Suicide, often increasing among youth, linked with infant feeding practices

by DP Meulenberg*

Contents:

Introduction:  Youth suicide has been greatly increasing among youth in the U.S. and some other countries in recent decades, prompting efforts to reduce it, with little success.

Section 1:  Association between youth suicides and infant feeding type.

Section 2:  Developmental toxins that have become highly prevalent in much infant feeding in high-income countries in the last half century.

Section 2.a:  Recognized vulnerability of development to toxins during the early postnatal period;

Section 2.b:  Presence of developmental toxins in typical infant feeding in quantities far exceeding established safe doses;

Section 2.c:  Evidence of neuro-developmental toxicity;

Section 2.d:  Greatly amplified exposure of developing infants to toxins, depending on type of feeding;

Section 2.e:  Recognized long-term effects of PCBs and dioxins that are relevant to mental health:

  -- damage to the blood-brain barrier by PCBs;

  -- endocrine disruption, including reduction of testosterone and alteration of sexual orientation, related to suicidality.

Section 3:  A closer look at the link between suicide rates and breastfeeding rates.

The pattern of high or low breastfeeding predicting high or low suicides among youth seems to apply in all average cases among high-income countries;

in every case where a high-suicide country doesn't have a high breastfeeding rate among youth, there appear to be unusually strong cultural or national risk factors that increase the likelihood of suicide.

Section 4: A surprising coincidence between a low year in breastfeeding rates and the birth year related to a low point in later suicides

Section 5: Is it time for a re-examination of the case for breastfeeding, as applied to high-income countries?

Introduction:  Suicide in the U.S. was a sufficiently serious problem at the beginning of the 21st century that the U.S. Institute of Medicine was motivated to publish a 512-page book in 2002 entitled, Reducing Suicide:  a National Imperative.¹   In 2001, the Harvard Institute of Economic Research devoted an entire publication to the subject indicated by its title: Explaining the Rise in Youth Suicide.²  Since those years, the already major problems addressed in those publications have increased:  suicides in the U.S. grew steadily, a total of 31%, between 2001 and 2017.³  The suicide rate for white children and teens between 10 and 17 increased 70% between 2006 and 2016, according to the U.S. Centers for Disease Control and Prevention.⁴  Judging by the huge (40%) unexplained increase in "unintentional injury" deaths in the U.S. between 1999 and 2017,^4a the number of actual (but un-acknowledged) suicides has almost certainly been even greater than indicated just above.  Among U.S. students in grades 9-12 during 2013-14, 13.6% made a plan about how they would attempt suicide in the previous 12 months, and 8% actually attempted suicide one or more times in the previous 12 months.⁵  That indicates an extremely large number of American youth in serious mental distress.

There have been national initiatives in 28 countries that have been aimed at reducing suicides, including (a) restrictions on lethal means and (b) early identification and treatment of depression.⁶  So even in countries where declines have been reported in completed suicides, the underlying mental problems that lead to suicidal thinking among young people may well have been continuing unabated or even increasing.

Section 1:  Association between youth suicides and infant feeding type:

A 2009 publication provides information about youth suicides among countries of the OECD, presented in the chart below, indicating greatly varying rates internationally.

Fig. 1

Above is from Doing Better for Children, OECD 2009, Ch. 2, at https://www.oecd.org/social/family/43570328.pdf

There are reasons to question the accuracy of the reporting of suicides in various countries, such as varying amounts of stigmatization associated with suicide;⁷ but some studies have concluded that, despite reporting issues, suicide data are comparable across countries.⁸

Another chart provided by the OECD presented data about exclusive breastfeeding among very much the same group of countries, for three different durations, of which the three-month duration is the most complete.  This is worth a closer look, to compare with higher and lower suicide rates in Figure 1.

Fig. 2

Above chart accessed at https://www.oecd.org/els/family/43136964.pdf

We can see a relationship that may at first seem surprising:

Of the countries in the top third of breastfeeding rates, a majority (Iceland, Norway, Australia and New Zealand) are also in the top third of suicide rates.

Of the countries in the bottom third of breastfeeding rates, a majority (U.K., Mexico, Italy and Netherlands), are also in the bottom third of suicide rates. 

So we see what might be a pattern formed by the majorities in both the high and the low groups, judging by comparing the above two charts.  These charts permit only a rough comparison, especially since the breastfeeding data is too recent to apply directly to the infancies of the 15-19-year-olds whose suicides are represented in Figure 1.  But what we see is sufficient to arouse curiosity about a possible biological relationship between youth suicide and developmental toxins that are recognized to be present in human milk in industrialized countries (see Section 2); we can look more closely later at possible correlations internationally between suicide rates and breastfeeding rates (Section 3).

The upcoming Section 2 will show that there does appear to be good evidence about neurodevelopmental toxins in human milk in developed countries in concentrations that imply a plausible relationship to later suicidal tendencies.  Section 3 will deal with various cultural and national risk factors for suicide, which are relevant to a pattern relating suicides to infant feeding history.  

Section 2:  Certain developmental toxins have become highly prevalent in much infant feeding in high-income countries in the last half century:

Bear in mind that Figures 1 and 2 above provided data for countries that are members of the OECD (Organization for Economic Cooperation and Development).  As can be seen in the chart below, the average of the per-capita national incomes of OECD countries (the blue line) is many times the averages for middle- and low-income countries (the green and maroon lines).

Fig. 3

(The above found at https://read.oecd-ilibrary.org/education/trends-shaping-education-2016/gap-between-richer-and-poorer-regions-widens_trends_edu-2016-graph7-en#page1)

Industrialization leads not only to higher national incomes but also to pollution; pollution-reduction efforts are unevenly effective, and contamination from the past tends to persist in the environment.  Pollution from traffic emissions would be expected to be higher in countries where there are more cars per capita (therefore in OECD countries).  

Note in Figure 3 above that the income gap between the OECD countries and the rest of the world has become large only since the mid-20th century.  A basic element of much of the economic development that led to the income gap has been production of chemicals, which rose dramatically during that same period.

Fig. 3.a

Chemicals enter the human environment during production, when in use in consumer products and buildings, (especially) during combustion, and while present in landfills.  So children who have grown up in OECD countries during the more recent decades would have been likely, during their vulnerable developmental periods, to be exposed to unprecedentedly large amounts of certain environmental pollutants, compared with children in earlier times.  Specifics will follow.

Section 2.a:  Recognized vulnerability of development to toxins during the early postnatal period:

There is considerable evidence from authoritative sources (including the U.S. National Academy of Sciences, the U.S. Agency for Toxic Substances and Disease Registry (ATSDR), and the EPA) verifying the special vulnerability of neurological development to toxins during the early-postnatal period.⁹ So we should consider how toxins ingested during infancy might relate to mental health many years after infancy.  Relevant information on this topic is provided in The Faroes Statement, which was by 23 authors from around the world, many of whom were highly-published experts; this statement was an outcome of a conference sponsored by seven health- and environment-related agencies of the U.S. and European governments and WHO.  Those authors were deeply concerned about the special "susceptibility of early development" to environmental toxins; they referred to the "foetus and small child as highly vulnerable populations," pointing out that chemical exposures during early postnatal life may predispose to disease during adolescence and adult life.  PCBs were one of the few specific chemicals about which they expressed concern.¹⁰

Also see the discussion of EPA-recognized postnatal effects of PBDEs later in Section 2.b.

Section 2.b: Presence of developmental toxins in typical infant feeding in quantities far exceeding established safe doses:

It is of interest to look at data about levels of some developmental toxins that are recognized to be present in typical infant feeding in concentrations that exceed established safe levels; see below.

Fig. 4

(Above condensed from 2017 study at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5225187)

Update on the basis for the calculated safe levels (dashed vertical red lines) shown above:  In 2001, the European Commission’s Scientific Committee on Food set a safe level for dioxins and dioxin-like PCBs that was similar to the level determined by WHO in 2001, which was the standard that was in effect during the WHO surveys results of which are shown above.¹¹

  However, in November of 2018, the European Food Safety Authority (EFSA) issued a revised statement of tolerable intake that was seven times lower than that established in 2001 by its predecessor Committee, based on new data and on improved assessment methods.¹² So the updated exceedances of tolerable intakes of these toxins, according to the best currently-available evidence and research methods, are probably many times the already major exceedances shown in the charts above.  There is also substantial other evidence, from the U.S. and other developed countries, indicating that exposures of breastfed infants to both PCBs and dioxins in recent decades have exceeded established safe levels by scores to hundreds of times.^{13, 14}

PCBs are ranked by the U.S. Agency for Toxic Substances and Disease Registry as being among the top 5 priority hazardous substances.¹⁵  Dioxin is "often called the most toxic man-made chemical," as stated in a document of the EPA, with no question expressed about the correctness of that assessment. ¹⁶ Exposures to developmental toxins such as these during early childhood have been increasingly recognized to have major effects later in life, as discussed earlier in the Faroes Statement.

PCBs and dioxins have been declining in many countries' environments since the 1970's; but they are called persistent for good reason, and they continue to be emitted, typically by combustion processes, including vehicular emissions.  As shown in surveys from the 2000's in Figure 4 above (and in the accompanying text), those toxins are still present in typical human milk in concentrations greatly exceeding established safe levels.  And they are much more highly present in environments of developed than of developing countries.^16a

Other hazardous chemicals to which vulnerable, developing infants have been exposed only beginning in the mid-20th century: 

The chart below is not about substances related to depression and social problems that are directly linked with suicide, but it does deal with chemicals that

    a) are relatively new in the environment, beginning in about the mid-20th century,

    b) have been found to become part of human milk in concentrations that vary in relation to effects on neurological development, and

    c) apparently affect mental development in ways that could affect a person's satisfaction with life.

Fig. 4.a Correlation between infant DDT exposures and test scores in 10 countries and 14 German states

This chart can also be accessed as of July 2019 at https://pdfs.semanticscholar.org/3420/8edaf63e7068c2b2e4970a52109ffd030ef3.pdf

Although DDT has been banned for most uses in most developed countries, its continued use (for malaria control and agriculture) in developing countries means that it is widely present not only there but also in developed countries in a high percentage of fruits, vegetables, and farm-raised seafood consumed, since much of that is imported.¹⁷

The fact that concentrations of DDT in human milk correlate with mental development doesn't mean that human milk is the chief pathway for these apparently harmful exposures to developing children; but there are good reasons to see that breastfeeding is, in fact, the chief pathway for DDT to children, as follows:

  -- Concentrations of DDT (and some PCBs) were found to be ten times as high in breastfed infants as in bottle-fed infants after six months of breastfeeding, in a 2005 study in Germany;¹⁸

--- Organochlorine concentrations (including metabolites of DDT) were found to be still four times as high in breastfed infants as in bottle-fed infants at age four, and still over twice as high at age 14; those findings were from a 2015 study in a western country (Spain) in which DDT was banned in 1977.¹⁹

  -- Quoting from a publication of a commission of the U.S. National Academy of Sciences, “measurements have consistently demonstrated that no pesticides are detected in finished infant formulas.  These invariably negative analytical findings are attributable to ingredient selection and processing procedures that reduce the potential for pesticide residues to appear in the finished product.”²⁰ In 2013, the U.S. Department of Agriculture reported testing over 300 samples of infant formula and finding no detectable pesticide in 100% of dairy-based formula tested and in 99.4% of samples of soy-based formula that were tested.²¹

PCBs, dioxins and PBDEs in traffic emissions:  In a 2013 U.S. study of PCB concentrations in carpet dust in homes at various distances from possible pollution sources, PCB concentrations were found to be about five times as high in homes within 600 yards from major roads in Los Angeles as they were in homes that were over 1100 yards from those roads;²²  In a study in Colombia, measurements of PCBs and dioxins taken near vehicular sources were found to be almost six times as high as measurements made over a mile farther away.²³.   Similar results concerning PCBs in traffic emissions were found in a study in Stockholm, Sweden.²⁴.

Dioxins:  A 2009 Czech study found "dramatic decreases" in concentrations of pollutants (including dioxins) in soil according to distances from roadways.  Concentrations next to roadways were found to be as high as in industrially-polluted areas; and the concentrations of dioxins were found to decrease, stepwise, with progressive distances from roadways up to the last distance measured.²⁵

PBDEs, which are chemical relatives of PCBs and best known as flame retardants, are similar to PCBs in that they are

   a) toxins that can cause impairment, being listed in the TENDR group of the six toxins of greatest concern,²⁶ and

   b) produced by combustion, including in vehicle engines.

Fig. 4.b

During the period (beginning in the 1970's) when PCBs and dioxins were declining in environments, PBDEs were rapidly increasing.

PBDEs are apparently produced in vehicle emissions in even greater amounts than PCBs.  A Taiwanese study found that concentrations of PBDEs in vehicle exhausts were 17 to 140 times as high as concentrations of PCBs, in the different vehicles tested.²⁷ (When reading that, remember from above how high PCBs have been found to be in vehicle emissions.)  In a 2010 study, the PBDE emission rate from tailpipe exhaust of just one unleaded-gas-fueled vehicle was found to be about four times higher than that from one U.S. house and garage.²⁸  (Bear in mind that U.S. houses, usually containing many flame-retardant-treated furnishings and electronics, are themselves substantial sources of PBDE dust.²⁹

So OECD countries (with their higher income levels) would have distinctly large numbers of

   a) vehicles emitting PBDEs, PCBs and dioxins and

   b) residences containing many flame-retardant-treated furnishings and electronics -- emitting PBDE dust.  That would mean that long-term neurological effects of infant exposures to PBDEs would be especially likely to show up in a chart (such as Figure 1) that shows adverse outcomes specifically in OECD countries. 

In a discussion of PBDEs, the EPA refers to those toxins' “adverse neurobehavioral effects following exposure during the postnatal period."  (The italics, not in the original, were added here to reinforce the point that these chemicals are known to have adverse neurodevelopmental effects resulting from exposures occurring after birth; that emphasis was added because prenatal exposures seem to draw inappropriately predominant attention; see text next to Figure 5.)  The EPA clearly sees those effects of PBDEs as being serious; they refer to neurobehavioral effects of PBDE exposures as being a “critical endpoint of concern.”³⁰

A typical adult's intakes of PBDEs are recognized to be mostly from dust,³¹ which would include traffic-related dust as well as dust from flame-retardant-treated furnishings and electronics.

Specifics about PCBs as developmental toxins contained in traffic-related pollution:

According to the U.S. Agency for Toxic Substances and Disease Registry, "PCBs are readily absorbed through the gastrointestinal tract, respiratory system and skin," followed by distribution to and accumulation in adipose tissue.³² (The respiratory system and skin would therefore be effective means for human intake of PCBs from traffic emissions.)  PCBs are stored in breast milk fat, resulting in their being excreted in the milk during lactation. The ATSDR document also points out, "Transfer of PCBs via breast milk can be considerable and, like prenatal exposure, has the potential to contribute to altered development." (p. 381)  

In studies published as of 2010, PCBs had been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. ATSDR, according to the Oregon Department of Environmental Quality.¹⁴  The studies on which the just-mentioned figures were based were probably not conducted specifically in high-traffic areas, so the average exceedance of the minimal risk levels would very likely be even higher for families living near major roads.

Section 2.c:  Evidence of neuro-developmental toxicity:  

PCBs: According to the Washington State Department of Ecology, there is considerable evidence indicating that PCBs "impact normal brain development."  Based on a review of many studies related to effects of PCBs on development, an expert in this field summarized, "The general conclusion is that the higher the child’s exposure to PCBs in early life, the lower the IQ and the more the child exhibits anti-social behavior, depression, and attention deficit hyper-activity disorder-type symptoms."³³

The reader should consider the relevance of exposure to toxins that lead to depression and anti-social behavior, in our discussion of exposures that could be linked with suicides.  The link between depression and suicide is well-recognized, and confirmed in multiple studies;³⁴ a meta-analysis of four studies found a 20-fold increased risk of suicide among those with major depressive disorder.³⁵  And, according to a 2010 study, increased suicide risk may typically follow social withdrawal and breakdown of social bonds.³⁶  Also, the reduced IQ and the attention deficit hyperactivity disorder that are linked with developmental PCB exposure would lead to more difficulties and worse outcomes in both school and work life, probably decreasing life satisfaction and increasing likelihood of suicidal tendencies.

PBDEs:  A U.S. study published in 2017 states that flame retardants (mainly PBDEs) in preschool children "were found to be linked with both more negative and less positive social behavior," and "this represents substantial risk for difficulty with academics, social relationships, and mental health."³⁷ As discussed above concerning effects of PCBs, negative social behavior and reduced mental health are recognized to be relevant to suicidal tendencies.

Neurodevelopmental effects of dioxins:  See the later section on Endocrine (hormone) disruption.

Section 2.d:  Greatly amplified exposure of developing infants to toxins, depending on type of feeding:

One study (by a team of researchers who are authors of a total of over 740 studies and articles) calculated that 91% of a typical U.S. breastfed infant’s total exposure to PBDEs was from breast milk.³⁸ Assuming such a percentage, a maximum of 9% of an infant's PBDE exposure would normally come via all of the pathways that lead directly from the environment; ten times that amount would be transferred via breastfeeding. That implies that a breastfed infant receives a ten-fold magnification of environmental exposures to PBDEs.

Another way of describing what takes place:  Two experts on toxins involved in child development reported in 2006 that “Persistent lipophilic substances, including specific pesticides and halogenated industrial compounds, such as PCBs (chemical relatives of PBDEs), accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”³⁹

According to data concerning the specific type of PBDE (BDE 209) that has been the most widespread type in recent years, especially in vehicle emissions, concentrations of that chemical have been found to be 800 to 9000 times as high in typical human milk as in infant formula.⁴⁰

The concentrating effect of lactation in relation to PBDEs and their chemical relatives, PCBs and dioxins, has also been observed in many other studies.⁴¹

………………..

A WHO/ UNICEF publication⁴² discusses the presence of PCBs and dioxins in breast milk and acknowledges that "there is evidence that these compounds can cause developmental neurotoxicity."  The publication goes on to say (p. 241), "Nevertheless, although relatively large amounts of PCBs and dioxins can be ingested by a breastfed infant, as yet no adverse effects have been found that outweigh the positive effects of breastfeeding on infant development."  No references or evidence are offered in support of that, which is a good indication that the statement lacks scientific basis; the publication does contain 372 references, in accord with the recognized need to provide evidence to support statements in science; so failure to provide evidence in this case strongly implies absence of supporting evidence.

The WHO/ UNICEF publication goes on to state (p. 242), "the risk of exposure through breast-milk is much less than that during the fetal period."  The only reference offered to support that statement is a publication in which the most relevant passages say that a working group concluded (in 1993) that "prenatal exposure appears more detrimental than postnatal;"  and elsewhere, "in utero exposure is likely to have been more significant…."^16a  So the original source is tentative about whether a prenatal-postnatal difference even exists, and it says nothing to imply that any possible differences are major.  But that is picked up by other authors (who are promoting a certain view) and inflated to become a risk that "is," and a risk that "is much less" after birth than during the fetal period.  The serious concerns expressed by the original source about risks of breastfeeding are indicated by its statement that studies "are urgently needed to assess the possible long term health hazards to the newborn and growing infant from the intake of contaminated breast milk."  But the later statement by other authors drawing on that source ignored the expression of urgent need for studies of long-term hazards.  This sort of distortion and half-truth becomes a basis on which people decide that it is reasonable to (indefinitely) continue feeding infants a substance that is undisputedly high in developmental toxins. 

Fig. 5

As indicated by multiple studies in more recent years (see on the right and below), exposures to PCBs (as well as dioxins) are now recognized to actually be far greater after birth, via breast milk, compared with prenatal exposures; and those far greater exposures occur during a period of recognized high developmental vulnerability. (Section 2.a)

The U.S. Agency for Toxic Substances and Disease Registry (ATSDR), in support of its statement that "the amount of PCBs transferred to offspring is expected to be higher during lactation than during gestation," refers to a laboratory experiment as an example:  "In female rats administered PCBs before gestation, an average of 0.003% of the administered dose was transferred to the fetus, whereas 5% was transferred to sucklings."⁴³  That works out to lactational transfer of PCBs over 1600 times greater than gestational transfer, resulting from the same original prenatal exposure; this is a ratio that the ATSDR obviously considers to be relevant to how human lactational exposure compares with human gestational exposure to those toxins.  Studies of humans have found lactational transfers of developmental toxins to be hundreds of times greater than gestational transfers.⁴⁴

.Fig. 6

All of this is relevant to a discussion of the association between breastfeeding and youth suicide, since

   a) PCBs and dioxins are typically present in human milk in developed countries in concentrations that far exceed established safe levels (as seen in Figure 4 above) and since

   b) both chemicals are known to be toxic to neurological development (Sections 2.c and 2.e), and

   c) the postnatal period is recognized to be a time of high vulnerability to developmental toxins. (Section 2.a)

Notice in Figures 5 through 8 and in the quotation from the ATSDR substantial evidence indicating that exposures to these chemicals are recognized to be far greater via lactation compared with trans-placental exposures.  In these charts from studies by several different research groups, levels of PCBs or dioxins in the infant are always seen to be low at birth, after which they either

  (a) increase rapidly as long as breastfeeding continues, typically reaching levels several times those at birth, or

  (b) decline during infancy if breastfeeding is not taking place.

Fig. 7

Fig. 8

Section 2.e:  Recognized long-term effects of PCBs and dioxins that are relevant to mental health:

Fig. 9

Damage to the blood-brain-barrier:  In a 2009 study,⁴⁵ mice were administered PCBs in doses that resulted in a plasma PCB level that is comparable to the levels found in some human populations that have received brief exposures to PCBs.⁴⁶   Shown in this chart is disruption of the blood brain barrier by three types of PCBs administered in that study: The right-hand three bars represent measures of permeability of the blood brain barriers of the PCB-dosed test animals, compared with permeability in the control animals that received only the vehicle (represented by bar on far left). Other studies provide additional evidence of the harmful effect of PCBs on the blood-brain-barrier.⁴⁷

It is not difficult to think of reasons why the condition of the blood-brain barrier is important to mental health, especially as the child grows older.  The brain is particularly vulnerable to damage by toxins, which is why the barrier evolved among animals, including homo sapiens.  Lack of a normally-effective barrier is likely to go unnoticed during the relatively sheltered existence of early childhood; but harmful levels of toxins can accumulate in the brain over the years due to a compromised barrier, especially by the time a youth has spent more time in the outside world engaging in exposure-increasing activities -- such as those related to vehicles, alcohol consumption, and many occupations.

Endocrine (hormone) disruption:

According to the ATSDR, "Depending on dose and duration, PCBs can disrupt the production and disposition of thyroid hormones at a variety of levels;"⁴⁸ and also, "it is agreed that the potential exists for these compounds (PCBs) to affect the synthesis, secretion, transport, binding, action, or elimination of natural hormones in the body...."⁴⁹ Dioxins, also, have been found to have adverse hormonal effects.⁵⁰  According to a publication of the National Academies Press, it has been found in animal testing that lactational exposure to dioxins reduces the weight of and secretions of  the pituitary gland;⁵¹ the pituitary gland plays an important role in balancing hormone levels in the body^50,51a as well as in production of sex hormones.⁵²

As a general indication of the strong relevance of the pituitary gland to suicidal tendencies, it is noteworthy that, in the 2002 National Academies book, Reducing Suicide: a National Imperative,⁵³  the index includes the word "pituitary" in  eight different places.  One of the book's findings was, "Dysregulation of one of the body’s primary stress response systems, the hypothalamic-pituitary-adrenal (HPA) axis, appears associated with suicidality across psychiatric diagnoses."  We do not need to go into detail in order to understand that functioning of the pituitary gland is significantly related to mental health in ways that are relevant to suicide.  Bear in mind (from above) that breastfed infants are exposed to toxins that reduce the size and secretions of the pituitary gland, with the toxins being received in doses many times in excess of established safe levels (Section 2.b).  This should be seen as relevant to a discussion of suicide rates.

Symptoms of hypopituitarianism include depression, low mood, nausea, and exhaustion.⁵⁴  Clearly, these are feelings (very possibly resulting from lactational exposure to dioxins) that, if continued, are not conducive to making a person look forward to continuing life.

All males have some estrogen and all females have some testosterone, but in different proportions. We should consider effects of altered balances of sex hormones, which may result from

  a) dioxin's effect on the pituitary gland (see above), and from

  b) PCBs' effects on the body's production of hormones in general (see earlier).  There are many different variations of PCBs, which have been found variously to have masculinizing, de-masculinizing, feminizing, or de-feminizing effects^52a and/or estrogenic or anti-estrogenic effects.^52b

Altered balances of these hormones might cause some individuals to have sexual orientations that don't fit in with the overall culture of which they are part, or with strongly-held views of family and other people.  Some evidence has shown that environmentally relevant exposures to certain other chemicals (such as PCBs) could affect brain sexualization.⁵⁵ When reading the above, bear in mind that breastfed infants are exposed to dioxins and PCBs in concentrations exceeding established safe doses by scores to hundreds of times. (Section 2.b)  This is relevant to a discussion of suicide, given the finding in a 1998 study in the American Journal of Public Health that male bisexuality/ homosexuality is associated with a seven-fold increased odds of suicide attempt;⁵⁶ a report of the U.S. Department of Health and Human Services stated that gay and lesbian youth were two to three times more likely to attempt suicide than other young people.⁵⁷

Major lactational exposures to endocrine-disrupting chemicals also come during a specific time period when sexual orientation is apparently being determined within the brain.  According to a 2008 article in Proceedings of the National Academy of Sciences, "Current evidence indicates that sexual differentiation of the human brain occurs during fetal and neonatal development."^57a  According to a 2013 study, animal research has indicated that the critical time for sexual differentiation of the brain occurs when differences in testosterone are highest between sexes;^57b related to that, there is a period of elevated testosterone in males beginning shortly after birth and peaking 3-4 months later (Fig. 1 of above ref.); going by the above generalization from animal research, that (along with the 2008 article mentioned above) would imply that critical sexual differentiation of the brain takes place during early postnatal months. According to other authors, neonatal exposure to the sex steroid hormones, estradiol and testosterone, is considered to be crucial for normal sex-typical sexual differentiation of the brain and behavior.^57c  Exposure to PCBs, specifically, during development has been found to alter adult reproductive and other sexually dimorphic behaviors.^57c

The CDC has pointed out that gonadal atrophy has been observed in animal studies of exposures to dioxin-like chemicals.⁵⁸  That agency also states that various different forms of PCBs and dioxins can reduce testosterone levels as well as having either estrogenic or anti-estrogenic effects; remember similar statements from the ATSDR^52b and research scienstists ^52a   And according to a publication of the EPA, "it is well established that PCBs, including both dioxin-like and non-dioxin-like congeners… may affect endocrine systems in vertebrates." (p. 15)^58a

Aside from effects related to hormonal imbalances and thereby to suicidal tendencies, many studies have found that lower testosterone is also associated with depression,⁵⁹ another risk factor for suicide. Anxiety and decreased quality of life are other outcomes, reasonably related to suicidality, that have been associated with lowered testosterone.⁶⁰

...............................

It should be emphasized that testosterone-reducing effects of PCBs and dioxins, and those toxins' effects on the blood-brain barrier and pituitary gland, are well substantiated.  And we should remember that

   (a) PCBs and dioxins in human milk have been authoritatively found to exceed established safe levels by scores to hundreds of times (see Figure 4 and accompanying text), and also

   (b) infancy is a stage at which development is unusually vulnerable to long-term effects of environmental toxins. (see Section 2.a)

Endocrine effects of PBDEs:  A 2013 study found a 9.4% decrease in testosterone levels with each interquartile increase in deca-BDE concentration in house dust, with a fairly high level of statistical significance (p-value - .02).⁶¹ (Other studies have found results compatible with that study's findings.⁶²) The above has special importance in that deca-BDEs were still in wide use in consumer electronic products and home furnishings until 2015, and will long be part of human environments and exposures. Putting the interquartile differences into other words, the above means that the rather common difference in household PBDE dust levels between the bottom quarter and the top quarter of this kind of population would be associated with a 28% (3 times 9.4%) reduction in testosterone levels.   We should consider how much the reduction in testosterone would be if comparing PBDE dust levels in the top 10% with dust levels prevailing before PBDEs entered human environments just a few decades ago.

The above is especially significant in that testosterone is important to male neurological development.⁶³

Remember (from Section 2.d) that, for breastfed infants at a time of developmental vulnerability, direct exposures to PBDEs from the environment are one-tenth of the exposures that occur via breastfeeding.

Section 3:  A closer look at the link between suicide rates and breastfeeding rates, among countries:

As discussed in Section 1, looking at a preliminary comparison, most of the high-breastfeeding countries of the OECD are seen to have high suicide rates among 15-to-19-year-olds, and most of the low-breastfeeding countries have low suicide rates in that age group.  So a closer look at the data is justified, especially now that we have seen (in Section 2) that toxins recognized to be present in human milk in high concentrations in developed countries have been found to have effects plausibly related to youth suicide.

Fig. 1 repeated

Note above that four countries that had high suicide rates in recent times (Iceland, Austria, Norway and Finland) can be seen just below to have had high breastfeeding rates during the relevant early years (figures farthest to the right, below); those were years during which adverse developmental effects resulting from toxins in infant feeding may have led to later mental health problems among the 15-19-year-olds whose suicide data is shown above.

Fig. 11

Three of the other countries in the high-suicide group (Australia, Poland, and New Zealand), which were not included in Figure 11 just above, did apparently also have high breastfeeding rates during the years of the infancies of the youths whose later suicides contributed to the data in Figure 1, as follows:

Australia:  48% breastfeeding at 6 months, as of the year (1995) for which there is apparently the earliest reported data,⁶⁴

New Zealand:  56% breastfeeding at 6 months, as of 1990-1991,⁶⁵

Poland:  58% breastfeeding at 6 months, as of the year (1997) for which there is apparently the earliest reported data.⁶⁶

So, of the ten countries in the top third of suicide rates among the 29 OECD countries, a total of seven apparently had high breastfeeding rates during the time of the infancies of 15-19-year-olds who later had high suicide rates.

Japan was a near-miss to the high-suicide top third:  According to data from a 1991 publication, Japan had a 52% breastfeeding rate at 6 months, which was over twice the rate in the U.S., aligning Japan with the high-breastfeeding/ high suicide pattern.⁶⁷

It is of interest to look closer at the three countries that didn't fit into the high-breastfeeding/ high-suicide pattern:  Belgium, Ireland, and Canada.

Belgium:  Belgium has the world’s most liberal law on physician-assisted suicide, which is not just for the terminally ill; patients with psychiatric conditions, even children, can request euthanasia.  Surveys in Belgium show overwhelming public support for this policy.⁶⁸  In the large Belgian region, Flanders, euthanasia accounts for nearly 5% of all deaths.⁶⁹ So it should be of no surprise that Belgium has the highest overall suicide rate in Western Europe⁷⁰ as well as one of the highest suicide rates in the 15-19 age group, as shown in Figure 1.  So it appears that, as a risk factor for suicide, breastfeeding is less strong than a culture that is very unusually receptive to suicide.

Canada:  Low exposure to sunlight is likely to have a depressive effect, especially on sensitive people; it is probably not coincidental that four of the ten high-suicide OECD countries are far northern -- farther north than 53 degrees latitude.(Iceland, Norway and Finland) or largely that far north (Canada).⁷¹  In addition, Aboriginal youth on reserves in Canada are 5 to 6 times more likely to die of suicide than their peers in the general population;⁷²  this could affect the overall youth suicide rate, since Aboriginal peoples constitute a significant percentage of Canada's population (4.9%),⁷³ with a higher percentage among young people.⁷²

Ireland:  Alcohol appears to be a specific problem related to suicide in Ireland.  In a survey in Northern Ireland, alcohol was above the legal limit in 41% of the suicide cases; percentages were especially high among young people.  A close link between alcohol abuse and suicide has been found in many studies in many countries (including Ireland), pointing to a likely causal relationship, especially among adolescents;⁷⁴ a 10-fold increase in suicides among those with alcohol-dependence was found in a meta-analysis of 12 studies.⁷⁵ A WHO survey found Ireland to be second in the world in binge drinking,⁷⁶ a practice that is especially common among Irish teenagers.⁷⁷

So it should not be surprising that youths in Ireland would have an above-average suicide rate, basically because of misuse of alcohol, despite having had below-average exposures to neurodevelopmental toxins during their infancies.

Fig. 1 repeated

Low-suicide OECD countries (the bottom third, above):

At first, one sees what might appear to be a beneficial effect of greater sun exposure, judging by the countries shown at the low-suicide end of the chart above.  Greece, Portugal, Italy, and Spain are all southern European -- all just south of 45 degrees latitude; and low-suicide Mexico is even farther to the south.⁷⁸  But many higher-suicide countries are also less than 45 degrees of latitude from the equator:  Japan, Korea, New Zealand, Australia, and most of the U.S.  So it appears that, once a certain minimum of sun exposure prevails, additional sunlight may have little or no additional effect in reducing suicides.

But there does seem to be a risk factor that is very consistently associated with the pattern discussed here, of low breastfeeding during infancies being linked with low suicide in the late teenage years.  One can look at each country in the low-suicide group in Figure 1 (repeated above) and then see its low 6-month breastfeeding rate toward the right end of the chart just below -- except that France and Mexico are discussed farther  down.  (The right end of this chart is the relevant place to look, to show data for the years -- around 1988-1993 -- of the infancies of youths whose suicides are shown in Figure 1.)

Fig. 11 repeated

Data in this table taken from table at WHO European Health for All Database at https://gateway.euro.who.int/en/datasets/european-health-for-all-database/, following directions above.

France:  Apparently there were no breastfeeding surveys conducted in France during the 1980's and 1990's, so no data for France is included above.  But there is ample evidence indicating mostly negative attitudes toward breastfeeding in France before 2000, so it is extremely likely that French breastfeeding rates were low during those decades.⁷⁹

Mexico:   A publication of 1992 stated that Mexico had one of the lowest breastfeeding initiation rates in the developing world.⁸⁰   Aside from Mexico's position in relation to the developing world, bear in mind that the principal concern of this article is effects of toxins that are generally more prevalent in human milk in developed countries (Section 1).

To sum up the above:

All ten of the lowest youth-suicide countries in the OECD appear to have had low breastfeeding rates during the period when those youths would have been infants. 

Of the ten highest youth-suicide countries in the OECD, seven had high breastfeeding rates during the period when those youths would have been infants.  The other three countries had either

  --  what are probably the world's most tolerant national attitudes toward voluntarily ending one's own life (in the case of Belgium), or

  -- an exceptionally high level among teenagers of alcohol misuse, a known strong risk factor for suicide (Ireland), or

  -- a substantial minority with a 500%-600% increased rate of suicide among its youth, as well as a latitude range characterized by considerably reduced sunlight (Canada).

Summarizing:  High or low exposures via the breastfeeding pathway predicted high or low suicide rates in 17 out of the 20 grouped countries.  In the few cases in which the breastfeeding exposures did not align with later suicide rates, other risk factors have been unusually prevalent in the country of interest.

So there is reason to give careful consideration to adverse effects of the recognized developmental toxins that are known to be present in human milk.

Section 4: A surprising coincidence between a low year in breastfeeding rates and the birth year related to a low point in later suicides

Notice (below left) a representation of the trend in suicides among U.S. 15-19-year-olds after 2000, as published in the Journal of the American Medical Association.  This can be compared with historical U.S. breastfeeding rates on the right.

Fig. 12.a-b

Notice above that the shape of the relevant section of the 6-months breastfeeding trend line (after 1982) is especially similar to the suicide trend line, tracking about 17 years earlier.

A plausible causal connection?  When trying to determine whether the above was just a chance coincidence, bear in mind that it has been authoritatively recognized that toxic exposures in early childhood can lead to adverse health outcomes in later life (Section 2.a), that breastfed infants in developed countries are typically exposed to PCBs and dioxins in amounts far exceeding established safe levels (Sections 2.b and 2.d), that such toxins may lead to depression and anti-social behavior, both of which have been linked with suicide (Section 2.c), and that those toxins have been found to damage the brain's protective barrier and to have hormonal effects that could lead to suicidal behavior. (Section 2.e)

It is also of interest to look at another, related dataset, below, to see which birth years may have been relevant to later suicidal inclinations.  This data applies to suicide plans, a problem that (compared with completed suicides) applies to a much larger percentage of the population -- 3.7% of 18-to-25-year-olds in 2017.

Fig. 13

We should focus on the upper trend line, which applies to the 18-25 age group, with average age of 21.5.  Subtract 21.5 from the first year of the marked upturn in suicide plans within that group (2012), to see that 1990-91 was the birth year at the beginning of a long-term upward trend in later suicide plans of those children.

So this is a second dataset, providing data about a different, much more widespread suicide-related outcome, and dealing with a different age group, which pointed to essentially the same birth year as the turning point at the beginning of a long-term adverse trend.  And, as seen in Figure 12.b above, that birth year was also when breastfeeding rates were starting to turn upward in the U.S.  The reader may wish to review the paragraph not far above, "A plausible causal connection?"

Section 5:  Is it time for a re-examination of the case for breastfeeding, as applied to high-income countries?

Actually, a better question would be, "is it time for a first-time-ever, balanced consideration of the case for breastfeeding in high-income countries?"  It appears that there has not yet been a rational consideration of this important matter, giving even minimal attention to evidence of adverse effects of the toxins that are authoritatively recognized to be present in human milk.

The American Academy of Pediatrics would probably be the logical U.S. organization to carry out a proper examination of this question, given its area of medical specialization.  But what it has published in this area is essentially entirely one-sided, providing no mention of the serious toxins that are authoritatively recognized to be present in typical human milk (especially in developed countries) in quantities greatly exceeding established safe levels (see Section 2.b); the word "toxin" does not appear even once in the text of its ten-page document, "Breastfeeding and the Use of Human Milk,"⁸¹ even though the AAP does not dispute the considerable evidence about such toxins in human milk. (see Appendix A)  The U.S. Surgeon General would be another presumptive likely source of a balanced consideration of this matter; but, again, the major breastfeeding statement from that office, issued by the Surgeon General in 2011,⁸² does not mention the word "toxin" even once and therefore cannot be considered to be a rational, balanced consideration of the matter.

However, Surgeon General Regina Benjamin did, toward the rear of her publication, provide an acknowledgement that helps reveal the weakness of the case in favor of breastfeeding.  The document points out (p. 33) that research on the health outcomes of different modes of infant feeding is limited to observational studies.⁸² The leading authorities on medical evidence have determined that evidence from observational studies is predominantly of low quality, with evidence from only exceptional ones reaching a medium level of quality.  One such determination has been provided by Dr. Gordon Guyatt and an international team of 14 associates;⁸³ Dr. Guyatt is chief editor of the American Medical Association’s Manual for Evidence-based Clinical Practice, in which 26 pages are devoted to examples of studies (almost all of which were observational) that were later refuted by high-quality studies.⁸⁴

A similar assessment of the low quality of evidence from observational studies has been provided by the other chief authority on medical evidence, Dr. David Sackett,⁸⁵ writing about “the disastrous inadequacy of lesser evidence,” in reference to findings from observational studies.⁸⁶  Dr. Sackett was said by the British Medical Journal to have been "widely regarded as 'the father of evidence-based medicine.'"⁸⁷

When people choose or decide not to choose an intervention, such as breastfeeding, that introduces "confounding" due to different types of people choosing one or the other alternative.  Specifically, mothers of higher socio-economic status in the U.S. and various other countries (people with better health-related circumstances) are much more likely to choose to breastfeed than mothers of lower status;⁸⁸ similarly, women who adhere to medical guidelines and who therefore also have better health habits in general (the "Adherer effect"⁸⁹) are also unusually likely to breastfeed.  In both cases, this causes confounding as to what are the real causes of the differing health outcomes.  Better child health is found to be associated with breastfeeding, and inferential conclusions are typically drawn on the basis of those associations; but the associations could well be caused by the confounders.  Defenders of observational studies say that they can control or adjust for confounders, but according to Rory Collins, an epidemiologist at Oxford University, “you can’t measure these things with precision so you will tend to under-correct for them. And you can’t correct for things that you can’t measure.”⁹⁰

There can be no doubt that "adherers" among mothers would be very predominantly breastfeeders, considering the strong promotion of breastfeeding that comes from the medical community⁹¹ as well as from many seemingly-informed private citizens.  The adherer effect stood out in the case of hormone replacement therapy (HRT).  This therapy was found in many observational studies to be beneficial for women who faithfully complied with it.  As of the mid-1990s, the American Heart Association, the American College of Physicians, and the American College of Obstetricians and Gynecologists had all concluded that the beneficial effects of HRT were sufficiently well established that it could be recommended to older women as a means of warding off heart disease and osteoporosis.⁹²  A 2004 meta-analysis concluded, after examination of 31 studies on the topic, that HRT therapy led to a large reduction in heart disease.⁹³

But when results came in from randomized studies, the study type recognized to be able to provide high quality evidence, it was found that outcomes of the HRT therapy were actually worse rather than better.  According to a New York Times article quoting Dr. Jerome Avorn, a Harvard epidemiologist, the observational studies may have inadvertently focused their attention specifically on the “Girl Scouts in the group, the compliant ongoing users, who are probably doing a lot of other preventive things as well.”⁹²   There are good reasons why the leading authorities on medical evidence have such low opinions of observational studies; such studies are thrown off by confounders such as the adherer effect.

Given the weakness of evidence from observational studies, attempts have been made to get around the confounding effects of the kind of mothers who do and the kind of mothers who do not choose to breastfeed, and of their home environments, by introducing randomized exposure to breastfeeding promotion.  The largest study yet conducted on the health effects of breastfeeding, published in the Journal of the American Medical Association, was also the only such study that has utilized an element of randomization:  the PROBIT study conducted in Belarus, with over 17,000 mother-infant pairs, following the children's outcomes at stages up to age 16.⁹⁴  The researchers gathered data concerning an experimental group whose breastfeeding rates were greatly increased by major promotion of breastfeeding, comparing that with data from a control group whose breastfeeding was relatively minimal.  The study found that risk of overweight/obesity at age 16 was significantly increased (odds ratio of 1.14) among children who had been breastfed for longer terms, compared with children who had received less breastfeeding.  This result contrasted strongly with results of various observational studies that have found obesity to be reduced by breastfeeding, findings that the authors of the PROBIT study attributed to confounding that typically distorts findings of observational studies.  Also, outcomes at age 16 (in the latest phase of the PROBIT study) were seen to be better predictors of long-term health than results at the young ages at which data is gathered in most studies.

The authors pointed out that their analysis "likely underestimates the magnitude of effect of breastfeeding exclusivity and duration (italics added), owing to overlap in breastfeeding between the randomized groups – many intervention mothers did not exclusively breastfeed for 3 or 6 months, and some control mothers did."   So the true increase in obesity resulting from breastfeeding is likely to be even higher than as found in this study, according to the authors.  They also suggested that the reason for increased obesity resulting from breastfeeding might be hormones in breast milk altering the child's lipid metabolism, thereby increasing body fat in later life; the authors cited a study in the Journal of Nutrition in support of that idea.

The above (apparent) correction of a typical belief about breastfeeding's effects also fits well with what has happened with obesity prevalence in the U.S. in recent decades, while breastfeeding has been greatly increasing.  Note (in Figure 12.b) that breastfeeding at 6 months in the U.S. increased more than six-fold between 1970 and 2000, then see (below) what happened in child obesity in the years after 1976:

Fig. 14

The more-than tripling of child obesity during these years is very compatible with the dramatic increases in breastfeeding that took place after 1970.

Sibling studies, which are the other principal means of trying to determine effects of an exposure such as breastfeeding while avoiding confounding, have also arrived at findings of interest.  If one sibling is breastfed and the other is not, comparisons of outcomes of those "discordant" siblings should not be distorted by differences between families in areas such as nutrition, adherence to health guidelines, and residence in neighborhoods with varying levels of environmental toxins. 

In a sibling study of breastfeeding effects (Colen and Ramey, 2014⁹⁵), based on thorough analysis of 25 years of data from the National Longitudinal Survey of Youth (NLSY), using breastfeeding data obtained within two years of birth and focusing on longer-term health effects, the authors found the following:  the same pattern was indicated by two different approaches in the analysis, "whereby estimates of the effect of breastfeeding on a diverse set of childhood outcomes are substantially attenuated toward zero when we rely on sibling comparisons."  Estimates of breastfeeding's effects on obesity, based on breastfeeding duration, switched from reduction of obesity (when between-family differences were present) to increase of obesity when comparisons were made between discordant siblings.  Some other health outcomes of breastfeeding, also, switched from favorable to unfavorable when comparisons were changed to the between-discordant-sibling method of comparison.  Poorer outcomes in asthma were found to be consistently associated with breastfeeding duration across all methods of comparing the data.   The authors pointed out that their findings "are consistent with those from a small but growing literature that seeks to more accurately assess the association between breastfeeding and child health and wellbeing."

Fig. 15

The poorer outcomes in asthma that were found to be consistently associated with breastfeeding duration, across all methods of comparing the data in the Colen and Ramey study, are supported by the historical data in the above chart, in line with historical increases in breastfeeding. (see Figure 12.b).

None of the regression coefficients in the above study reached statistical significance.  However, the true effects of breastfeeding may well be worse for the child than as found in this study; the authors pointed out that, despite the discordant sibling method of comparison, there could still be bias in favor of the breastfed infants:  "All of the scenarios we can call to mind in which siblings are differently fed favor the breastfed sibling – for example, sibling A is born full-term and breastfed while sibling B is born preterm and bottle-fed."⁹⁵  So the true effects of breastfeeding could well be even worse than as found in this study.

A follow-up PROBIT study investigated data about 16-year-old children in the two groups that had received or not received the randomized promotion of breastfeeding, resulting in findings of interest.⁹⁶  (Similarly to an earlier stage of the PROBIT study, the authors described this phase as "the largest randomized trial in the area of human lactation," but this time including "a high follow-up rate to age 16 years.")  Neurocognitive function in seven different areas was assessed by means of a computerized, self-administered test.  It was found that children in the intervention (higher-breastfed) group had slightly higher scores in the verbal area (1.4 points difference), but there were no significant differences in other areas.  Higher verbal scores had also been found when the children had been tested at age 6.5, but the difference was "substantially smaller" at age 16.  Noting the authors' observation that long-term effects of breastfeeding on neurocognitive development decrease substantially with advancing age, a likely outcome to consider is eventual total disappearance of even that minimal breastfeeding advantage by adulthood, following more exposure to non-maternal influences.  The authors acknowledged that better verbal function in breastfed children might be explained by factors such as more verbal exchange during breastfeeding compared with bottle feeding, in support of which they cited two studies.

Even if the slight verbal advantage should persist into later years, this study (incorporating randomized increase of breastfeeding as well as being outstandingly large) provides excellent basis for disregarding the findings of the many observational studies, with their recognized problem of confounding, that have found overall cognitive benefits of breastfeeding.

Again, actual historical data about levels of neurological problems aligns well with the  updated knowledge about neuro-developmental effects of breastfeeding.   But demonstrating that alignment becomes too lengthy to include here, so that section has been made into Appendix B, conveniently accessible near the end of this article.

Studies finding autism to be higher in association with greater duration of breastfeeding:

A 2011 study that investigated data from all 50 U.S. states and 51 U.S. counties found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."⁹⁷

Note that, according to the EPA, “Epidemiologic studies of exposed human populations provide the most convincing evidence of human health effects.”⁹⁸ Also, a dose-response relationship between an exposure and a health outcome is considered to be especially significant evidence to support a finding of cause and effect.  One example of a dose-response relationship, as found in an epidemiological study by a well-published scientist (R.J. Shamberger), was quoted in the previous paragraph.  This finding was even more significant in that it was based on investigation of a very large, diversely-populated geographic area (all 50 U.S. states), and it also applied in relation to numerous smaller-scale units (51 counties). 

Additional support for a causal connection between breastfeeding and autism was provided by three additional, relatively recent studies, with a dose-response relationship being apparent in the overall view of those three studies, with increasing odds of autism in parallel with greater durations of breastfeeding.

-- In a 2011 Canadian study of a population of over 125,000 (Dodds et al.), using discharge from the hospital as the dividing line for breastfeeding exposure, there was a 20% higher autism rate among the breastfed children than among non-breastfed children.⁹⁹

  -- In a 2009 U.K. study, the duration of breastfeeding that was assessed was four weeks versus less than four weeks.  65% of the autism cases had received exclusive breastfeeding for at least four weeks; that should be compared with only about 28% of the general U.K. infant population receiving that much breastfeeding.  That meant a 130% higher odds of having had that much breastfeeding, among those with autism.¹⁰⁰

  -- In a 2010 American study in Kentucky by an MD/PhD team, the duration of breastfeeding used for comparison was six months.  37% of autism cases had received that much breastfeeding, compared with 13% of the controls, indicating an approximately 185% (37%/13%) greater likelihood that the autism cases would have had more breastfeeding.  The p-value was .003, implying three chances out of a thousand that the finding was a result of chance occurrence.¹⁰¹

In the Dodds study, significantly increased odds of autism were found in relation to breastfeeding as determined by three different ways of analyzing the data, and the odds of autism in relation to breastfeeding increased with each improvement in the analysis.⁹⁹

For additional studies relating breastfeeding to autism, see Section 4 of www.pollution-effects.info.

Childhood cancer incidence:  Promoters of breastfeeding point to (observational) studies that have found childhood leukemia incidence to be reduced by breastfeeding.  That should prompt a question about other types of cancer.  See some data (from cancer.gov) below about childhood and total cancer incidences in recent decades, during which breastfeeding greatly increased (Figure 12.b)

One can see that childhood cancer incidence increased significantly through the decades during which breastfeeding greatly increased.  But we see on the left that cancer in the total population (even including the increases in childhood cancer) was declining after 1991.  So we should consider any carcinogens to which children may have been exposed, to which the adult population has not been so exposed.

We should then note that multiple studies have found PCB exposures to be associated with various types of cancer,¹⁰² and PCBs are classified by the IARC as carcinogens and by the EPA as probable carcinogens.  Dioxins are known carcinogens.  Remember from Section 2.b that PCBs and dioxins have been found to be present in typical human milk in concentrations scores to hundreds of times established safe levels.

*About the author:

As the author of the above, my role has not been to carry out original research, but instead it has been to read through very large amounts of scientific research that has already been completed on the subjects of environmental toxins and infant development, and then to summarize the relevant findings; my aim has been to put this information into a form that enables readers to make better-informed decisions related to these matters.  The original research articles and government reports on this subject (my sources) are extremely numerous, often very lengthy, and are usually written in a form and stored in locations such that the general public is normally unable to learn from them. 

My main qualification for writing these publications is ability to find and pull together large amounts of scientific evidence from authoritative sources and to condense the most significant parts into a form that is reasonably understandable to the general public and also sufficiently accurate as to be useful to interested professionals. My educational background included challenging courses in biology and chemistry in which I did very well, but at least as important has been an ability to correctly summarize in plain English large amounts of scientific material.  I scored in the top one percent in standardized tests in high school, graduated cum laude from Oberlin College, and stood in the top third of my class at Harvard Business School.  

There were important aspects of the business school case-study method that have been helpful in making my work more useful than much or most of what has been written on this subject, as follows:   After carefully studying large amounts of printed matter on a subject, one is expected to come up with well-considered recommendations that can be defended against criticisms from all directions.  The expected criticisms ingrain the habits of (a) maintaining accuracy in what one says, and (b) not making recommendations unless one can support them with good evidence and logical reasoning.  Established policies receive little respect if they can’t be well supported as part of a free give-and-take of conflicting evidence and reasoning.  That approach is especially relevant to the position statements on breastfeeding of the American Academy of Pediatrics and the American Academy of Family Physicians, which statements cite only evidence that has been

   (a) selected, while in no way acknowledging the considerable contrary evidence,^a1 and

(b) of a kind that has been authoritatively determined to be of low quality. (See the paragraphs dealing with observational studies.)

When a brief summary of material that conflicts with their breastfeeding positions is repeatedly presented to the physicians’ associations, along with a question or two about the basis for their breastfeeding recommendations, those associations never respond.  That says a great deal about how well their positions on breastfeeding can stand up to scrutiny.

The credibility of the contents of the above article is based on the authoritative sources that are referred to in the references: The sources are mainly U.S. government health-related agencies and reputable academic researchers (typically highly-published authors) writing in peer-reviewed journals; those sources are essentially always referred to in footnotes that follow anything that is said in the text that is not common knowledge.  In most cases a link is provided that allows easy referral to the original source(s) of the information.  If there is not a working link, you can normally use your cursor to select a non-working link or the title of the document, then copy it (control - c usually does that), then “paste” it (control - v) into an open slot at the top of your browser, for taking you to the website where the original, authoritative source of the information can be found.  

The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source.  Write to dm@pollutionaction.org.  I will quickly correct anything found to be inaccurate.

Comments or questions on the above are invited, including criticisms if they are specific, and will usually receive a response.  At the next link are past comments and questions from a number of readers, including eight doctors, followed by our responses.  Some of the doctors have been critical but others have been substantially in agreement with us (including one with children with asthma, one who says she has delivered thousands of babies, and one with a son with autism); they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications.  Topics discussed in that section include about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option.  To read the above, go to www.pollutionaction.org/comments.htm

In criticisms, please point out any specific passages that you feel are not accurately based on authoritative sources (as cited) or that do not logically follow from the evidence presented.  Note that the author of this article feels no obligation to present the pro-breastfeeding case as long as the medical associations and other promoters of breastfeeding fail to inform parents about the developmental toxins that are, without dispute, present in high concentrations in human milk. Please e-mail criticisms or other comments to dm@pollutionaction.org.  Most will receive a reply.

For a more complete statement about the author and Pollution Action, please go to www.pollutionaction.org. 

Don Meulenberg

Pollution Action

Shenandoah, VA, USA

Appendix A:  Exposures that far exceed established safe levels:

The American Academy of Pediatrics and the American Academy of Family Physicians, both of which strongly advocate breastfeeding, do not deny that PCBs and dioxins are transferred to infants via breastfeeding in quantities that far exceed established safe levels.  In an August, 2018 letter to the AAP, the author of this article wrote the following, based on considerable evidence from authoritative sources, which were cited:  "PCBs have been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry.^4,6  Dioxins have been found to be present in typical U.S. human milk in concentrations exceeding the EPA’s RfD (estimated reasonably safe dose) by scores to hundreds of times.^5,6  PCBs have been found to have long-term effects including cancer^7,9 and damage to the blood-brain barrier; ⁸ dioxins have been found to have long-term effects including cancer, heart disease, reproductive abnormalities, and immunity deficits.^9,10 "

The letter requested a response from the AAP that would contradict the above based on peer-reviewed scientific evidence, and offered $5,000 to compensate for the time required to write a response.  (The financial offer was due to the lack of response to several earlier, similar letters to both the AAP and the American Academy of Family Physicians.)  Return receipt for the letter was requested and received from the U.S. Postal Service, and (despite offer to place the funds in escrow to assure payment upon receipt of reply) as of over six months later, no response has been received.  Any organization that promotes breastfeeding (such as the AAP) should have responded if the statements quoted above were not well-substantiated or if there existed scientific evidence that could contradict the substance of the letter that was received.

Likewise, there has been no reply to a similar letter to the AAP (dated Oct. 5, 2018) with similar financial offer to compensate for a science-based, contradictory response, stating, "Of toxins with recognized long-term effects, none are known to be ingested or inhaled by U.S. infants in doses beyond established safe levels, except for toxins that are transferred via breast milk."  Again, return receipt for the letter was received, and again (after over five months) there has been no response and no sign of disagreement with the statement in quotes.

Appendix B:

Actual historical data about neurological problems aligns with the (apparently) corrected view of neuro-developmental effects of breastfeeding.  The chart below shows mental impairment data for 8-year-old children after 1991.  Among the different classifications of impairment shown, there were both decreases and increases, with decreases being somewhat greater than increases during the 1996-2000 period, resulting in a small decline in overall mental impairment during those years.

Fig. 16

So, among 8-year-olds who were born in 1988 and within a few years thereafter (their outcomes are shown beginning at 1996), there was an overall minor decline in mental impairment levels taking place during those years. (The numbers shown permit simple calculations to reveal the net decline taking place during those years.)  But, with the declines in two categories starting to come to an end after 2000, while increases continued in the other categories, there was a transition from decreases to increases in overall impairment among 8-year-olds beginning soon after 2000. 

Subtracting 8 from the transition year, 2000, the early 1990's can be seen to have been the birth years of the 8-year-olds whose cognitive impairments were starting to increase in 2000.  Note how this fits with the transition in breastfeeding in about 1990, as seen in Figure 12.b.

References:

1) Institute of Medicine 2002. Reducing Suicide: A National Imperative. Washington, DC: The National Academies Press, at http://nap.edu/10398

2) Harvard Institute of Economic Research: Explaining the Rise in Youth Suicide, 2001, Harvard University, at https://canadiancrc.com/pdfs/harvard_discussion_paper_no_1917.pdf

3) NIH (U.S. National Institute of Mental Health) web page:  Suicide, Figure 1 and separate text, accessed 5/27/2019 at https://www.nimh.nih.gov/health/statistics/suicide.shtml

4) USA Today:  Teen suicide is soaring. Do spotty mental health and addiction treatment share blame?, Mar. 19, 2018, at https://www.usatoday.com/story/news/politics/2018/03/19/teen-suicide-soaring-do-spotty-mental-health-and-addiction-treatment-share-blame/428148002/

See alsohttps://www.kidsdata.org/topic/213/youthsuicide-rate/trend#fmt=2311&loc=1&tf=48,93

4a)  CDC National Center  for Health Statistics release 7/172019:  Unintentional Injury Death Rates in Rural and Urban Areas: United States, 1999–2017

5) CDC Suicide Fact sheet, 2015, at https://www.cdc.gov/violenceprevention/pdf/suicide-datasheet-a.pdf

6)  McNicolas, Suicide in Europe: an on-going public health concern, Soc. psihijat. Vol. 45 (2017) No. 1,  pp. 22-29

7) Kapusta et al., Declining Autopsy Rates and Suicide Misclassification, Arch Gen Psychiatry/Vol 68 (NO. 10), OCT 2011

8)  OECD Family Database, CO4.4:  Teenage suicides, at https://www.oecd.org/els/family/CO_4_4_Teenage-Suicide.pdf

9) See Section 2.a of http://www.pollution-effects.info/

10) Grandjean et al., The Faroes Statement: Human Health Effects of Developmental Exposure to Chemicals in Our Environment, Basic and Clinical Pharmacology and Toxicology, Volume 102, Issue 2, February 2008 at http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2007.00114.x/full

11) Scientific statement on the health-based guidance values for dioxins and dioxin-like PCBs, European Food Safety Authority, EFSA Journal, 2015, at https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2015.4124

    -- Also European Food Safety Authority Panel on Contaminants in the Food Chain (CONTAM), Risk for animal and human health related to the presence of dioxins and dioxin-like PCBs in feed and food, Nov. 2018, at https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2018.5333

12) European Food Safety Authority:  Dioxins and related PCBs: tolerable intake level updated, Nov. 2018, at https://www.efsa.europa.eu/en/press/news/181120

13) Re: EPA’s RfD for dioxin:   At www.epa.gov/iris/supdocs/dioxinv1sup.pdf  in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day."  (that is, O.7 pg of TEQ/kg-d)  

 Re: breastfed infants’ exposures to dioxins, in U.S. and internationally:

- Arisawa et al., Background exposure to PCDDs/PCDFs/PCBs and its potential health effects : a review of epidemiologic studies, The Journal of Medical Investigation Vol. 52 2005, at https://www.jstage.jst.go.jp/article/jmi/52/1%2C2/52_1%2C2_10/_pdf

- Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Vol. 110 No. 6, June 2002,  Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download, indicating 242 pg of TEQ/kg-d at initiation of breastfeeding. 

   Also see Patandin et al. in ref 84c for other U.S. information.

 - Wittsiepe J, PCDD/F and dioxin-like PCB in human blood and milk from German mothers. Chemosphere. 2007 Apr;67(9):S286-94. Epub 2007 Jan 10. www.ncbi.nlm.nih.gov/pubmed/17217986

- Focant et al., Levels of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls in human milk from different regions of France,  Science of The Total Environment, Volumes 452–453, 1 May 2013, Pages 155–162  abstract at http://www.sciencedirect.com/science/article/pii/S0048969713002404

- Yang J, et al., PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants. Chemosphere. 2002 Jan;46(3):419-28. At www.ncbi.nlm.nih.gov/pubmed/11829398

- Bencko V et al.,  Exposure of breast-fed children in the Czech Republic to PCDDs, PCDFs, and dioxin-like PCBs. Environ Toxicol Pharmacol. 2004 Nov;18(2):83-90. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/21782737/

- Nakatani T, et al., Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and coplanar polychlorinated biphenyls in human milk in Osaka City, Japan   Arch Environ Contam Toxicol. 2005 Jul;49(1):131-40. Epub 2005 Jun 22.  Found at http://www.ncbi.nlm.nih.gov/pubmed/15983863

- Deng B, et al., Levels and profiles of PCDD/Fs, PCBs in mothers' milk in Shenzhen of China: estimation of breast-fed infants' intakes.Environ Int. 2012 Jul;42:47-52.. At  www.ncbi.nlm.nih.gov/pubmed/21531025

- Chovancová J, et al., PCDD, PCDF, PCB and PBDE concentrations in breast milk of mothers residing in selected areas of Slovakia   Chemosphere. 2011 May;83(10):1383-90. doi: 10.1016/j.  At  www.ncbi.nlm.nih.gov/pubmed/21474162

- J Grigg,  Environmental toxins; their impact on children’s health, Arch Dis Child 2004;89:244-250 doi:10.1136/adc.2002.022202 at http://adc.bmj.com/content/89/3/244.full

14) Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (near very end) at http://www.deq.state.or.us/lq/pubs/docs/cu/HumanHealthRiskAssessmentGuidance.pdf  “The doses of PCBs that a breastfeeding infant may be expected to receive, given breast milk PCB concentrations measured in the literature, are presented in table 1. These doses range from 0.0019 to 0.0081 mg/kg/day and are 63-270 times higher than ATSDR’s minimal risk level (0.00003 mg/kg/day) for PCB exposures that last between 15 and 364 days.”

15)  ATSDR's Substance Priority List, at https://www.atsdr.cdc.gov/spl/

16) EPA: HEALTH CONSEQUENCES OF DIOXIN EXPOSURE, at https://cfpub.epa.gov/si/si_public_record_Report.cfm?Lab=NHEERL&dirEntryId=171623

16a) Schutz et al., GEMS/Food International Dietary Survey:  Infant Exposure to Organochlorine Contaminants from Breast Milk, WHO, 1998, at https://apps.who.int/iris/bitstream/handle/10665/64097/WHO_FSF_FOS_98.4.pdf?sequence=1&isAllowed=y

17) Boumann et al., Malaria Control Insecticide Residues in Breast Milk: The Need to Consider Infant Health Risks, Environmental Health Perspectives, Vol. 117, No. 10, Oct. 2009, at http://ehp.niehs.nih.gov/0900605/

Also see Section 4.a of www.autism-studies.info.

18) Lackmann et al., [Lactational transfer of presumed carcinogenic and teratogenic organochlorine compounds within the first six months of life], Z.Geburtshilfe Neonatal, 2005 Oct;209(5):186-91.at http://www.ncbi.nlm.nih.gov/pubmed/16317629

19) Fig. 3 of Gascon and eight others:  Temporal trends in concentrations and total serum burdens of organochlorine compounds from birth until adolescence and the role of breastfeeding, Environment International, Volume 74, January 2015, Pages 144–151, at http://www.sciencedirect.com/science/article/pii/S0160412014003043 )

20) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, p. 232

21) USDA, Pesticide Data Program, Annual Summary, 2013,  Appendix L, at http://www.ams.usda.gov/sites/default/files/media/2013%20PDP%20Anuual%20Summary.pdf

22) DellaValle et al., Environmental determinants of polychlorinated biphenyl concentrations in residential carpet dust, Environ Sci Technol. 2013 Sep 17; 47(18): 10405–10414. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076890  the p-value for this finding was <.01, indicating a high level of statistical significance.

23) Cortés et al., PCDD/PCDF and dl-PCB in the ambient air of a tropical Andean city:  passive and active sampling measurements near industrial and vehicular pollution sources, Sci Total Environ. <#> 2014 Sep 1 at https://www.ncbi.nlm.nih.gov/pubmed/24555963  Note that PCDD/F is a designation for what is more commonly referred to as dioxins

24) Ishaq et al., PCBs, PCNs, PCDD/Fs, PAHs and Cl-PAHs in air and water particulate  samples--patterns and variations, in Chemosphere  March 2003 at https://www.researchgate.net/publication/10934371_PCBs_PCNs_PCDDFs_PAHs_and_Cl-PAHs_in_air_and_water_particulate_samples--patterns_and_variations

25) .Štěpánková et al., Dioxin-Like and Endocrine Disruptive Activity of Traffic-Contaminated Soil Samples,  Arch Environ Contam Toxicol (2009),  at https://www.researchgate.net/publication/26259547_Dioxin-Like_and_Endocrine_Disruptive_Activity_of_Traffic-Contaminated_Soil_Samples;  specifically, Table 3, 1st column re dioxins.

26) Project TENDR: Targeting Environmental Neuro-Developmental Risks The TENDR Consensus Statement, Environ Health Perspect. 2016 Jul; 124(7): A118–A122. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937840

27) Re presence of PBDEs in vehicular emissions, citing two other studies as well as its own findings about PBDEs in vehicular emissions, see Lien-Te Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters,  Aerosol and Air Quality Research, at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf ;

    Re PBDEs being produced in vehicle emissions in larger amounts than PCBs, see Table 3, Total PCBs and Table 4, Total (PBDEs), ("before" in both cases), noting that PBDEs are shown in nanograms, which must be multiplied by 1000 to be equivalent to the picograms by which the PCBs are quantified.

28) Wang et al., Emission estimation and congener-specific characterization of polybrominated diphenyl ethers from various stationary and mobile sources, Environmental Pollution, Vol. 158, Issue 10, Oct. 2010, at http://www.sciencedirect.com/science/article/pii/S0269749110002769

29) State of Oregon web page on PBDEs at http://public.health.oregon.gov/HealthyEnvironments/HealthyNeighborhoods/ToxicSubstances/Pages/pbde.aspx) 

30) 2009 EPA Polybrominated Diphenyl Ethers Action Plan at  http://www.epa.gov/sites/production/files/2015-09/documents/pbdes_ap_2009_1230_final.pdf, p. 12.  Quoting from p. 12:   "Children’s Health:

PBDEs are a concern for children’s health. The most sensitive outcome of PBDE exposure is adverse neurobehavioral effects following exposure during the postnatal period."

31) Pp. 160, 161 of EPA document on Biomonitoring (PBDEs) at https://www.epa.gov/sites/production/files/2015-05/documents/biomonitoring-pbdes.pdf     See also  Jones-Otazo, Is House Dust the Missing Exposure Pathway for PBDEs? An Analysis of the Urban Fate and Human Exposure to PBDEs, Environ. Sci. Technol. June 15, 2005 at http://pubs.acs.org/doi/abs/10.1021/es048267b

32) P. 417 of U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf  Also p. 411: "PCBs are readily absorbed through the gastrointestinal tract, respiratory system, and skin."     p. 179 of U.S. ATSDR, Persistent chemicals found in breast milk, Appendix A, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf  "...studies of humans and animals exposed to airborne PCBs provide qualitative information that inhaled PCBs can be absorbed (ATSDR 2000). Ingested PCBs appear to be efficiently absorbed based on studies of infants consuming PCBs in their mothers’ breast milk and studies of animals indicating retention percentages ranging from 60 to 100% of ingested doses."

33)  D.O. Carpenter, Polychlorinated Biphenyls (PCBs): Routes of Exposure and Effects on Human Health, in Reviews on environmental health,  21(1):1-23 · January 2006, at https://www.researchgate.net/publication/7081925_Polychlorinated_Biphenyls_PCBs_Routes_of_Exposure_and_Effects_on_Human_Health

34) Rihmer et al., Suicide in Hungary -- epidemiological and clinical perspectives, Ann Gen Psychiatry, 2013, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3698008/

35) Ferrari et al., The Burden Attributable to Mental and Substance Use Disorders as Risk Factors for Suicide: Findings from the Global Burden of Disease Study 2010, PLoS ONE, at https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091936#s1

36) Pompii et al., Suicidal Behavior and Alcohol Abuse, Int J Environ Res Public Health, 2010, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872355/

37) Lipscomb et al., Cross-sectional study of social behaviors in preschool children and exposure to flame retardants, Environ Health v.16; 2017 at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343384/

38) Johnson-Restrepo et al., An assessment of sources and pathways of human exposure to polybrominated diphenyl ethers in the United States, Chemosphere, 2009 Jul;76(4):542-8. doi: 10.1016/j.chemosphere.2009.02.068. Epub 2009 Apr 5.  at http://www.ncbi.nlm.nih.gov/pubmed/19349061

39) Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf p. 2 

-- Also see see Section 2.b of http://www.pollution-effects.info

40) Food and beverages” row in Table 1 of Health Canada:  Human Health State of the Science Report on Decabromodiphenyl Ether (decaBDE), Dec. 2012,  at https://www.ec.gc.ca/ese-ees/92D49BA9-4B11-4C56-BDB0-9A725C5F688E/DecaBDE%20-%20Final%20SoS%20-%20EN.pdf  Note that, although decaBDE can consist of more than just BDE 209, the two are in practice so similar that the two designations are often used interchangeably. (Costa et al., Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?  Neurotoxicology. 2011 Jan)

41) See Section 2.a of www.pollution-effects.info

42) Michaelsen et al., Feeding and Nutrition of Infants and Young Children, WHO Europe/UNICEF, WHO Regional Publications European Series, No. 87,  p. 241, at http://www.euro.who.int/__data/assets/pdf_file/0004/98302/WS_115_2000FE.pdf

43) U.S. ATSDR, Persistent chemicals found in breast milk,  Appendix A, p. 180, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf

44)  Kommission “Human-Biomonitoring” des Umweltbundesamtes:  Stoffmonographie PCB - Referenzwerte für Blut, Section 8.3., found within https://www.umweltbundesamt.de/sites/default/files/medien/377/dokumente/pcbblut.pdf, website of Umwelt Bundes Amt (German Federal Environmental Office). The text drawn on says, " "Die derzeit durchschnittlich vom Erwachsenen täglich aufgenommene Menge an PCB (ca. 0,02 μg PCB/kg KG [13]) liegt deutlich unter der ATD von 1 μg PCB/kg KG. Der gestillte Säugling erhält dagegen eine deutlich höhere PCB-Zufuhr (3 μg PCB/kg KG.", which Bing Translator respectably translates as " "The amount taken daily average currently by the adults of PCB (approx. 0.02 μg PCB/kg bw [13]) is well below the ATD of 1 μg PCB/kg. The breastfed infant, however, receives a significantly higher PCB intake (3 μg PCB/kg bw.)"

 ---Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. 2006 October; 114(10): 1515–1520. Published online 2006 July 13. doi: 10.1289/ehp.9121PMCID: PMC1626425   at https://www.ncbi.nlm.nih.gov/pubmed/17035135

45) Seelbach et al., Polychlorinated Biphenyls Disrupt Blood–Brain Barrier Integrity and Promote Brain Metastasis Formation, Environ Health Perspect., 2010 Apr; 118(4): 479–484. Published online 2009 Oct 28.  At https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854723/

46) Choi et al., Exercise Attenuates PCB-Induced Changes in the Mouse Gut Microbiome, Environ Health Perspect/; DOI:10.1289/ehp.1306534 at https://ehp.niehs.nih.gov/1306534/

47) Eum et al., Pcbs and Tight Junction Expression, Environ Toxicol Pharmacol, 2009, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2346445/

Selvakumar et al., Polychlorinated biphenyls impair blood-brain barrier integrity via disruption of tight junction proteins in cerebrum, cerebellum and hippocampus of female Wistar rats: neuropotential role of quercetin, Hum Exp. Toxicol., 2013, at https://www.ncbi.nlm.nih.gov/pubmed/23155198

48) U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, p. 123,  at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf

49) Page 372 of ATSDR publication above

50) Texas Spine and Neurosurgery Center web page at https://www.texasspineandneurosurgerycenter.com/pituitary-adenomas/

51) National Academies Press:  Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Chapter: 6 Noncancer End Points, at https://www.nap.edu/read/11688/chapter/9

51a) National Library of Medicine web page, How does the pituitary gland work? at https://www.ncbi.nlm.nih.gov/books/NBK279389/

52) https://www.hopkinsmedicine.org/healthlibrary/conditions/endocrinology/hormones_and_the_endocrine_system_85,P00402

52a) Wilson and Davies, The control of sexual differentiation of the reproductive system and brain, Reproduction, 2007, at  https://rep.bioscientifica.com/view/journals/rep/133/2/1330331.xml

Also see ATSDR document in 52b.

52b) U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf

53) Institute of Medicine 2002. Reducing Suicide: A National Imperative, Washington, DC: The National Academies Press, at http://nap.edu/10398

54)  What are pituitary symptoms?, Pituitary Foundation, at https://www.pituitary.org.uk/information/symptoms,-diagnosis-and-tests/symptoms/

Also  Merck Manual web page on hypopituitarism at https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/hypopituitarism

55) WHO:  State of the Science:  Endocrine Disrupting Chemicals - 2012, p. 119 State of the Science of Endocrine Disrupting Chemicals - 2012, accessible at https://www.who.int/ceh/publications/endocrine/en/

56) Remafedi et al., The Relationship between Suicide Risk and Sexual Orientation: Results of a Population-Based Study, American Journal of Public Health, 1998, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1508407/pdf/amjph00013-0059.pdf

57) Feinleib, Report of the Secretary's Task Force on Youth Suicide. Volume 3: Prevention and Interventions in Youth Suicide, p. 3-10, DHHS. Alcohol, Drug Abuse, and Mental Health Administration Jan 89

57a)  Swaab, Sexual orientation and its basis in brain structure and function, PNAS, 2008, at https://www.pnas.org/content/105/30/10273

57b) Auyeung et al., Prenatal and postnatal hormone effects on the human brain and cognition, Eur J Physiol, 2013

57c) Walker and Gore, Endocrine-Disrupting Chemicals and the Brain, in: Endocrine-Disrupting Chemicals: From Basic Research to Clinical Practice,

Edited by: A. C. Gore © Humana Press Inc., Totowa, NJ, at http://eknygos.lsmuni.lt/springer/631/63-109.pdf

58)  CDC National Biomonitoring Program:  Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls, at https://www.cdc.gov/biomonitoring/DioxinLikeChemicals_BiomonitoringSummary.html , it may be necessary to select "General information" to reach the relevant text.

58a) EPA:  Non-Dioxin-Like PCBs: Effects and Consideration In Ecological Risk Assessment (2003), at https://www.epa.gov/risk/non-dioxin-pcbs-effects-and-consideration-ecological-risk-assessment

59)  Khera, Patients with testosterone deficit syndrome and depression, Arch. Esp.Urol, 2013, at https://www.ncbi.nlm.nih.gov/pubmed/24047633

Also Harvard Medical School:  Testosterone — What It Does And Doesn't Do, Harvard Health Publishing, Published: July, 2015   at https://www.health.harvard.edu/drugs-and-medications/testosterone--what-it-does-and-doesnt-do

60) Aydogan et al., Increased frequency of anxiety, depression, quality of life and sexual life in young hypogonadotropic hypogonadal males and impacts of testosterone replacement therapy on these conditions, Endocr J, 2012, at https://www.ncbi.nlm.nih.gov/pubmed/22972022

61) Johnson et al., Associations between brominated flame retardants in house dust and hormone levels in men, Sci Total Environ. 2013 Feb 15; Table 3, PMCID: PMC3572297, 445-446: 177–184.at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572297/

62) Akutsu et al., Polybrominated diphenyl ethers in human serum and sperm quality. Bull Environ Contam Toxicol. <#> 2008 Apr;80(4) at https://www.ncbi.nlm.nih.gov/pubmed/18320132        Costa and Giordano, Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants,  2008  Neurotoxicology   National Center for Biotechnology Information,  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/)

63) Judy L . Cameron, Dept. of Psychiatry, Neuroscience, and Cell Biology and Physiology, University of Pittsburgh, in "Effects of Sex Hormones on Brain Development," Chapter 5 of Handbook of Developmental Cognitive Neuroscience, MIT Press, 2001, edited by Charles A. Nelson and Monica Luciana.

Also Stephen B. Klein and B. Michael Thorne in Biological Psychology (2006), Worth Publishers, p. 390

64) Amir et al., Breastfeeding in Victoria: A Report, Mother & Child, La Trobe University, 2010, at https://www.education.vic.gov.au/Documents/childhood/professionals/health/breastfeedvic.pdf 

65)  Essex et al., Breastfeeding rates in New Zealand in the first 6 months and the reasons for stopping, N.Z. Med J., 1995,

66)  WHO/ UNICEF:  Comparative Analysis of implementation of the Innocenti Declaration, Annex 1, at https://apps.who.int/iris/bitstream/handle/10665/108153/E63687.pdf?sequence=1

67) Rickard (University College Dublin), The Shame of Breast-Feeding? An Aspect of Irish Culture in Historical Perspective, at http://www.ucd.ie/pages/97/rickard.html

68) The right to die in Belgium:  An inside look.   Megan Thompson, PBS NewsHour, Jan 15, 2015

69) The Death Treatment:  When should people with a non-terminal illness be helped to die? By Rachel Aviv, The New Yorker, June 22, 2015, at https://www.newyorker.com/magazine/2015/06/22/the-death-treatment

70)  The Bulletin:  Belgian suicide rate is 'dismally high', according to WHO, at https://www.thebulletin.be/belgian-suicide-rate-dismally-high-according-who

71) See world latitude map at https://www.mapsofindia.com/worldmap/latitude-longitude.html  See also Davis and Lowell, Evidence That Latitude is Directly Related to Variation in Suicide Rates, Can J Psychiatry 

72) Kirmayer et al., Suicide in Canadian Aboriginal Populations: Emerging Trends in Research and Intervention, at https://www.mcgill.ca/tcpsych/files/tcpsych/Report1.pdf

73) Statistics Canada at https://www150.statcan.gc.ca/n1/daily-quotidien/171025/dq171025a-eng.htm

74)  Walsh and Walsh, Suicide in Ireland: The Influence of Alcohol and Unemployment, The Economic and Social Review, Vol. 42, 2011, see especially Figures 2 and 3.       

Pompii et al., Suicidal Behavior and Alcohol Abuse, Int J Environ Res Public Health, 2010, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872355/

Also Ganz and Sher, Suicidal behavior in adolescents with comorbid depression and alcohol abuse, Minerva Pediatrica 2009, at https://www.minervamedica.it/en/journals/minerva-pediatrica/article.php?cod=R15Y2009N03A0333

75) Ferrari et al., The Burden Attributable to Mental and Substance Use Disorders as Risk Factors for Suicide: Findings from the Global Burden of Disease Study 2010, PLoS ONE, at https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091936#s1

76)  Ireland Bill Aims to Crack Down on Excessive Drinking With Health Warning Labels, NY Times, Oct. 6, 2018, at https://www.nytimes.com/2018/10/06/world/europe/ireland-drinking-bill.html

77)  Matt Cooper:  Why do we normalize underage binge drinking in Ireland?  Today FM, at https://www.todayfm.com/podcasts/today-fm/why-do-we-normalise-underage-binge-drinking-in-ireland

How much do we drink? Alcohol Ireland, at https://alcoholireland.ie/facts/how-much-do-we-drink/

Also  Alcohol, suicide and mental health, Alcohol Action Ireland, at https://alcoholireland.ie/facts/mental-health-and-suicide/

78) See world latitude map at https://www.mapsofindia.com/worldmap/latitude-longitude.html

79) Cassidy (Ed.), Ethnographies of Breastfeeding: Cultural Contexts and Confrontations , Bloomsbury Publishing, At https://books.google.com/books?id=acbuBQAAQBAJ&pg=PA64&dq=OECD+breastfeeding&hl=en&sa=X&ved=0ahUKEwjK2ua2p_3iAhUFVN8KHY7ZBFUQ6AEIVDAI#v=onepage&q=OECD%20breastfeeding&f=false

80) Perez-Escamilla and Dewey, The epidemiology of breast-feeding in Mexico: rural vs. urban areas, Bull.Pan.Am.Health.Organ, 1992, at https://www.ncbi.nlm.nih.gov/pubmed/1600435

81)  Section on Breastfeeding, Pediatrics, 2012, 129, e827, orig. published online Feb. 27, 2012, at http://pediatrics.aappublications.org/content/129/3/e827.full.html

82) The Surgeon General's Call to Action to Support Breastfeeding, 2011,  U.S. Department of Health and Human Services, Washington, D.C., 2011

83) Figure 2 in Guyatt et al., GRADE guidelines:  1. Introduction -- GRADE evidence profiles and summary of findings tables, Journal of Clinical Epidemiology, at http://www.jclinepi.com/article/S0895-4356(10)00330-6/pdf

84) Dr. Gordon Guyatt is chief editor of User’s Guides to the Medical Literature:  A Manual for Evidence-based Clinical Practice, 2nd Edition (3rd is upcoming), copyright  American Medical Association, published by McGraw Hill.

85)  In a review in the Journal of the Medical Library Association, only two guides are recommended for use by physicians in evaluating evidence in medical literature, one of which is the one edited by Guyatt et al., already referred to, and the other of which is by Dr. Sackett. (Journal of the Medical Library Association, Oct. 2002, User’s Guide to the Medical Literature:  A Manual for Evidence-Based Clinical Practice, Review by Rebecca Graves, at httpi://www.ncbi.nlm.nih.gov/pmc/articles/PMC128970) 

86) Writing in The Canadian Medical Association Journal, as quoted in “Do We Really Know What Makes Us Healthy?” New York Times, published: September 16, 2007  at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?pagewanted=2&_r=0

87) BMJ 2015;350:h2639, at  https://www.bmj.com/content/350/bmj.h2639

88) The Surgeon General’s Call to Action to Support Breastfeeding 2011, Table 2, at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf

89)  Simpson et al., A meta-analysis of the association between adherence to drug therapy and mortality, BMJ 2006; 333 doi: at http://www.bmj.com/content/333/7557/15

90) Gary Taubes, Do We Really Know What Makes Us Healthy?  The New York Times Magazine, Sept. 16, 2007,  at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?_r=0 

Also see O'Neil and 7 others, Observational evidence and strength of evidence domains: case examples, Biomed Central: Systematic Reviews, at https://systematicreviewsjournal.biomedcentral.com/articles/10.1186/2046-4053-3-35

91) This can be verified by going to the websites of the AAP (American Academy of Pediatrics), AAFP (American Academy of Family Physicians) and ACOG (American Congress of Obstetricians and Gynecologists) and seeing their breastfeeding position papers.

92)  Gary Taubes, Do We Really Know What Makes Us Healthy?  The New York Times Magazine, Sept. 16, 2007,  at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?_r=0

93)  Lawlor et al,  Commentary: The hormone replacement–coronary heart disease conundrum: is this the death of observational epidemiology? International Journal of Epidemiology, v. 33, Issue 3, June 2004, Oxford University Press, at https://academic.oup.com/ije/article/33/3/464/716652

     Also  Stampfer et al., Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence, International Journal of Epidemiology, Volume 33, Issue 3, 1 June 2004, Pages 445–453, at https://www.ncbi.nlm.nih.gov/pubmed/1826173 

94) Martin et al., Effects of promoting longer-term and exclusive breastfeeding on adolescent adiposity, blood pressure, and longitudinal growth trajectories: evidence from the PROBIT cluster-randomized trial, JAMA Pediatr, 2017

95) Colen and Ramey, Is Breast Truly Best? Estimating the Effect of Breastfeeding on Long-term Child Wellbeing in the United States Using Sibling Comparisons, Soc.Sci.Med. 2014, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077166/

96) Yang et al., Breastfeeding during infancy and neurocognitive function in adolescence: 16-year follow-up of the PROBIT cluster-randomized trial, PLOS, 2018, at https://journals.plos.org/plosmedicine/article/file?id=10.1371/journal.pmed.1002554&type=printable

97)  Shamberger, R.J., Autism rates associated with nutrition and the WIC program, J Am Coll Nutr. 2011 Oct;30(5):348-53.  Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621   An image of part of the article is shown below, since it may be expensive for many readers to see the complete study.

98) EPA, The Effects of Great Lakes Contaminants on Human Health, Report to Congress, Section III, p. 12 (bottom) and again on p. 16, at http://nepis.epa.gov/Exe/ZyNET.exe/2000BSHI.txt?ZyActionD=ZyDocument&Client=EPA&Index=1995%20Thru%201999&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&UseQField=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5CZYFILES%5CINDEX%20DATA%5C95THRU99%5CTXT%5C00000002%5C2000BSHI.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=p%7Cf&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=10&ZyEntry=20

99) Dodds et al., The Role of Prenatal, Obstetric and Neonatal Factors in the Development of Autism, J Autism Dev Disord (July 2011) 41:891–902  DOI 10.1007/s10803-010-1114-8, Table 6, at http://link.springer.com/article/10.1007/s10803-010-1114-8?no-access=true (This article is available only by subscription or $40 payment, so the reader may be satisfied to see the chart provided below, taken from the article.)  This 2010 Canadian study, drawing data from a population-based “clinically-rich perinatal database,” investigated a very large population, nearly 130,000 births.  Data from almost 127,000 of those children (those without identified genetic risk of autism) went into the study’s finding that there was a 20 - 25% increased risk of autism among children who were breastfed at discharge from the hospital. 

Observe in the chart below that

   a) significantly increased odds of autism were found in relation to breastfeeding as determined by three different ways of analyzing the data (from different tables, as brought together below), and

   b) the odds of autism in relation to breastfeeding increased with each improvement in the analysis, starting with basic data, then advancing to include consideration of other variables that could affect the outcome, and finally refining the data in a way that makes it most relevant to the great majority of the population (those with low genetic susceptibility).

100) Whitely et al., Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14  Autism Insights 2009:1 3-17  at https://www.academia.edu/17814363/Trends_in_Developmental_Behavioral_and_somatic_Factors_by_Diagnostic_sub-group_in_pervasive_Developmental_Disorders_A_Follow-up_Analysis.  This study found that 65% of autism cases had been exclusively breastfed for at least four weeks; the authors looked at a comparison figure of 54%, but that figure was unrealistically high, since it came from a study (Pontin et al.) of breastfeeding by mothers largely from “more affluent families”, who breastfeed at unusually high rates in the U.K.   For breastfeeding prevalence data that would apply to the general U.K. population, the authors of the Pontin study referred the reader to Infant Feeding 1995 (Foster et al.); examination of the data in that book reveals that a figure in the upper 20%’s would apply for the equivalent period (just after four weeks). That is also as was found in the U.K. Infant Feeding Survey - UK, 2010 Publication date: November 20, 2012, Chapter 2, Figure 2.13, at http://www.hscic.gov.uk/catalogue/PUB08694/ifs-uk-2010-chap2-inc-prev-dur.pdf

101)  Breastfeeding and Autism  P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, PhD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot  https://imfar.confex.com/imfr/2010/webprogram/Paper6362.html)   This study found a 37% rate of breastfeeding at six months among children diagnosed with autism, as compared with 13% in the control group. 

102) CDC:  Biomonitoring Summary:  Non-Dioxin-Like Polychlorinated Biphenyls, at https://www.cdc.gov/biomonitoring/NDL-PCBs_BiomonitoringSummary.html