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Metabolic Acidosis In Liver Failure

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What is BASAL METABOLIC RATE? What does BASAL METABOLIC RATE mean? BASAL METABOLIC RATE meaning - BASAL METABOLIC RATE definition - BASAL METABOLIC RATE explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. Basal metabolic rate (BMR) is the minimal rate of energy expenditure per unit time by endothermic animals at rest. It is reported in energy units per unit time ranging from watt (joule/second) to ml O2/min or joule per hour per kg body mass J/(hkg)). Proper measurement requires a strict set of criteria be met. These criteria include being in a physically and psychologically undisturbed state, in a thermally neutral environment, while in the post-absorptive state (i.e., not actively digesting food). In bradymetabolic animals, such as fish and reptiles, the equivalent term standard metabolic rate (SMR) is used. It follows the same criteria as BMR, but requires the documentation of the temperature at which the metabolic rate was measured. This makes BMR a variant of standard metabolic rate measurement that excludes the temperature data, a practice that has led to problems in defining "standard" rates of metabolism for many mammals. Metabolism comprises the processes that the body needs to function. Basal metabolic rate is the amount of energy expressed in calories that a person needs to keep the body functioning at rest. Some of those processes are breathing, blood circulation, controlling body temperature, cell growth, brain and nerve function, and contraction of muscles. Basal metabolic rate (BMR) affects the rate that a person burns calories and ultimately whether that individual maintains, gains, or loses weight. The basal metabolic rate accounts for about 60 to 75% of the daily calorie expenditure by individuals. It is influenced by several factors. BMR typically declines by 12% per decade after age 20, mostly due to loss of fat-free mass, although the variability between individuals is high. The body's generation of heat is known as thermogenesis and it can be measured to determine the amount of energy expended. BMR generally decreases with age and with the decrease in lean body mass (as may happen with aging). Increasing muscle mass has the effect of increasing BMR. Aerobic (resistance) fitness level, a product of cardiovascular exercise, while previously thought to have effect on BMR, has been shown in the 1990s not to correlate with BMR when adjusted for fat-free body mass. But anaerobic exercise does increase resting energy consumption (see "aerobic vs. anaerobic exercise"). Illness, previously consumed food and beverages, environmental temperature, and stress levels can affect one's overall energy expenditure as well as one's BMR. BMR is measured under very restrictive circumstances when a person is awake. An accurate BMR measurement requires that the person's sympathetic nervous system not be stimulated, a condition which requires complete rest. A more common measurement, which uses less strict criteria, is resting metabolic rate (RMR).

Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>

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  1. coreycorndog

    I posted to r/askscience for the hell of it but really this answer is all I needed.

  2. tinkan

    I think it's a pretty straight-forward yes. There is no other energy source other than stored fat and metabolic processes are conserved amongst all animals. The bear must rely on metabolizing the fat stores and that will involve ketosis (the brain likes ketones, it doesn't/can't use FFA - this is why people say the brain prefers glucose but it's really a misnomer. There are no lipid stores in the brain and free fatty acids are not soluble enough in the blood nor are they going to be able to cross the blood brain barrier. This physical barrier means brain cells can not rely on FFA for energy. Thus, FFA are converted in a more blood soluble fat energy molecule, the ketone. In short, the brain does not "require" glucose to function. It just needs time to adapt to ketone usage.)
    Just be forewarned AskScience harbors some anti-keto sentiments that we know to be false (such as loving to bring up the ketoacidosis reason or kidney troubles). But they would probably give you a better answer than us.

  3. Sporkfortuna

    IIRC, Bear recycles his urine during the long winter months.
    "Stuck in a cave, better..."

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The Electron Transport Chain & complexes I-IV that pump protons out of the Mitochondria by the transfer of the electrons carried on NADH & FADH2 to maintain the concentration gradient of the protons "high in the intermembrane space & low in the matrix of the Mitochondria" this video is made by HarvardX on edX https://goo.gl/KDZmML http://bit.ly/2hqwmRB

Hypoketotic Hypoglycemia, Metabolic Acidosis, Toxic Liver Disease: Causes & Diagnoses | Symptoma.com

Causes of metabolic acidosis There are many causes. [patient.info] Diseases and drugs that impair mitochondrial function can cause lactic acidosis. [merckmanuals.com] metabolic , Metabolic acidosis NOS , Metabolic Acidoses , Acidosis, Metabolic , Acidoses, Metabolic , Metabolic Acidosis , acidosis metabolic , metabolic acidosis disorder [fpnotebook.com] Also, severe electrolye abnormalities (hyponatremia, hypophosphatemia, hypokalemia, hypomagnesemia, also metabolic acidosis). [errolozdalga.com] Progress in liver diseases . 3 : 28298. [en.wikipedia.org] Instead of being harmlessly metabolized and bound to glucuronates and sulfates, excessive acetaminophen compounds enter CYP protein-mediated metabolic reactions in the liver [lecturio.com] Long Chain Hydroxyacyl-CoA Dehydrogenase Deficiency Treatment : It is important to avoid fasting to prevent hypoketotic hypoglycemia. [emilytam.com] Clinical considerations: Poor feeding, vomiting, lethargy Hypoglycemia Metabolic acidosis Hepatomegaly Cardiac insufficiency History of sudden unexpected death in a sibling [archildrens.org] Symptoms associated with LCHAD deficiency are due to low levels of energy and the toxic build-up of fatty acid Continue reading >>

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  1. kamaboko

    Hello,
    I've been on a Keto diet now for nine weeks. I am not diabetic. I'd just like to burn off some stomach fat. That said, I am simply starving at 20g of carbs per day. I've been using keto sticks to measure my ketosis levels (and yes I am aware that these sticks may not be the most accurate testing measure, but I'm not going to get a blood analysis every week). If I go beyond 20g per day, according to the keto stick results, I get thrown out of ketosis. How on earth does one stay at or below 20g of carbs per day? I should also say, prior to this diet, I was rarely a meat eater. I don't like bacon (pork or chicken varieties). Chicken and fish was always my choice.
    Prior to every meal I drink an 8oz glass of water with apple cider vinegar. I read this helps with digestion. I also drink lemon water throughout the day.
    Vegetables such as spinach or broccoli take my stomach forever to breakdown. I'm constantly bloated.
    Honestly, this has been a living Hell. What am I doing wrong?
    Typical day...
    Breakfast: Three AA large eggs and three slices of bacon.
    Lunch: Three cups of spinach. A half pound of ground beef with taco seasoning mix. Two tbsp of sour cream.
    Dinner. Three cups of spinach. Five ounces of chicken. One avocado. One roma tomato.
    Snacks are usually mozzarella or cheddar cheese sticks.

    Thanks,
    K



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    Summarize This Topic

  2. Brook

    This is going to be counterintuitive, but try going zero carb. Decide on a period of time like 3 weeks or 30 days, and eat no plant material at all for that period, then reassess. Some people find zero carb much easier to do than trying to stay very low carb. Figure you are going to est 2-3 times your current amount of meat. Eat all you want whenever you are hungry, but strictly from the animal kingdom. As much as you want of meat, fish, eggs. You can also have small amounts of cream, and full fat cheese, but view them as sides to meat, fish, or eggs.

  3. Jeff

    Fat to satiety. If you're hungry, add more fat. It's a wonderful way to deal with hunger pangs. I eat salami with cream cheese until I feel full. More bacon, butter with your avocado, or fatty cheeses. Don't be afraid to add more fat! Wishing you well.

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Acid-base And Potassium Disorders In Liver Disease

Northwestern University, Feinberg school of Medicine, Chicago Acid-base and potassium disorders occur frequently in the setting of liver disease. As the liver's metabolic function worsens, particularly in the setting of renal dysfunction, hemodynamic compromise, and hepatic encephalopathy, acid-base disorders ensue. The most common acid-base disorder is respiratory alkalosis. Metabolic acidosis alone or in combination with respiratory alkalosis also is common. Acid-base disorders in patients with liver disease are complex. The urine anion gap may help to distinguish between chronic respiratory alkalosis and hyperchloremic metabolic acidosis when a blood gas is not available. A negative urine anion gap helps to rule out chronic respiratory alkalosis. In this disorder a positive urine anion gap is expected owing to suppressed urinary acidification. Distal renal tubular acidosis occurs in autoimmune liver disease such as primary biliary cirrhosis, but often is a functional defect from impaired distal sodium delivery. Potassium disorders are often the result of the therapies used to treat advanced liver disease. Do you want to read the rest of this article? ... Patients with decompens Continue reading >>

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  1. <7%

    Do Ketogenic Diets Slow Metabolism?

    I have had insomnia for close to two decades and amazingly, very few things helped as much as a keto diet. At first, I thought this was odd but later I read about many other people who had better sleep while on KETO. Also, I read somewhwere -may be on Lyle's board- that KETO diets slow down the metabolism via reduction in T3 and T4 secretion and this is one of the reasons they help you preserve muscle mass. So is this true? Do they actually decrease T3 and T4 levels? If not, what is the better sleep attributable to?
    Sub7

  2. Eileen

    I don't think keto diets slow metabolism any more than other diets, and probably less, since it preserves muscle better, which works to keep up the metabolism.
    I've also found I sleep better in keto, and wake constantly when I'm doing a carb-up. I think it's just the effect of the insulin spikes and dips that wake me up when I eat carbs, rather than something special about keto.

  3. leenmeen

    Eileen, you might be interested in this: beneficial effect of keto diet on the sleep disorder narcolepsy has been reported in the medical literature:
    ---
    Husain AM, et al. Diet therapy for narcolepsy. Neurology, 22 June 2004; 62 (12): 2300-2302
    Abstract�
    The effects of a low-carbohydrate, ketogenic diet (LCKD) on sleepiness and other narcolepsy symptoms were studied. Nine patients with narcolepsy were asked to adhere to the Atkins� diet plan, and their symptoms were assessed using the Narcolepsy Symptom Status Questionnaire (NSSQ). The NSSQ�Total score decreased by 18% from 161.9 to 133.5 (p = 0.0019) over 8 weeks. Patients with narcolepsy experienced modest improvements in daytime sleepiness on an LCKD.
    Narcolepsy is a syndrome characterized by excessive daytime sleepiness (EDS), cataplexy, sleep paralysis, and hypnagogic hallucinations. However, despite optimal pharmacologic management, daytime sleepiness persists in many patients. The effect of diet on the sleep�wake cycle in narcolepsy has not been studied in detail. We examined the effect of a low-carbohydrate, ketogenic diet (LCKD) on daytime sleepiness in patients with narcolepsy already on optimal doses of stimulant medications.
    Methods.
    Patients were recruited from the narcolepsy clinic at the Veterans Affairs Medical Center, Durham, NC. Inclusion criteria consisted of a diagnosis of narcolepsy with continued daytime sleepiness despite optimal stimulant therapy. Narcolepsy was defined as the presence of EDS with either unequivocal cataplexy or presence of at least two sleep-onset REM periods on a Multiple Sleep Latency Test (MSLT). 1 Additionally, patients had to have a body mass index (BMI) of at least 20 kg/m2 and agree to modify their diet per instructions. Patients were excluded if they were pregnant or nursing or had a serious medical condition.
    Diet instructions for the LCKD were derived from a popular lay press book, Dr. Atkins� New Diet Revolution. 2 Patients were instructed to restrict carbohydrate intake to <20 g/day. They were advised to take a standard multivitamin and drink copious fluids daily. Follow-up group visits occurred every other week for 8 weeks. Patients were instructed not to change their stimulant medication dosage.
    Sleepiness was measured at baseline and weeks 2, 4, and 8 using three validated self-administered scales: the Narcolepsy Symptoms Severity Questionnaire (NSSQ), the Epworth Sleepiness Scale (ESS), and the Stanford Sleepiness Scale (SSS). 3,4 Adherence to the diet intervention was measured by self-report and urinary ketones. Patients self-monitored urine ketone levels with dipsticks at the same time daily using the following semiquantitative scale: 0 = none, 1 = trace (up to 5 mg/dL), 2 = small (5 to 40 mg/dL), 3 = moderate (40 to 80 mg/dL), 4 = large-80 (80 to 160 mg/dL), 5 = large-160 (>160 mg/dL). The mean level of urine ketones for each week was calculated for each patient. Weight and vital signs were measured at each visit. A fasting lipid profile and routine serum chemistries were obtained at baseline and study termination.
    Linear mixed-effects models, with a random intercept and time (i.e., week) as a fixed effect, were used to analyze the effect of the diet on sleepiness symptoms as measured by the NSSQ, ESS, and SSS. Paired t-tests, or Wilcoxon signed-rank tests where appropriate, were used to compare baseline to week 8 vital and laboratory measurements for the eight participants who completed the study. A p value of <=0.05 was considered significant. Analyses were performed using SAS Statistical Software (version 8.02; SAS Institute, Cary, NC).
    Results.
    Nine patients were recruited for the study. The mean � SD age was 47.6 � 10.9 years; eight were men, seven were African American, two were Caucasian. The mean body weight at baseline was 100.9 � 19.8 kg, and the mean BMI was 32.8 � 6.9 kg/m2. One subject dropped out after 4 weeks owing to inability to adhere to the diet.
    Significant improvements were seen on the NSSQ�Total score and the following subscales: Sleepiness, Sleep Attacks, and Sleep Paralysis (table;figure 1). The Total score on the NSSQ decreased by 18% from 161.9 at baseline to 133.5 at week 8 (p = 0.0019). In addition, the Sleepiness Subscale score decreased by 22% from 51.0 to 39.6 (p = 0.017), the Sleep Attacks Subscale score decreased by 13% from 46.0 to 40.0 (p = 0.016), and the Sleep Paralysis Subscale score decreased by 24% from 21.1 to 16.0 (p = 0.015). The ESS and SSS did not change significantly over the 8-week duration of the study.
    Graphic
    Table Predicted scores* on sleep questionnaires
    Graphic
    Figure 1. Predicted mean scores of Narcolepsy Symptom Status Questionnaire (NSSQ) subscales by linear mixed-effects model. Diamonds = Sleepiness; squares = Sleep Attacks; triangles = Cataplexy; x�s = Sleep Paralysis; circles = Vivid Dreams.
    The mean number of days since the previous visit that participants were not adherent to the diet increased from 0.3 � 0.5 day at week 2 to 1.3 � 1.3 days at week 8. The mean urine ketone levels by self-testing increased from 0 at baseline to 2.8 � 0.6 at week 1, peaked at 3.7 � 0.9 at week 2, and declined gradually to a plateau at 2.8 � 1.1 at week 8 (figure 2). Over the 8 weeks, body weight decreased from 99.3 � 20.7 kg at baseline to 92.2 � 19.8 kg (p < 0.0001). No adverse changes were noted in blood pressure, serum lipid profiles, or serum chemistry tests.
    Graphic
    Figure 2. Mean (SE) urine ketone levels for each week (n = 9 for weeks 0 to 4, n = 8 for weeks 5 to 8). Urine ketone scale: 0 = none, 1 = trace (up to 5 mg/dL), 2 = small (5 to 40 mg/dL), 3 = moderate (40 to 80 mg/dL), 4 = large-80 (80 to 160 mg/dL); 5 = large-160 (>160 mg/dL).
    There were no serious adverse events reported during this study. Four patients (44%) had transient side effects (headache, leg cramps, irritability, and difficulty with concentration); however, none was severe enough to prompt discontinuation of the study or the diet. No patient reported a worsening of daytime sleepiness.
    Discussion.
    EDS is often debilitating for patients with narcolepsy. Many patients continue to experience daytime sleepiness despite the optimal use of stimulant medications. Another treatment commonly recommended to narcolepsy patients is dietary modification, even though its effect has not been studied prospectively.
    In the current study, dietary modification resulted in significant improvements of narcolepsy symptoms as measured by the NSSQ. The NSSQ�Total score decreased by 18% after 8 weeks of treatment, whereas the Sleepiness Subscale score decreased by 22%, Sleep Attacks Subscale by 13%, and Sleep Paralysis Subscale by 24%.
    Serum ketones are one potential mechanism for the observed effect on narcolepsy symptoms, although the pathway involved has not been identified. Urinary ketones were highest in the first 2 weeks and then decreased somewhat to plateau at week 8. A similar pattern of ketonuria with this diet has been noted previously. 5 The most likely reason for the gradual decline in urine ketones is that subjects increased their carbohydrate intake. Alternatively, it is possible that the body adjusts physiologically to reduced carbohydrate intake.
    Another intriguing mechanism to consider involves the role of orexin (hypocretin). Patients with narcolepsy have been shown to have impaired orexin signaling. 6 Hypoglycemia tends to activate orexin-containing neurons. 7 It is possible that the LCKD, by inducing relative hypoglycemia (blood glucose lower than baseline), increases the activation of orexin-containing neurons, which in turn improves daytime sleepiness.
    Dietary effects on sleep and fatigue have been evaluated in other situations. In one study, volunteers without a sleep disorder who consumed a high-carbohydrate, low-fat diet spent less time in slow wave sleep than those who consumed either a balanced or a low-carbohydrate, high-fat diet. 8 In a review of occupational sleep and fatigue, the authors noted that simple carbohydrates produce a transient increase in alertness, followed by a decrease in alertness after a few hours. 9 These studies support the view that diet influences sleep and that carbohydrates may exacerbate sleepiness in certain individuals.
    One possible limitation of this study was the method used to measure daytime sleepiness. The gold standard for measuring the degree of daytime sleepiness is the MSLT. This test was not employed for this study because of the considerable cost and time required for its use. It can be argued that daytime alertness may have improved because of decreases in body weight. As this variable was not controlled in this study, it remains a possibility, although benefits were noted by patients early in the study before substantial weight loss occurred. Though this study suggests that dietary therapy may improve daytime sleepiness, a randomized trial with a comparison intervention is needed to determine if weight loss or other factors contributed to the observed improvements in sleepiness symptoms.

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