here are some abstracts from my collection, I think they may be relevant to the discussion here.
Ok, these authors state that ketosis is bodyís response to starvation. Should we widen up our definition of Ďstarvation dietsí, to include high calorie low carb intake diets, not only low calorie intake, into that category? This article is excellent in its overview of the goodness of ketosis.
Ketone bodies, potential therapeutic uses.
Veech RL, Chance B, Kashiwaya Y, Lardy HA, Cahill GF Jr.
Unit on Metabolic Control, LMMB/NIAAA, Rockville, Maryland, USA.
Ketosis, meaning elevation of D-beta-hydroxybutyrate (R-3hydroxybutyrate) and acetoacetate, has been central to starving man's survival by providing nonglucose substrate to his evolutionarily hypertrophied brain, sparing muscle from destruction for glucose synthesis. Surprisingly, D-beta-hydroxybutyrate (abbreviated "betaOHB") may also provide a more efficient source of energy for brain per unit oxygen, supported by the same phenomenon noted in the isolated working perfused rat heart and in sperm. It has also been shown to decrease cell death in two human neuronal cultures, one a model of Alzheimer's and the other of Parkinson's disease. These observations raise the possibility that a number of neurologic disorders, genetic and acquired, might benefit by ketosis. Other beneficial effects from betaOHB include an increased energy of ATP hydrolysis (deltaG') and its linked ionic gradients. This may be significant in drug-resistant epilepsy and in injury and anoxic states. The ability of betaOHB to oxidize co-enzyme Q and reduce NADP+ may also be important in decreasing free radical damage. Clinical maneuvers for increasing blood levels of betaOHB to 2-5 mmol may require synthetic esters or polymers of betaOHB taken orally, probably 100 to 150 g or more daily. This necessitates advances in food-science technology to provide at least enough orally acceptable synthetic material for animal and possibly subsequent clinical testing. The other major need is to bring the technology for the analysis of multiple metabolic "phenotypes" up to the level of sophistication of the instrumentation used, for example, in gene science or in structural biology. This technical strategy will be critical to the characterization of polygenic disorders by enhancing the knowledge gained from gene analysis and from the subsequent steps and modifications of the protein products themselves.
This article overviews bruising side effect of the ketogenic diets. I experienced it myself.
Bruising and the ketogenic diet: evidence for diet-induced changes in platelet function.
Berry-Kravis E, Booth G, Taylor A, Valentino LA.
Department of Pediatrics, RUSH-Presbyterian-St Luke's Medical Center, Chicago, IL 60612, USA. eberrykr~rush.edu
Excessive bruising is a symptom noted by parents of some children treated with the ketogenic diet for epilepsy control, although this side effect is not reported in the literature. We evaluated our cohort of current and past diet-treated patients for symptoms of bruising or bleeding through chart review and prospective screening at clinic follow-up visits. A significant increase in bruising or other minor bleeding was reported and/or observed in 16 of 51 patients (31.4%). There were no differences in sex distribution or number of anticonvulsants used between patients with bruising/bleeding and those without this symptom, although the group with bruising/bleeding was significantly younger. No specific anticonvulsant was associated with bruising/bleeding. Six patients with diet-induced bruising/bleeding underwent an investigation for bleeding diathesis. Five of these patients had prolonged bleeding times and all had diminished responsiveness to various platelet aggregating agents, with no evidence of a release defect. The abnormalities all normalized in the 1 patient tested after ceasing the diet. No patients had serious hemorrhage. One patient had mild von Willebrand disease, which had been asymptomatic before diet initiation. Some patients were Stimate responsive, suggesting a treatment for more severe bouts of symptoms. These data suggest that a ketogenic diet-related bleeding tendency occurs in about one third of treated patients owing to preexisting factors defining susceptibility in combination with diet-induced depression of platelet responsiveness, possibly related to changes in platelet membrane lipid composition and/or concentration and resultant effects on function of membrane-embedded proteins. Patients on the diet undergoing anticoagulation or surgery should be evaluated carefully for symptoms of bleeding tendency.
I post this abstract here only because I mentioned this article in another post of mine on this board, didnít want to leave that info unreferenced.
Acute pancreatitis causing death in a child on the ketogenic diet.
Stewart WA, Gordon K, Camfield P.
Department of Pediatrics, Dalhousie University, IWK Health Centre, Halifax, Nova Scotia. wastewar~is.dal.ca
The ketogenic diet has demonstrated good efficacy in children with pharmacologically resistant seizures. Relatively few serious complications have been reported in the more than 70 years in which the diet has been used. We report a child who developed acute pancreatitis and died. A 9-year-old girl had a seizure disorder with associated developmental delay owing to glucose transport protein deficiency. The ketogenic diet with medium chain triglyceride oil had been initiated shortly after diagnosis in infancy. She was not on anticonvulsants. She presented in coma with decreased respiratory effort and shock, requiring resuscitation. Investigations were consistent with pancreatitis. Despite fluid resuscitation and inotropic support, she had prolonged hypotension and acidosis. She subsequently had a cardiac arrest and died. A postmortem examination confirmed hemorrhagic pancreatitis. Hypertriglyceridemia is a risk factor for developing acute pancreatitis. The high fat content of the ketogenic diet often causes hyperlipidemia. The outcome for this patient raises concern regarding a potential consequence of the ketogenic diet.
Authors of this article do not seem to think that higher carbohydrates diets are bad as long as carbs come from the low glycemic sources, they believe that the caloric excess is to blame. They also engage in evolutionary speculations, gosh, everyone is suddenly interested in using evolutionary statements to support their arguments!
The 'carnivore connection'-evolutionary aspects of insulin resistance.
Colagiuri S, Miller JB.
Department of Endocrinology, Diabetes and Metabolism, Prince of Wales Hospital, Sydney, Australia.
Insulin resistance is common and is determined by physiological (aging, physical fitness), pathological (obesity) and genetic factors. The metabolic compensatory response to insulin resistance is hyperinsulinaemia, the primary purpose of which is to maintain normal glucose tolerance. The 'carnivore connection' postulates a critical role for the quantity of dietary protein and carbohydrate and the change in the glycaemic index of dietary carbohydrate in the evolution of insulin resistance and hyperinsulinaemia. Insulin resistance offered survival and reproductive advantages during the Ice Ages which dominated human evolution, during which a high-protein low-carbohydrate diet was consumed. Following the end of the last Ice Age and the advent of agriculture, dietary carbohydrate increased. Although this resulted in a sharp increase in the quantity of carbohydrate consumed, these traditional carbohydrate foods had a low glycaemic index and produced only modest increases in plasma insulin. The industrial revolution changed the quality of dietary carbohydrate. The milling of cereals made starch more digestible and postprandial glycaemic and insulin responses increased 2-3 fold compared with coarsely ground flour or whole grains. This combination of insulin resistance and hyperinsulinaemia is a common feature of many modern day diseases. Over the last 50 y the explosion of convenience and takeaway 'fast foods' has exposed most populations to caloric intakes far in excess of daily energy requirements and the resulting obesity has been a major factor in increasing the prevalence of insulin resistance.
Well, athletes, you are safe with your higher protein consumption, according to this study.
Do regular high protein diets have potential health risks on kidney function in athletes?
Poortmans JR, Dellalieux O.
Department of Physiological Chemistry, Institute of Physical Education and Kinesiotherapy, Free University of Brussels, Belgium.
Excess protein and amino acid intake have been recognized as hazardous potential implications for kidney function, leading to progressive impairment of this organ. It has been suggested in the literature, without clear evidence, that high protein intake by athletes has no harmful consequences on renal function. This study investigated body-builders (BB) and other well-trained athletes (OA) with high and medium protein intake, respectively, in order to shed light on this issue. The athletes underwent a 7-day nutrition record analysis as well as blood sample and urine collection to determine the potential renal consequences of a high protein intake. The data revealed that despite higher plasma concentration of uric acid and calcium, Group BB had renal clearances of creatinine, urea, and albumin that were within the normal range. The nitrogen balance for both groups became positive when daily protein intake exceeded 1.26 g.kg but there were no correlations between protein intake and creatinine clearance, albumin excretion rate, and calcium excretion rate. To conclude, it appears that protein intake under 2. 8 g.kg does not impair renal function in well-trained athletes as indicated by the measures of renal function used in this study
This article supports high protein intake as long as alkali buffers are included in oneís diet.
Excess dietary protein can adversely affect bone.
Barzel US, Massey LK.
Division of Endocrinology and Metabolism, Department of Medicine, Montefiore Medical Center and The Albert Einstein College of Medicine, Bronx, NY 10467, USA.
The average American diet, which is high in protein and low in fruits and vegetables, generates a large amount of acid, mainly as sulfates and phosphates. The kidneys respond to this dietary acid challenge with net acid excretion, as well as ammonium and titratable acid excretion. Concurrently, the skeleton supplies buffer by active resorption of bone. Indeed, calciuria is directly related to net acid excretion. Different food proteins differ greatly in their potential acid load, and therefore in their acidogenic effect. A diet high in acid-ash proteins causes excessive calcium loss because of its acidogenic content. The addition of exogenous buffers, as chemical salts or as fruits and vegetables, to a high protein diet results in a less acid urine, a reduction in net acid excretion, reduced ammonium and titratable acid excretion, and decreased calciuria. Bone resorption may be halted, and bone accretion may actually occur. Alkali buffers, whether chemical salts or dietary fruits and vegetables high in potassium, reverse acid-induced obligatory urinary calcium loss. We conclude that excessive dietary protein from foods with high potential renal acid load adversely affects bone, unless buffered by the consumption of alkali-rich foods or supplements.
This article may explain why those who are on a ketogenic diet have trouble maintaining the state of ketosis, itís the butter, folks! Up your omega-3ís intake!
Dietary fat, ketosis, and seizure resistance in rats on the ketogenic diet.
Likhodii SS, Musa K, Mendonca A, Dell C, Burnham WM, Cunnane SC.
Departments of Nutritional Sciences and Pharmacology and Bloorview Epilepsy Research Program, Faculty of Medicine, University of Toronto, Toronto, Canada. sergei.likhodi~utoronto.ca
PURPOSE: Fat is the major component of the ketogenic diet (KD), yet no studies have examined whether the type of fat used in the diet can be optimized to provide additional benefits. The purpose of the present experiments was to compare the efficiency of different fats in inducing ketosis and affording seizure resistance. METHODS: The effects of KDs that incorporate lard, butter, medium-chain triglycerides (MCT), or flaxseed oil or a mixture of the latter three fats were examined in rats fed KD for up to 98 days. The maximal electroshock (MES) or pentylenetetrazole (PTZ) threshold tests were used to assess seizure susceptibility in two separate experiments. RESULTS: The rank order of induced ketosis was MCT > mixture > or = flaxseed oil > or = lard = butter > or = control. MES failed to reveal anticonvulsant effects, but the PTZ test indicated that up to 50% of rats fed the KD were seizure protected (p < 0.05). The measures of seizure protection, seizure incidence and score, did not correlate, however, with the level of ketosis in the range of 0. 7-5.2 mmol/L for beta-hydroxybutyrate. In the long-term study, flaxseed oil KD maintained stable ketosis throughout 98 days, whereas ketones declined with lard and butter KD to the control level. CONCLUSIONS: Seizure protection with the versions of the KD did not improve with the higher level of ketosis. The focus of the KD improvement, therefore, is not the achievement of higher ketosis per se but rather designing a diet that provides steady ketosis, exploits advantages of certain fats for neurological development or seizure protection via a nonketogenic mechanism, and is nutritionally balanced.