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Autism Spectrum Disorder is a neurodevelopmental disorder that causes individuals to have challenges with social skills, circular behavior patterns, speech, and nonverbal communication. It is termed a “spectrum disorder" due, in part, to the seemingly innumerable count of presentations that it can take. The U.S. Center for Disease Control, (CDC), estimated in 2014 that 1 in 68 children in the United States would be diagnosed with the disorder, and that number is thought to be even higher in boys. This demonstrates a 119.4% increase in the prevalence of ASD since 2000, which is nothing short of alarming.
And yet, presently, there is no definitive treatment for Autism Spectrum Disorder in the U.S., (ASD), because, presently, there is no definitive cause, either. But with that said, a vast plethora of theories have been proposed since the first incidence of its formal diagnosis in 1933. While I do not endorse any of these causes, personally, some of these include, (in no particular order):
· pregnancy and/or delivery complications
· maternal nutrition, (pre-partum)
· nutrition of the child during infancy, (post-partum)
· exposure to certain viruses
· exposure to certain vaccines
· atypical brain development
· exposure to various teratogens (in-utero)
· immune deficiency
· immune overstimulation
· food allergies
· “bad” parenting
· traumatic experiences
· comorbid mental illness
· older-aged fathers
· exposure to television
Historically, both genetic variations, and variations in the gut microbiome, (dysbiosis), have been strongly associated with ASD. So too has been both the consumption of genetically modified organisms, (GMOs), (specifically, due to the presence, therein, of the herbicide glyphosate), and nutrient deficiencies. The great vaccination debate began years ago, and in the minds of many, swiftly crashed, with no possibility for redemption. This is fine with me, but I don’t rule out the environmental cause theory, entirely. One of the strongest, most undeniable theories around, in my opinion, is perhaps the one least publicized: that exposure to glyphosate, over time, leads to intestinal permeability, (i.e., “leaky gut syndrome”), and that this, in turn, leads to profound, and possibly abrupt, epigenetic changes, as well as significant, systemic inflammation, thereby leading to the development of ASD – in infancy/childhood - and with it, nutritional deficiencies, (hence the correlation, there). Knowing what we know about human genomics - that the phenotypic traits, (e.g., physical, behavioral, mental), of an individual are direct expressions of his or her genes - epigenetic modulation easily becomes a compelling consideration when examining Autism Spectrum Disorder (ASD) etiology.
Over the past decade, the body of research supporting the epigenetic modulation potential of the gut microbiome, and illuminating the mechanisms of action(s) that occur(s), has become more and more robust. And from this research, it has been gathered by those who mind it that environmental toxins, stress, nutrition, and a myriad of other non-genetic factors, play a significant role in gene activity, whereby epigenetic modulation of gene expression, (by way of “DNA methylation, posttranslational modification of histone proteins, [gene] silencing,” or any of the other identified biological processes implicated in epigenetic change), occurs as a direct response (Paul, Barnes, et. al., 2015). Microbiologists, geneticists, and the like, are being pulled toward the somewhat-freshly evolved field of epigenetics, the theory behind which elicits a new framework for understanding how abnormal physiological, neurological, and emotional conditions come to manifest. This comes, at least in part, from the rapidly climbing incidence rates of virtually all types of disease and disorder, least deniably of which being those of the mental sort. ASD, while not classified exclusively as a mental disorder the way that depression and anxiety are, no matter the variation, is widely treated as one. Understood to be a group of neurodevelopmental disorders, or more specifically, pervasive developmental disorders, (PDD), ASD is “characterized by impairments in communication, reciprocal social interaction, and restricted repetitive behaviors or interests” (Faras, Ateeqi, & Tidmarsh, 2010). It would not be far fetched, therefore, to propose the idea that an impaired gut microbiome, in the mother, the child, or both, could have the potential to illicit a presentation of the disorder.
Much research has observed strong, “significant associations between ASD and genetic factors” (Jiao, et. al., 2011). In fact, one such study in 2011, which employed a quasi-experimental design, the Child Autism Rating Scale, (CARS), and predictive models, generated by machine-learning techniques, managed to demonstrate that single nucleotide polymorphisms could potentially be used to predict symptom severity in ASD children. Single nucleotide polymorphisms, (SNPs), are “genetic markers that enable researchers to search for genes associated with complex diseases,” and ASD has been associated with many of them, some of which include GABRA4, GABRA2, and GABRB1 (Jiao, et. al., 2011). Operating from this base, the researchers in this study took 118 children with ASD, and put each of them into one of two groups: the mild/moderate ASD group, or the severe ASD group. Genomic DNA was, then, extracted from the peripheral blood leukocytes of each participant, and diagnostic models were generated, whereby model-generation bias was avoided by the utilization of machine-learning methods. Previous to this, behavior had been the gold standard for ASD diagnosis, whereas this study undertook the first ever attempt at creating a diagnostic tool centered in gene sequencing. Ultimately, the results supported the hypothesis that genotyping on specific SNPs could predict ASD symptom severity, and thereby bolstering the notion that ASD is genetically linked.
To expound further on the notion that ASD is a phenotypic expression of genetic abnormality, reference ought to be made to the 2017 book, “Deep Nutrition.” In their expansive work, delineating precisely how nutrition impacts genetic expression, Dr. Cate Shanahan, MD, and her husband, report that “in 2007, a consortium of geneticists investigating autism boldly announced that the disease was not genetic in the traditional sense of the word,” but that, rather, children with ASD possess “new gene mutations, never before expressed in their family line” (Shanahan & Shanahan, 2017). The authors venture on, noting the incidence of these mutations, and recalling how, in 2012, a study published findings that a duplication of the gene at a specific “hotspot,” (“regions of the human genome where the DNA strand is tightly coiled around organizing proteins called histones”), on chromosome 7, results in the development of ASD, while the deletion of the same gene results in Williams Syndrome. This is a profound finding, especially given that, while ASD children present with extremely antisocial tendencies, children with Williams Syndrome are so uniquely gregarious that they will often socialize with anyone. The main idea, here, is that the genetic mutations being seen in ASD are spontaneous in the progeny, and thus, completely new to the gene pool. So, extrapolating from this, we arrive at the idea that some sort of environmental factor is having an enormously powerful effect upon the genetic profiles of children, today.
While it does manifest most noticeably as a mental impairment, ASD often presents with physiological abnormalities, as well. “Cross-sectional data from the 2003-2004 National Survey of Children's Health indicate[d] that children with ASD were 40% more likely to be obese compared to typically developing children,” an extremely significant statistic (Kral, Eriksen, Souders, & Pinto-Martin, 2013). And it has repeatedly been seen that children with ASD present with both abnormal eating practices, and unusual, and/or limited, dietary choices, but additionally, ASD has, time-and-again, been observed as positively correlating with the co-occurrence of numerous food sensitivities, (whereby “sensitivity” denotes the elicitation of an immunological response, rather than a histamine response, such as what is seen in food allergies, i.e., in the traditional sense). Moreover, key nutrient deficiencies, possibly by way of the malabsorption of key micronutrients, have been implicated in ASD, and as has been glyphosate-based herbicide exposure, (by way of GMO food intake). Finally, the comorbidity of ASD and gastrointestinal symptoms is both uncanny, and undeniable. Given the number of food-related variables associated with ASD, one would be remiss to overlook the potential of nutrition as being that “enormously powerful” environmental factor. One specific gastrointestinal condition, intestinal permeability, (otherwise referred to as “leaky gut syndrome”), is particularly compelling. Not only has intestinal permeability been shown to cause both nutrient malabsorption, and food sensitivities, it has also been shown to be caused by glyphosate exposure. And, as two researchers reported in their review of a study that examined the evidence supporting a link between autism and glyphosate, both “leaky gut syndrome,” and “gut flora alterations have been well-documented in autism” (Je & Seneff, 2015). Taking this into account, it would seem probable that the nutrition of both mother and child, before, during, and after gestation, could potentially play a profound role in ASD development.
In a 2016 study examining the similarities and differences between mothers with ASD children, and mothers with children of typical development, (TD), a survey was conducted in order to gauge the perceptions of the mothers. Specifically, the study aimed to gather data surrounding their perceptions of four different mealtime outcomes: “nutritional intake, stress, time, and assistance given” (Crowe, Freeze, Provost, King, & Sanders, 2016). For the study, 24 mothers of ASD children and 24 mothers of TD children, (whereby all of these children were of pre-school age), were surveyed. The findings were such that the mothers of ASD children, overall, were less satisfied with the four outcomes being looked at. The outcome of interest to the current proposal is that of nutrition. While no overt flaws are apparent, one unanswered question that this researcher has is: what sort of nutritional outcome were these mothers hoping for? Today, most people consider adequate nutrition to be a matter of sufficient caloric intake, but this study was not conducted to assess for individual opinions on what constitutes the optimal diet. The current study, therefore, aims to illuminate this a bit, so that information can be gathered as to the need for educating the lay-public. Further research into the maternal perceptions, as they pertain to older children, or siblings, could be conducted in the future.
In a 2013 review of the literature that had targeted the patterned “eating behaviors, diet quality, and gastrointestinal symptoms” in children with ASD, the authors hoped to demonstrate how robust the existing evidence is for a correlation between these factors and ASD, suggesting that the role of nutrition is highly indicated (Kral, Eriksen, Souders, & Pinto-Martin, 2013). They go on to discuss the altered gut floras, and characteristic intestinal permeability, frequently observed in children with ASD, and throughout, present a wealth of credible information gathered by previously conducted, peer-reviewed studies. Rather than suggesting that these children’s guts were already altered prior to birth, the authors suggest that their highly restricted diets may be the cause of their less-than-diverse gut microbiomes, and offer that more research into how to best correct unusual eating behaviors, and food neophobias, is dire for the neurodevelopment of ASD children. The study proposed, herein, however, will take the opposite approach.
A study in 1995, operating from the burgeoning anecdotal evidence suggesting that autistic behaviors are improved when dairy and wheat are eliminated from the diet, was conducted to observe whether or not an association would be had between immunological responses to certain foods, and ASD (Lucarelli, Zingoni, et. al., 1995). 36 adult patients previously diagnosed with ASD were chosen for the study, but gender was not matched, as the majority of the participants (30 out of 36) were biologically male. After exposing the participants to a variety of different foods, immune response was measured by way of serum blood levels of immunoglobulin proteins, (i.e., IgG, IgA, and IgM). The authors, however, ultimately conceded in their discussion that although they observed associations between the variables, the hypothesis could not be outright accepted due to both the small size of the study, as well as the broad differences in symptomatology. A larger scale longitudinal study could be conducted in the future to investigate this hypothesis further, and with greater precision.
Keto Baking Co. products are 100% non-GMO because I could never handle my conscience being fraught with worry, and guilt that there was glyphosate on the foods I'm offering to people as "healthy."
Stay tuned next week for Part 2!
Crowe, T. K., Freeze, B., Provost, E., King, L., & Sanders, M. (2016). Maternal Perceptions of Nutrition, Stress, Time, and Assistance during Mealtimes: Similarities and Differences between Mothers of Children with Autism Spectrum Disorders and Mothers of Children with Typical Development. Journal Of Occupational Therapy, Schools & Early Intervention, 9(3), 242-257.
Faras, H., Al Ateeqi, N., & Tidmarsh, L. (2010). Autism spectrum disorders. Annals of Saudi Medicine, 30(4), 295–300. http://doi.org/10.4103/0256-4947.65261
Je, B., & Seneff, S. (2015). The Possible Link between Autism and Glyphosate Acting as Glycine Mimetic - A Review of Evidence from the Literature with Analysis. Journal of Molecular and Genetic Medicine, 09(04). doi:10.4172/1747-0862.1000187
Jiao, Y., Chen, R., Ke, X., Cheng, L., Chu, K., Lu, Z., & Herskovits, E. H. (2011). Single Nucleotide Polymorphisms Predict Symptom Severity of Autism Spectrum Disorder. Journal of Autism and Developmental Disorders, 42(6), 971-983. doi:10.1007/s10803-011-1327-5
Kral, T. V., Eriksen, W. T., Souders, M. C., & Pinto-Martin, J. A. (2013). Eating Behaviors, Diet Quality, and Gastrointestinal Symptoms in Children With Autism Spectrum Disorders: A Brief Review. Journal of Pediatric Nursing, 28(6), 548-556. doi:10.1016/j.pedn.2013.01.008
Lucarelli, S., Zingoni, A., Ferruzzi, F., Giardini, O., Quintieri, F., Barbato, M., . . . Cardi, E. (1995). Food Allergy and Infantile Autism. Panminerva Medica, 37(3), 137-141. Retrieved May 11, 2017, from https://www.researchgate.net/profile/Maria_Barbato/publication/14338163_Food_allergy_and_infantile_autism/links/56e468ff08aedb4cc8ac24c8.pdf.
Mulle, J. G., Sharp, W. G., & Cubells, J. F. (2013). The Gut Microbiome: A New Frontier in Autism Research. Current Psychiatry Reports, 15(2). doi:10.1007/s11920-012-0337-0
Paul, B., Barnes, S., Demark-Wahnefried, W., Morrow, C., Salvador, C., Skibola, C., & Tollefsbol, T. O. (2015). Influences of diet and the gut microbiome on epigenetic modulation in cancer and other diseases. Clinical Epigenetics, 7, 112. http://doi.org/10.1186/s13148-015-0144-7
Shanahan, C., & Shanahan, L. (2017). Deep nutrition: why your genes need traditional food. New York: Flatiron Books.
Sure you can! Have some avocado, coconut, olives, cacao, coffee, lemons, limes, or tomato? All systems go! Just remember that fruits are carbohydrates, first and foremost, (except for, arguably, the coconut), so don't go overboard. Granted, lemons and limes are virtually sugar and calorie free, so those can be considered "freebies," so-to-speak. Oh, shoot...not what you had in mind?
In the three years that I've been ketotic, I've probably fielded this question at least a hundred times. Family, friends, coworkers, roommates, and classmates of mine all seem to get either a) concerned, or b) shocked in disbelief, when I tell them, or remind them, that "yup, I still don't eat fruit," (at least not the kinds of fruit that they are most likely thinking of). In these scenarios, I don't bother to get specific because the word "fruit" is synonymous with "sweet," at least in the context of a juxtaposition with vegetables; so even though most people know that avocados and tomatoes are fruits, those types simply aren't the types that they're referring to when they inquire as to the frequency, (or lack thereof), of my fructose-containing-flesh consumption. Sometimes, I will say that I eat coconut, but that's about as far as I'll expound on the subject, unless someone is genuinely interested in keto, or is overtly trying to glean nutrition advice.
So on that note, back to the fruit question. Oh yeah, but what about berries? If you're reading this blog, then you likely aren't new to keto, so I won't bother explaining what countless others have already explained much better than I could: why we don't eat high sugar, low fiber fruits, such as apples, bananas, and oranges. But berries - those are fine, right? Au contraire, my keto friends - not all berries are made equally, and therefore, not all berries are keto-friendly. For example, quite often, I see people say that blueberries are fine to consume on a ketogenic diet. I, personally, respond to this with caution.
Below is a chart comparing the nutrition of common berries: raspberry, blackberry, cranberry, strawberry, elderberry, blueberry, goji, and acai, all of which are sandwiched between two reference fruits: the coconut on the "GO!" side, (i.e., green), and the banana on the "STOP!" side, (i.e., red). The nutrition information given is per 100 gram serving, and is the most up-to-date, USDA certified info.
Berry Nutrition Comparison Chart
As you can plainly tell, the raspberry, with its 4 grams of sugar, 6 grams of fiber, 6 net carbs, and 1 gram of fat, is on the far left side. I gave it the #1 best berry for Keto rating, (despite that it has 1 net carb more than the blackberry), because it has 1 gram of fat more than the blackberry, and 1 gram of sugar, less. This could lead me into a discussion on why net carbs are not the whole picture, but aiming to keep these blogs short, I will save that for a future one. Just keep this is mind, and know the shorthand, which is that fiber and fat content help to blunt the glycemic response, and that glycemic response is best kept as low as possible when attempting to be in a ketotic state.
I chose to use raspberry as the flavor of "jelly" in our Peanut Butter & Jelly Thumbprint Gra-POW! Cookie Granola for this reason. But admittedly, not just for this reason - it also happens to be my favorite of the berries, flavor-wise, anyway. The third and final reason is that it's just plain traditional.
The traditional jam, or jelly, to use in this glorious cookie is raspberry.
Now, that said, I decided that adding a carton of raspberries to the mix would be just a bit too carb-y to offer as a ketogenic food. It didn't sit right in my heart, in other words. Instead, I experimented with raspberry powder and raspberry oil/extract in order to bring the same flavor to the table, while skimping on the sugar content. Ultimately, my goal is use similar methods to bring other fruity flavors into our future products, so if you miss fruit on your ketogenic diet, please stay tuned!