Download Him him him him him him him imagine if you will go and explore

Him him him him him him him imagine if you will go and explore yourself and perhaps put yourself
maybe 100 years ago and you're exploring the confidence perhaps larger on the African continent for
example you in your course of your explorations going from village to village sure you come across a
village were a good percentage of the people have a substantial physical performance there's obviously
questions why perhaps this village showed this part of the country which are exploring a comment or
exploring has this malformation perhaps not others this puts us in the event the frame of mind perhaps
to be detectives of human disease and especially in this case for today's lecture foodborne disease while
going to do today in today's lecturers talk about naturally occurring toxicants toxins the crew naturally in
many foodstuffs across the globe and how they perform in the role as ecologic agents of foodborne
disease are learning objectives here today going to do is when examined the etiology or causation of
human disease as it is related to naturally occurring foodborne toxicants where try to understand the
complex nature of foods in terms of their chemical makeup we tend to think of foods in terms of their
protein and carbohydrates we've introduced in the plant kingdom we have a secondary chemical
compounds for various reasons these are typically the chemical compounds that cause foodborne
toxicant induced disease when explore a range of foodborne disease and what were going to do or what
you're going to do perhaps this is explore is try to do a little bit of detective work you got a disease
manifestation what in the local diet is perhaps causing the disease manifestation foregoing explore
some of the major foodborne diseases including goiter tropical ataxia neuropathy or cayenne tropical
amblyopia laugher is a very famous disease and some of their linkages in terms of the chemical linkages
to foodborne toxicants when you finish off looking at a range of natural food toxicants that exist out in
the human diet and their direct involvement in is not necessarily disease classification could sometimes
a grouping of diseases in terms of the complexity of food most of us understand that carbohydrates
proteins lipids segments in terms than nutrient value of food the most important part of it why we get
our energies in the synthetic precursors to the molecules of life from our diet less concerned perhaps
are we about the non-nutrient aspects of the food although sometimes the non-nutrient aspects
actually drives it's the color of the taste and unfortunately sometimes these secondary compounds
always also are intoxicating the non-nutrient aspects of food or so we can have as food additives will
combine things either a low scale sort of food preparation are very exotic or synthetic food additives
these can occur as secondary chemicals that are natural can also be contaminants or processing
chemicals in terms of the numbers of non-nutrient chemicals we find in different foods give your range
of these can be in the hundreds in these the chemicals that we've been able to identify and typically is a
real challenge to find out what chemical of this entire range is actually the active ingredient if you will
disease vector in terms of food borne intoxication and this also gives you an idea as we go back to
revisiting things like food additives and pesticide residues in food and as well environmental
contaminants that it is a challenge to decipher this complex makeup of chemicals as consortium of
chemicals to find out again one that we're looking for and this is the challenge of analytical toxicology so
I would imagine that you fewer explore without modern analytical toxicology your task of finding the
causes of a foodborne intoxication would be a particular challenge sorcerers as we should all have a
tremendous amount of respect scientists and physicians the public health officials. Decades ago perhaps
even several hundred years ago in some cases linked particular types of food to particular disease
manifestations now terms of the natural toxicants in human disease will go through several including
the classification compounds a cause goiter or going we talked briefly in several segments several
lectures about Simon Genet glycosides will talk about the causation of laughter is we've introduced in a
couple of slides and various presentations in this course lectins and their toxic properties as we have
also talked about various types of alkaloids will repeat some of those to do emphasis but to draw
attention to its physiological effects will introduce a protease and that inhibitors and vasoactive amines
with briefly talked about vasoactive amines we haven't referred to them as vasoactive amines and so
will talk about them and how they change your physiology glycogen set is a very visible disease
manifestation on this class of chemicals contribute to the growth of quarters quarter is a very large
sharp growth on the thyroid is seen in this particular image is fairly noticeable disease manifestation
glycogen so come to us from compounds in the Christopher I the Brassica species Insurer kale turnips
typically in the seats and not much in the leaves if you combine presentation of these foodborne
chemicals with iodine deficiency this will enhance the presentation of a quarter endpoint now the
Christopher I are the class of the plants that actually have naturally occurring satellites of these are file
sides said their characteristic of these plants the diets of many people many parts of the world have the
salutes in there because they have cruciferous plants in their diet whether it be the mustard said the hot
spicy's spices that we eats here in this country or in the East cabbage and root vegetables in Europe and
the Americas various wheels like rapeseed oil were the various cultivars currently used for oils such as
canola oil were Canadian oil is a rapeseed oil were the glucosinolates have been bred out of its were no
longer is so what would be regarded as a toxic food oil these are undesirable compounds because of the
toxicity of the bitter taste of this compound and the toxicity of the breakdown products in these
breakdown products are of concern in terms of quarter development greater Jenna compounds are
going trends are formed from these breakdown products of glucosinolates by file coast cities of the
metabolites are acted on nitriles thiocyanate's and oxazole with the downward trends work on the
thyroid and we know that the thyroid gland actually excretes several thyroid hormones that are very
active in terms of flow hormonal balance in the human body thyroxine try Ido triiodothyronine and
thyroglobulin are the main hormones associated with the thyroid is controlled by the hypothalamus and
to a Terry the hypothalamus produces thyrotropin releasing hormone or TRH dissimulation to return to
release by more thyroid stimulating hormone or TS HS can be helpful because of the of the jargon
medical jargon and number syllables amazed to use the abbreviations that TSH will promote the uptake
of iodine in the synthesis of GH and police of GYN triiodothyronine which feedback to reduce the TSH
the thyroid hormones also affect oxygen consumption cardiovascular function on neuromuscular
activity: a strong: cholesterol metabolism and cerebral function as well as growth developments of this
is important thyroid system hormonal system in terms of growth and development of the now greater
Jones and courtroom and thiourea inhibits TY synthesis and what happens is the thiocyanate's in the
auctions oxazole gene and nitriles inhibit uptake of iodine by the thyroid is a lack of iodine causes this
physical enlargement and it causes this tissue to hypo vascular rate to trap more iodine and that you so
this growth referred to as goiter known terms of testing for the presence of the origins in the diet and
the presentation of the quarter disease typically it's associated with the clinical analysis of the way to
the histology of the thyroid the growth rate of the patient animal terms of perhaps being stunted in
growth because of the importance of thyroid hormones to growth and development as well as the
iodine concentration in the blood in the thyroid tissues there is a away a clinical measurement
diagnostic in terms of the feeding the individual or dosing individual with iodine compounds and
mentoring that uptake and that's typically done with radioactive iodine known terms of sleep
presentation of another sort of foodborne disease psychogenic glycosides are category events is
widespread because of the widespread consumption of many plants that produce these chemical
compounds primary and this is Cassano which is stable in in Africa and in South America and a little bit in
Asia are various glycosides associated with these; Linda Maron during the Maron in the lima bean these
glycosides have a toxic endpoint because they can produce hydrogen cyanide cyanide will interact with
oxygen transport systems software roots also known as the many awkward yucca depending on where
your apt is a woody shrub is a perennial of the root is actually harvested there are many varieties out
there some more bitter than others in the bitterness is typically associated with higher levels of of the
cyanide compounds is an annual crop and various cultivars coupled with environmental conditions such
as drought and food preparation will actually be significant for whether or not the cardio glide cardiac
glycosides level is higher or low now the topic toxic chemical in cytogenetic glycosides is hydrogen
cyanide in this HCN is released when the plant is chewed or chopped what happens is the physical
action releases a couple of enzymes they don't will go your days and hydroxy nitrile lysates are released
these acts synergistically to release the HCN in the gut this is basic generic chemical structure of a
psychogenic glycosides now in terms of flow food preparation communities and cultures that use solve
the roots know that there needs to be certain types of preparation to remove the toxicants what
happens in terms of preparation is that especially the larger roots need to be soaking in water chop and
water for a period of time and this hydrolysis of some of the action releases it the cassava flour is
sometimes ground and then treated water prior to use intestinal bacteria nor what the active agents in
terms of residual cytogenetic glycosides that might be in their converting it to HCN even if the enzymes
have been deactivated by soaking water another vector for psychogenic glycosides in the diet is Laetrile
this is actually used as a drug anticancer compound of slowly marginal repute it's not approved in the US
so extracted from apricot pits and there have been instances of several deaths associated with this
compound known terms of the mechanism of acute cyanide poisoning what happens is it shuts down
cellular respiration and therefore energy metabolism in mitochondria it does this by finding ferric iron
the binding capacity of cyanide or scion needs to iron is substantial and it can then be used for transport
of oxygen so it's a competitive in this binds iron on cytochrome oxidase in Krebs cycle the middle of a
lethal dose is about .5 to 3.5 mg of HCN per kilogram of body weight and symptoms of acute cyanide
poisoning are muscular paralysis mental confusion respiratory distress it's typically presents with rapid
onset the treatment to interestingly enough if we recall our conversations about nitrate nitrite toxic
doses where nitrate and actually reduction to tonight's right actually is an oxidizing agent that oxidizes
ferrous iron to ferric iron in fact in acute cyanide poisoning the antidote to few will the treatments is
perhaps another toxicants we use nitrites to convert hemoglobin with ferrous iron to met hemoglobin
ferric iron and what this particular chemical reaction does this since releases some of the cyanide from
the cytochrome oxidase what you can do them in terms of follow-up therapies if file sulfate is around
file sulfate will bind with cyanide to form a less a more innocuous chemical called thiocyanate that is
nonreactive in terms of cytochrome oxidase irons in terms of chronic cyanide poisoning this is quite a bit
difference this occurs in areas of cassava in the diet term exposure chronic exposure is not particularly
well understood and fate may be more complex than psychogenic glycosides are two disorders
associated with chronic cyanide poisoning from cassava this is tropical ataxia neuropathy and tropical
amblyopia now TA and reports its common name console cruise in many tropical areas is most prevalent
in west Africa it's an atrophy of the optic nerve ataxia or inability to walk and not mental disorders are
some the clinical signs associated with gonzo there is a high prevalence of goiter in these individuals will
we find terms of the clinical observations is that there are low levels of sulfur containing amino acids in
the individuals affected with this particular disease and there's elevated plasma file scion eight which is
a goiter June now terms of some of the dietary modifiers that may impact chronic cyanide please
poisoning we find that if there is adequate iodine in the diet. There is no goiter and by the way most of
you that thereby salt notice that the commercially sold as iodine's iodized salt this itemization this food
additive if you will of common table salt is so closely related to the need to put iodine into diets that are
deficient in that particular mineral malnutrition terms of the cyanide to talk cyanide poisoning impact
malnutrition increases the neurological effects protein deficient diets also modify it in terms of lack of
these particular sulfur containing amino acids these help convert cyanide to thiocyanate in terms of the
chemical reactivity's now the second category of diseases tropical amblyopia this is an atrophy of the
optic nerve yields were vision and ultimately blindness Africa and South America were cassava is
significant staple in the diet are the primary geographical locations for this particular disease it is
reproducible in lab animals the next category of disease around talk about in terms of linking a particular
foodstuff of foodborne toxicants to disease is laughter was laughter is a results from the consumption of
certain types of peace especially laugher settles these are referred to in by common names as Sawgrass
peas are blue sweet peas there primarily restricted to various areas where this is a part of the diet in
Asia and Africa this is a very well-known neurodegenerative disease results from the presence of two
compounds in these peas there's an enzyme inhibitor will refer to his BAP and ensuring the structure
here momentarily and also neurotoxic amino acid Odette and again will show you that your moment
this is a popular food plants are not only for human consumption but for food animal consumption
because it's a hardy plant very drought resistant because of the prevalence in the history laughter is a
new cultivars of related plants are being developed to minimize the amounts of these particular
chemical compounds these naturally occurring toxicants in the laughter is has two forms of this
particular disease osteoblast tourism which occurs mostly in animals and neural laughter is which
presents in humans noun osteoblast tourism we find bone deformations characteristic weakness and
arterial walls and connective tissues this is typically in terms of dose response studies been associated
with the chemical BAP enter beta oh terrible amino group you nitrile on this is shown structurally down
in the bottom here this again is a complement of these peas osteoblast tourism terms the mechanism
VPN will inhibit license oxidase enzymes in this figure enzyme is needed to help cross-linked collagen
collagen is a structural components in this helps us in terms of tissues and strength it's a main
complement of various connective tissues and bones and that's why you get the disabilities associated
with the structuralism is neural aphorism is what presents most commonly in humans begin this comes
from the chronic consumption of the saddest variety of presents with the paralysis of the legs followed
by general weakness and muscular rigidity some refer to it as a young man disease and this may be
because of the relative dietary loading in terms of body size to and during the developmental cycle of
individuals there appears to be a sudden onset of the disease that starts with calf muscle spasms there
has not been inadequate animal model developed for neural aphorism in terms of its presentation
humans it's been associated with old Or oxo alpha diamine appropriate like acid ODD P I give you the
structure here on this particular slide in terms of neural aphorism in in in humans the etiologic agents
may be hope he he its found without this particular species of peas OPEC fears and interferes with
normal function of the nerve synapse it inhibits uptake of glutamic acid there is no animal model in
terms of a true understanding of this particular disease another sort of the presentation of the disease is
from neurotoxic cholinesterase inhibitors in our target organ toxicology and several case studies we
presented we talked about various types of cholinesterase visitors especially those that present in the
human diet are found in a variety of plants including the alkaloids and potato tomato plants send a
plants as well we find its originally in terms of the prototypical cholinesterase inhibitor in the West
African Calabar bean we talked about in one of our case studies because we talked about the Faisal stick
mean drug that has been used as a cholinesterase inhibitor when we have a patient that has been
exposed to cholinergic type toxicants this particular the phytochemical is a natural carb family
remember that car bandmates are a class of cholinesterase inhibiting pesticides and soon a certain
sense here this is a natural carb family therefore a natural insecticide that is present in a foodstuff in
terms of other cholinesterase inhibitors in the human diet from the soul and I we have the study this
comes to us in potatoes I have a structural representation of the molecule on the slide in the earliest
parts the century in the previous century potatoes in many cultures so Western cultures especially were
considered to be toxic because the cultivars at that time had relatively high levels of stolen and they did
present in terms of the normal presentation of chorus esterase in addition and just generalized illness
headaches associated with the awkward levels of the glycol alkaloids in potatoes so run from 2200 ppm
wet weight FDA has an upper tolerance of 200 ppm we recall in terms of our discussion here intrusive
for the greeting by traditional breeding of a potato variety: happy that was actually presented for
approval as a chipping variety Cato to USDA until it was discovered that it had significant amounts of
Celine alkaloids greater 300 ppm therefore this particular variety was fraught with strong from the
marketplace the greatest concentration of potato alkaloids and Salinas one of them is in the PO and
around us plaster sprouts what mom told you about the greening is in fact to truly about sprouted
potatoes that they have enhanced amounts of these alkaloids is it going to harm you significantly
probably not might give you a tummy ache or headache Possibly so upon your particular sensitivity is
only levels are increased with the sunlight and so that's why are you store potatoes in a dark space if
you take russet Burbank potato put the light for five days you stimulate remembering that a potato was
a living organism that in response to that life starts its production the salinity levels start rising 250 700
ppm five days so the toxicity markers that we have this is a green in terms of potential social what we
find in terms of the Celine in the human foods it does have five documented human toxicity and death
potato sprouts have high concentration sprouted potatoes and green potatoes all have higher levels
than recommended the presentation of disease includes gastric pain nausea vomiting hyper stingier
increased and accelerated respiration and there have been there about two of six Sundance in terms of
people look at exposed to high concentrations in potatoes now terms of a case study this was a case
with potatoes that had 420 ppm total alkaloid contents about 50% of the alkaloids in these potatoes was
so owning in this case was 200 of the 420 ppm with that that calculation you'd only need to consume 1
kg of 2.2 pounds of potato for toxicity only due to sully this may also act synergistically with other glycol
alkaloids or actively with other glycol alkaloids like a chicken in the animal LD50 for Celine is 500 to 1000
mg per kilogram of body weight sows can be hard to get a significant LD 50 type dose in terms of
humans from consumption but probably enough to make you quite feel our next category of the
naturally occurring tops concerned that we are concerned with disease are vasoactive amines which
talked about a few these in the course so far what we find these compounds are the highest in aged
cheese of beer and wine and they are responsible for some people's intolerance or food intolerance
associated with these particular food groups are low levels but they're still present in some foods such
as banana tomato avocado spinach oranges we find them and spoiled me if you remember our food
allergy discussions and the presentation of strong boys and strong boy toxins for the disease
manifestation called scrum boy talks closest these are vasoactive amines are primarily histamine visa
amines associated with vasoactive amines are sometimes also referred to as pressor amines because
they do impacts cause vasoconstriction and hypertension are increased blood pressure there also called
catecholamines we find them in my meat and fish of the bacterial action and the initial states of the flow
spoilage future semen cadaver in order to vasoactive amines in banana and avocado they present as
dopamine and to remain to remain being one of the ones that quite high in some foods catecholamine
neurotransmitters that are found in foods are norepinephrine dopamine and serotonin in the structures
of these vasoactive amines are at the bottom slide now we got problem with vasoactive active amines
because of their metabolism and its effects on people using certain types of medications vasoactive
amines are acted on by monoamine oxidase MAO this particular enzyme is widely distributed in the
body is important in many vile transformations it does impact of vasoactive amines by breaking them
down some individuals so that have clinical depression are treated with drugs called MAO inhibitors you
sometimes will see labels on foods that might have a high level of vasoactive amines warning individuals
are on the strokes that there there is the presence of of these particular chemicals when you do have a
call exposure to the vasopressin amines and food mostly to remain perhaps and she's what you find is
that the MAO inhibitor figures actually decreased the ability to file transformative grade these amines
and therefore they can have all of the physiological effects the increase in blood pressure and perhaps
hyperventilation in terms of the some of the mechanisms of vasoactive amines in one study tyramine we
find that it has little bit of an indirect action it actually displaces normal catecholamines in non-nerve
granules I show a picture here of a nerve granules it can lead to chronic hypertension this can be a
severe presentation the presence of MAO inhibitors the vasoactive amines are found in food at
relatively some foods at relatively high concentrations especially cheese tyramine two 2000 ppm
avocado and 25 ppm we find serotonin in banana pulp at 30 ppm avocado and typical typically most
food sources are less than 10 ppm and finally in terms of some of the symptoms of vasoactive amines
hypertension can be mild to severe depending better sensitivity it can be linked to migraine headaches
these food groups are some of the foods that are counseled individuals in terms of food avoidance for
response to migraine headaches are rarely you can see the presentation of intracranial bleeding or
death with swift populations that are very sensitive to this class of compounds next category of naturally
occurring food toxicants is the eliciting alkaloids if you recall with spoken of the PAs several times in
food toxicology this semester this presents itself as a problem in food animals forge because grazing
animals to have access to some of the plants of the toxic plants that do contain PAs but we do get them
into human subpopulations through exposure via either a toxic incident will talk about a case study that
happened totally understand about a decade ago or through cultural food types for instance Native
Americans or other sort of subgroups that actually each specific foods and those foods happen.
Relatively high and pure eliciting alkaloids these levels of these alkaloids can occur in some plants at a
significantly high levels about 5% dry weight there were hundred different conferences great diversity of
chemical structure and outcome the PAs that outcome is typically associated with hepatotoxicity in
some form most human exposure does occur from herbal teas we talked about comfrey tea that is not
commonly available nowadays but you can still find it to them being sold this those have eliciting
alkaloids in it typically though what you find in terms even toxic hostesses crop or foodstuff
contamination we do have the ability to have low-level exposure in terms of the metabolites from milk
or meat but she is usually the main vector terms of the fragrances and tastes of some of the plants for
common tea or medicinal herbal tea applications one of these is Bush tea use in Jamaica there is a
decreased use of comfrey comfrey has astringent properties and still was used to and wound dressing
one of the concerns we have over your eliciting alkaloids is the carcinogenicity because of its red activity
with liver hepatocytes one of the ways we see the progression of liver toxicity is to feel occlusive disease
with your eliciting alkaloids this is an occlusive lesion is produced in some of hepatic veins cycles of
lesions being lesions that block the flow this particular obliterating and though phlebitis actually stops or
inhibits flow of blood into the liver that it leads to edema narrowing and occlusion of the ruling on the
pathways within the liver atrophy and finally necrosis of liver cells from lack of energy resources due to
block blood flow portal hypertension terms of the backup of blood flow from the portal vein is another
diagnostic criteria for video clips of disease in Tajikistan in 1992 there was an episode of widespread per
eliciting alkaloids toxicity what happened this particular cases there is a military blockade that
essentially ended with a week late wheat harvest the weeds were able to thrive in the wheat fields and
the week was contaminated with the seeds of heliotrope this is a particular alkaloids eliciting alkaloids
generating species first cases of the illness occurred about six weeks after contaminated bread was
consumed by individuals by the spring of 1993 there had been more than 33,900 cases of illness patients
in stage one of illness had abdominal pain nausea vomiting and age and stage II they had enlarged livers
in stage III they had the assignees or an extended distended abdomen in end-stage final stage there was
hepatic encephalopathy essentially necrotizing destruction of the tissue of liver itself the case of tally in
this particular incident the ratio of the tallies was 1.3% and the fatalities appeared to increase with age
another class of compounds that has direct impact on human diseases is one that is under study are the
anti-nutritional compounds known as protease inhibitors of these particular compounds are found in
legumes greens potatoes a pleasant onions or mode of action is to inhibit gastric enzymes that break
down various proteins such as a consumer protease type enzymes the toxicity studies that we found
that out animals we really don't know how these chemicals of these previous others affect humans it's
somewhat unclear what we do find is that there is evidence for pancreatic hypertrophy were we find a
hyper section of amino hyper secretion of amino acid rich proteins on this will lead to an amino acid
deficiency and some growth retardation of due to the court declined nutritional status we see that this
particular mode of action disease endpoint has a similar mechanism of laughter is there other possible
natural toxicants in the human diets are too many to talk about the inner class like food toxicology some
of these in terms of the ones we use quite often are exposed to quite often Units alkaloids various
chemical compounds in terms of flavors and fragrances and spices licorice and it makes Sassafras licorice
root is pictured here and then the final elections that are found in many foods some of these natural
toxicants and specific doses impurities can actually be used as medicinals some of these have significant
undesirable effects of your coffee drinker and you drink caffeine we spoke before in the course about
the father being alkaloids in the presentation of fathers in these alkaloids of icing, lysine and they cause
of fabless and people that have an enzyme deficiency of glucose six phosphate dehydrogenase this
happens in some segments black Africans being one subpopulations the presentation of far clinical signs
include headaches and dizziness nausea some yachting's vomiting and insists abdominal pain fever there
can be a subsidence of symptoms at this point in time in some the real presentation of acute hemolytic
anemia where the actual red blood cells release of their hemoglobin and all kidney problems will follow
these are the structures of the father being alkaloids aside, by scene by scene collectives or another
category of flow naturally occurring toxicants we've introduced before these are proteins are
glycoproteins on the combine various types of carbohydrates in the figure at the bottom of the slide you
can see a poultry lectins that actually is binding complexation with the lactose in this particular model
some of this binding capacity of lectins will cause cells to nature club together this is not just not a good
thing in terms of human health there are some blood type assays in terms of nation assays that look at
the cleanliness of your blog if you will what the motive action in terms of lectins it's not perfectly well
understood it appears to decrease nutrient absorption from intestinal cells there are over 800 species of
plants that are lectins sources we also get them from animal tissues some of the sources include black
beans soy beans lima beans and kidney beans the example I used in previous lecture some of problems
associated with collectives in terms of because they they interrupt the nutritional transport that can
cause growth retardation for consumption of raw product some of these are very toxic you probably
have heard of ricin in these days of terrorism and potential for chemical warfare ricin is elected and that
comes from the castor bean the rat LD50 is .05 mg per kilogram or 15 µg per kilogram very is highly toxic
phytochemical is responsible for growth retardation in cases where 1/2 to 1% of the diets is black beans
or soybeans heating will destroy toxicity and as we spoke before uncooked or undercooked beans can
be a source of selected toxicity mechanism of action for lectins it's so unknown there seems to be a
complex motive action in terms of leading to disease we do know that there is an action where it
prevents nutrient uptake there is apparent that floor involvement and there apparently is an immune
come on perhaps in terms of an allergic sort of response and progression of disease what this does is
give us finally a Lisa looks into the presentation of disease among the follow-through in terms of the
determining the causation of the disease from a naturally occurring toxic this gives us a little bit of
thought way to sort of understand the balance of naturally occurring chemicals in the human food chain
with the synthetic chemicals that do appear contaminate the human food chain gives us food for
thought if you pardon that image in terms of the relative saw that the media gives in terms of synthetic
chemicals in the human food chain versus some of these naturally occurring hard to blame nature words
it's very easy to blame perhaps the manufacturers of synthetic chemicals and perhaps rightfully so
people or individuals or companies that pollute the environment
will follow through with more analyses in terms of our explorations in the sources pathways receptors
controls food toxicology for lifetime for lunch