Gut biota never recover from antibiotics: Damages future generations

Heidi Stevenson
Activist Post
Wed, 05 Jun 2013 16:07 CDT

The misuse of antibiotics is not only causing new, never-before known diseases like E. coli and MRSA, the flesh-eating bacteria, it’s also destroying the gut biome with devastating effects on our ability to deal with infections and destroying our ability to absorb nutrients from food. 

Emerging research shows that the harmful effects of antibiotics go much further than the development of drug resistant diseases. The beneficial bacteria lost to antibiotics, along with disease-inducing bacteria, do not fully recover. Worse, flora lost by a mother is also lost to her babies. The missing beneficial gut bacteria are likely a major factor behind much of the chronic disease experienced today. The continuous use of antibiotics is resulting in each generation experiencing worse health than their parents. 

Martin Blaser, the author of a report in the prestigious journal Naturewrites:

Antibiotics kill the bacteria we do want, as well as those we don’t. These long-term changes to the beneficial bacteria within people’s bodies may even increase our susceptibility to infections and disease.Overuse of antibiotics could be fuelling the dramatic increase in conditions such as obesity, type 1 diabetes, inflammatory bowel disease, allergies and asthma, which have more than doubled in many populations.

Without even considering the development of superbugs, we’re now seeing clear documentation that the overall long term effects of antibiotics are devastatingly harmful to our health. Speaking to ABC News, Blaser said:

Antibiotics are miraculous. They’ve changed health and medicine over the last 70 years. But when doctors prescribe antibiotics, it is based on the belief that there are no long-term effects. We’ve seen evidence that suggests antibiotics may permanently change the beneficial bacteria that we’re carrying. [Emphasis my own.]

Notice that term, permanent. Without factoring in the potential risks in the casual use of antibiotics, it now looks like conventional medicine is creating several pandemics of some of the worst chronic diseases known. 

Mass Use of Antibiotics 

By the time a child reaches age 18 in the industrialized world, the chances are he or she has been given 10-20 courses of antibiotics. That misuse continues into adulthood, and they’re casually prescribed to pregnant women. 

That’s where the situation grows ever worse. Part of normal childbirth is a baby’s passage through the birth canal – where it’s exposed to its first dose of beneficial bacteria. (This should give pause to anyone considering a caesarian birth that isn’t absolutely necessary.) 

When a mother’s microbiota is deficient, her child is born to that deficiency. The evidence now appears to show that, once a probiotic deficiency exists, it is never recovered – and it’s passed down the generations. Therefore, each generation is likely to suffer from poorer health than the parents enjoyed. 

Costs of Antibiotic-Induced Chronic Conditions 

Healthcare costs rise and rise in treating this chronic ill health. Consider the pandemic status of diabetes and asthma in children today. Those diseases were extremely rare 50 years ago, and now they’re literally routine. Yet, the focus continues to be on treatment – which increasingly lines the pockets of Big Pharma and doctors. 

The search for cause has practically been ignored, even in the face of rising rates of chronic illness. Instead, treatment is the touchstone. Ever more toxic methods of suppressing symptoms, while hiding adverse effects, are researched and pushed on conventional medicine’s victims. 

Two of the most critical functions in health are drastically compromised in enormous numbers of today’s children. The ability to metabolize food and the ability to breathe are being stolen from this generation. Yet the treatment they’re receiving for this poor health does nothing to make them well. It only masks the symptoms and makes their children even sicker! 

On top of those losses, children suffer from allergies, their bodies’ inability to distinguish between disease-inducing agents and harmless substances. They suffer from autoimmune disorders, their bodies’ inability to distinguish between foreign substances and parts of their own bodies. 

Has there ever been a generation of children whose inherent health has been so devastated by the very medical system that is supposedly responsible for their health? 

Iatrogenic Disease 

Iatrogenic disorders are health problems caused by medical errors. They are now officially the third-leading cause of death in the United States. But those numbers do not include early deaths from diabetes, asthma, allergies, chronic bowel disorders, or cancer – all of which have been documented as results of antibiotic use – nor are the miseries suffered by the people burdened with them reckoned in the iatrogenic toll. 

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Is the Ketogenic Diet the cure for multiple diseases?

Health Impact News
Sat, 08 Jun 2013 21:37 CDT

The ketogenic diet was developed at John Hopkins hospital in the 1920s as a natural cure for epilepsy, when drugs failed. It is a high fat diet restricting carbohydrates. The diet fell out of favor during the anti-saturated fat campaign started in the U.S. and codified into official government dietary advice in the 1970s as a result of the McGovern Report. It is still official government dietary policy today, due to the influence of the vegetable oil industry which produces their products from the highly subsidized corn and soy bean crops. 

The Ketogenic Diet in some form or another has been labeled by many different names in recent times, and started gaining traction again with Dr. Atkins and the low-carb fad diets that became popular about 8 to 10 years ago. Today’s latest fad diet, the “paelo diet” is another example of a diet based on the ketogenic principles. 

This diet is not new, however, as it was seen as a therapeutic diet that produced better results than drugs in treating epilepsy way back in the 1920s. Today, the diet is being studied in the medical community with applications to all kinds of diseases. Of course, most of the medical interest in the diet is to try and develop a line of “ketone” drugs to mimic the diet. Ketones, which our body can produce during fasting or “starvation,” is an alternative energy source for those who are insulin resistant. Insulin resistance is increasingly being seen as a major cause of many diseases. 

When the Atkins diet gained media popularity several years ago, many critics complained that there were no long-term studies done on the diet. However, there are plenty of studies on the Ketogenic Diet and there has never been any negative effects recorded from long-term use. One study is here. Epidemiological studies on populations that eat high saturated fat diets also abound. So with no side effects from a natural diet, it is highly unlikely that any pharmaceutical products will see the same success the Ketogenic Diet is seeing today. 

The research that is starting to be published on the effectiveness of the Ketogenic Diet in curing disease is nothing less than amazing. This study below is a survey of the diet’s use in a variety of neurological diseases. 

The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders 

Carl E. Stafstrom1,2 and Jong M. Rho3,4,

Front Pharmacol
. 2012; 3: 59. 

Abstract 

Dietary and metabolic therapies have been attempted in a wide variety of neurological diseases, including epilepsy, headache, neurotrauma, Alzheimer disease, Parkinson disease, sleep disorders, brain cancer, autism, pain, and multiple sclerosis. The impetus for using various diets to treat – or at least ameliorate symptoms of – these disorders stems from both a lack of effectiveness of pharmacological therapies, and also the intrinsic appeal of implementing a more “natural” treatment. The enormous spectrum of pathophysiological mechanisms underlying the aforementioned diseases would suggest a degree of complexity that cannot be impacted universally by any single dietary treatment. Yet, it is conceivable that alterations in certain dietary constituents could affect the course and impact the outcome of these brain disorders. Further, it is possible that a final common neurometabolic pathway might be influenced by a variety of dietary interventions. The most notable example of a dietary treatment with proven efficacy against a neurological condition is the high-fat, low-carbohydrate ketogenic diet (KD) used in patients with medically intractable epilepsy. While the mechanisms through which the KD works remain unclear, there is now compelling evidence that its efficacy is likely related to the normalization of aberrant energy metabolism. The concept that many neurological conditions are linked pathophysiologically to energy dysregulation could well provide a common research and experimental therapeutics platform, from which the course of several neurological diseases could be favorably influenced by dietary means. Here we provide an overview of studies using the KD in a wide panoply of neurologic disorders in which neuroprotection is an essential component. 

Introduction 

The ketogenic diet (KD) is now a proven therapy for drug-resistant epilepsy (Vining et al., 1998; Neal et al., 2008), and while the mechanisms underlying its anticonvulsant effects remain incompletely understood (Hartman et al., 2007; Bough and Stafstrom,2010; Rho and Stafstrom, 2011), there is mounting experimental evidence for its broad neuroprotective properties and in turn, emerging data supporting its use in multiple neurological disease states (Baranano and Hartman, 2008). Even in patients with medically refractory epilepsy who have remained seizure-free on the KD for 2 years or more, it is not uncommon for clinicians to observe that both anticonvulsant medications and the diet can be successfully discontinued without recrudescence of seizures (Freeman et al., 2007). This intriguing clinical observation forms the basis of the hypothesis that the KD may possess anti-epileptogenic properties. 

This review article explores the rationale for using the KD and related dietary treatments in neurological disorders outside of epilepsy, and summarizes the clinical experience to date. An underlying theme of such diet-based therapies is that nutrients and metabolic substrates can exert profound effects on neuronal plasticity, modifying neural circuits and cellular properties to enhance and normalize function. At a fundamental level, any disease in which the pathogenesis is influenced by abnormalities in cellular energy utilization – and this implies almost every known condition – would theoretically be amenable to the KD. It is important to acknowledge that much of the data discussed here are preliminary and anecdotal, and hence need to be validated by well-controlled prospective studies. Nevertheless, that diet and nutrition should influence brain function should not be altogether surprising, and there are already abundant clinical and laboratory data linking defects in energy metabolism to a wide variety of disease states (Waldbaum and Patel, 2010; Roth et al., 2011; Schiff et al., 2011). Thus, the potential for interesting and novel applications of the KD and related dietary therapies is almost limitless (Stafstrom, 2004). 

Neuroprotective Role of the KD 

Over the past decade, investigators have identified numerous mechanisms through which the KD may provide neuroprotective activity. While a comprehensive discussion of such mechanisms is beyond the scope of this chapter, a brief discussion is warranted as such actions are intimately related to disorders that share the common feature of progressive neurodegeneration and/or cellular bioenergetic dysfunction. The reader is referred to recent reviews for more details on this subject (Gasior et al.,2006; Acharya et al., 2008; Masino and Geiger, 2008). 

Two hallmark features of KD treatment are the rise in ketone body production by the liver and a reduction in blood glucose levels. The elevation of ketones is largely a consequence of fatty acid oxidation. Specific polyunsaturated fatty acids (PUFAs) such as arachidonic acid, docosahexaenoic acid, and eicosapentaenoic acid, might themselves regulate neuronal membrane excitability by blocking voltage-gated sodium and calcium channels (Voskuyl and Vreugdenhil, 2001), reducing inflammation through activation of peroxisome proliferator-activated receptors (PPARs; Cullingford, 2008; Jeong et al., 2011), or inducing expression of mitochondrial uncoupling proteins which reduce reactive oxygen species (ROS) production (Bough et al., 2006; Kim do and Rho, 2008). Ketone bodies themselves have been shown to possess neuroprotective properties, by raising ATP levels and reducing ROS production through enhanced NADH oxidation and inhibition of mitochondrial permeability transition (mPT; Kim do et al., 2007). Along similar lines of improved bioenergetics, the KD has been shown to stimulate mitochondrial biogenesis, resulting in stabilized synaptic function (Bough et al., 2006). 

The second major biochemical feature of the KD is the decrease in glycolytic flux. Reduction of glycolysis is an essential feature of calorie restriction, which has been shown to suppress seizures (Greene et al., 2001) as well as prolong the lifespan of numerous species, including primates (Kemnitz, 2011; Redman and Ravussin, 2011). While the link between calorie restriction and KD mechanisms remain controversial (Yamada, 2008; Maalouf et al., 2009), it is clear that both treatments result in reduction of blood glucose, likely involving reduced glycolytic flux. In that regard, 2-deoxy-d-glucose (2DG), an analog of glucose that blocks phosphoglucose isomerase and hence inhibits glycolysis, has been shown to block epileptogenesis in the rat kindling model by decreasing the expression of brain-derived neurotrophic factor (BDNF) and its principal receptor, tyrosine kinase B (TrkB; Garriga-Canut et al., 2006). Several other important mechanisms contribute to the neuroprotective consequences of calorie restriction, including improved mitochondrial function and decreased oxidative stress (similar to that seen with ketones and PUFAs), decreased activity of pro-apoptotic factors, and inhibition of inflammatory mediators such as interleukins and tumor necrosis factor alpha (TNFα; Maalouf et al., 2009). 

In the end, there are likely many other mechanisms that could contribute to the neuroprotective properties of the KD. Many of these mechanisms are thought to relate principally to the KD’s anticonvulsant effects, but some if not all of them could contribute to cellular homeostasis and preventing neuronal injury or dysfunction. An important caveat, however, is that yet unidentified mechanisms may operate in diseases outside of epilepsy, and this possibility presents further opportunities for examining the pleiotropic effects of this metabolism-based therapy at a mechanistic level. 

The KD in Epilepsy 

There is no longer any doubt that the KD is effective in ameliorating seizures in patients, especially children, with medically refractory epilepsy (Vining, 1999; Neal et al., 2008; Freeman et al., 2009). After its introduction in 1920, the KD was used as a first or second-line treatment for severe childhood epilepsy. With the introduction of anticonvulsant medications in convenient pill form, the use of the KD waned, only to resurge later in the early 1990s, due largely to the efforts of concerned parents who brought the diet back to greater public awareness (Wheless, 2008). Recent years have witnessed a remarkable surge in research on the KD, including basic science efforts as well as clinical protocols and trials (Kim do and Rho, 2008; Neal et al.,2008; Kessler et al., 2011). The KD has now become an integral part of the armamentarium of most major epilepsy centers throughout the world (Kossoff and McGrogan, 2005). 

The KD in Aging 

Aging involves the gradual decrease in function, and at times outright degeneration, of neurons and neural circuits. It is possible that by altering energy metabolism with the KD, rates of degeneration of certain neural structures and functions might be slowed (Balietti et al., 2010a). However, KDs may induce differential morphological effects in structures such as the hippocampus, perhaps as a consequence of region-specific neuronal vulnerability during the late aging process (Balietti et al., 2008). Specifically, it has been shown that the medium-chain triglyceride (MCT) form of the KD may induce detrimental synaptic changes in CA1 stratum moleculare, but beneficial effects in the outer molecular layer of the dentate gyrus (Balietti et al., 2008). In MCT-fed aged rats compared to aged rats receiving a normal diet, mitochondrial density and function in cerebellar Purkinje cells were significantly increased, suggesting that the KD can rescue age-related mitochondrial dysfunction (Balietti et al.,2010b). These observations imply certain risks, but also potential benefits of the KD for the aging brain. However, the fact that the KD reduces oxidative stress and its downstream consequences provides a reasonable rationale for considering this type of treatment to retard the adverse consequences during aging (Freemantle et al., 2009). As an example, T-maze and object recognition performance were improved in aged rats by KD administration, suggesting a potential functional benefit in cognition (Xu et al., 2010). Finally, it should be noted that because of its similarities to calorie restriction (as noted above), the KD is likely to involve other neuroprotective mechanisms that could ameliorate pathological aging – especially when occurring in the context of neurodegeneration (Contestabile, 2009). 

The KD in Alzheimer Disease 

There is growing realization that neuronal excitability is enhanced in patients with Alzheimer disease (AD; Noebels, 2011; Roberson et al., 2011). While the essential pathological processes of AD involves neuronal degeneration with accumulation of abnormal cellular products such as fibrillary plaques and tangles, recent evidence points to alterations in the function of extant neural circuits and mitochondrial homeostasis (Kapogiannis and Mattson, 2011). This view is bolstered by the higher incidence of seizures in patients with AD as compared to the unaffected population (Palop and Mucke, 2009). Therefore, there is a rationale for hypothesizing that the KD might have a beneficial role in patients with AD (Balietti et al., 2010a), in addition to the potential benefits to the aging process as noted above. One should note, importantly, that if ketone bodies are indeed the primary mediators that counter aging and neurodegeneration in AD, implementation of the KD should be tempered by known age-related differences in the production and extraction of ketones (i.e., this is more efficient in young animals), as well as age-specific regional differences in ketone utilization within the brain (Nehlig, 1999). 

Clinical studies to date have been equivocal but promising. A randomized double-blind, placebo-controlled trial of a MCT KD resulted in significantly improved cognitive functioning in APOε4-negative patients with AD but not in patients with a APOε4 mutation (Henderson et al., 2009). In this study, the primary cognitive end-points measured were the mean change from baseline in the AD Assessment Scale-Cognitive subscale, and global scores in the AD Cooperative Study – Clinical Global Impression of Change (Henderson et al., 2009). This significant clinical improvement was considered to be secondary to improved mitochondrial function, since ketone bodies (specifically, beta-hydroxybutyrate or BHB) have been shown to protect against the toxic effects of β-amyloid on neurons in culture (Kashiwaya et al., 2000). Alternatively, the KD may actually decrease amounts of β-amyloid deposition (VanderAuwera et al., 2005). Interestingly, other diets such as the Mediterranean diet are showing some promise in AD (Gu et al., 2010), possibly through a reduction in systemic inflammation and improved metabolic profiles. 

Recent studies have shown a closer linkage of AD to epilepsy. For example, animal models of AD exhibit neuronal hyperexcitability and enhanced propensity to seizures (Palop et al., 2007; Roberson et al., 2011); these models may ultimately allow for detailed analyses of both cognitive and anticonvulsant effects of the KD or other dietary manipulations such as calorie restriction. Transgenic AD mice fed 2DG demonstrated better mitochondrial function, less oxidative stress, and reduced expression of amyloid precursor protein and β-amyloid compared to control animals (Yao et al., 2011). 

Another pathophysiological mechanism hypothesized to operate in AD ties together altered mitochondrial function and glucose metabolism, i.e., accumulation of advanced glycation endproducts (AGE; Srikanth et al., 2011). AGE accumulation is a process of normal aging that is accelerated in AD; proteins are non-enzymatically glycosylated and this cross-linking of proteins accentuates their dysfunction. One proposed mechanism is increased ROS and free radical formation, which, as discussed above, hampers mitochondrial function. The intriguing possibility that AGE inhibitors (e.g., aminoguanidine, tenilsetam, carnosine) could act in concert with the KD or antioxidants in retarding AD progression remains speculative at this time. 

Thus, there is growing evidence that the KD may be an effective treatment for AD through a variety of metabolism-induced mechanisms that reduce oxidative stress and neuroinflammation, and enhance bioenergetic profiles – largely through enhanced mitochondrial functioning. However, caution should be exercised in extrapolating findings in animals to humans, as discrepancies in terms of both clinical efficacy and untoward side-effects have been noted. For example, adverse reactions to calorie restriction have been reported in some rodent models (Maalouf et al., 2009), and in hippocampus, abnormal morphological synaptic changes have been observed in CA1 stratum moleculare (Balietti et al., 2008). 

The KD in Parkinson Disease 

The primary pathophysiology in Parkinson disease (PD) is excitotoxic degeneration of dopaminergic neurons in the substantia nigra, leading to abnormalities of movement, and to an increasing extent, in cognition and other cortical functions. How could the KD benefit patients with PD? Based on the recognition that ketone bodies may bypass defects in mitochondrial complex I activity that have been implicated in PD, a small clinical study demonstrated that 5 of 7 affected patients showed improved scores on a standard PD rating scale (Vanitallie et al., 2005); however, given the small sample size, a placebo effect cannot be ruled out. In animal models of PD produced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), BHB administration ameliorated the mitochondrial respiratory chain damage that ordinarily results from that toxin (Kashiwaya et al., 2000). Additional evidence supporting the potential benefits of ketone bodies in PD is provided by in vitro experiments demonstrating the protective effects of these substrates against mitochondrial respiratory chain dysfunction induced exogenously by complex I and II inhibitors rotenone and 3-nitropropionic acid, respectively (Kim do et al., 2010), and even anti-inflammatory actions of the KD on MPTP-induced neurotoxicity (Yang and Cheng, 2010). It would be of interest to determine whether commercially available treatments that augment ketonemia – e.g., the MCT-based formulation used in a recent Alzheimer’s clinical trial (Henderson et al., 2009) – might benefit patients with PD. 

The KD in Amyotrophic Lateral Sclerosis 

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive disease due to degeneration of motor neurons of the cortex and anterior horn of the spinal cord. As a consequence, voluntary motor activity gradually deteriorates, leaving the affected individual profoundly weak despite largely retained cognitive functioning. The essential pathophysiological mechanisms that underlie this relentless disorder are yet to be fully elucidated, but similar to other neurodegenerative disorders, the involvement of energy-producing systems likely play a role and mitochondrial dysfunction probably contributes to disease pathogenesis. In this regard, the KD may be a promising adjunctive treatment for this devastating disease (Siva, 2006), as evidenced in a mouse model of ALS, produced by knocking out the gene encoding the copper/zinc superoxide dismutase SOD1-G93A, causing progressive muscle weakness and death by respiratory failure. Administration of a KD to these mutant mice led to both histological (higher motor neuron counts) and functional improvements (preserved motor function on the rotorod test) compared to non-KD fed animals (Zhao et al., 2006). However, the KD did not extend survival time compared to non-KD fed control mice. Mitochondria from these mutant mice demonstrated increased ATP synthesis, countering the inhibition of complex I of the electron transport chain. It is important to note that approximately 20% of the familial cases of ALS have SOD1 mutations, and hence the possibility arises that the KD may be of benefit to patients with ALS. 

One potentially important consideration in this regard – applicable to all neurodegenerative diseases – is determining whether timing of intervention is crucial for a protective effect by KD treatment. Neurological disorders in late stages of progression may have such extreme neuronal dysfunction and death to allow a “re-fueling” with metabolic substrates to help recover integrity and function. Certainly, this appears to be the case in a small pilot study of KD treatment in patients with Lafora body disease (Cardinali et al., 2006). 

The Kd in Cancer 

Cells that exhibit the most active metabolic rates (i.e., cancer cells) are most sensitive to the lack of metabolic energy to fuel their activity, a well-recognized biochemical phenomenon known as the Warburg effect. Theoretically, depriving rapidly dividing, highly metabolic cancer cells of their usual fuel supply, e.g., glucose (by use of the KD or 2DG), could be clinically therapeutic (Aft et al., 2002; Pelicano et al., 2006; Otto et al., 2008). Despite this well documented cellular observation, the KD has only recently been considered as a clinical treatment in the oncology field. 

Pioneering work by Seyfried et al. (2011) over the past decade has shown that animals with experimentally produced brain tumors placed on a KD exhibit markedly decreased tumor growth rates, and these remarkable effects appear to be a consequence of calorie restriction (i.e., reduced blood glucose levels) rather than KD-induced ketosis (i.e., fatty acid oxidation) as the principal mechanism. Other investigators have found similar effects of the KD in animal models. One group found that the KD reduces ROS production in malignant glioma cells, and gene microarray expression profiling demonstrated that the KD induces an overall reversion to patterns seen in non-tumor specimens and a reduction in the expression of genes encoding signal transduction pathways and growth factors known to be involved in glioma growth (Stafford et al., 2010). It is also interesting to note that PPARα-activated by nutrients such as fatty acids – is now a target for developing anti-cancer drugs that target mitochondrial metabolism (Grabacka et al., 2010). 

While clinical validation of this phenomenon is not yet forthcoming, there are several case reports suggesting that the KD may be efficacious in humans with brain tumors. Nebeling et al. (1995) reported beneficial effects of an MCT-based diet in two pediatric patients with advanced stage malignant astrocytomas. More recently, Zuccoli et al. (2010) described a case study of an elderly woman with glioblastoma multiforme who was treated with standard radiotherapy plus concomitant temozolomide therapy together with a calorie-restricted KD, and a complete absence of brain tumor tissue was noted on FDT – PET and MRI imaging after 2months of treatment – results the authors attributed in part to the adjunctive dietary treatment. Further, in a pilot trial of the KD in 16 patients with advanced metastatic tumors, six individuals reported improved emotional functioning and less insomnia, indicating that in some instances, the KD may lead to improved quality of life (Schmidt et al., 2011). In contrast, a retrospective examination of five patients with tuberous sclerosis complex treated with the KD indicated either a lack of tumor suppression or further tumor growth (Chu-Shore et al., 2010). Thus, it may be that distinct tumor types within different organ systems may respond differently to the KD or other dietary treatments and that such differences may reflect variations in the metabolic vulnerability of specific tumor types, perhaps through intrinsic differences in the expression of metabolism-related genes (Stafford et al., 2010). 

The KD in Stroke 

To date, no clinical trials of the KD have been performed in patients with stroke, but several animal studies of hypoxia-ischemia support the potential beneficial effect of the diet. Most of these models entail pre-treatment with the KD (or with BHB), resulting in decreased structural and functional damage from the stroke. For example, Tai et al. (2008) utilized a cardiac arrest model in rats and found significantly reduced Fluoro-Jade staining in animals that underwent 25 days of pre-treatment with the KD. These investigators later determined that these effects were not due to involvement of plasmalemmal ATP-sensitive potassium channels (Tai et al., 2009), which have been implicated in ketone body action (Ma et al., 2007). Other researchers have hypothesized that the neuroprotective properties of ketone bodies might be related to up-regulation of hypoxia inducible factor (HIF1-α) which is important in angiogenesis and anti-apoptotic activity (Puchowicz et al., 2008). In that study, pre-treatment with BHB (via intraventricular infusion, followed by middle cerebral artery occlusion) led to significant increases in brain succinate content, as well as elevations in HIF1-α and Bcl-2, an anti-apoptotic protein. To be clinically meaningful, of course, a positive effect must be demonstrable after, and not before, an ischemic event. Nevertheless, such studies imply that biochemical alterations that favor energy metabolism would be protective against acute forms of severe brain injury. 

The KD in Mitochondrial Disorders 

As mentioned above, given the growing evidence that the KD enhances mitochondrial functioning and biogenesis (Bough et al.,2006; Maalouf et al., 2009; Kim do et al., 2010), it is logical to ask whether patients with known mitochondrial cytopathies might derive a benefit from the KD and/or ketone bodies such as BHB. At the same time, it must be considered that inherent mitochondrial dysfunction might predispose individuals to adverse toxicities from high fatty acid loads that could overwhelm β-oxidation within the mitochondrial matrix. Experimental data described above attest to significant improvements in mitochondrial function, and many lines of evidence point to the rationale of therapeutically targeting mitochondrial bioenergetics for other disease states (Wallace et al., 2010), but is there any clinical evidence in patients with intrinsic mitochondrial disorders? Kang et al. (2007) reported that the KD was both safe and effective in 14 pediatric patients with established mitochondrial defects in complexes I, II, and IV, all of whom had medically intractable epilepsy. These authors observed that half of these patients became seizure-free on the KD, and only four patients failed to respond. Hence, these preliminary data suggest that the KD is not necessarily contraindicated in patients with mitochondrial respiratory chain abnormalities. However, KD treatment is not recommended in individuals with primary carnitine deficiencies [including mutations in carnitine palmitoyl transferase (CPT) I or II and mitochondrial translocase] and fatty acid β-oxidation abnormalities (e.g., medium-chain acyl dehydrogenase deficiency; Kossoff et al., 2009). Thus, it is critical to determine the specific mitochondrial defect when considering treatment with the KD, to avert clinical deterioration. 

The KD in Brain Trauma 

Unfortunately, the incidence of brain injury is increasing in both civilian and military contexts. Brain injury, either due to a penetrating injury or to blunt/blast trauma, can lead to severe cognitive and motor consequences. Further, the occurrence of epilepsy months to years following brain trauma adds to the morbidity of affected individuals, and speaks to the emergence of hyperexcitable neuronal circuits over time. Hence, in light of the clinical problem of post-traumatic epileptogenesis and the fact that the KD can reduce seizure activity, the notion has emerged that dietary therapy might ameliorate brain injury and possibly, long-term consequences such as epilepsy. 

Several recent animal studies support this idea, and investigators have principally focused on ketone bodies (Prins, 2008a). Using a controlled cortical impact (CCI) injury model, Prins et al. (2005) showed that pre-treatment with a KD significantly reduced cortical contusion volume in an age-related manner that correlated with maturation-dependent differences in cerebral metabolism and ketone utilization. Later, they showed that cognitive and motor functioning was also improved with KD treatment (Appelberg et al., 2009). Further, using a weight drop model, Hu et al. (2009) showed that the KD pre-treatment reduced Bcl-2 (also known as Bax) mRNA and protein levels 72h after trauma, indicating that apoptotic neurodegeneration could be prevented with this diet. Consistent with these observations, it was found that fasting – which shares the key feature of ketosis with the KD – led to significant tissue sparing in brain following CCI injury, and that again ketosis (with improved mitochondrial functioning) rather than the relative hypoglycemia seen with fasting was the important determinant of neuroprotection (Davis et al., 2008). 

With respect to anti-epileptogenesis following head injury, the data regarding KD effects are mixed. KD treatment – either before or after fluid percussion injury in rats – did not alter later seizure sensitivity to fluorothyl, even though the degree of hippocampal cell loss was reduced by pre- but not post-treatment (Schwartzkroin et al., 2010). Similarly, in the lithium – pilocarpine model of temporal lobe epilepsy, KD treatment prior to induction led to morphological neuroprotection in the hippocampus but did not affect latency to onset of spontaneous recurrent seizures (Linard et al., 2010). In contrast, Jiang et al. (2012) recently reported that the KD increased after-discharge thresholds and reduced generalized seizure occurrence in a rat amygdala kindling model. Thus, at this juncture, there is no consensus regarding whether the KD is anti-epileptogenic following a variety of traumatic insults and manipulations. However, given the recent finding that the KD inhibits the mammalian target of rapamycin (mTOR) pathway (McDaniel et al., 2011), which has been linked to modulation of epileptogenesis (McDaniel and Wong, 2011), further studies in different animal models are clearly warranted. What is unambiguous, nevertheless, is the age-dependence of the effects of the KD in ameliorating the consequences of head injury (Prins, 2008b; Deng-Bryant et al., 2011). 

The KD in Psychiatric Disorders (Depression) 

Mood stabilizing properties of the KD have been hypothesized (El-Mallakh and Paskitti, 2001), but no clinical studies have been conducted as of this writing. The potential role of the KD in depression has been studied in the forced choice model of depression in rats, which led to a beneficial effect similar to that afforded by conventional antidepressants (Murphy et al., 2004; Murphy and Burnham, 2006). 

The KD in Autism 

Autism is a neurodevelopmental disorder that affects language development and social function. The heterogeneous etiologies leading to autism spectrum disorders, plus the uncertainty about what causes autism in the majority of “idiopathic” cases, has hampered the development of a universally beneficial treatment, aside from symptomatic treatment of autism-related behaviors such as aggression or anxiety. Now, limited clinical evidence raises the intriguing possibility that the KD might be helpful to alleviate some of the abnormal behaviors seen in children with autism spectrum disorders. Using a KD variant consisting of MCT, 10 of 18 autistic children demonstrated moderate or significant behavioral improvement (by a blinded rater) after a 6-month trial of providing the diet for 4weeks of KD diet treatment alternating with 2weeks of normal diet, in 6-week cycles (Evangeliou et al., 2003). This study was carried out on the island of Crete, where the frequency of autism is high but the possibility of genetic inbreeding is also significant. Therefore, these findings need to be interpreted cautiously and larger longitudinal studies are needed. The potential involvement of adenosine, an endogenous neuromodulator and anticonvulsant, in ameliorating autistic behaviors raises the possibility of overlap with KD mechanisms (Masino et al., 2011). As a caveat, many children with autism poorly tolerate changes in dietary and other routines, which could impact implementation of dietary therapies, which require strict adherence. 

The KD in Migraine 

Migraine is a paroxysmal neurological disorder having considerable clinical phenotypic overlap with epilepsy (Rogawski, 2008). Although the intrinsic mechanisms underlying seizures and migraine attacks differ in many fundamental respects, there are theoretical reasons to consider the KD for chronic migraine. Both disorders involve paroxysmal excitability changes in the brain, and there is considerable overlap in the array of pharmacological agents used to treat these conditions. Although it might seem unlikely that an individual with migraine would undertake such a complicated dietary regimen as the KD, in light of suboptimal alternatives, this choice is worthy of consideration, particularly in the medically refractory population (Maggioni et al., 2011). 

Interestingly, the first report of using the KD for migraine came in 1928, only a few years after the diet’s first use for epilepsy (Schnabel, 1928). Nine of 28 patients reported “some improvement,” although the validity of this clinical study is uncertain and some patients admitted poor compliance. Compliance might be better with the less restrictive modified Atkins diet, which has also shown promise for migraine treatment (Kossoff et al., 2010). Other case reports exist but there are no large clinical series or trials. Notwithstanding this limitation, laboratory investigations have found that both short-term and long-term treatment with either MCT or long-chain triglyceride forms of the KD resulted in a significant reduction in the velocity of cortical spreading depression (CSD) velocity in immature rats (de Almeida Rabello Oliveira et al., 2008). Another intriguing aspect of this study was the observation that triheptanoin – an anaplerotic substrate that enhances tricarboxylic acid cycle function – had a notable effect in retarding CSD, consistent with a later report that triheptanoin supplementation raised pentylenetetrazol tonic seizure threshold and delayed the development of corneal kindled seizures (Willis et al., 2010). 

Summary 

Despite the relative lack of clinical data, there is an emerging literature supporting the broad use of the KD (and its variants) against a variety of neurological conditions. These preliminary studies are largely based on the fundamental idea that metabolic shifts may lead to neuroprotective actions (Gasior et al., 2006; Maalouf et al., 2009). How can a simple dietary change lead to improvement in disorders with such a huge span of pathophysiological mechanisms? Alterations in energy metabolism appear to be a common theme. So while the mechanisms through which the KD exerts such effects are likely diverse (Maalouf et al.,2009; Rho and Stafstrom, 2011), there may indeed be one or more common final pathways that are mechanistically shared. Ultimately, the details of how that altered metabolism reduces neuronal excitability, abrogates ongoing neurodegeneration, or mitigates functional disability remain unknown. Herein lay rich opportunities for further investigation, in both the laboratory and the clinic, in the broad realm of translational neurosciences. 

Conflict of Interest Statement 

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. 

Read the full study here 

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  86. Waldbaum S., Patel M. (2010). Mitochondrial dysfunction and oxidative stress: a contributing link to acquired epilepsy? J. Bioenerg. Biomembr. 42, 449 – 455. doi: 10.1007/s10863-010-9320-9. [PMC free article] [PubMed] [Cross Ref]
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The 9 Foods You Should Never Eat

1. Canned Tomatoes

BPA is a toxic chemical linked to reproductive abnormalities, neurological effects, heightened risk of breast and prostate cancers, diabetes, heart disease and more. To avoid this hazardous chemical, avoid canned foods entirely and stick to fresh fruits and vegetables, or switch over to brands that use glass containers instead—especially for acidic foods like tomatoes.

2. Processed Meats

Deli meats are typically made with meats from animals given growth hormones, antibiotics and other veterinary drugs. These meats also typically contain sodium nitrite and other chemical flavorings and dyes. Processed should be avoided entirely as processed meats increase your risk of cancer, and NO amount of processed meat is “safe.” Fresh organically-raised grass-fed or pastured meats, or wild caught salmon are healthier options.

3. Margarine

There are a myriad of unhealthy components to margarine and other butter impostors, including trans fats, free radicals, emulsifiers and preservatives, hexane and other toxic solvents. Raw milk butter, when made from grass-fed cows, is rich in beneficial conjugated linoleic acid (CLA), which is known to help fight cancer and diabetes.

4. Vegetable Oils

Vegetable oils are highly processed, and when consumed in large amounts, they distort the important omega-6 to omega-3 ratio. Vegetable oils can oxidize good cholesterol, turning it into bad cholesterol. Coconut oil is best for cooking as it is not very susceptible to heat damage. It’s also one of the most unique and beneficial fats for your body. Olive oil is easily damaged by heat and is best reserved for drizzling cold over salad.

5. Microwave Popcorn

Microwave popcorn bags are lined with PFOA, and when they are heated the compound leaches onto the popcorn. These chemicals are part of an expanding group of chemicals known to disrupt your endocrine system and affect your sex hormones. The EPA has ruled PFCs as “likely carcinogens,” and has stated that PFOA “poses developmental and reproductive risks to humans.”

6. Non-Organic Potatoes and Other Fresh Produce Known for High Pesticide Contamination

Your best bet is to buy only organic fruits and vegetables, as synthetic agricultural chemicals are not permissible under the USDA organic rules. That said, not all conventionally grown fruits and vegetables are subjected to the same amount of pesticide load. Fruits and vegetables with the highest pesticide load, making them the most important to buy or grow organically, include apples, cucumbers, spinach, kale and potatoes.

7. Table Salt

Regular ‘table salt’ and the salt found in processed foods are NOT identical to the salt your body really needs. Table salt contains chemicals like ferrocyanide and aluminosilicate, and added iodine, while natural salt contains many naturally occurring minerals, including trace minerals like silicon, phosphorous and vanadium. My favorite is Himalayan salt, which contains about 84 trace minerals your body needs.

8. Soy Protein Isolate and Other Unfermented Soy Products

Most soybeans grown in the US are genetically engineered (GE) to be “Roundup Ready.” The active ingredient in Roundup is glyphosate, which disrupts cellular function and can induce many of our modern diseases, including autism. Unfermented soy has also been linked to malnutrition, digestive distress, immune-system breakdown, thyroid dysfunction, cognitive decline, reproductive disorders and infertility—even cancer and heart disease. The only soy with health benefits is organic soy that has been properly fermented, at which point their beneficial properties become available to your digestive system.

9. Artificial Sweeteners

Artificial sweeteners such as aspartame can stimulate your appetite, increase carbohydrate cravings, and stimulate fat storage and weight gain. The methanol formed in aspartame can wreak havoc with sensitive proteins and DNA in your body, as humans do not have the protective mechanism that allows methanol to be broken down into harmless formic acid. Toxicology testing on animals is a flawed model, as animals have this protective mechanism while humans do not, so the results do not fully apply to people.

 

Exposing the truth about GMOs


Michael Thomas
exposingthetruth.co
Mon, 27 May 2013 15:58 CDT

One of the hottest and most controversial issues in the world today is genetic engineering. With protests against Monsanto on May 25th in over 400 cities, people have shown that this is a topic they truly care about. Largely, the stances are highly polarized with opponents saying it is all cancer causing, poisonous, and environmentally dangerous and supporters saying it is wonderful, improving yield and making everyone except “anti-science” opponents happy. 

The problem with polarized positions is they almost always miss the reality of the issue and avoid talking about the general facts. Polarized texts instead skip directly to the evidence supporting their position. But, in real life, I think it is important to lay out exactly what we are talking about before we try to say if it is “good” or “bad.” 

The first question we have to address, before we talk about the potential and danger of genetic modification, is what exactly is genetic modification? If you want to avoid the science, you can just skip the next 3 paragraphs. Otherwise, I can advise continuing to read, using the sources I provide, or using a search engine. 

In the modern context we are talking about the introduction of foreign genetic material, almost always coding for a protein – which are molecular workhorses capable of doing everything from binding with other proteins to changing what DNA is activated or not (nuclear receptors), to themselves performing reactions and either creating or breaking down molecules-, which is introduced into the genome through a double-strand break and insertion (what I call “splice-in”), or through homologous DNA recombination (meaning it trades bases, or DNA, with a target strand inside the cell). 

This means that using existing techniques we are often inserting a new piece of code, complete with its own regulatory mechanisms (transcription factors), into the cell and inducing a targeted double-strand break and insertion with endonucleases, something like TAL-effectors, and hoping this doesn’t accidentally alter any important regulatory or coding elements. 

Newer methods allow homologous DNA exchange, but switching out bases (which we can perceive as letters, which together make words – amino acids- which then form sentences – proteins-) from existing code depends on us actually understanding all the roles existing code is playing: which we often do not. So in both cases we risk tampering with existing code and risk current genetic information being lost. But, this risk can be minimized by selecting for redundant code, meaning little risk of disabling something entirely. 

But, current usage has not been sufficiently responsible and in fact viral DNA containing an extra Cmv promoter and gene sequence (Gene VI) has recently been found in almost all GM crops. This seems to be able to activate transcription or expression of any cellular mRNA (Ryabova et al, 2002), meaning it can lead to the production of the wrong proteins. Gene VI also codes for a protein which does, among other things, suppress RNA silencing processes: it weakens the body’s reaction against viruses (Haas et al. 2008). Gene VI even makes plants less capable of defending against bacteria (Love et al. 2012). Unfortunately, this sequence was found in all of Monsanto’s transgene crops, and this, many years after they had already been approved in the US (Podevin & du Jardin, 2012). 

Now that we know what we are talking about, we can ask ourselves: is this safe? Well, is anything in science inherently safe or dangerous? It really all depends on what you are doing, how you are going about it, and what, if any, precautions you take. 

I don’t think we can regard all genetic modification as being equal. Huge successes in the realm of unicellular genetic modification have been seen, for instance using modified yeast to produce insulin or other molecules which would otherwise require complex industrial processes to create (for instance in the realm of fuel alternatives). This use of genetic modification, isolated from the natural world, seems to only bring benefits. 

Unfortunately, a lot of the efforts towards modifying multicellular organisms like plants have relied on genetic resistance to endocrine disruptors -disrupt metabolism and internal processes- or toxins. This means that their use and usefulness dependson the simultaneous use of a chemical which will do ecological damage. These chemicals remove competition for the plants by killing anything lacking resistance-genes (for instance Glyphosate aka Roundup), they do this by destroying their metabolism. These chemicals are often, if not always, non-selective and thus will wreak havoc on the metabolism of anything unlucky enough to come into contact with these chemicals. 

This toxicity also includes mammals, with 2 year rat studies showing a significantly higher death rate of 2-3x more than normal, liver congestions and necrosis were 2.5 – 5.5 times higher, tumor risk in males 4x higher, and more kidney deficiencies than normal. (Seralini et al, 2012). 

The arguments used against this fact is that destruents (which are the most important part of the ecological cycle since they turn dead organic matter – with carbon- into inorganic – without carbon- material for plants to use) like bacteria, Earthworms and other parts of the soil ecology will adapt relatively quickly to this, that the effects are likely limited, and that the doses we consume of them in our produce are relatively small. 

But, none of those arguments are fully valid: only some destruents will adapt but many will invariably disappear from the soil at least temporarily (years), since none of these chemicals degrade quickly. This makes the soil less fertile for future generations. 

If that was not enough to convince us to avoid GM pest control, Bt toxin plants are often mentioned – plants which produce their own insecticide- along with the statement that they have led to reduced pesticide use. Now, to be truthful, the absolute worldwide use of insecticides has sunk since the introduction of Bt organisms. But, the overall use of pesticides and herbicides has continued to rise, especially as resistance develops in the “target” populations and making Bt less effective. 

This has likely contributed to the continued death of the bees: Colony Collapse Disorder, which currently wipes out approx 30-40% of colonies every year (15% is acceptable at the end of winter). Of course, the disorder may also be related to the use of monocultures, which is intensified by the use of total herbicides like Roundup. In the end, it is likely a mix of both the chemicals and the monocultures. 

Now, the thing is that these Bt toxins are actually not even harmless to mammals (Portilho et al., 2013) and we need to ask ourselves about the ecological sense in creating something which cannot be eaten by the other organisms in the ecosystem. 

Now, before we say that genetic engineering is inherently bad, there are in fact more responsible ways to use this technology even in the realm of multicellular organisms. A really good example is the “golden rice” which is rice with an added enzyme to produce beta-carotine (basically Vitamin A, which we cannot synthesize ourselves). The research was done relatively transparently, seed created and distributed at cost or for free. The rice is even shown to contain more vitamin A than spinach (Tang, 2012). 

Meanwhile the World Health Organization advises the continuation of supplement programs instead of giving the people a way to produce the vitamins they need in their own soil. The anti-GM movement has also so far been largely inclined to oppose all genetic modification and lump golden rice in with roundup-ready corn. 

Unfortunately, while Monsanto has the economic power to push their products through, even block labeling in certain nations (e.g the US, where despite public support for labeling, the senate blocked an amendment 71-to-27 which would have allowedstates to label GMOs if they wanted to, on Thursday May 23rd, 2013) general suspicion of genetic engineering has led to the use of this rice also being opposed, despite the fact that no new chemicals would be needed in its use, and that the new gene actually has a beneficial ecological role. 

We are being misled. The world is not black and white, and we cannot lump an entire branch of science together with those abusing it. Luckily, the world may be open to waking up to this fact. Recent global protests have seen millions marching against Monsanto, not against genetic modification. 

As always the issues are goals, methods, responsibility, and transparency. Companies like DuPont and Monsanto are not here to help the world’s farmers, they are not there to help feed us. The people making the decisions, as always in an LLC(Limited Liability Company), are not even responsible for any consequences they cause through the company’s actions. They even have personal interest in reducing transparency so they can hinder people from finding out about problems or mistakes for long enough that they can become filthy rich. 

They were producing poisons (including Agent Orange) since before they were working to supposedly feed the world. They work very hard to try to discredit all the studies I have linked in this article, but I encourage you to read the studies yourself. If anything, the fact the data is open for us all to see, and their methods of analysis, gives me more faith in them than in Monsanto, who has famously misrepresented and even falsified data in the past (e.g PCBs, Roundup) and has monetary interest in ignoring the warnings. 

Both a recent New York Times article and a Forbes rebuttal concentrated on the economic values of Monsanto’s crops, cherry-picking economic data. What is strange is how this discussion has been so railroaded into the realm of statistics instead of real world ecological and health consequences. 

So, are GMOs bad? In my opinion, there are some wonderful applications for this technology that have little or limited risk for negative consequences. Meanwhile, the way the technology is being used at the moment, in tandem with dangerous chemicals, is obviously not acceptable. It may be a good idea to not only forbid the patenting of genes, as some companies are trying to do in regard to the human genome, but to make genetic engineering efforts: data, methods, and analysis, publically available. Only then can we help insure that decisions are not being made independent of the data, to help prevent decisions being made only in light of the profit margin. 

Sources

  1. Seralini et al, 2012. sciencedirect.com
  2. Portilho et al., 2013. gmoevidence.com [PDF]
  3. TAL Effector-Nucleotide Targeter (TALE-NT) 2.0: tools for TAL effector design and target prediction – TAL-effectors (“splice-in”)
  4. Genetic engineering using homologous recombination – recombination (replacing bases)
  5. Regulators Discover a Hidden Viral Gene in Commercial GMO Crops – viral genes in GMOs
  6. β-Carotene in Golden Rice is as good as β-carotene in oil at providing vitamin A to children – Golden rice
  7. Tang, 2012. β-Carotene in Golden Rice is as good as β-carotene in oil at providing vitamin A to children Golden rice.
  8. GMO labelling blocked in senate

About the author 

Michael Thomas: I come from Boston, Massachusetts, but currently live in Germany, where I study biology. I am politically active and am working on creating my own political movement based on the idea of the government and politicians being almost totally transparent, and localized/decentralized decision making.

 

Breeding the nutrition out of our food


Jo Robinson
New York Times
Sat, 25 May 2013 15:34 CDT

We like the idea that food can be the answer to our ills, that if we eat nutritious foods we won’t need medicine or supplements. We have valued this notion for a long, long time. The Greek physician Hippocrates proclaimed nearly 2,500 years ago: “Let food be thy medicine and medicine be thy food.” Today, medical experts concur. If we heap our plates with fresh fruits and vegetables, they tell us, we will come closer to optimum health. 

This health directive needs to be revised. If we want to get maximum health benefits from fruits and vegetables, we must choose the right varieties. Studies published within the past 15 years show that much of our produce is relatively low in phytonutrients, which are the compounds with the potential to reduce the risk of four of our modern scourges:cancer, cardiovascular disease, diabetes and dementia. The loss of these beneficial nutrients did not begin 50 or 100 years ago, as many assume. Unwittingly, we have been stripping phytonutrients from our diet since we stopped foraging for wild plants some 10,000 years ago and became farmers. 

These insights have been made possible by new technology that has allowed researchers to compare the phytonutrient content of wild plants with the produce in our supermarkets. The results are startling. 

Wild dandelions, once a springtime treat for Native Americans, have seven times more phytonutrients than spinach, which we consider a “superfood.” A purple potato native to Peru has 28 times more cancer-fighting anthocyanins than common russet potatoes. One species of apple has a staggering 100 times more phytonutrients than the Golden Delicious displayed in our supermarkets. 

Were the people who foraged for these wild foods healthier than we are today? They did not live nearly as long as we do, but growing evidence suggests that they were much less likely to die from degenerative diseases, even the minority who lived 70 years and more. The primary cause of death for most adults, according to anthropologists, was injury and infections. 

Each fruit and vegetable in our stores has a unique history of nutrient loss, I’ve discovered, but there are two common themes. Throughout the ages, our farming ancestors have chosen the least bitter plants to grow in their gardens. It is now known that many of the most beneficial phytonutrients have a bitter, sour or astringent taste. Second, early farmers favored plants that were relatively low in fiber and high in sugar, starch and oil. These energy-dense plants were pleasurable to eat and provided the calories needed to fuel a strenuous lifestyle. The more palatable our fruits and vegetables became, however, the less advantageous they were for our health. 

The sweet corn that we serve at summer dinners illustrates both of these trends. The wild ancestor of our present-day corn is a grassy plant called teosinte. It is hard to see the family resemblance. Teosinte is a bushy plant with short spikes of grain instead of ears, and each spike has only 5 to 12 kernels. The kernels are encased in shells so dense you’d need a hammer to crack them open. Once you extract the kernels, you wonder why you bothered. The dry tidbit of food is a lot of starch and little sugar. Teosinte has 10 times more protein than the corn we eat today, but it was not soft or sweet enough to tempt our ancestors. 

Over several thousand years, teosinte underwent several spontaneous mutations. Nature’s rewriting of the genome freed the kernels of their cases and turned a spike of grain into a cob with kernels of many colors. Our ancestors decided that this transformed corn was tasty enough to plant in their gardens. By the 1400s, corn was central to the diet of people living throughout Mexico and the Americas. 

When European colonists first arrived in North America, they came upon what they called “Indian corn.” John Winthrop Jr., governor of the colony of Connecticut in the mid-1600s, observed that American Indians grew “corne with great variety of colours,” citing “red, yellow, blew, olive colour, and greenish, and some very black and some of intermediate degrees.” A few centuries later, we would learn that black, red and blue corn is rich in anthocyanins. Anthocyanins have the potential to fight cancer, calm inflammation, lower cholesterol and blood pressure, protect the aging brain, and reduce the risk of obesity, diabetes and cardiovascular disease. 

European settlers were content with this colorful corn until the summer of 1779 when they found something more delectable – a yellow variety with sweeter and more tender kernels. This unusual variety came to light that year after George Washington ordered a scorched-earth campaign against Iroquois tribes. While the militia was destroying the food caches of the Iroquois and burning their crops, soldiers came across a field of extra-sweet yellow corn. According to one account, a lieutenant named Richard Bagnal took home some seeds to share with others. Our old-fashioned sweet corn is a direct descendant of these spoils of war. 

Up until this time, nature had been the primary change agent in remaking corn. Farmers began to play a more active role in the 19th century. In 1836, Noyes Darling, a onetime mayor of New Haven, and a gentleman farmer, was the first to use scientific methods to breed a new variety of corn. His goal was to create a sweet, all-white variety that was “fit for boiling” by mid-July. 

He succeeded, noting with pride that he had rid sweet corn of “the disadvantage of being yellow.” 

The disadvantage of being yellow, we now know, had been an advantage to human health. Corn with deep yellow kernels, including the yellow corn available in our grocery stores, has nearly 60 times more beta-carotene than white corn, valuable because it turns to Vitamin A in the body, which helps vision and the immune system. 

Supersweet corn, which now outsells all other kinds of corn, was derived from spontaneous mutations that were selected for their high sugar content. In 1959, a geneticist named John Laughnan was studying a handful of mutant kernels and popped a few into his mouth. He was startled by their intense sweetness. Lab tests showed that they were up to 10 times sweeter than ordinary sweet corn. 

Mr. Laughnan was not a plant breeder, but he realized at once that this mutant corn would revolutionize the sweet corn industry. He became an entrepreneur overnight and spent years developing commercial varieties of supersweet corn. His first hybrids began to be sold in 1961. 

Within one generation, the new extra sugary varieties eclipsed old-fashioned sweet corn in the marketplace. Build a sweeter fruit or vegetable – by any means – and we will come. Today, most of the fresh corn in our supermarkets is extra-sweet. The kernels are either white, pale yellow, or a combination of the two. The sweetest varieties approach 40 percent sugar, bringing new meaning to the words “candy corn.” Only a handful of farmers in the United States specialize in multicolored Indian corn, and it is generally sold for seasonal decorations, not food. 

We’ve reduced the nutrients and increased the sugar and starch content of hundreds of other fruits and vegetables. How can we begin to recoup the losses? 

Here are some suggestions to get you started. Select corn with deep yellow kernels. To recapture the lost anthocyanins and beta-carotene, cook with blue, red or purple cornmeal, which is available in some supermarkets and on the Internet. Make a stack of blue cornmeal pancakes for Sunday breakfast and top with maple syrup. 

In the lettuce section, look for arugula. Arugula, also called salad rocket, is very similar to its wild ancestor. Some varieties were domesticated as recently as the 1970s, thousands of years after most fruits and vegetables had come under our sway. The greens are rich in cancer-fighting compounds called glucosinolates and higher in antioxidant activity than many green lettuces. 

Scallions, or green onions, are jewels of nutrition hiding in plain sight. They resemble wild onions and are just as good for you. Remarkably, they have more than five times more phytonutrients than many common onions do. The green portions of scallions are more nutritious than the white bulbs, so use the entire plant. Herbs are wild plants incognito. We’ve long valued them for their intense flavors and aroma, which is why they’ve not been given a flavor makeover. Because we’ve left them well enough alone, their phytonutrient content has remained intact. 

Experiment with using large quantities of mild-tasting fresh herbs. Add one cup of mixed chopped Italian parsley and basil to a pound of ground grass-fed beef or poultry to make “herb-burgers.” Herbs bring back missing phytonutrients and a touch of wild flavor as well. 

The United States Department of Agriculture exerts far more effort developing disease-resistant fruits and vegetables than creating new varieties to enhance the disease resistance of consumers. In fact, I’ve interviewed U.S.D.A. plant breeders who have spent a decade or more developing a new variety of pear or carrot without once measuring its nutritional content. 

We can’t increase the health benefits of our produce if we don’t know which nutrients it contains. Ultimately, we need more than an admonition to eat a greater quantity of fruits and vegetables: we need more fruits and vegetables that have the nutrients we require for optimum health. 

About the author 

Jo Robinson is the author of the forthcoming book Eating on the Wild Side: The Missing Link to Optimum Health.

Diabetes Blood-Glucose Level Lowered 6% With Two Teaspoons of Household Item

Controlling glucose levels for people who have type 2 diabetes or have a hard time with their waking glucose counts might be as easy to fix as a 30-second organic solution at bedtime.

And, in contrast to expensive pharmaceuticals your doctor might prescribe, this solution is found in the aisles of practically every grocery store in the world- and is inexpensive.

For many years, the benefits of adding apple cider vinegar to mealtimes for diabetics has been shown in countless studies, but a different timing of ingestion was recently studied by Researchers at Arizona State University.

Instead of looking at the effects of vinegar on glucose levels after it had been included at mealtime, they wanted to see if there would be an effect when 2 tablespoons were taken at bedtime.

Measuring glucose levels of participants who were not taking insulin therapy at the time of the study, the scientists were able to show that taking apple cider vinegar at bedtime had a noticeable effect on waking blood glucose levels.

In fact, the participants in the study showed an average improvement of more than 6% in waking levels after just 2 days.

Participants took the vinegar with an ounce of cheese at bedtime, but changed nothing else about their diets. The control group that ate the cheese and only had water, not vinegar, showed no improvement.

Good way to consume apple cider vinegar is to add 2 tablespoons in half a glass (full glass if you dislike the taste) of water. Many health experts also claim that apple cider vinegar with ‘mother’ (not filtered as much) is better.