A High Fat, Low Carb Keto BarHIGH-FAT, LOW-CARB
The vast majority of bars are high in net carbs (carbs that raise blood sugar) and low in fat. In contrast, IQ BARs contain ~10g of healthy fats and just 4g of net carbs. Read up on why we chose this macronutritional profile below!
IQ BARs contain ~12g of healthy fats and just 3g of net carbs. Read up on why we chose this macronutritional profile below!
FATS HAVE BEEN LINKED TO BRAIN BENEFITSFATS ARE LINKED TO BRAIN BENEFITS
- The brain is literally made of fat (it’s 70% fat)
- Vitamins key to brain health need fat for absorption
- Studies have linked fat with lower rates of Alzheimer’s
- A high-fat diet is used to treat neurological disease
CARBS HAVE BEEN LINKED TO BRAIN DECLINECARBS ARE LINKED TO BRAIN DECLINE
- Studies have linked carbs with higher rates of brain impairment and smaller critical brain structures
Fats Support Slow-burning Energy
- Fat is essential to produce energy and survive
- Fat has 2X+ the potential energy per gram vs. carbs
- MCTs (fats in IQ BARs) digest into efficient brain fuel
- Fats burn in a non-volatile fashion through the day
Carbs Burn Fast And Cause “crashes”
- Non-fiber carbs rapidly convert into blood sugar, causing an eventual crash and other symptoms
FATS SUPPORT A HEALTHY BODY WEIGHT
- Studies have shown high-fat diets to drive weight loss
- Major diets like Paleo, Whole30®, Keto prioritize fat
- Fat consumption doesn’t promote fat retention
- Fat consumption counteracts feelings of hunger
Carbs Support Weight Gain
- High carb intake creates excess glucose and insulin in the blood; glucose then converts to body fat
A Gluten, Dairy, Soy-free BarGluten/Dairy/Soy-Free
We exclude gluten, dairy, and soy from IQ BARs because we want people with allergies to enjoy our products and compounds in substances have been linked with negative health outcomes. While these links are still debated, we always err on the side of caution!
We exclude these compounds for those with allergies and because they’ve been linked with negative health outcomes. We will always err on the side of caution!
Why Exclude Gluten?
- Gluten causes inflammation in those who are sensitive to it – a substantial portion of the population
- Studies have correlated chronic inflammation with cognitive dysfunction, depression, dementia, and other negative brain conditions
- Studies have also directly correlated celiac disease (severe gluten sensitivity) with progressive cognitive impairment
Why Exclude Dairy?
- A protein in dairy called A1 beta casein causes inflammation in those who are sensitive to it – a substantial portion of the population
- Studies have correlated casein from dairy with cancer formation and growth in animal studies
- Lactose, a sugar in dairy, is one of the leading allergies in the world – up to 65% of humans has a reduced ability to digest lactose
Why Exclude Soy?
- Soy is high in phytates, compounds that bind to brain-critical minerals like magnesium and make them unavailable for absorption.
- Soy is high in isoflavones, compounds that fluctuate estrogen levels; studies have correlated estrogen imbalance with cancer and infertility.
- A longitudian study correlated soy consumption with elevated levels of cognitive impairment, brain shrinkage, and Alzheimer’s.
Used in Chinese medicine for millennia, the Lion’s Mane mushroom is widely championed for its potential brain benefits. It’s perhaps best known for its demonstrated ability to boost nerve growth factor (NGF) across a host of animal studies.  NGF promotes the generation of new neurons, the growth, maintenance, and survival of existing neurons, and the reversal of injury-induced nerve damage.  In vitro research has shown Lion’s Mane to also promote neurite outgrowth, a process by which neurons create more expansive cellular connections. 
Unsurprisingly, healthier neurons appear to improve brain function! A landmark 2009 study found that when a group of 50- to 80-year-old Japanese men and women regularly consumed Lion’s Mane tablets for weeks at a time, they scored significantly higher than a control group in cognitive function testing. A subsequent 2017 study found that mice demonstrated superior spatial short-term and visual recognition memory after consuming the mushroom.  Perhaps the strongest animal research on this topic is that which has shown Lion’s Mane to protect against neurodegenerative diseases like Alzheimer’s and Parkinson’s.    
Lion’s Mane also appears to have strong anti-oxidant properties. Several in vitro studies in the last five years have shown the mushroom to be highly adept at “scavenging” (i.e., disabling) free radicals and reducing genes’ expression of chemicals that promote inflammation.    Lion’s Mane has also been linked with a reduction in fatigue, anxiety, and depression, in part due to its anti-oxidant capabilities.   These “feel-good” benefits are likely the biggest reason Lion’s Mane is cropping up everywhere these days!
Medium Chain Triglycerides (MCT’s) are a powerful alternative brain energy source to carbohydrates and longer-chain saturated fats. When most fats are digested, they are broken down in the intestines, circulated in the bloodstream, and finally metabolized in the liver. In contrast, MCTs are sent directly from the small intestine to the liver where they are broken down quickly and easily into compounds called ketones. While ketones provide near-instant energy to the brain in much the same way that blood sugar from carbohydrates does, they are released in a far more sustainable, crash-free stream.
Extensive literature indicates that MCT’s provide not just cognitive energy, but a higher quality of cognition as well. For instance, a 2004 study found that adults with mild cognitive impairment (MCI) were far more adept at paragraph recall after having taken just a single dose of MCT oil.  A 2010 study took an extended treatment approach, finding that dogs given an MCT-supplemented diet over eight months vastly outperformed their peers across a battery of cognitive tests covering learning ability, visuospatial function, and attention.  In 2015, researchers also found that dogs’ neurons were more capable of metabolizing energy when they were given MCT dosage over a two-month period. 
Additionally, MCT’s has been repeatedly shown to have brain-protective properties. For instance, in 2014, Canadian scientists found that neurons exposed to amyloid proteins - which play a pivotal role in neurodegeneration - have significantly higher survival rates, and lower mitochondrial damage rates, when they are exposed to MCT-rich coconut oil.  Furthermore, when compared to other oils with antioxidant properties like copra oil, olive oil, and sunflower oil, a 2013 study found that coconut oil attenuated oxidative damage in rat brains to the greatest degree.  Given these findings, MCT’s are commonly cited by those in the food community working to debunk the outdated myth that saturated fats are categorically “unhealthy”.
If there was a brain nutrient rockstar, it would be omega-3 fatty acids. On top of energizing the brain, omega-3’s are a primary structural component of the organ itself, representing 8% of its total weight, and the majority of the weight of substructures like neuronal plasma membranes.  Moreover, greater consumption of these acids has been found to correlate with higher gray matter volume in critical components of the brain - especially in its memory center, the hippocampus.   A major driver of this correlation is omega-3’s apparent capacity to induce creation of brain-derived neurotrophic factor (BDNF), a protein that supports new neuron formation. Despite these benefits, 70% of Americans are omega-3 deficient. 
Omega-3 consumption has been linked to more than just larger brains - it has also correlated with greater memory retention, capacity to learn, and neuronal plasticity. Two 2012 studies found that working memories of both younger (aged 18-25) and older (aged 51-72) adults improved when omega-3 pills were taken for extended periods of time.   Further, studies focusing on 4-10 year-olds found that omega-3 intake was associated with improved reading ability, listening comprehension and vocabulary acquisition, and activation of the prefrontal cortex.    Finally, across animal studies where brain injury occurred, omega-3’s corresponded with greater plasticity through reductions in oxidative damage, learning impairment, and cellular homeostasis disruptions.   
One of omega-3 fatty acids’ greatest conferred benefits is counteracting free radicals and inflammation that contribute to a whole host of maladies from brain fog to stroke. Omega-3’s accomplish this feat by signaling the body to mass-produce the antioxidant protein Nrf2 and “mediator” molecules that prevent, halt, and resolve inflammation.     The impact of these biological mechanisms has been shown to be substantial across structural and emotional cognitive outcomes. For instance, a 2007 study tracked over 8,000 healthy older adults and found that those who regularly ingested omega-3-rich oils were 60% less likely to develop dementia than others.  Additional studies have found that consumers of omega-3’s are less likely to be anxious or depressed.  Long story short: omega-3’s do it all.
Flavonoids are one of the reasons people feel “sharp” after consuming colorful fruits and vegetables. When ingested, these compounds signal the body to prioritize cognitive resources and functionality. For instance, flavonoids have been shown to drive greater blood flow to the brain.    They also appear to increase density of (i.e., strengthen) synaptic connections between neurons, and to activate new inter-neuron signaling pathways.   More fortified, efficient connectivity ultimately drives improved cognition. Across human studies measuring processing speed, executive function, working memory, and learning, flavonoids have been shown to cause significant improvements.   
Flavonoids have also been shown to confer energy, stamina, and nimbleness to the brain. A 2006 study found that healthy young adults who consumed drinks containing cocoa flavonoids self-reported reduced mental fatigue after a period of sustained demand, in addition to outperforming controls across a battery of cognitive performance tests.  A 2016 study came to similar conclusions, finding that healthy middle-aged men who consumed a flavonoid-rich drink self-reported higher alertness than controls, and exhibited better executive function and psychomotor speed.  A 2003 study made the additional discovery that older female subjects who consumed flavonoid-rich Pueraria lobata root appeared to have increased flexible thinking (i.e., ability to switch cognitive tasks). 
The brain is not just more functional and active on flavonoids though - it is also better fortified against oxidation, inflammation, neurodegeneration, and depressed mood. The compound’s most widely cited impact is its capacity to both directly neutralize free radicals, and indirectly offset them by facilitating mass-activation of antioxidant Nrf2 proteins in the body.   Similarly, flavonoids have been shown to both prevent and remediate inflammatory enzymes and their byproducts . And, long-term consumption appears to pay off; studies show that consuming flavonoid-rich foods like berries, green tea, and cocoa over decades correlates with lower rates of cognitive decline.    The cherry on top? Across both humans and animals, flavonoids appear to make all creatures happier.  
Vitamin E is a powerful antioxidant that serves a critical role in protecting the brain over time. Neuronal cell membranes are comprised of fats and cholesterol that are highly susceptible to oxidation and inflammation caused by free radicals. Vitamin E embeds itself into these cell membranes and effectively shields them against free radicals, thus preventing chain reactions of structural damage. Despite vitamin E’s capacity to drastically slow the cognitive aging process, well over 90% of adults in America do not consume adequate quantities of the nutrient. 
Most studies on the brain impacts of vitamin E focus on cognitive degradation in the older adult population. For instance, studies conducted in 2002 and 1999 found that healthy, elderly subjects with high vitamin E intakes performed significantly better than others on mental function questionnaires and memory tests.  Another 2002 study found subjects in the highest quintile of vitamin E intake had a 36% reduction in the rate of cognitive decline relative to the lowest quintile - equivalent to an age decrease of 8-9 years.  Finally, a 2011 study linked vitamin E intake to specific brain disorders, finding the risk of mild cognitive impairment (MCI) was 15% lower in adults with the highest levels of vitamin E, and that both MCI and Alzheimer’s disease were correlated with vitamin E damage markers. 
Structural protection offered by vitamin E appears to affect more than just cognition. Tests done on mice have shown that when the animals’ diets are supplemented with vitamin E, they showed markedly improved acrobatic prowess and spatial awareness, and lived 40% longer than their peers . Other medical investigations have found vitamin E to confer benefits to the human heart and immune system - researchers have shown association between vitamin E consumption and decreased risk of heart attack, death from heart disease, and upper respiratory tract infections, including the common cold.   
Choline – considered an essential nutrient by the Institute of Medicine – is perhaps the most underappreciated brain compound in existence. First and foremost, we need it to properly form brain cells. Choline is a critical component of our neurons’ membranes, and without it, our cells’ structural integrity breaks down.  Additionally, choline metabolizes into key messenger chemicals like acetylcholine, which our brains require to regulate muscle control, memory, and mood.  While the body can produce choline in the liver, it cannot generate enough to meet our needs. Thus, without dietary choline consumption, our brain structure and function degrades.
In addition to neuron health, choline also appears to have a positive impact on memory. For instance, in a landmark 2011 study conducted across 1,391 healthy subjects, researchers found a strong correlation between choline intake and performance on verbal and visual memory tests.  Additional studies have found that subjects with memory deficits, as well as those who have experienced traumatic brain injury, benefit from a memory-boosting and neuro-protective impact from choline consumption.    A wealth of animal research also suggests that choline consumption proactively prevents memory decline if taken regularly. 
Finally, a choline-rich diet has been linked across numerous studies to a heightened level of attention. A 2012 study powerfully demonstrated such a link. In it, a group of healthy women were broken into three groups over the course of a month – one that consumed a placebo, one that consumed 250mg of choline a day, and one that consumed 500mg a day. Not only did the 250mg group perform better than the placebo group on attentional tests, but the 500mg group performed the best of all!  Many believe the correlation between choline and focus is due to choline’s role in the creation of dopamine and norepinephrine, neurotransmitters needed for focus and various thinking processes. 
Not only is the brain the fattiest organ in the body (at 70% fat), but vitamins critical to brain health - like A, D, E and K - cannot be absorbed without dietary fat. Thus, it’s no surprise that a high-fat diet correlates with cognitive health benefits. In our Functional Nutrients section, we detail benefits of specific fats like omega-3’s. In addition, though, numerous studies have uncovered positive long-term effects of high-fat diets in general. For instance, a seminal 1998 post-mortem study found that control patients had vastly greater fat content in their cerebrospinal fluid relative to Alzheimer’s patients.  A more recent, 2012 study found that older people whose diets were highest in fats were 42% less likely to develop mild cognitive impairment (MCI), a condition widely considered to be a precursor of Alzheimer’s. 
Perhaps the greatest testament to fat’s beneficial cognitive impact is that it is regularly used to treat serious neurological conditions. For instance, a high-fat, “ketogenic” diet has been used to treat epileptic seizures for thousands of years, and has, according to recent studies, led to an up-to-90% reduction in seizure frequency for many patients.   Another 2005 study found that Parkinson’s disease patients experienced a 43% reduction in Unified Parkinson’s Disease Rating Scale scores after being on a high-fat diet.  A 2014 study even found that a ketogenic diet counteracted migraines, reducing their frequency by 76% and their length of attack by 82%.  Thus, when presented with biological assailants, it appears the brain craves the same compound it is comprised of: fat.
Chronic carbohydrate intake, on the other hand, has been linked with adverse cognitive outcomes. In the aforementioned 2012 study on MCI, subjects in the highest-carb group were nearly four times more likely to be impaired than those in the high-fat group . A second 2012 study found that healthy, non-diabetic subjects with the highest blood glucose levels - a hallmark of high carb consumption - had smaller hippocampi and amygdalae, brain structures critical to memory and emotion.  To help us understand many of the reasons why carb-induced blood sugar spikes can injure the brain, neurologist David Perlmutter gets specific in his 2013 best-selling book Grain Brain: When your blood sugar increases, there’s an immediate depletion of the neurotransmitters serotonin, epinephrine, norepinephrine, GABA, and dopamine. At the same time, B-complex vitamins, which are needed to make those neurotransmitters (and a few hundred other things), get used up. Magnesium levels also diminish, and this handicaps both your nervous system and liver. In addition, high blood sugar triggers a reaction called ‘glycation,’...the biological process whereby glucose, proteins, and certain fats become tangled together, causing tissues and cells to become stiff and inflexible, including those in the brain
Fat has served as a primary bodily and cognitive energy source for over 99% of humans’ two-and-a-half million year evolution. Our hunter-gatherer ancestors thrived on a diet consisting of roughly 75% fat, and it wasn’t until 10,000 years ago - a blip in our species’ history - that modern agriculture introduced fat-displacing foods like grains to the human diet. Moreover, it wasn’t until the 1970’s, when the US Senate Committee on Nutrition and Human Needs began pushing carbohydrates (largely through their “Dietary Goals for the United States”), that the low-fat diet gained serious traction in America. Thus, from an evolutionary standpoint, it’s fair to say we are still “pre-programmed” to run on fat, and there’s quite a bit of research to support that position.
For one, fat is essential to survival. Were we to go entirely fat-free, we would perish. By contrast, carbs are non-essential, as our bodies can generate their derivative glucose from protein via gluconeogenesis. In addition, fat offers a highly concentrated form of energy, with more than double the potential energy per gram that carbs and protein offer. That energy, when delivered through fat-derived ketone bodies, is also highly efficient. As Harvard Medical School professor George Cahill notes: “Studies have shown that beta-hydroxybutyrate, the principal ketone, is not just a fuel, but a superfuel, more efficiently producing ATP energy than glucose.”  As an example, Cahill cites an animal study showing ketones to provide unmatched contractility (strength and vigor) in the heart per unit of oxygen consumed. 
Fat is also the longest-lasting, most even-burning form of macronutrient energy. When the body burns fat, it draws on a virtually endless source of fuel. Because fat doesn’t need to be stored with water - as carbohydrates do - even the leanest of bodies can retain up to 100,000 calories of it (by contrast, we can store just a few thousand calories of carb-derived glycogen). Thus, it makes sense that a body at rest or engaged in moderately-intense exercise draws the majority of its energy from free fatty acids and muscle triglycerides.  Moreover, because fat consumption does not meaningfully elevate blood glucose, a higher-fat diet can spare our bodies from volatility in energy levels. Unlike carbohydrate metabolism, fat metabolism is a slow-release process with an effectively bottomless reserve fuel tank.
Some in the health, nutrition, and fitness spaces have deemed carbohydrates to be the human body and brain’s preferred source of fuel. Here, we’ll address two arguments commonly made by those who assert this position, and provide IQ BAR’s responses to these arguments:
Pro-Carb Argument #1: Our body metabolizes carbohydrates before fats. Thus, carbohydrates must be our body’s preferred fuel source.
IQ BAR’s Take: If this logic was valid, our bodies’ truly preferred energy source would be alcohol. After all, when we consume alcohol with food, our body metabolizes the alcohol before any other energy source - carbohydrates included. Of course, we all know alcohol is not a desirable energy source, and has numerous deleterious health impacts when consumed at volume. Moreover, a primary reason our body burns carbs before fat is our need to keep blood glucose levels from becoming poisonously high after a meal. The point here is that we at IQ BAR feel the moniker of “preferred energy source” should not be defined by speed of metabolism, but rather by factors such as how dense, clean-burning, and efficiently stored the energy source is. And, in all of these categories, fat is the clear frontrunner.
Pro-Carb Argument #2: The brain runs almost exclusively on glucose, and cannot use fatty acids as fuel. Thus, carbohydrates must be our brain’s preferred fuel source.
IQ BAR’s Take: Our brain does, in fact, run almost exclusively on glucose when we consume a high-carb diet, and it is true that fatty acids cannot be burned as brain fuel, as they cannot pass the blood-brain barrier. However, when glucose and its stored form glycogen are low, the liver readily converts fatty acids into ketone bodies, which can displace glucose as a primary (and arguably more efficient) source of brain fuel. Furthermore, when medium-chain triglycerides (MCT’s) are consumed, they are converted by the liver into meaningful quantities of brain-fueling ketones regardless of carbohydrate and glycogen levels.  Some brain cells do require glucose-based energy, though this does not have to come from carbs - it can be generated by breaking down proteins and other compounds via gluconeogenesis.
Unfortunately, when most people think of the word “fat”, images of obesity are conjured. Yet consuming a high-fat diet has actually been shown to correlate with weight-loss, not gain. Numerous studies have shown that a high-fat diet results in far greater weight loss than a low-fat diet     . The true driver of fat accumulation and retention appears to be the carbohydrate. Of course this is by no means a novel realization. Hugely popular modern weight-loss regimens like the Atkins, Paleo, Whole-30, and ketogenic diets are all predicated on the same principle: cut the carbs. So what is it about carbohydrates that cause us to get fat?
After ingestion, carbs are converted into glucose and enter the bloodstream. Only some of this glucose can be burned for energy - our pancreas secretes insulin into the blood to ferry the excess into liver, fat, and muscle cells that convert some of it into glycogen, and much of it into fat. Insulin also promotes the formation of new fat cells, and the retention of fat via several mechanisms. First, it facilitates triglyceride formation in fat cells by increasing volumes of cellular glycerol. Second, it stimulates fatty-acid-attracting enzyme lipoprotein lipase (LPL) in fat cells, causing them to grow, and tempers LPL in muscle cells, reducing their ability to burn fatty acids. Third, it suppresses hormone-sensitive lipase (HSL), an enzyme that breaks down fat cell triglycerides into fatty acids that can enter the blood and be used for fuel.
Fat ingestion, by contrast, does not trigger meaningful insulin release, and thus does not promote fat retention. When we consume a high-fat meal, triglycerides enter the blood (via chylomicron particles) where they are either broken down into fatty acids and used for energy by muscle cells, broken down and stored in muscle and fat cells, or transformed into other substances in the liver and recycled back into the blood. However, because this meal does not upregulate insulin and re-balance LPL and HSL to support fat retention, the fat we temporarily store after eating can easily flow back into the blood to be burned for energy between meals. Moreover, a high-fat diet has been shown to temper the hunger hormone ghrelin, and correlate with lower reported hunger levels, keeping our appetite in check.  
Evidence linking chronic inflammation to cognitive dysfunction, depression, dementia, and other negative brain conditions is mounting.       Thus, it stands to reason that consumption of compounds that incite inflammation put us at risk. Literature suggests that gluten - a sticky protein that entered the human diet just 10,000 years ago - is one such compound for those with sensitivity to it. A landmark 2006 study identified notable overlap between patients with celiac disease (severe gluten sensitivity) and progressive cognitive decline. The study concluded “a possible association exists between progressive cognitive impairment and celiac disease, given the temporal relationship and the relatively high frequency of ataxia and peripheral neuropathy, more commonly associated with celiac disease.” 
So what exactly happens when a gluten-sensitive person consumes the sticky protein? Once in the small intestine, a component of gluten called gliadin instigates the mass-production of anti-gliadin antibodies. These antibodies then bind with gliadin molecules, and cause a class of immune cells called T cells to produce inflammatory cytokine chemicals that destroy villi - critical intestinal protrusions that absorb the nutrients we consume. Repeated damage to villi often results in Leaky Gut Syndrome, autoimmune disease, and a whole host of other maladies. In addition, strong evidence exists that cytokines correlate with a series of cognitive disorders.     Moreover, anti-gliadin antibodies are also capable of binding with proteins in the brain, resulting in even greater cytokine production. 
At this point, you may be thinking: “I don’t have gluten sensitivity, so none of this applies to me.” If so, we implore you to heed two realities. First, the vast majority of gluten sensitivity and celiac disease cases go undetected because most carriers experience no short-term symptoms.   As gastroenterologist Dr. Rodney Ford states in his 2009 article, The Gluten Syndrome: A Neurological Disease, “the crucial point...is that gluten-sensitivity can also be associated with neurological symptoms in patients who do not have any mucosal gut damage (that is, without celiac disease).”  Second, although researchers struggle to estimate just how large the population of gluten-sensitive individuals is, some experts like neurobiologist Dr. Aristo Vojdani suggest as much as 30% of Western populations are at risk. 
Like grains, animal dairy was a recent addition to the human diet, entering ~7,500 years ago. And, while health implications of dairy are debated, much of the scientific community takes issue with a protein similar to gluten that manifested in dairy just several thousand years ago: A1 beta casein. The first knock on this protein is that it breaks down into opiate-like compounds called casomorphins that correlate with inflammation when those with sensitivity digest it. For instance, a 2014 study demonstrated increased levels of the inflammatory biomarker calprotectin in a subset of participants who consumed A1 beta casein.  Far more research on casomorphins’ inflammatory effects has been conducted on rats and mice, with several studies linking A1 beta casein to the inflammatory biomarker myeloperoxidase.  
Researchers have also found correlations between A1 beta casein and a host of inflammatory conditions. Perhaps the most ardent critic of casein is Dr. T. Colin Campbell, who ran a series of studies in the 1980’s in which he found that rats developed liver lesions at an alarming rate when their diet exceeded 10-12% casein.    Dr. Campbell even wrote a book on this topic called The China Study in which he states: "Casein is the most relevant chemical carcinogen" that has ever been identified. Recent research gives potential credence to such claims - for instance, a 2014 study linked casein with growth in prostate cancer cells.  Other research has linked casein sensitivity to cognitive disorders. A 2010 study found a significant correlation between casein antibodies and major depressive disorders and schizophrenia. 
Another often-discussed, though less controversial, component of dairy is a sugar called lactose. Lactose intolerance is one of the leading allergies in the US and across the globe. According to the National Institutes of Health, “approximately 65 percent of the human population has a reduced ability to digest lactose after infancy…[and] about 30 million American adults have some degree of lactose intolerance by age 20.”   One frequently-cited hypothesis for why this aversion to lactose is so widespread is that the human genome has not sufficiently evolved to adapt to continued animal dairy consumption. While lactose has not been shown to correlate with disease when consumed by those sensitive to it, it can produce painful and distressing symptoms such as abdominal pain, bloating, diarrhea, and indigestion.
Soybeans were domesticated by Chinese farmers just several thousand years ago, and a staggering 90+% of soy grown in the US is genetically modified from its original structure.  Furthermore, while it is true that certain East Asian societies with long-living populations consume large quantities of soy (a fact the soy industry readily trumpets), the forms of soy these populations consume - organic fermented miso, natto, and tempeh - have markedly different nutritional profiles than the soy most frequently consumed by Americans. For one, the unfermented soy Americans consume is far higher in phytates, compounds that bind to brain-critical minerals like zinc, iron, and magnesium and make them unavailable for absorption in the human gut.
Soybeans are also high in isoflavones, which function as phytoestrogens that activate estrogen receptors in the body. Phytoestrogens can elevate or mitigate estrogen levels, depending on natural levels at time of consumption.  Estrogen disruption is concerning, given animal studies have linked soy isoflavones’ impact to breast cancer, and human studies have linked it to increased proliferation of breast cells most likely to become cancerous.      In men, isoflavone-induced estrogen increases have been shown to reduce fertility.  Further, a longitudinal study on Japanese-American men found that those who consumed the most tofu during mid-life had higher rates of cognitive impairment, brain shrinkage, and Alzheimer’s.  Study conductors implicated isoflavones as perpetrators of this cognitive decline.
Soy isoflavones also function as goitrogens, meaning they can disrupt proper thyroid function. For instance, they have been shown to interfere with thyroid peroxidase, the enzyme responsible for adding iodine during thyroid hormone production.   Animal and infant studies have also shown that high levels of soy consumption can induce development of goiter - a condition in which the thyroid becomes enlarged - unless a proper amount of iodine is consumed in tandem.       Furthermore, while research on soy’s effect on hypothyroidism (an underactive thyroid gland, which often results in fatigue, coldness, and weight gain) is limited, some literature suggests that managing this condition can be complicated by a high-soy diet.