Author Archives: Bix

Study: BPA Levels In Humans Dramatically Underestimated, Urgent Need To Reassess Regulatory Limits

BPA: Have Flawed Analytical Techniques Compromised Risk Assessments?, The Lancet Diabetes and Endocrinology, 5 December 2019

The conclusion from our analyses is that previous studies using indirect techniques requiring deconjugation underestimated actual human levels of BPA. Accordingly, we undertook a comparative analysis of 29 urine samples from pregnant women in their second trimester using both indirect and direct methods (figure C; appendix pp 1–2). Using the direct method, we obtained a geometric mean for these urine samples of 51·99 ng/mL total BPA, 44-times higher than the latest geometric mean for adults in the USA reported by the National Health and Nutrition Examination Survey (NHANES).10

Importantly, disparity between indirect and direct results increased substantially as exposure increased (figure D and E). Because pregnancy induces physiological changes that might affect metabolism of BPA, we also compared indirect and direct measurements on urine samples from five adult men and five non-pregnant women (figure C). The same trends were evident in this small sample (appendix p 3) and, as in the samples from the pregnant women, the difference in BPA levels was a reflection of the inability of the indirect method to accurately measure the levels of metabolites of BPA.

Indirect analytical methods have provided the bulk of data on human BPA levels. To our knowledge, our data provide the first evidence that this is a flawed analytical tool for measurement of BPA levels.

Importantly, because estimates of human exposure have been based almost exclusively on data from indirect methods, these findings provide compelling evidence that human exposure to BPA is far higher than has been assumed previously.

Because negligible exposure levels have been a cornerstone of regulatory decisions, including the FDA conclusion that BPA poses little health risk, the present data raise urgent concerns that risks to human health have also been dramatically underestimated.

In addition to offering a new dimension to the dispute over the safety of BPA and structural analogues that have replaced it, our findings have broader implications. Currently, measurements of a wide range of chemicals, including replacement bisphenols, other environmental phenols (eg, parabens, benzophenone, triclosan), and phthalate metabolites rely on indirect methods.8 Thus, the problem identified here for BPA might extend to other environmental contaminants.

Look at those graphs! The orange one … the one on the left is what was thought we had in us: negligible. The one on the right is what is actually in us. For that blue-and-purple graph, bottom right, you can’t even SEE the green bar that reflects our presumed load, but it’s there.

Endocrine disruptors are so dangerous because they imitate hormones in our bodies (see below). BPA is a xenoestrogen. You only need a tiny bit of these mimicking hormones to have an effect … like weight gain, insulin resistance and diabetes, impaired mental development in infants (when mother is exposed during pregnancy). It is imperative that we reduce our exposure to these chemicals.


Exposed: How willful blindness keeps BPA on shelves and contaminating our bodies, Environmental Health News, 19 November 2019 investigation finds regulatory push to discredit independent evidence of harm while favoring pro-industry science despite significant shortcomings.

Federal tests ‘dramatically’ undercount BPA and other chemical exposures, Environmental Health News, 6 December 2019
Researchers say federal agencies use highly inaccurate tests to estimate exposure to BPA—findings that extend to multiple other harmful chemicals that get into our bodies.

War-Related Decreases In Fat Consumption Caused A Decrease In Death From Diabetes

The top graph shows that during war-related food rationing people died less from diabetes. The bottom graph shows that those lower death rates were attributable to a lower fat, high-carb diet. I transcribed parts that stood out for me. I especially like what he said about immigrants and genetics.

Discussion On The Cause Of Diabetes, Proceedings of the Royal Society of Medicine, May 1949

During wars the diabetic death rate tends to fall. Closer analysis reveals that this is related, not to actual war, but to food shortage, for no such decrease occurs in belligerent countries whose food supplies are unaffected while it falls significantly in neutrals subject to privation. This association is evident in the comparative mortality indices for England and Wales (fig.1) which show that the falls are co-terminous with food restriction rather than hostilities.

Figure 1. England and Wales. Diabetic mortality: comparative mortality indices (1938 basis).

In World War II food restrictions began in 1940 and have not yet been ameliorated. If such restrictions affect mortality a lag time of at least a year would be expected before their effects became manifest. Fig. 2 shows the changes in the daily, per capita, consumption of different foods from the diet of 1939 to the diet of today [2]. Below is given the change in female diabetic mortality; the female rate being chosen as less influenced by mobilization, the curve being antedated one year to allow for the time lag. The protein curve bears no relation to the mortality curve; a possible correlation – direct in one inverse in the other – may exist for the calorie or carbohydrate curves; but the correlation between the mortality and fat consumption curves is striking.

Figure 2. England and Wales. Food consumption and female diabetic deaths.

There is a mass of evidence with similar import [1]. The progressive rise in diabetic mortality in Western countries during the last fifty years coincides with a gradual change towards higher fat and lower carbohydrate diets, the protein and calorie values have altered little. The diabetic mortality rate is high in countries whose diets tend to be high in fat and poor in carbohydrate; and low where the opposite tendency prevails. The fall in diabetic mortality in World War I was related to a fall in fat and rise in carbohydrate intake. The higher urban, as compared with the rural, diabetic mortality is associated with a higher fat and lower carbohydrate consumption in towns. Diabetic mortality rises with economic position and, simultaneously, dietary habits change so that a greater proportion of fat and less carbohydrate is taken. Race is not a predominant factor in determining diabetic mortality. Immigrant races manifest the mortality rate of their new country in proportion as they acquire its dietary habits.

There thus seems to be a universal relation between diet and diabetic mortality. The dietetic factor most closely related is fat consumption.

The general explanation suggested for the data available in 1935 was to the following effect:
[1] Susceptibility and hereditary predisposition undoubtedly play a part in the etiology of diabetes but it is difficult to explain the great variations in diabetic mortality, during the last thirty years, by widespread distributions in the distribution of hereditary susceptibility. A more reasonable explanation is that susceptibility is widespread and that the increasing pressure of some environmental factor is disclosing its prevalence. It seems possible that diet is this external factor. Any population will contain an unknown number of individuals of varying susceptibility. When the diet of their country is rich in carbohydrate and poor in fat it will provoke diabetes only in the most susceptible. But if the diet changes progressively towards a higher calorie, higher fat and lower carbohydrate diet it will provoke diabetes in less and less susceptible individuals and the incidence of diabetes in a population will continue to reflect the dietary habits. The new data presented in this paper strengthen these conclusions.

Professor H. P. Himsworth

We’ve known that diabetes is caused by eating too much fat for SEVENTY YEARS. I’ve been writing about it (along with presenting studies) for at least a decade. It is exasperating that people choose not to apply it.

My gratitude goes to Dr. McDougall for highlighting the top graph in his 2012 newsletter which prompted me to read further.

Donovan, “Catch The Wind”

In the chilly hours and minutes
Of uncertainty, I want to be
In the warm hold of your loving mind

To feel you all around me
And to take your hand along the sand
Ah, but I may as well try and catch the wind

When sundown pales the sky
I want to hide a while behind your smile
And everywhere I’d look your eyes I’d find

For me to love you now
Would be the sweetest thing ‘twould make me sing
Ah, but I may as well try and catch the wind

Di di di di, di di di di
Di di di di, di di di di
Di di di

When rain has hung the leaves with tears
I want you near to kill my fears
To help me to leave all my blues behind

For standin’ in your heart
Is where I want to be and long to be
Ah, but I may as well try and catch the wind

Ah, but I may as well try and catch the wind

“Catch the Wind” was Donovan’s first released song, released as a single in the United Kingdom on 12 March 1965, when he was 18 years old.

Active Ingredient In Roundup “The Most Important Causal Factor” In Celiac Disease And Gluten Intolerance

Glyphosate, Pathways To Modern Diseases II: Celiac Sprue And Gluten Intolerance, Interdisciplinary Toxicology, December 2013

Celiac disease and gluten intolerance are just one part of the glyphosate picture. But let’s just look at them for a moment:

So, as glyphosate/Roundup use increased, the incidence of celiac disease and intestinal infections increased. The paper explained why the increase in disease was not simply due to increased reporting from better diagnostic tools.

This is a big paper, lots of mechanisms, 271 references. There’s a lot here. This is from the abstract:

Celiac disease, and, more generally, gluten intolerance, is a growing problem worldwide, but especially in North America and Europe, where an estimated 5% of the population now suffers from it. Symptoms include nausea, diarrhea, skin rashes, macrocytic anemia and depression. It is a multifactorial disease associated with numerous nutritional deficiencies as well as reproductive issues and increased risk to thyroid disease, kidney failure and cancer.

So, celiac disease is on the rise, in parallel to glyphosate/Roundup use. They ruled out disease increase from increased reporting due to better diagnostic tools.

Here, we propose that glyphosate, the active ingredient in the herbicide, Roundup®, is the most important causal factor in this epidemic.

Fish exposed to glyphosate develop digestive problems that are reminiscent of celiac disease.

Celiac disease is associated with imbalances in gut bacteria that can be fully explained by the known effects of glyphosate on gut bacteria.

Characteristics of celiac disease point to impairment in many cytochrome P450 enzymes, which are involved with detoxifying environmental toxins, activating vitamin D3, catabolizing vitamin A, and maintaining bile acid production and sulfate supplies to the gut. Glyphosate is known to inhibit cytochrome P450 enzymes.

Deficiencies in iron, cobalt, molybdenum, copper and other rare metals associated with celiac disease can be attributed to glyphosate’s strong ability to chelate these elements.

Deficiencies in tryptophan, tyrosine, methionine and selenomethionine associated with celiac disease match glyphosate’s known depletion of these amino acids.

Celiac disease patients have an increased risk to non-Hodgkin’s lymphoma, which has also been implicated in glyphosate exposure.

Reproductive issues associated with celiac disease, such as infertility, miscarriages, and birth defects, can also be explained by glyphosate.

Glyphosate residues in wheat and other crops are likely increasing recently due to the growing practice of crop desiccation just prior to the harvest.

We argue that the practice of “ripening” sugar cane with glyphosate may explain the recent surge in kidney failure among agricultural workers in Central America.

We conclude with a plea to governments to reconsider policies regarding the safety of glyphosate residues in foods.

We have to stop consuming – breathing, eating, drinking – glyphosate. As I have been saying for years, buying organic is a smoke screen. There’s so much of this in use now that it contaminates organic crops. Remember this? — > Bob’s Red Mill Faces Class Action Lawsuit over Glyphosate Weedkiller Contamination. In one study, some of the highest levels of glyphosate were found in organic eggs because glyphosate bioaccumulates.

The EPA is trying to weasel out of responsibility by setting limits for glyphosate in food that are ridiculously high. Endocrine disruptors like glyphosate, according to the Endocrine Society, cause abnormalities at “even infinitesimally low levels.” Lower doses, in fact, are more hormonally disrupting than higher doses.

In July of this year, a statement by the International Federation of Gynecology and Obstetrics (FIGO) concluded: “We recommend that glyphosate exposure to populations should end with a full global phase out.”

This is what we’re up against:

Intermittent Fasting Has Drawbacks

[After a year], LDL cholesterol in the intermittent fasting group ended up 10% higher than the constant calorie-restriction group despite the exact same loss of body fat.

Even with proactive medication reduction, advice to immediately break the fast should sugars drop too low, and weekly medical supervision, type 2 diabetics fasting even just two days a week were twice as likely to suffer from hypoglycemic episodes compared to an unfasted control group.”

Even just fasting for a day can significantly slow the clearance of some drugs (like the blood-thinning drug coumadin).

Steve McCurry, Known For His Portrait Of The “Afghan Girl,” Has A New Book About Animals

Steve McCurry’s Photos Show The Complex Relationship Between Humans And Animals, CNN, 8 November 2019

Click to enlarge.

A boy rests against a cow in Kathmandu, Nepal, 2013. Credit: © 2019 Steve McCurry, Long Island City, NY

A Mahout and his elephant at a sanctuary. Chiang Mai, Thailand, 2010. Credit: © 2019 Steve McCurry, Long Island City, NY

… McCurry hopes, too, that his images will inspire a greater respect for animals, and a desire to address the dire predictions of mass extinction caused by human activity.

“This is an unimaginable catastrophe, but one that is sadly coming to fruition. We are losing species every year; wildlife is being decimated to the point where in a few years some species will cease to exist in their natural habitats.”

Below is Sharbat Gula, the Afghan Girl, at Nasir Bagh refugee camp near Peshawar, Pakistan. By Steve McCurry, December 1984.

This photograph was the cover of The National Geographic magazine the following year.

Endocrine Disruptors Cause Abnormalities At “Even Infinitesimally Low Levels”

People can become overweight, develop type 2 diabetes, heart disease, fertility problems, immune disorders, respiratory diseases, cancers, and a host of other chronic ailments, in part, because of the chemicals to which they are exposed. That’s what the Endocrine Society, the world’s oldest, largest, and most active organization devoted to hormone research has been saying for over a decade. Your diet probably would have worked better a hundred years ago.

EDC-2: The Endocrine Society’s Second Scientific Statement on Endocrine-Disrupting Chemicals, Endocrine Reviews, December 2015

All those letters in red on the left side of this diagram are abbreviations for chemicals we’re exposed to every day. I’ve listed some sources for those chemicals at the bottom of this post. T2DM is type 2 diabetes.

The Endocrine Society’s first Scientific Statement in 2009 provided a wake-up call to the scientific community about how environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans—especially during development—may lay the foundations for disease later in life.

At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, and epigenetic changes, thereby producing effects in exposed individuals as well as their descendants.

Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans.

In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems.

The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings can be much better translated to human health. Armed with this information, researchers, physicians, and other healthcare providers can guide regulators and policymakers as they make responsible decisions.

About that “low-dose effects” highlight, from their first report:

Even infinitesimally low levels of exposure — indeed, any level of exposure at all — may cause endocrine or reproductive abnormalities, particularly if exposure occurs during a critical developmental window (10). Surprisingly, low doses may even exert more potent effects than higher doses. Second, EDCs may exert nontraditional dose-response curves, such as inverted-U or U-shaped curves (11). Both of these concepts have been known for hormone and neurotransmitter actions, but only in the past decade have they begun to be appreciated for EDCs.

We are being continually bombarded by many sources. The amount of chemicals in our bodies has never been seen in the history of humanity. We are one big experiment:

Single exposures are not representative of more common widespread persistent exposure to a broad mix of indoor and outdoor chemicals and contaminants. Industrialized areas are typically characterized by contamination from a wide range of industrial chemicals that may leach into soil and groundwater. These complex mixtures enter the food chain and accumulate in animals higher up the food chain such as humans, American bald eagles, polar bears, and other predatory animals. Exposure occurs through drinking contaminated water, breathing contaminated air, ingesting food, or contacting contaminated soil. People who work with pesticides, fungicides, and industrial chemicals are at particularly high risk for exposure and thus for developing a reproductive or endocrine abnormality.

Right? So, when it comes to endocrine disruptors, basic assumptions about dose-response goes out the window. Don’t let the government tell you that there is a certain threshold below which these chemicals won’t affect us. It’s simply not true.

Some sources for endocrine disruptors:

Bisphenol A (BPA):

  • Canned foods, because most metal cans are lined with a sealant containing BPA
  • Water and other beverage bottles
  • Baby bottles, sippy cups, baby pacifiers
  • Other hard, clear plastic food containers
  • Cash register receipts
  • Eyeglass lenses and safety glasses
  • CDs and DVDs


  • Coatings on pharmaceutical pills and nutritional supplements
  • Shampoo, soap, perfumes, nail polish, hair spray, aftershave lotions, moisterizers
  • Pesticides
  • Toys
  • Vinyl flooring and wall coverings
  • Siding and roofing materials
  • Food packaging
  • Detergents and lubricating oils
  • Medical devices, e.g. blood bags and tubing
  • Wire and cable
  • Coated fabrics
  • Rain boots and other footwear
  • Garden hoses and outdoor furniture

Persistent Organic Pollutants (POPs). This is a group of pollutants including DDT, PCBs, dioxins, furans, hexachlorobenzene. They are used as pesticides, solvents, pharmaceuticals, and industrial chemicals. They are called persistent because they don’t break down easily in the environment.

  • Consumption of animal foods considered greatest contributor (as POPs move up the food chain, they increase in concentration = bioaccumulation)
  • Pesticides, insecticides
  • Cigarette smoke
  • Vehicle exhaust
  • Paints
  • Indoor and outdoor dust and air

By the way, Roundup is an endocrine disruptor.