Medical Hypotheses 114 (2018) 13–17

Contents lists available at ScienceDirect

Medical Hypotheses
journal homepage: www.elsevier.com/locate/mehy

Optimise the microbial flora with milk and yoghurt to prevent disease T

James A. Morris
Royal Lancaster Infirmary, Lancaster LA1 4RP, United Kingdom

A R T I C L E I N F O A B S T R A C T

Keywords: Pathogenic bacteria, which are temporary or permanent members of our microbial flora, cause or contribute to a
Milk wide range of human disease at all ages. Conditions include Alzheimer’s disease, atherosclerosis, diabetes
Yoghurt mellitus, obesity, cancer, autoimmunity and psychosis, amongst others. The mechanism of damage is in-
Atherosclerosis flammation which can be chronic or acute. An optimal microbial flora includes a wide range of pathogenic
Senile dementia
bacteria in low dose. This allows specific immunity to be developed and maintained with minimal inflammatory
Cancer
Autoimmunity
damage. Human milk has evolved to deliver an optimal microbial flora to the infant. Cow’s milk has the po-
Psychosis tential, following appropriate fortification, to maintain an optimal human microbial flora throughout life.
Diabetes mellitus Yoghurt is a fermented milk product in which bacteria normally present in milk convert sugars to lactic acid. The
acid suppresses the growth of pathogens in the oral cavity, oropharynx and oesophagus. Thus yoghurt can
restore an optimal flora in these regions in the short term. Since bacteria are transported between epithelial
surfaces, yoghurt will also optimise the flora elsewhere. The judicious use of milk and yogurt could prevent a
high proportion of human disease.

Introduction
The hypothesis that low dose, early, mucosal exposure to patho-
genic bacteria will reduce the frequency of microbial disease has been
published previously [1]. The concept is based on the observation that
the clinical severity of disease caused by bacteria and viruses is in-
creased if first exposure is delayed beyond childhood, and if the in-
fecting dose is high [2–4]. Furthermore the mucosal surfaces of the
enteric tract, in particular, are richly endowed with lymphatic tissue
early in life and the information processing capacity to generate an
effective immune response is optimal at this time. The hypothesis also
included the prediction that in the 21st century we will re-discover the
germ theory of disease. That germs cause most disease and genes act in
complex networks to prevent disease. The interaction between germs
and genes leading to, not only the range of infections described in
standard textbooks, but also atherosclerosis, Alzheimer’s disease, car-
cinoma, diabetes mellitus, depression, psychosis, autoimmunity and
many more. In fact the full range of human disease except trauma. This
bold assertion was supported by evidence at the time of publication
[4–10] and additional evidence has been gathered since publication
[11,12].
In order to prevent disease we envisaged the development of an
enteric coated pill containing a mixture of commensal and pathogenic
bacteria [1]. The pill would be taken by mouth and the bacteria would
be released in the small intestine and would eventually populate the
colon. The total dose of bacteria would not be high, but the major
component would be commensals and there would only be a small dose
of pathogens. The pill would be precisely formulated and varied from
day to day or week to week so that infants would meet all the common
pathogens in the first year of life. The pill would then be continued
throughout life and formulated to maintain an optimal commensal flora
and a wide range of pathogens. The commensals would keep the pa-
thogens in check and the presence of pathogens would maintain im-
munity. In addition to the enteric coated pill we envisaged that nasal
sprays of low doses of epidemic viruses might be required from time to
time. Furthermore it might be necessary to use lotions and creams
containing commensal skin bacteria to establish and maintain an op-
timal skin flora. This is all very involved but worthwhile if it were to
prevent disease and prolong active life.
A point we failed to make in the original publication is as follows: if
low dose early mucosal exposure is an effective way of reducing disease
then surely a mechanism to achieve this goal would have evolved
naturally. It has and the medium is milk. Mammalian milk, including
human milk, contains bacteria [13–18]. These are not contaminants.
They are selected from other epithelial surfaces and carried through the
blood to be actively secreted into milk. The composition of the bacterial
flora of human milk varies between individuals, by geography and
through lactation. It is also early days in the analysis and the methods
are still in development but it appears that the majority of bacteria are
commensals. They include the lactose fermenting bacteria which are
used to make natural yoghurt (lactobacilli, bifidobacteria and lactose
fermenting streptococci). But in addition to the commensals there are

E-mail address: Jim.A.Morris@mbht.nhs.uk.

https://doi.org/10.1016/j.mehy.2018.02.031
Received 20 January 2018; Accepted 25 February 2018
0306-9877/ © 2018 The Author. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
J.A. Morris
low doses of pathogens. Thus it appears that milk and yoghurt have the
potential to achieve our aim of preventing disease by developing an
optimal microbial flora.
The microbial flora
There are of the order of 1015 bacterial cells on or within the surface
of the body [19]. The majority resides in the colon, but there are bac-
teria on every epithelial surface. The concept of on the surface is ob-
vious and it applies to all commensal bacteria. But there are some
bacteria which grow within the surface [12]. These include pathogens
such as Staphylocccus aureus, which can grow on the keratin surface of
the skin, but can also grow between the squamous epithelial cells of the
skin. S. aureus also grows within the skin adnexal glands (eccrine, se-
baceous and apocrine). Once again it can be on the surface or between
the epithelial cells and therefore within the surface. Bacteria within the
surface are in direct continuity with the systemic circulation and can
induce inflammation. This is one way in which pathogens can cause
chronic low grade damage over many years contributing to degen-
erative disease [12].
The vagina is lined by non keratinizing stratified squamous epi-
thelium. The surface cells contain glycogen which is metabolized by
surface lactobacilli to lactic acid. The acid pH inhibits the growth of
pathogenic staphylococci and streptococci. Thus an optimal commensal
flora protects the vagina from infection. This is the simplest and best
characterized example of the interaction of commensal and pathogenic
bacteria. In the colon the flora is much more complicated with up to
800 different species [19]. But the principle of a stable ecological
system with commensal species dominating and inhibiting the growth
of pathogens still applies. The pathogens maintain immunity but only if
they are in direct contact with the systemic circulation and therefore
growth within the surface might be more extensive than currently
known. Pathogens can also invade the blood stream. In most cases they
are rapidly cleared by neutrophils in the post capillary venules of the
lung or by phagocytes in the sinusoids of the spleen [20]. These epi-
sodes of transient bacteraemia are clinically silent. But if the bacteria
grow more quickly than they are removed, septicaemia occurs and
provokes clinically overt sepsis.
Bacteria enter the body through the oral cavity in food and drink.
They also enter the upper respiratory tract in inhaled air, and these
bacteria are then carried into the oropharynx by nasociliary action. The
lining of the oral cavity, oropharynx and oesophagus is non keratinized
squamous epithelium, as in the vagina. Bacteria can grow on and within
this epithelium. There are also deep crypts within the tonsils within
which bacteria can grow. Many bacteria are destroyed by stomach acid,
but the upper small intestine contains bacteria and they increase in
numbers as they transit to the colon. Bacteria can also alight on the
external skin surface and extend into the skin adnexal glands. There is
also transit of bacteria through the blood from one epithelial lined
surface to another. This certainly occurs in the case of breast milk. But
the extent to which the ducts of the non lactating breast, the pancreas
and prostate are colonized by direct extension from the surface or from
the blood is unclear.
Probiotics and yoghurt
Metchnikoff, the Nobel laureate who discovered phagocytosis, first
popularized the consumption of yoghurt as a health food [21]. He
studied the distribution of centenarians in Europe and noted there were
more in Greece and the Balkans than in Northern Europe. Bulgaria in
particular was noted for a long lived healthy population of peasants
whose diet included yoghurt. He postulated that natural fermentation
of milk, producing an acid product, would suppress fermentation by
bacteria in the colon. The absorption of toxic products from the colon
would, therefore, be reduced and their harmful effects in causing dis-
ease and aging would be ameliorated. But in many ways yoghurt, as a
14
Medical Hypotheses 114 (2018) 13–17
health food, has been a disappointment. Yoghurt consumption has a
minimal effect on the composition of the bacterial flora in the colon
[22]. Furthermore, the idea, that absorption of toxic products from the
colon is a major cause of disease, is no longer accepted. The bacteria
used to produce yoghurt, however, are the basis of probiotic therapies
and these have been extensively investigated [22,23]. It is difficult to
summarise the results because the trials use different combinations of
bacteria and varying doses in a wide range of conditions. In general
there are small positive effects in most trials.
I believe it is time to re-evaluate the role of natural yoghurt [12]. It
contains far fewer bacteria than the therapeutic probiotic preparations
but it generates an acid environment which is essential for suppressing
the growth of pathogenic bacteria. This is certainly the situation in the
vagina and probably will apply to the oral cavity, oropharynx and oe-
sophagus which have a similar lining. Daily consumption of yoghurt is
likely to change the flora around the teeth and in the tonsillar crypts in
the short term. It will also determine the flora in the small intestine and
perhaps influence the resident bacteria at other sites by blood borne
transfer from the oral cavity. It won’t affect the colonic flora in the short
term but it could in the longer term.
Hypotheses and predictions
Chronic inflammation is a risk factor for a range of diseases of
middle and later life, such as atherosclerosis [6], Alzheimer’s disease
[5], type 2 diabetes mellitus [24], endogenous depression [25,26] and
obesity [27]. Dental caries and chronic periodontitis are amongst the
commonest inflammatory conditions and they are associated with the
aforementioned diseases [28]. Dental infections are caused by a wide
range of pathogenic bacteria, including pathogenic streptococci such as
Streptococcus mutans. Pathogenic staphylococci and streptococci also
grow in the tonsillar crypts and within the squamous epithelium of the
oropharynx. The inflammatory response is designed to specifically de-
stroy pathogenic bacteria with as little damage to the host as possible.
But the cytokine molecules released during inflammation are designed
to damage all biological material and therefore some damage to host
tissues is inevitable [12]. Systemic release of cytokines will therefore
damage endothelial cells, hence atherosclerosis, and perhaps directly
damage neurons, hence Alzheimer’s disease.
Staphylococcus aureus grows within the surface epithelium and is
therefore in direct contact with the immune system. Many strains of this
organism secrete pyrogenic toxins which act as superantigens. They
directly stimulate T cells and lead to a non-targeted inflammatory re-
sponse. This means maximal damage to the host with minimal damage
to the bacteria [12]. We all have antibodies to these superantigens and
therefore we all must be frequently exposed [29–31]. This makes S.
aureus carriage a prime candidate for a pathogenic role in the above
conditions. The secretion of pyrogenic toxins into the blood leads to the
formation of immune complexes with their specific anti-toxin IgG an-
tibody. These complexes are secreted in the urine [32,33] . This is an
active process as the complexes are far too large to be passively filtered
by the glomeruli. Thus measurement of urinary IgG and identification
of the toxins is theoretically possible.
The experimental approach envisaged is an observational study of
patients in the early stages of the above conditions. The patients would
consume yoghurt daily for several months and the effects on the mi-
crobial flora of the oral cavity, inflammatory markers, urinary IgG and
the progression of the disease would be assessed. It is likely that yo-
ghurt will take time to have an effect on the flora, particularly around
the teeth and in the tonsillar crypts. Furthermore success in the case of
Alzheimer’s disease and atherosclerosis would be slowing progression
of the condition rather then any marked improvement. The response in
endogenous depression might be more gratifying and perhaps should be
tried first.
The winter months in the UK bring an increased number of viral
respiratory tract infections followed by an increase in the number of
J.A. Morris
hospital admissions and an increase in the number of deaths in the
community. I have conducted many autopsy examinations on people
who have died in these circumstances, but I have rarely attributed
death to viral infection. The hospital admissions and deaths are due to
heart attacks, strokes, sepsis and pneumonia caused by secondary
growth of pathogenic staphylococci and streptococci in the respiratory
tract and oropharynx. Regular consumption of yoghurt could have a
marked effect on winter deaths and greatly reduce the burden on the
health service.
The most likely explanation for the cause of autoimmune disease is
that the auto-antibodies are provoked by molecular mimicry with
bacteria of the normal body flora [4,34]. These conditions, character-
istically, show a course of exacerbation and remission. Exacerbations
are presumably associated with periods of re-exposure or increased
carriage, and remissions with reduced carriage. Furthermore to main-
tain auto-antibodies over the long term the immune system must be in
direct contact with the bacteria and the causative organisms are likely
to be pathogens growing within the surface rather than on it. The use of
yoghurt to reduce pathogen carriage could therefore be successful in
reducing exacerbations and prolonging remissions.
Rheumatoid arthritis is an immune complex mediated disease in
which there is exciting new evidence that the immune complexes
contain staphylococcal antigens. These patients have a high frequency
of staphylococcal toxins in the urine [35] and this implies that they are
present in the blood as immune complexes with anti-toxin IgG. Redu-
cing staphylococcal carriage in these patients could prevent the disease.
Changes in social conditions can have profound effects on our flora
and lead to marked changes in the frequency of disease. In technolo-
gically advanced societies good quality plumbing delivers hot and cold
water to baths and showers. Daily washing with bactericidal soap then
washes off the surface bacteria and gives a competitive advantage to
bacteria, such as S. aureus, which are deeper in the skin. The result is an
epidemic of eczema, asthma, hay fever, and type 1 diabetes mellitus –
the so called diseases of the “hygiene hypothesis” [36–38]. Probiotics
can prevent eczema [39,40], probably by suppressing the growth of S.
aureus. I suspect that yoghurt will be as successful. Yoghurt might also
prevent asthma and type 1 diabetes mellitus. S. aureus has a growth
advantage when blood glucose rises. There will therefore be an evolu-
tionary advantage to any organism that could damage the beta cells of
the Islets of Langerhans in the pancreas or directly interfere with insulin
action. Since bacteria evolve rapidly it is highly likely that such a me-
chanism exists. Thus the hypothesis is that S. aureus causes type 1
diabetes mellitus by provoking the production of auto-antibodies that
damage beta cells. In a similar way S. aureus might cause type 2 dia-
betes mellitus by secreting toxins that interfere with insulin and or
damage beta cells. Suppressing S. aureus carriage might, therefore be
successful in preventing both types 1 and 2 diabetes mellitus [11].
The epidemic of obesity is also a cause of considerable concern. I
doubt that it is due to moral failings or the sins of gluttony and sloth, as
implied in many articles in the general press. Instead I would con-
centrate on the systems that regulate appetite and match intake of
calories to their expenditure. Modern farming techniques are designed
to increase weight gain in animals, and the selective approach will also
select for bacteria that promote weight gain. The latter mechanism
would involve producing molecules or provoking the formation of auto-
antibodies that directly or indirectly stimulate appetite. The bacterial
flora of animals will spread to humans and we could be experiencing a
hidden change in the composition of our flora. Once again the bacteria
that secrete molecules into the body and provoke auto-antibodies are
likely to be those in direct contact with the systemic circulation. The
short cut to identifying the causative bacteria is to measure IgG in the
urine and if it is present to try to identify the antigen of the IgG immune
complex [11]. Auto-antibodies to regulatory peptides, provoked by our
bacterial flora, are in fact common [34].
Normal wear and tear to our bones and joints will cause micro-
fractures in bone and cartilage which are quickly repaired and
15
Medical Hypotheses 114 (2018) 13–17
remodeled. But what if the tiny bleeds that accompany the micro-
fractures contain pathogenic bacteria from the oral cavity: bacteria that
are adapted to grow and survive on the surface of dentine and to de-
stroy periodontal ligaments. This could lead to local inflammation in
the bone and joint and impair repair and remodeling. Once again a trial
of yoghurt seems worthwhile.
Our ideas of the nature of cancer have changed in recent years
[41,42]. The conventional idea that malignant cells have acquired
mutations in growth control genes leading to clinical cancer is correct.
But this is secondary to local destruction of the epithelial stem cell
hierarchy by chronic inflammation. Multiple stem cells then divide
without a quiescent phase and acquire mutations leading to multiple
malignant clones. Most of the clones die out but an occasional clone
survives to form a clinical cancer. The likely cause of cancer in the
breast, prostate and pancreas is therefore a pathogenic bacterial flora in
the ducts. Women who complete a pregnancy early in life and breast-
feed the infant will acquire a breast duct flora of lactose fermenting
bacteria. These women have a reduced risk of breast cancer and
therefore the lactic acid forming bacterial flora is protective [43,44].
Regular consumption of yoghurt could in theory have a similar effect
but it will be difficult to test. The same might apply to the prostate and
pancreas. At least it should be possible to ascertain if regular con-
sumption of yoghurt will alter the bacterial flora in prostate secretions.
Mother’s milk has evolved to nourish the infant and to provide it
with an optimal bacterial flora. But milk will only have an optimal flora
if the mother’s flora is optimal. Technological change influences our
flora and we cannot assume that mothers do have an optimal flora in
our society at present. Bacteria are carried from the epithelial surfaces
of the pregnant female to the breast and to the placenta. These bacteria
include pathogens from the oral cavity, particularly if dentition is poor.
Could this be relevant to pre-eclamptic toxaemia; a common but enig-
matic condition of unknown cause? There is clearly a case to monitor
the bacterial flora in pregnancy and consider the role of yoghurt in
modifying the flora.
I can construct similar hypotheses for a broad range of other con-
ditions including acne, Crohn’s disease and gastro-intestinal reflux
disease (GORD). Will yoghurt consumption decrease the carriage of
Propionibacterium acnes in the oral cavity and skin? Will modification of
the oesophageal flora reduce the degree of inflammation associated
with GORD, improving symptoms and reducing the risk of carcinoma?
Modification of the oesophageal flora will change the flora in the small
intestine and therefore could decrease the risk of Crohn’s disease. In fact
whenever we are faced with a common inflammatory disease of un-
known cause we should consider the possibility of a bacterial cause and
investigate by searching for bacterial antigens in the urine [11]. A trial
of yoghurt is then worthwhile because to date there are no recorded
downsides.
Discussion
I have used the term “microbial flora’ rather than the more modern
term “microbiota” throughout this article. This is because the concept
of the microbiota is often linked to the idea that the gut bacteria work
together as a complex organism interacting positively with the colon
and the immune system to preserve health. There is much to commend
this idea, but in this article I have emphasized the role of competition in
keeping pathogens in check. This is an ecological concept and therefore
the term “microbial flora” is more appropriate. It is also somewhat
simplistic to talk of commensals and pathogens as distinct, because all
bacteria are potentially pathogenic and there is in fact a spectrum of
behaviour. But if we are to make progress in the short term towards
preventing disease it is essential that we focus on suppressing the
growth of known pathogens, such as S. aureus, and augmenting the
growth of known commensals, such as the lactic acid producing bac-
teria.
Many readers will be skeptical of the claim that milk and yoghurt
J.A. Morris
could have such potential to prevent disease. They are certainly not
new products and their health benefits have been investigated [45–49].
Epidemiological studies of milk and yoghurt consumption are, however,
fraught with difficulties. It is not possible to get an accurate assessment
of the amount consumed over long periods, and the commercial pro-
ducts of yoghurt in particular vary greatly. Most yoghurts on the su-
permarket shelves are low fat and sweetened by sugar; ideal for
growing pathogens rather than suppressing them. Furthermore we do
not know to what extent modern milk, produced by modern farming
technique, has an optimal composition of bacteria. Overall, however, it
appears that milk and yoghurt are good for health [49]. Consumption of
these products is associated with reduced risk of obesity and diabetes
mellitus. They are less harmful for atherosclerosis and its complications
than previously assumed and might even be beneficial. There are also
negative associations with cancer risk, particularly colon and breast.
The potential of epidemiological studies to answer key questions is,
however, limited. The thesis presented above is that we should focus on
the potential of milk and yoghurt to modify the microbial flora and then
determine the effect of the changed flora on general health.
Milk has evolved to provide the infant with an optimal bacterial
flora. What we need to consider is the possibility that we could main-
tain an optimal flora throughout life by daily consumption of milk and
yoghurt. Determining the optimal flora at each stage of life will be a
major task, one that will take many years of detailed research. We al-
ready know, however, that pathogens in high dose are damaging but in
low dose might be beneficial. We also know that inflammation caused
by pathogens is responsible for a wide range of disease [1,11,12]. Fi-
nally there are sound theoretical reasons, and there is increasing ex-
perimental evidence, that regular consumption of yoghurt can suppress
the growth of many of the pathogens. Thus the first practical step is to
observe the effects of yoghurt consumption on the wide range of con-
ditions listed above. There is reason to believe that this could have a
marked effect on human health in the short term.
Regular consumption of milk is also likely to be beneficial to health.
But we do need to determine the bacterial composition of cow’s milk in
much more detail. The composition is likely to vary by breed, by the
phase of lactation, and by the conditions in which the cows are reared
and kept. The optimum for cows might not be the optimum for humans,
but there is a reasonable chance that they are not in practice too dis-
similar. Perhaps in the longer term we will look towards fortifying milk,
after pasteurization, with a range of bacteria in appropriate dose to
approximate the optimum.
Mapping the bacterial flora is a major task, with up to 800 potential
species and many strains per species. Furthermore there is a large
number of micro-environments including around the teeth, tonsillar
crypts, and varying epithelial surfaces. But there are fewer pathogens
and it is sensible to concentrate on these initially. Focusing on the oral
cavity rather than the colonic flora will also help in the early stages.
Considerable help in this process arises from the observation that im-
mune complexes formed in response to inflammation caused by pa-
thogens within the surface are secreted actively by the kidney and
appear in the urine. Thus there is the possibility that the antigen of the
immune complex can be determined by mass spectrometry and the
causative bacteria in turn identified [11,12].
Dr Weston Price was one of the first to study the link between poor
dentition and chronic systemic disease [50]. His ideas had a mixed
reception, but now his words seem prophetic as an explosion of re-
search publications on the oral flora, periodontitis and systemic disease
emerge from laboratories in every part of the world. Bacteria around
the teeth cause local inflammation but also spread through the blood
stream to cause systemic inflammation. It seems a little odd that it has
taken us so long to realize a simple truth – optimize the oral flora to
prevent disease.
16
Medical Hypotheses 114 (2018) 13–17
Conflict of interest
None.
References
[1] Morris JA, Harrison LM, Lauder RM, Telford DR, Neary R. Low dose, early mucosal
exposure will minimize the risk of microbial disease. Med Hypotheses
2012;79:630–4.
[2] Heath CW, Brodsky AL, Potolsky AI. Infectious mononucleosis in a general popu-
lation. Am J Epidemiol 1972;95:46–52.
[3] Nathanson N, Martin JR. The epidemiology of poliomyelitis: enigmas surrounding
its appearance, epidimicity, and disappearance. Am J Epidemol 1979;110:672–92.
[4] Morris JA. Autoimmunity: a decision theory model. J Clin Pathol 1987;40:210–5.
[5] Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and
Alzheimer’s disease. Neurobiol Aging 2000;21:383–421.
[6] Libby P. Inflammation in atherosclerosis. Nature 2002;420:868–74.
[7] Morris JA, Harrison LM, Biswas J, Telford DR. Transient bacteraemia; a possible
cause of life threatening events. Med Hypotheses 2007;69:1032–9.
[8] Morris JA, Harrison LM, Brodison A, Lauder RM. Sudden infant death syndrome and
cardiac arrhythmias. Future Cardiol 2009;5:201–7.
[9] Warren-Gash C, Bhaskaran K, Hayward A. Circulating influenza virus, climatic
factors, and acute myocardial infarction: a time series study in England and Wales
and Hong Kong. J Infect Dis 2011;203:1710–8.
[10] Tlaskalova-Hogenova H, Stepankova R, Kozakova H, et al. The role of the gut mi-
crobiota (commensal bacteria) and the mucosal barrier in the pathogenesis of in-
flammatory and autoimmune diseases and cancer/; contribution of germ-free and
gnotobiotic animal models of human diseases. Cell Mol Immunol 2011;8:110–20.
[11] Morris JA. Re-discovering the germ theory of disease: a major role for proteomics. J
Proteom Bioinform 2016;9:84–6.
[12] Morris JA. Staphylococcus aureus bacteraemia: a hidden factor in the pathogenesis of
human disease. JSM Microbiol 2017;5:1037–9.
[13] Martin R, Langa S, Reviriego C, Jimenez E, Marin ML, Xaus J, et al. Human milk is a
source of lactic acid bacteria for the infant gut. J Pediatr 2003;143:754–8.
[14] Gueimonde M, Laitinen K, Salminen S, Isolauri E. Breast milk: a source of bifido-
bacteria for infant gut development and maturation? Neonatology 2007;92:64–6.
[15] Jimenez E, Fernandez L, Maldonado A, Martin R, Olivares M, Xaus J, et al. Oral
administration of lactobacilli isolated form breast milk as an alternative for the
treatment of infectious mastitis during lactation. Appl Environ Microbiol
2008;74:4650–5.
[16] Rodtiquez JM. The origin of human milk bacteria: is there a bacterial entero-
mammary pathway during late pregnancy and lactation? Adv Nutr 2014:779–84.
[17] Jost T, Lacroix C, Braegger C, Chassard C. Impact of human milk bacteria and
oligosaccharides on neonatal gut microbiota establishment and gut health. Nutr Rev
2015;73:426–37.
[18] McGuire MK, McGuire MA. Got bacteria? The astounding, yet not-so surprising,
microbiome of human milk. Curr Opin Biotechnol 2017;44:63–8.
[19] Tannock GW. New perceptions of the gut microbiota: implications for future re-
search. Gastroenterol clin N Am 2005;34:361–82.
[20] Morris JA, Harrison LM, Biswas J, Telford DR. Transient bacteraemia: a possible
cause of sudden life threatening events. Med Hypotheses 2007;69:1032–9.
[21] Metchnikoff E. The prolongation of life. New York: Putnam & Sons; 1908.
[22] Doron S, Snydman DR, Gorbach SL. Lactobacillus GG: bacteriology and clinical
application. Gastroenterol N Am 2005;34:483–98.
[23] Floch MH, Montrose DC. Use of probiotics in humans: an analysis of the literature.
Gastroenterol Clin N Am 2005;34:547–70.
[24] Badawi A, Kip A, Haddad P, Cole DEC, Bibiani GC, El-Sohemy A, et al. Type 2
diabetes mellitus inflammation: prospects for bio-markers of risk and nutritional
intervention. Diabetes Metab Syndr Obes 2010;3:173–86.
[25] Almond M. Depression and inflammation: examining the link. Current Psychiatry
2013;12:24–32.
[26] Zunszain P, Hepgul N, Pariante CM. Inflammation and depression. Curr Topics
Behav Neurosci 2013;14:135–51.
[27] Monteiro R, Azevedo I. Chronic inflammation in obesity and the metabolic syn-
drome. Mediators Inflamm 2010. http://dx.doi.org/10.1155/2010/289645.
[28] Shaik MM, Ahmad S, Gan SH, Abuzenadah AM, Ahmad E, Tabrez S, et al. How do
periodontal infections affect the onset of Alzheimer’s disease? CNS Neurol Disord
Drug Targets 2014;13:460–6.
[29] Harrison LM, Morris JA, Bishop LA, Lauder RM, Taylor CA, Telford DR. Detection of
specific antibodies in cord blood, infant and maternal saliva, and breast milk to
staphylococcal toxins implicated in sudden infant death syndrome (SIDS). FEMS
Immunol Med Microbiol 2004;42:94–104.
[30] Harrison LM, Morris JA, Lauder RM, Tellford DR. The effect of Staphylococcus aureus
carriage in late pregnancy on antibody levels to staphylococcal toxins in cord blood
and breast milk. FEMS Immunol Med Microbiol 2008;54:137–43.
[31] Harrison LM, Morris JA, Lauder RM, Telford DR. Staphylococcal pyrogenic toxins in
infant urine samples: a possible marker of transient bacteraemia. J Clin Pathol
2009;62:735–8.
[32] Price FS. Analysis of urine as a marker of Staphylococcus aureus bacteraemia during
intensive care. Lancaster University; 2013. MSc thesis.
[33] Bull KL. Analysis of urine for Staphyloccus aureus toxin alpha haemolysin and
immunoglobulin as markers of infection. Lancaster University; 2014. MSc thesis.
[34] Morris JA, Broughton SJ, Wessels Q. Microbes, molecular mimicry and molecules of
mood and motivation. Med Hypotheses 2016;87:40–3.
J.A. Morris
[35] Grace L. Detection of staphylococcal enterotoxins in patients with rheumatoid ar-
thritis or closed fractures. Lancaster University; 2016. PhD thesis.
[36] Strachen DP. Hay fever, hygiene and household size. Br Med J 1989;299:1259–60.
[37] Strachen DP, Harkin LS, Johnston IDA, Anderson HR. Childhood antecedents of
allergic sensitization in young British adults. J Allergy Clin Immunol 1997;99:6–12.
[38] Marshall AL, Chetwynd A, Morris JA, Placzek M, Smith C, Olabi A, et al. Type 1
diabetes mellitus in childhood: a matched case control study in Lancashire and
Cumbria, UK. Diab Med 2004;21:1035–40.
[39] Kalliomaki M, Salminen S, Arvilommi H, Kero P, Kaskinen P, Isolauri E. Probiotics
in primary prevention of atopic disease: a randomized placebo controlled trial.
Lancet 2001;357:1076–9.
[40] Kalliomaki M, Salminen S, Poussa T, Arvilommi H, Isolauri E. Probiotics and pre-
vention of atopic disease: 4 year follow up of a randomized placebo controlled trial.
Lancet 2003;361:1869–71.
[41] Morris JA. The hierarchical model of stem cell genesis explains the man mouse
paradox, Peto’s paradox, the red cell paradox and Wright’s enigma. Med Hypotheses
2014;83:713–7.
[42] Begum N-M, Morris JA. Solutions to Peto’s paradoxes and to Wright’s enigma have
implications for cancer prevention. JOJ Immun Virol 2017;1(4):555568. http://dx.
doi.org/10.19080/JOJIV.2017.01.555568.
[43] Kelsey JL, Gammon MD, John EM. Reproductive factors and breast cancer.
17
Medical Hypotheses 114 (2018) 13–17
Epidemiol Rev 1993;15:36–47.
[44] Lipworth L. Epidemiology of breast cancer. Eur J Cancer Prev 1995;4:7–30.
[45] Babio N, Becerra-Tomas N, Martinez-Gonzalez MA, Corella D, Estruch R, Ros E,
et al. Consumption of yoghurt, low fat dairy products is associated with lower risk
of metabolic syndrome in an elderly Mediterranean population. J Nutr
2015;145:2308–16.
[46] Crichton GE, Alkerwi A. Dairy food intake is positively associated with cardiovas-
cular health: findings from observations of cardiovascular risk factors in
Luxembourg study. Nutr Res 2014;34:1036–44.
[47] Thorning TK, Bertram HC, Bonjour JP, De Groot L, Dupont D, Feeney E, et al. Whole
dairy matrix or single nutrients in assessment of health effects: current evidence and
knowledge gaps. Am J Clin Nutr 2017;105:1033–45.
[48] Drouin-Chartier JP, Brassard D, Tessier-Grenier M, Cote JA, Labonte ME, Desroches
S, et al. Systematic review of the association between dairy product consumption
and risk of cardiovascular related clinical outcomes. Adv Nutr 2016;7:1026–40.
[49] Thorning TK, Raben A, Tholstrup T, Soedamah-Muthu SS, Givens J, Astrup A. Milk
and dairy products: good or bad for human health? An assessment of the totality of
scientific evidence. Food Nutr Res 2016;60. http://dx.doi.org/10.3402/fnr.v60.
32527.
[50] Price WAV. Dental infections, oral and systemic. Cleveland, Ohio: Penton
Publishing Company; 1923.