Low carb high fat diet sample menu card,lose weight diet running,weight loss meal plan australia,60 lb weight loss success stories - PDF 2016

11.01.2016
Before you binge out on pasta dinners and bagel breakfasts, you might want to take a serious look at what researchers are reporting about “carbo-loading” before a marathon or long endurance event. When muscles can access fat as fuel during a race, glycogen stores are spared and saved for use later down the road – this means “hitting the wall” or “bonking” can be delayed and perhaps even avoided completely.
A new pre-race nutrition paradigm that combines the two ‘loading’ approaches is being recommended by experts in the sports performance field.  Here’s the plan in a nutshell. After 10 days of eating low-carb, high-fat foods, switch to a traditional “carbo-load” diet that incorporates 70 percent of calories from carbohydrates for the next three days. This ensures that your glycogen levels are as high as they can be and are raring to go on race day. A study conducted by the University of Cape Town in South Africa implemented this 10-day ‘fat-load’ followed by 3-day ‘carbo-load’ plan on a group of experienced cyclists. 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.
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.
When the Atkins diet gained media popularity several years ago, many critics complained that there were no long-term studies done on the diet.
The research that is starting to be published on the effectiveness of the Ketogenic Diet in curing disease is nothing less than amazing. 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. 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.
Over the past decade, investigators have identified numerous mechanisms through which the KD may provide neuroprotective activity. Two hallmark features of KD treatment are the rise in ketone body production by the liver and a reduction in blood glucose levels.
In the end, there are likely many other mechanisms that could contribute to the neuroprotective properties of the KD. Aging involves the gradual decrease in function, and at times outright degeneration, of neurons and neural circuits.
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. 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.
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.
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. 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. 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. Unfortunately, the incidence of brain injury is increasing in both civilian and military contexts. Several recent animal studies support this idea, and investigators have principally focused on ketone bodies (Prins, 2008a). With respect to anti-epileptogenesis following head injury, the data regarding KD effects are mixed. 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. Autism is a neurodevelopmental disorder that affects language development and social function.
Migraine is a paroxysmal neurological disorder having considerable clinical phenotypic overlap with epilepsy (Rogawski, 2008). 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). 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. 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. The days of high-carb diets may be over – well, make that modified — for athletes who want to perform their best on race day, or so says the March 2013 issue of Competitor magazine. About two weeks out from an endurance event, aim to get about 65 percent of calories from fats and continue this high-fat intake for 10 days. After a moderate two-hour warm-up, the athletes were able to complete a 20k time trial 4.5 percent faster following the new diet protocol. Today, the diet is being studied in the medical community with applications to all kinds of diseases.
However, there are plenty of studies on the Ketogenic Diet and there has never been any negative effects recorded from long-term use. 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.
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).
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. 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. After its introduction in 1920, the KD was used as a first or second-line treatment for severe childhood epilepsy. 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).
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). A randomized double-blind, placebo-controlled trial of a MCT KD resulted in significantly improved cognitive functioning in APO?4-negative patients with AD but not in patients with a APO?4 mutation (Henderson et al., 2009). 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. 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.
As a consequence, voluntary motor activity gradually deteriorates, leaving the affected individual profoundly weak despite largely retained cognitive functioning. 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. Most of these models entail pre-treatment with the KD (or with BHB), resulting in decreased structural and functional damage from the stroke. 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 ?-oxidation within the mitochondrial matrix.
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).


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. 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.
Nine of 28 patients reported "some improvement," although the validity of this clinical study is uncertain and some patients admitted poor compliance.
New research is suggesting that a low-carb diet may actually have benefits because it trains an athlete’s muscles to be better fat burners. Training day after day on a low-carb diet can leave a runner feeling sluggish and slow because glycogen stores never get topped off. This “hall pass” to eat fats doesn’t mean you can pig out on pizza and ding-dongs all day, or really any day. Instead, top off your tank with high-quality, healthy carbs including whole-grain pastas, breads, and rice along with plenty of fruits and veggies (but, of course, cut the fiber intake 24 hours before event). Today's latest fad diet, the "paelo diet" is another example of a diet based on the ketogenic principles.
Of course, most of the medical interest in the diet is to try and develop a line of "ketone" drugs to mimic the diet. 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. This intriguing clinical observation forms the basis of the hypothesis that the KD may possess anti-epileptogenic properties. 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. 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. 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). 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). This view is bolstered by the higher incidence of seizures in patients with AD as compared to the unaffected population (Palop and Mucke, 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). Transgenic AD mice fed 2DG demonstrated better mitochondrial function, less oxidative stress, and reduced expression of amyloid precursor protein and ?-amyloid compared to control animals (Yao et al., 2011).
One proposed mechanism is increased ROS and free radical formation, which, as discussed above, hampers mitochondrial function.
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.
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). Despite this well documented cellular observation, the KD has only recently been considered as a clinical treatment in the oncology field. 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?
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.
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).
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. 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. Compliance might be better with the less restrictive modified Atkins diet, which has also shown promise for migraine treatment (Kossoff et al., 2010). How can a simple dietary change lead to improvement in disorders with such a huge span of pathophysiological mechanisms? Ketogenic diets: an historical antiepieptic therapy with promising potentialities for the aging brain.
A ketogenic diet increases succinic dehydrogenase (SDH) activity and recovers age-related decrease in numeric density of SDH-positive mitochondria in cerebellar Purkinje cells of late-adult rats.
Ketogenic diets cause opposing changes in synaptic morphology in CA1 hippocampus and dentate gyrus of late-adult rats. Benefits of caloric restriction on brain aging and related pathological states: understanding mechanisms to devise novel therapies. Peroxisome proliferator-activated receptor alpha and the ketogenic diet.Epilepsia 49(Suppl. Peroxisome proliferator activated receptor ? ligands as anti-cancer drugs targeting mitochondrial metabolism.
Plus, there hasn’t been any irrefutable, one hundred percent conclusive proof that removing carbs from the diet improves endurance performance. Quality fats from healthy oils, nuts, meats, avocados, whole milk, cheese, eggs, and fatty fish are what should be on the table. Ketones, which our body can produce during fasting or "starvation," is an alternative energy source for those who are insulin resistant. Yet, it is conceivable that alterations in certain dietary constituents could affect the course and impact the outcome of these brain disorders. 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. 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). 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. 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 ?-amyloid on neurons in culture (Kashiwaya et al., 2000).
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). 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). 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. Later, they showed that cognitive and motor functioning was also improved with KD treatment (Appelberg et al., 2009).
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). 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). In fact, one study at the University of Birmingham in England found that low-carb runners (41% carbs) reported more fatigue and showed reductions in performance than their high-carb counterparts (65% carbs) during intensive training runs.


During this phase, your body will learn how to tap into fat stores for fuel; and, your training won’t suffer much because you’ll be tapering down anyway.
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. 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. Further, it is possible that a final common neurometabolic pathway might be influenced by a variety of dietary interventions. 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 KD has now become an integral part of the armamentarium of most major epilepsy centers throughout the world (Kossoff and McGrogan, 2005). 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). Alternatively, the KD may actually decrease amounts of ?-amyloid deposition (VanderAuwera et al., 2005).
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).
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). It is also interesting to note that PPAR?-activated by nutrients such as fatty acids - is now a target for developing anti-cancer drugs that target mitochondrial metabolism (Grabacka et al., 2010). 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.
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). 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.
Thus, the potential for interesting and novel applications of the KD and related dietary therapies is almost limitless (Stafstrom, 2004). These observations imply certain risks, but also potential benefits of the KD for the aging brain. 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.
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). Other researchers have hypothesized that the neuroprotective properties of ketone bodies might be related to up-regulation of hypoxia inducible factor (HIF1-?) which is important in angiogenesis and anti-apoptotic activity (Puchowicz et al., 2008). These authors observed that half of these patients became seizure-free on the KD, and only four patients failed to respond. Thus, at this juncture, there is no consensus regarding whether the KD is anti-epileptogenic following a variety of traumatic insults and manipulations.
Therefore, these findings need to be interpreted cautiously and larger longitudinal studies are needed. 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).
Ultimately, the details of how that altered metabolism reduces neuronal excitability, abrogates ongoing neurodegeneration, or mitigates functional disability remain unknown.
The effects of a ketogenic diet on behavioral outcome after controlled cortical impact injury in the juvenile and adult rat. Ketogenic diet prevents alterations in brain metabolism in young but not adult rats after traumatic brain injury. 2-Deoxy-D-glucose reduces epilepsy progression by NRSF-CtBP-dependent metabolic regulation of chromatin structure. Caloric restriction inhibits seizure susceptibility in epileptic EL mice by reducing blood glucose. 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.
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). Mitochondria from these mutant mice demonstrated increased ATP synthesis, countering the inhibition of complex I of the electron transport chain.
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). 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-? and Bcl-2, an anti-apoptotic protein.
Hence, these preliminary data suggest that the KD is not necessarily contraindicated in patients with mitochondrial respiratory chain abnormalities. 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). 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). Herein lay rich opportunities for further investigation, in both the laboratory and the clinic, in the broad realm of translational neurosciences.
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. 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). 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. 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). To be clinically meaningful, of course, a positive effect must be demonstrable after, and not before, an ischemic event.
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.
Here we provide an overview of studies using the KD in a wide panoply of neurologic disorders in which neuroprotection is an essential component. 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). Nevertheless, such studies imply that biochemical alterations that favor energy metabolism would be protective against acute forms of severe brain injury. Thus, it is critical to determine the specific mitochondrial defect when considering treatment with the KD, to avert clinical deterioration.




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