowly along the trigeminal nerves (V2 & V3), from mouth to brain, initially triggering Mild Cognitive Impairment and eventually "full-blown" AD?
It is noteworthy that parts of the brain most seriously damaged by AD, are located near the basal region of the brain, relatively close to the end of the trigeminal nerve.
2. Might special antibiotics offer preventive treatment and cure?
The motivation for this article is to draw attention to a new line of thinking about AD, which offers the prospect of a simple and inexpensive cure. However, it is important to stress that the "theory" presented here is HYPOTHETICAL and has not been subject to clinical test or peer review.
The new hypothesis asserts that the current epidemic of sporadic AD results from a behaviour-driven infection, initiated through unprotected oral sex (oral sex without use of a barrier eg without condom or dental dam).
*NB In this article, "AD" means "sporadic Alzheimer's Disease", as distinct from familial Alzheimer's Disease, the inherited (genetic) form of the illness, which accounts for no more than about 5% of cases.
It is important to be clear about the difference between "risk" and "cause". A host of risk factors have been suggested but, in common with many other neurological diseases, the underlying cause of AD remains a mystery - even after many years of intensive research. It is precisely because the underlying cause is unknown, that an effective treatment and cure has yet to be found.
SOME KEY POINTS
1. AD - an incurable and terminal neurodegenerative condition - mainly affects people aged 65+ but, according to the thesis here, it does not result directly from the ageing process. There are signs that the precursor of AD, MCI, appears in people as young as fifty. In other words, the process leading to full AD starts many years before the obvious signs of dementia appear.
There are more than 100 types of dementia of which AD is by far the commonmest, accounting for about 60-70% of all recorded cases. As many as 40-50% of those in the US & Europe aged 85+ have AD symptoms. As life expectancy continues to rise, there will be a huge increase in the number of cases. Estimates indicate that there are currently about 25 million sufferers world-wide - a figure that is forecast to quadruple by 2050. As to the cost of treatment and care, it is predicted that in the US alone it will eventually cripple the medicare system, and seriously harm the economy. One researcher in the US has called the scale of the problem "frightening".
2. According to the hypothesis, AD is caused by a sub-microscopic pathogen - probably a molecular toxin or toxins - contracted mainly, though perhaps not exclusively, through unprotected oral sex. The much discussed senile plaques, often found post-mortem in the brains of AD patients, are not the underlying cause of the disease - an assertion supported by the fact that some non-AD brains have been found that were full of plaques. Moreover, in summer 2008 a research group in the UK at Southampton University published findings, from a five-year study, which showed that removal of the plaques made no difference to the progress of the disease - in some cases the AD even accelerated!
3. The prevalence of oral sex (cunnilingus & fellatio) seems to have increased steadily, during the second half of the twentieth century, from about 40-50% of married couples in the US in the 1940s (according to Kinsey's Reports) to about 70-90% of sexually active individuals in the UK by 2000 (Ref 2). Oral sex is as old as humanity, but during the last century it became more widespread in the West as "Victorian morality", under whose strictures the subject was taboo, gradually relaxed. It seems that oral sex was "re-discovered" in the US in the 1920s (possibly associated with Hollywood and the "casting couch") but probably became much more widespread with the 'invisible' sexual revolution that took place during WWII, when oral sex would have been a form of contraception.
The US currently has about 5.3 million AD sufferers - roughly eleven times the official number in the UK, yet the population of the US is only about five times larger than the UK. This anomaly implies that the prevalence of AD in the US is twice that in the UK. However, diagnosis might be better in the US than the UK - which would mean that, in reality, AD is about twice as common in the UK as is currently believed about (450 thousand cases). Indeed, figures for Australia (about 250 thousand cases) suggest that the true number of cases in the UK is more likely to be around 700-900 thousand - consistent with US and AU figures.
When the disease was identified by Dr Alzheimer, in 1906, it was thought to be rare; however, a huge increase in prevalence has taken place since the 1970s, when there were only a few hundred-thousand cases in the US and when few outside the medical profession had even heard of the disease. AD is now by far the commonest of all serious neurological diseases. The rate of increase is one of the more alarming statistics, with about 100,000 new cases each year out of 11 million people aged 65+ in the UK. A doubling of AD cases has occured in the US within the last decade alone. There are an estimated 5 million new cases each year world-wide, though it is probable that many cases are undiagnosed.
4. The hypothesis implies that the toxin that triggers AD is universal - ie found in men and women everywhere - and is therefore most likely to be a component of urine. The likely toxin is urea. The reason for identifying urea is that one of the consequences of kidney failure is uremic poisoning - a condition which affects the brain. Uremic poisoning presents dementia symptoms, very similar to AD, which include: distortions of memory, thinking, speech, perception and emotional stability. It is posiible that in the brain, urea undergoes a catalytic reaction, decomposing mainly into ammonia. Ammonia is highly toxic in living systems and it is known to be especially dangerous inside the brain. Indeed, ammonia very seriously interferes with fundamental energy proccesses, especially in the base of the brain. If this hypothesis is correct, ammonia from "decomposed" urea is the toxin that causes sporadic AD.
Each day, an adult excretes about 0.5-1 mole of urea in urine. Hence, in one drop of urine the size of a pinhead (about 1 cubic mm), there are of the order 100,000 trillion molecules of urea. The brain contains about 100,000 million cells, so there are millions of urea molecules for every brain cell, in one tiny drop of urine. In the mouth, there might be millions of treponema bacteria, the number will vary greatly from one person to another. Nevertheless, the number of toxic molecules available for bacteria to transport to the brain, from just one drop of urine, is huge.
5. Bacteria "infected" with toxin enter the bloodstream through lesions in the mouth (tiny cuts, ulcers, abrasions etc) and find their way into the complex system of nerves (trigeminal nerves, V2 & V3) in and around the oral cavity. The toxin is transported very slowly, by the migrating treponemes, along the trigeminal nerves into the brainstem - a path that evades the blood-brain barrier (which normally prevents toxins entering the brain).
6. The key evidence that this transport mechanism exists (Ref 1) is that treponema denticola has been found, post-mortem, in 90% (18/20) of a sample of AD patients' brains** - compared with just 30% in a sample of non-AD brains. The latter figure, which is relatively high, implies that the bacteria are not themselves the fundamental cause of AD - they simply act as a "Trojan Horse" that carrys toxins into the brain. If treponema denticola alone were responsible for AD, everyone with the bacterium in the brain should have disease symptoms. It seems that, in the control sample in question, 30% did not. Moreover, the migration of treponema denticola from mouth to brain, via the trigeminal nerves, is a process that has always taken place in humans. So, the question is why wasn't AD a relatively common disease long before the 1970s, if treponemes alone are responsible?
*Treponema denticola is associated with gingivitis. It is estimated, by Harvard Medical School, that about 80% of the adult population is infected with the bacterium at some stage. Indeed, gum disease is just about the most common infection in the world. People with gum disease and those with missing teeth, are thought to have an enhanced risk of AD. It is noteworthy that although the Amish community in the US are known to have poor oral hygeine, resulting in an abundance of oral bacteria, they have low prevalence of AD. This again suggests that oral treponema are not, in themselves, the cause of AD.
**The "missing" 5% might be accounted for by familial AD. If so, it might mean that 100% of sporadic AD brains in the sample contained treponema denticola.
7. Entering the base of the brain from the root of the trigeminal nerve, after a journey lasting (perhaps?) 10-20 years and spanning many generations of bacteria, the toxin slowly builds up and starts to trigger a processes that results in the death of nerve cells. Perhaps acting as a catalyst, the toxin might initiate a cascade of secondary reactions which result in inflamation. In fact, brain inflamation is strongly associated with AD.
It is significant that the limbic system is located close to the root of the trigeminal nerve, and that functional impairments of the limbic system - which include short-term memory loss (hippocampus), impaired sense of smell (olfactory bulbs), reduced metabolism (hypothalamus) and loss of emotional stability (amygdala) - are associated with symptoms of AD. It is thought that loss of balance and problems with gait are early symptoms of AD - this might correspond with damage to pons, where the bacteria first enter the brainstem. The pineal gland, which controls sleep patterns, is also likely to be infected early in the disease process. Disturbed sleep pattern is an early symptom of AD.
8. Treponema migrate very slowly along nerves and inside brain tissue, so significant cognitive decline only appears many years after the initial infection, though very subtle signs of the disease are probably manifest long before the main symptoms appear. Once the bacteria leave the root of the trigeminal nerve, they migrate throughout the brain, eventually affecting every part; however, certain parts of the brain are more badly affected than others, in particular, regions close to the base of the brain.
9. AD takes a very long time to present obvious symptoms, partly because the bacteria move very slowly through nerve tissue, partly because it probably takes a long time to acquire sufficient toxin to trigger the disease and partly (perhaps) because the immune system keeps the infection under control. If the immune system is weakened - through ageing or illness - the disease is able to manifest itself in observable symptoms. Perhaps those with strong immune systems have less chance of developing the disease early, only presenting observable symptoms when very old. If so, those who remain fit and healthy probably tend to keep the infection at bay longer. It is also possible that those with good circulation, in the brain, will clean out toxins more effectively than those with poor circulation. This will help to stave off the disease.
10. None of the drugs developed so far has proven an effective treatment. The simplest explanation for the lack of efficacy is that the drugs have only dealt with symptoms of AD, not the underlying cause. This hypothesis, in identifying the underlying cause, suggests a preventive treatment and cure. By targeting powerful antibiotics on treponema in the mouth, jaw, trigeminal nerves and brain, it should be possible to kill the bacteria in situ, thereby halting the progress of the toxin and so arrest the development of symptoms. IF the hypothesis is correct, special ANTIBIOTICS administered early enough could provide a preventive treatment and cure.
The sudden, rapid increase in the number of AD cases, from a much lower prevalence prior to the 1980s, is one of the more puzzling aspects of the disease. The number of cases in the US has doubled in the last decade alone. Good circumstantial evidence implies that the AD epidemic is not a "natural" phenomenon and that the huge escalation in the number of cases, in the last thirty years especially, has been driven by human behaviour. This is suggested by comparison with the following behaviour-driven "epidemics": lung cancer and heavy smoking; cirrhosis of the liver and excessive alcohol consumption; skin cancer and unprotected sun-bathing; heart disease and high-colesterol diet; type II diabetes and sugar-rich diets; hypertension and salt in diet.
As with these examples, the number of AD cases has been increasing relentlessly for many years - with no sign of a slow-down or peak. It seems, therefore, that AD might be another example of a behaviour-driven epidemic. It is noteworthy that when Japanese settled in the US, before WWII, the prevalence of AD amongst them increased significantly over a number of years. Indeed, the prevalence of AD among Japanese Americans is about twice that among the native population in Japan. This suggests that sporadic AD is not driven by genetics nor is it driven by ageing itself - since the Japanese have just about the highest life expectancy in the world, yet significantly less AD prevalence than the US and Europe.
1. What sustained behaviour has been driving the AD epidemic?
2. Why did the epidemic appear to begin in the 1970s?
3. If AD is driven purely by ageing, why is prevalence in the "young" age-range (50-70) also showing signs of increase?
4. Why does AD seem to be more prevalent in urban communities than in rural ones?
The fact that the AD epidemic seems to have started in the 1970s suggests that the generation born around 1900 were the first, after the end of the Victorian era, to engage in oral sex in significant numbers. They would have been sexually experienced, mature people in the 1930s and during WWII. Thirty to forty years later, they became the first generation in modern times in which the number of AD cases began to grow significantly. This suggests an AD "lead-in" time ranging from about thirty to fifty years.
AD seems to be more prevalent in urban communities than rural ones. This might be because towns and cities tend to be more sexually dynamic and "adventurous" than rural communities. It is likely that the more oral sex partners an individual has, the greater the chance of developing AD. In the past, people in urban communities probably tended to have more oral sex partners than those living in rural areas.
Question 4. raises a secondary issue, which is the problem of detection and diagnosis. It is currently thought that only about 1 person in 1000 has AD at the age of 65 - the question is: how can we be sure? It is possible that many people aged 65 might have very subtle symptoms which, at present, cannot be detected - or which aren't currently recognised as precursors of AD. It is possible that far more than 1 person in 1000 has subtle, early symptoms of AD in their sixties, fifties or even late forties. If so, it would provide further evidence that AD does not suddenly "switch on" in old age, but that it is a disease which develops very slowly, over many years - decades, prior to the on-set of obvious clinical symptoms.
Conditions necessary for the transfer of toxin(s) to the brain of the person giving oral sex are:
1. Unprotected oral sex (no barrier - condom or dental dam).
2. Toxin in the genital region of the individual receiving oral sex - probably a toxin in urine.
3. Treponema denticola present in the mouth of the individual giving oral sex.
4. Lesions in the mouth of the individual giving oral sex.
These conditions are widespread in the general population, so transfer of the AD pathogen from genitals to brain is likely to be very common. If those conditions are met, the main factors which determine the probability of the individual developing AD symptoms are:
1. Number of occasions when unprotected oral sex took place
2. Time spent engaged in oral sex
3. Total dose of toxin received
4. Age at which oral sex started
5. Genetic susceptibility
6. Number of oral sex partners*
7. Lifetime of the individual in question
8. Serious health problems - especially weakened immune system/ circulation in the brain
* Although anecdotal it is perhaps significant, in the context of sexual partners, that Rita Hayworth, Norma Shearer and Iris Murdoch had something else in common apart from early on-set AD - a reputation for promiscuity.
According to a study by David Snowdon in the US, nuns get AD at a prevalence of about 30%, a figure which compares with about 40-50% among females of the general population in the same age range (80-100 years) - but how? It is noteworthy that, according to autobiographies of women who were fomerly nuns, an estimated 30-40% are lesbian. Oral sex is very common among lesbians. It is unknown whether lesbians, in general, have a higher than average prevalence of AD. But if AD is driven purely by ageing, why is it less prevalent in nuns than in women, generally, in the US and Europe?
It has been suggested that drinking alcoholic beverages and eating curry reduce the risk of developing AD. These observations might be explained by the fact that both oral activities introduce chemicals into the mouth that are toxic to bacteria - thereby reducing the size of any treponema colony that might be present. It has also been suggested that those who consume a lot of sugary foodstuffs are at greater risk - perhaps because sugar feeds bacterial colonies, thereby enhancing the dose and probability of infection. In respect of sugar, it is possible that the reason why diabetics seem to have an increased risk of AD is because, even with medication, blood-sugar is above normal levels much of the time. Increased sugar in saliva enhances the abundance of oral bacterial and so, all other things being equal, increases the chance of developing AD.
It is possible to habitually engage in unprotected oral sex and yet NOT contract AD - if treponema denticola is absent (in the case of about 20% the population) or, perhaps, if the individual performing oral sex has a strong immune system. There is very good evidence that AD causes inflamation in the brain - possibly due to an allergic reaction to the presence of a toxin. This is further evidence that AD results from an infection, not simply from growing old. Nevertheless, the fact that 40-50% of people aged 85+ have AD implies that anyone who regularly engages in unprotected oral sex is at very serious risk of the disease, if they live long enough. It seems that by 85-90 years of age, nearly all of those infected will have developed symptoms.
The population divides into two groups as far as oral sex is concerned: those for whom oral sex is inherent behaviour and those for whom oral sex is learned behaviour. The former group probably have a genetic predisposition to engage in oral sex, the latter group probably do not. Hence, there might be a genetic bias towards some people developing AD because in them, oral sex is an inherent behaviour.
Seven final points:
1. If the hypothesis is correct, the present annual rate of increase in the number of Alzheimer's patients in the UK (for example) should correlate strongly with the annual increase in the number of people who started to engage in unprotected oral sex during the last few decades.
The sexually 'active' population spans about forty years from about 20-60. This represents roughly 25 million people in the UK. The average rate of increase in prevalence of oral sex over the last fifty years has been about 1% p.a. (roughly, from 40% to 90%). Hence, in any given year the increase has been about 1% of 25 million + = 250,000 +. The current rate of AD cases in the UK is about 100,000 p.a., however, only about half the original cohort reaches the 65-90 age group. Hence, the rate of increase of AD would have been roughly double (200,000+ cases p.a.) if none of the original cohort had died in the meantime. The fact that these rates are so similar, suggests a strong link between the rising prevalence of oral sex and the growth in prevalence of AD, especially during the second half of the twentieth century.
If the prevalence of treponema denticola is about 80% of the adult population (according to Harvard Medical School) and the prevalence of oral sex is now near saturation, at about 95% of the sexually active population, it seems that up to 75% of the entire population will eventually be at risk of AD. About 800,000 individuals are born each year in the UK, which means that, at saturation, about 600,000 would eventually be at risk. Roughly half of those would probably die before reaching the 65-95 age group. Thus, about 300,000 would actually develop AD. In other words, at saturation, there would be about three times as many AD cases per year as there are now (100,000 pa in the UK).
2. When Alzheimer's patients in North America were given a course of antibiotics to treat an unrelated infection, the patients claimed that the AD symptoms appeared to improve - an observation which suggests that bacteria play a crucial role in the progress of the disease.
3. Research published in 2006, shows that cats* get a disease like human AD. The question is: what behaviour pattern do cats and humans have in common that could transfer a toxin causing AD? In other words, what behaviour has been increasing in human beings, during the last few decades, that mirrors habitual behaviour in cats? One only has to watch a cat clean itself to see the answer.
*It is noteworthy that although chimps are the closest animal relatives of humans, and although they possess one of the risk factor genes, they do not get AD. In fact, all primates develop senile plaques as they age, but none develop AD - even though, like humans, they have oral treponemes capable of migrating to the brain. However, primates do not make a habit of performing oral sex. Oral sex in the animal kingdom is very rare, it is a behaviour almost entirely confined to humans.
4. It is thought that individuals with gum disease have an enhanced risk of AD. This is probably due to enhanced levels of oral bacteria, especially treponema denticola. About 600 species of oral bacteria are known and, typically, there are about 100 million bacteria in each ml of saliva.
5. Treponema denticola causes gingivitis and is also responsible for certain kinds of cardiovascular disease. Thus, it would be expected that many patients with AD will have cardiovascular disease as well. In other words, AD and some cardiovascular diseases have a common cause. It is not that cardiovascular disease causes AD, it is simply that the diseases are correlated.
6. Kinsey found, in his 1940s reports on sexual behaviour, that the prevalence of oral sex in married American couples was about 45-50%. Those from the original surveys who have survived to the present are now 85+. Of that generation about 50% have dementia.
1. Although age is the most important risk factor, AD is caused not by the ageing process itself but by habitual behaviour: unprotected oral sex. Evidence: i) The prevalence ratio between US and UK. ii) Prevalence ratio between rural populations in India and China and developed nations esp. US. iii) Japanese immigrants to US have shown increased prevalence. iv) Prevalence has doubled in just one decade in the US. v) Prevalence seems to be increasing in the younger age group 50-70.
2. AD is caused by an infection, a pathogen carried via trigeminal nerves from mouth to brain, by treponema denticola (and possibly treponema genitalis). Evidence: Ref (1): 95% of sample of AD brains at autopsy had treponema denticola present. Sporadic AD does not have a direct genetic origin - as demonstrated by cases of identical twins where one twin develops sporadic AD while the other does not.
3. Oral treponemes are not themselves the cause of AD, they are only the vehicle carrying the toxin. Evidence: i) 30% of the control sample (Ref 1) had the bacteria present but no AD ii) treponema denticola must always have been present in the brains of older populations, in the past, at a time when AD was thought of as being uncommon.
4. Treponema denticola acquire the toxin causing AD, in the mouth, through unprotected oral sex. Thus, oral sex is driving the AD epidemic. Evidence: i) There are many possible toxins, which might cause neurological damage, in the genital region. ii) the rate at which AD is increasing, in the UK, is very similar to the rate at which oral sex has been increasing during the last fifty years in the UK.
5. Cats get AD like Humans, which suggests that the underlying cause is the same or similar. The AD epidemic appears to be behaviour-driven in humans, so it is likely to be behaviour-driven in cats. The behaviour common to cats and human, which could account for an orally acquired toxin, involves oral-genital contact - specifically, how cats clean themselves. It is noteworthy that although primates get senile plaques in the brain as they age, they do not get AD. Primates do not clean themselves like cats, nor do they engage in oral sex.
6. AD might be treated by administering antibiotics to kill treponema denticola, before it has chance to cause significant damage. Evidence: When AD patients in North America were given antibiotics to treat an unrelated infection, they reported an improvement in symptoms.
7. In societies and communities where oral sex has traditionally been uncommon, the prevalence of AD is low.
A) In rural villages in India only about 5% get AD. According to a survey into HIV/AIDS in the early 1990s, only about 5% of the villagers claimed to engage in oral sex.
B) In the Amish community in the US, where oral sex is forbidden by a strict religious code, the prevalence of AD is low.
C) Among the peoples of sub-Saharan Africa, who in the past regarded oral sex as unhygienic and as "something white people do", there is currently a low prevalence of AD relative to the US and Europe.
D) Older generations of Filipinos, who regarded oral sex as an abomination, appear to have very low prevalence of AD - based on statistics from AD diagnostic centres in California. Filipinos make up 7% of California's population but only 0.7% of AD cases, about 1/10th the number of cases that might be expected.
E) The Inuit tribes of North America have traditionally not engaged in fellatio, they too have low prevalence of AD.
F) Kashmir has a low prevalence of AD. Kashmir has traditionally been a very conservative Islamic state and conservative Islam tends to frown on oral sex. It is likely that, under those strict religious conditions, oral sex has been relatively uncommon.
G)The prevalence of AD in Japan is about 50% of that in the US and Europe. Currently, the Japanese seem to engage in oral sex only about half (or less) as much as people in the US and Europe.
* It is possible that Jamaica has low prevalence of AD, since Rastafarian law forbids oral sex. Whether AD prevalence is in fact low in Jamaica is unknown. However, in 2003 it was reported in a local newspaper that the prevalence of dementia in Jamaica was "lower than previously thought".
The above are diverse examples, involving very different peoples, yet they have two key things in common: low prevalence of AD and a tendency to abstain from oral sex. This seems to be key evidence, from around the world, indicative of a very strong link between unprotected oral sex and sporadic AD.
Until quite recently, oral sex was a difficult subject to discuss openly. It isn't easy to suggest - in all seriousness - that granny "lost her mind" because, many years earlier, she habitually engaged in oral sex! But in view of the devastating effect on sufferers, the tremendous burden placed on carers, the huge financial cost (often carried by relatives) and the vast number of people affected, it is imperative that the Alzheimer's "time-bomb" is defused as quickly as possible. To do so it is necessary to keep an open mind and consider all credible causes, however unpalatable they might be.
Today, a person aged 65 has a 1 in 3 chance of developing AD at some point in the remainder of their lifetime. That figure is set to double in the next thrity years. At such time, the majority of the population could expect to get AD - that's why it's so important to find an effective treatment as soon as possible.
More is spent managing AD than is spent treating all cancers, all heart disease and all strokes combined. The estimate of the total annual global cost is about $600 billion. This figure will exceed $ 1 trillion in the not too distant future - equivalent to a major banking crisis every year. The failure of many drugs trials, in recent years, suggests that current thinking about AD needs to be seriously reconsidered, if progress is to be made, hence the justification for this article.
Although controversial, the ideas outlined here are certainly worth further investigation, since they suggest the possibility of a simple and inexpensive treatment for a terminal disease that devastates the lives of millions and costs the global economy hundreds of billions every year.
In general, the more a hypothesis explains the more likely it is correct. Of course, the thesis presented here might be wrong; but can medical science - and society in general - ignore the possibility that it might be right?
1. Molecular and immunological evidence of Oral Treponema in the human brain and their association with Alzheimer's Disease.
Authors: Riviere G.R. Riviere K.H. Smith K.S.
In: Oral microbiology and immunology (2002) Vol 17 no2 pp 113-118
2. Statistics on sexual behaviour in the UK from NATSAL I and NATSAL II (the first and second national survey of sexual attitudes and lifestyles)