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Candida albicans alcohol,what is candida virus,time yeast infection clear up - Reviews

Author: admin, 14.03.2014

There are about a dozen recognized causes of intestinal dysbiosis (or dys-function of the microbiome, or inner ecology) and candida overgrowth (CO). Alcohol (ethanol, CH3CH2OH) tops the list of toxic substances encountered in forensic toxicology for the simple reason that heavy drinking and drunkenness are incriminated in many fatal accidents, trauma deaths, suicides, crimes of violence and antisocial behavior in general. A major problem associated with postmortem alcohol analysis is the risk that the alcohol, at least in part, was generated or destroyed between the time of death and the time of the autopsy or after taking the specimens and performing the toxicological analysis. The methods suitable for analyzing alcohol in postmortem specimens are essentially the same as those used when specimens are taken from living subjects, e.g. Quantitative methods for the determination of alcohol in blood and urine have been available for more than 1OO years. In the 1960s gas chromatographic (GC) methods were developed for the analysis of alcohol in blood and urine and these have dominated ever since. Gas chromatography coupled with the headspace sampling technique (HS-GC) still remains the method of choice for forensic analysis of alcohol in specimens from living and dead persons. Figure 1 Schematic diagram showing analysis of alcohol in biological samples by headspace gas chromatography with two different stationary phases (SP1 and SP2) for packing the chromatographic columns and two different internal standards (pro-pan-1-ol and t-butanol) for diluting the specimens prior to analysis.
Sometimes a rapid assessment of whether alcohol intoxication was a contributing factor in a person’s death is considered necessary.
Traces of alcohol occur naturally in body fluids as products of metabolism and also by the microbial fermentation of sugars in the gut. After drinking alcoholic beverages, the alcohol (ethanol) contained in beer, wine or spirits is diluted with the stomach contents before being absorbed and transported by the blood to all body organs and tissues. After drinking small doses of alcohol (one to two drinks) some of the alcohol might become metabolized in the stomach mucosa or during the first passage of the blood through the liver.
The blood-alcohol concentration reached after drinking alcoholic beverages depends on the amount consumed (dose), the speed of drinking, the rate of absorption from the gut and also on the person’s body weight, age and gender. Once absorbed from the gut, alcohol is transported via the portal vein to the liver where enzymes begin the process of breaking down the alcohol to clear it from the bloodstream. Alcohol and water mix together in all proportions and only a very small fraction of the total amount of alcohol absorbed into the blood penetrates into fatty tissue and bone. Table 3 gives the water contents of body fluids and tissues taken at postmortem and used for analysis of alcohol.
After absorption and distribution of alcohol are complete and the concentration in blood begins to decrease, the organs and tissue such as skeletal muscles return alcohol into the venous blood and peripheral circulation. Table 3 Average water-content of body fluids, organs and tissue in relation to the expected concentrations of alcohol. Fatalities caused by abuse of alcohol and drunkenness occur daily throughout the world and heavy drinkers and alcoholics are over-represented among individuals committing suicide. Deaths attributable to alcohol impairment include all kinds of accidents and especially road-traffic fatalities, which are the leading cause of death among people aged under 35 years for drivers, passengers and pedestrians.
The acute toxicity of alcohol is well documented for inexperienced drinkers who consume too much too quickly, leading to gross impairment and alcoholic coma. Some people consume large quantities of alcohol daily and build-up a pronounced central nervous system tolerance, which might explain the very high blood-alcohol concentration reported in autopsy material (4-5gl”1).
Examples of the biological specimens taken at autopsy and subsequently used for alcohol analysis are presented in Table 4.
The concentration of alcohol in a sample of postmortem blood can provide useful information about the BAC at the time of death and within limits the amount of alcohol the person might have consumed.
The effects of alcohol and other psychoactive substances on performance and behavior tend to be correlated with the concentrations infiltrating the brain and the person’s BAC provides the best indirect estimate of central nervous system (CNS) exposure to the drug.
Blood specimens submitted for alcohol analysis are often clotted and completely hemolyzed, and occasionally, also diluted with other biological fluids. The sampling tubes and containers used to collect and store postmortem specimens for alcohol analysis must contain sufficient sodium or potassium fluoride so that the final concentration of preservative is approximately 2%, wlw. Obtaining intracranial blood from a subdural or subarachnoid hematoma is one useful strategy to investigate whether the person had been drinking alcohol before receiving a blow to the head, fracture of the skull and cerebral hemorrhage.
If necessary, the blood-alcohol concentration determined at autopsy can be translated into the amount of alcohol in the body at the time of death. The concentration of alcohol in VH should exceed that of the femoral venous blood as there is roughly 10-20% more water in the eye fluid.
Figure 2 shows a scatter plot of the concentrations of alcohol in VH and in femoral venous blood in samples from 56 autopsies. The proper role of VH as a biological specimen for alcohol analysis in postmortem toxicology is to compare results with the BAC and thus to corroborate the presence of alcohol in the body at the time of death.
The UAClBAC ratio might give a hint about the status of alcohol absorption at the time of death, which could have forensic significance when fatal accidents are investigated. The main advantage of urine over blood is that invasion of the bladder by microbes and yeasts appears to be less of a problem and except in those cases with a history of diabetes, urine does not normally contain any significant amounts of sugar for alcohol fermentation. In aviation fatalities where polytraumatic deaths are the rule rather than the exception, drawing correct conclusions about alcohol consumption from analysis of a single specimen of blood or tissue is very difficult.
The CSF is mainly composed of water (97-99%) and the concentration of alcohol reaching CSF indicates the concentration that has passed through the brain giving an indication of pharmacological exposure. Figure 5 shows an example of the pharmacokinetic profiles of alcohol in venous blood and CSF obtained by lumbar puncture at various time intervals after subjects drank a moderate dose of alcohol in 5 min. The first choice of body fluids for postmortem alcohol analysis are femoral venous blood, bladder urine and vitreous humor (Table 4). Skeletal muscle contains glycogen which is converted into glucose after death providing an abundance of substrate for microbial synthesis of alcohol.
The stability of alcohol in blood after death is another problem faced when the analytical results are evaluated and a judgment is made about a person’s state of inebriation at the time of death. The mechanism of alcohol loss from tissues and body fluids after death might involve evaporation, enzymatic breakdown or microbiological degradation. Distinguishing antemortem ingestion of alcohol from postmortem synthesis has always been and still is a major dilemma for the forensic pathologist and toxicologist. Bodies recovered from water and incinerated cadavers present special problems when the results of forensic alcohol analysis are interpreted.
A multitude of microorganisms are capable of producing alcohol from endogenous and exogenous substrates. Postmortem diffusion relates to the movement or redistribution of alcohol andlor other drugs or their metabolites from one part of the body to another after death. Many factors need to be considered when the results of analyzing alcohol in postmortem materials are interpreted for medicolegal purposes. Although blood from a femoral vein has become the preferred specimen for toxicological analysis of alcohol and other drugs, this is not always possible owing to severe injuries to the body.
Much thought is needed when the results of postmortem blood-alcohol analysis are reported to the police because of the stigma attached to any suggestion that a deceased person was under the influence of alcohol. Reports from accident and emergency service departments worldwide provide ample evidence to support the negative impact of alcohol abuse and alcoholism in society.
However, difficulties arise when the concentration of alcohol in a postmortem blood specimen is interpreted and conclusions are drawn about a person’s state of inebriation at the time of death.
This becomes a major dilemma when decomposed bodies are examined and requests are made for alcohol analysis. Having a higher proportion of fat gives a higher BAC for the same dose of alcohol consumed because leaner individuals have more body water into which the alcohol can be diluted. The principal alcohol-metabolizing enzyme is class I hepatic alcohol dehydrogenase (ADH), which converts ethanol into a toxic metabolite, acetaldehyde.


Accordingly, the distribution of alcohol in body fluids and tissue after diffusion equilibrium is complete follows the distribution of water in the body.
These values provide a rough estimate of the relative concentration of alcohol expected in various biofluids and tissues because the ratios of the water content should correspond to the distribution ratios of alcohol provided that diffusion equilibrium of alcohol is complete. The venous blood therefore contains a somewhat higher concentration of alcohol than arterial blood when the blood-alcohol curve enters the postabsorptive stage. If the victim survives several hours after the trauma the concentration of alcohol in peripheral venous blood might have decreased to zero owing to metabolism occurring in the liver. This watery fluid makes an ideal specimen for forensic analysis of alcohol because of the isolated location of the sampling site, that is, the remoteness of the eyes from the gut, thus minimizing the risk of contamination with microorganisms or diffusion of alcohol from the stomach. The normal rate of urine production is 1mlmin-1 (60 ml h-1), but diuresis is enhanced after drinking alcohol especially when the BAC curve is rising. Figure 3 shows a plot of urine alcohol and blood alcohol in 21 subjects who first emptied their bladders and then drank a moderate dose of alcohol in the morning without having eaten breakfast. This suggests elimination of alcohol from the bloodstream owing to metabolism with a subsequent pooling of urine in the bladder. The combination of sugar, viable yeast or other microorganisms, and optimal time and temperature conditions leads to the formation of alcohol in urine within about 24-36 h after death; one molecule of glucose produces two molecules of ethanol and carbon dioxide during the fermentation process.
When these are not available other biological specimens or tissues are desirable and occasionally submitted for analysis of alcohol. Several reports indicate that alcohol is generated in muscle tissue within the first few days after death or during the time specimens are sent by mail to the laboratory for analysis. Both losses and increases in the concentration of alcohol are possible when a corpse is submerged in water for extended periods or burnt.
The main candidate is glucose, which increases in concentration after death, especially in the liver and skeletal muscles.
The stomach, portal vein and liver are the main sites from which alcohol can diffuse into the peri-cardial and pleural fluid, and less readily into the chambers of the intact heart and extremities. An appreciable increase or decrease in the concentration of alcohol suggests activity of microorganisms. These higher alcohols are produced in decomposing tissue and can therefore serve as indicators of postmortem synthesis of ethanol.
At the same time, a small fraction of the biogenic aldehyde is reduced to an alcohol metabolite 5-hydroxytryptophol (5HTOL) by the action of ADH or aldehyde reductase. Relating the measured postmortem BAC with an equivalent ante-mortem BAC and making a statement about whether a person had ingested alcohol before death is fraught with pitfalls. DietPoor food choices Is one of the main causes of candida overgrowth (CO) and intestinal dysbiosis. The impairment caused by overconsumption of alcoholic beverages explains many accidents in the home, in the workplace and on the roads. Translating a BAC determined at autopsy (called necropsy in UK) into the amount of alcohol in the body at the time of death is subject to considerable uncertainty. The blood-glucose concentration increases after death owing to mobilization and hydrolysis of glycogen stores in the liver and muscle tissue thus providing abundant substrate for microbial synthesis of alcohol.
The units used to report the concentration of alcohol determined in blood and other body fluids differ from country to country, e.g. In postmortem toxicology, the sampling variation and magnitude of site-to-site differences in blood alcohol concentration often exceeds these pure analytical variations. The electron-impact mass spectrum of ethanol shows prominent ion-fragments with a base peak at mlz 31 (common for primary alcohols), mlz 46 (molecular ion) and also at mlz 45 (molecular ion -1). One such method consists of a disposable dip-stick device, which was originally developed for the analysis of alcohol in saliva specimens from living subjects.
Since women tend to be smaller than men and also have more fatty tissue and less body water, a given amount of alcohol in a female drinker yields a higher BAC and a correspondingly greater effect on the brain (impairment) and more damage to organs and tissues. However, these arterial-venous differences in alcohol concentration lack significance in postmortem work. Because circulation in a cerebral blood clot is diminished or nonexistent the concentration of alcohol present should reflect the concentration in peripheral blood at an earlier point in time. The sampling and analysis of alcohol in vitreous humor (VH) is therefore highly recommended as a complement to taking blood samples for toxicological analysis and specimens of VH can be obtained without making a full autopsy. VH is also the most useful specimen for alcohol analysis whenever embalmed bodies are examined.
An alternative explanation is death occurring immediately after drinking a large amount of alcohol with the bladder containing an alcohol-free pool of urine. In aircraft accidents, there is always a bigger risk for postmortem synthesis of alcohol because of the abdominal trauma and microorganisms from the gut spread more quickly throughout the body.
CSF is a clean biological specimen well suited for the analysis of alcohol and other drugs. Alcohol is not evenly distributed in the brain owing to an uneven distribution of water so the results depend on which brain region was analyzed.
Loss of alcohol can occur in the interval between death and performing the postmortem examination, and from the time of autopsy to making the toxicological analysis.
Loss of alcohol from body fluids and tissue occur by dilution owing to high solubility in water as time after death increases. If necessary, the specimens of blood or tissue can be cultured and tests made for the presence of alcohol-producing species according to classical microbiological techniques. The number of people who die with high concentrations of alcohol in their stomachs has not been well established although it is generally thought to be rather few.
Translating the BAC into the amount of alcohol consumed is also subject to considerable uncertainty. Such intensive care treatments can alter the concentrations of alcohol in the various body compartments and complicate interpretation of toxicological results. Accordingly, measuring and interpreting the concentrations of alcohol in blood and other biological specimens are routine procedures in forensic medicine and toxicology. The limit of quantitation of alcohol in postmortem blood specimens under routine conditions is about 10mg100ml-1 (0.1 gl-1) and analytical results below this threshold are generally reported as negative in postmortem work. How fast alcohol enters the bloodstream depends on many variable factors, especially the speed of gastric emptying as controlled by the pyloric sphincter.
Gastric ADH differs from hepatic ADH in other respects such as the optimal Km and Vmax values for oxidation of alcohol. Indeed, alcohol intoxication or drug-alcohol interactions should not be overlooked when sudden natural deaths are investigated and screening of all out-of-hospital deaths for elevated blood-alcohol concentration has been suggested. Chronic intake of alcohol results in metabolic disturbances such as hypoglycemia, lactic acidosis and ketoacidosis. Thus, by comparing the alcohol concentration in subdural blood with, for example, femoral venous blood gives a clue about the person’s BAC at the time of the accident.
Comparing the concentration of alcohol in VH with the blood-alcohol concentration allows a check on whether postmortem synthesis of alcohol in the blood samples needs to be considered.
The negligible intercept (0.01 gl-1) indicates rapid equilibration of alcohol between blood and eye fluids with no pooling of the alcohol and a minimal concentration-time lag. Embalming fluids contain, among other things, formalin and also various alcohols (mainly methanol).
Higher urine-to-blood alcohol concentration (UACl BAC) ratios tend to be associated with low concentrations of alcohol, because like percentages the value of a ratio depends on the size of the denominator. Finding a UAClBAC ratio of 1.1 or less suggests that absorption and distribution of alcohol was incomplete and that the person might therefore have consumed alcohol within 2 h of death.


At zero BAC the mean UAC (y intercept) was 0.25gl-1, which indicates a pooling of urine in the bladder during which time the BAC continues to decrease owing to metabolism of alcohol in the liver. The concentration of alcohol measured in urine should not be used to estimate the concentration of alcohol in the body at the time of death. Table 6 lists some of the problems associated with the analysis and interpretation of alcohol concentrations in postmortem specimens.
The CSF is relatively protected from fermentation processes and is sufficiently isolated so that diffusion of alcohol from the stomach is not a major problem. This creates a pooling of alcohol in the lumbar fluid so the concentration of alcohol in lumbar CSF does not reflect the BAC at the time of death. Tissue such as liver, brain, kidney and skeletal muscle have also served as specimens for analysis of alcohol in postmortem toxicology. However, the results of these studies are confounded by inherent site-to-site variations in concentrations of alcohol, any life-saving medication administered and the possibility of postmortem diffusion taking place prior to autopsy.
The opportunity for postmortem synthesis of alcohol exists from the moment of death to the time of the autopsy. Evidence of mummification, skin slippage, bloating, purging, discoloration, maggots, and bad-smelling corpses give strong indications of decomposition and putrefaction making it all the more likely that any alcohol present was produced after death. For this reason the analysis of alcohol in stomach contents is a common practice in forensic toxicology to compare with blood-alcohol concentration thus providing a clue as to whether the person had died shortly after drinking alcohol. The wet-chemistry oxidation procedures were replaced by milder and more selective enzymatic oxidation in the 1950s and under these conditions only a few other alcohols (propan-1-ol, isopropanol, butan-1-ol) represented any real interference problem. Packed columns made from glass or stainless-steel tubes which are 2 m long and 3 mm internal diameter are still widely used for forensic alcohol analysis. These instruments offer excellent opportunities for unequivocal identification of alcohols and other volatiles in blood and tissue specimens obtained at postmortem as well as in the poisoned patient.
Although the results obtained with these quick and easy methods are less reliable than those obtained by gas chromatography, they at least indicate whether the person might have been under the influence of alcohol at the time of death.
Alcohol absorption is relatively slow through the stomach mucosa, which is less permeable to small molecules than the duodenal or jejunal mucosa. Moreover, liver and kidney have considerable enzymatic activity and the concentration of alcohol in these organs decreases for various periods of time after death owing to on-going metabolic processes.
Blood samples intended for alcohol analysis should not be taken from the pericardium, abdominal or thoracic cavities because at these anatomical locations there is an increased risk of contamination by alcohol spreading from the gut.
The postmortem diffusion of alcohol and other drugs is a recurring issue in postmortem toxicology when the analytical results are interpreted. However, low concentrations of alcohol in intracranial blood clots might have been produced by microbial activity, which underscores the need for obtaining supporting evidence of alcohol consumption such as the analysis of urine or vitreous humor. Good agreement has been observed for the concentrations of alcohol determined in VH retrieved from both eyeballs. Moreover, it remains feasible to sample VH for analysis of alcohol when the corpse has become moderately decomposed. The regression coefficient of 1.19 indicates that VH-alcohol is 19% higher than the corresponding blood alcohol concentration in this material. In contrast, a UAClBAC ratio of 1.3 or more indicates that the alcohol was already equilibrated in body fluids and tissues and that consumption had probably ended several hours before death. But even with blood specimens from living subjects taken in sterile 10 ml Vacutainer tubes containing 1% NaF as preservative and kept at 4°C for several months, the concentration of alcohol decreased at a rate of 0.03 gl-1 per month (3 mg 100 ml-1) on average. After biological specimens are sampled, any further production of alcohol can be blocked by keeping the specimens cold (4°C) and treating them with ~2% sodium or potassium fluoride.
Addition of a preservative and enzyme inhibitor such as sodium or potassium fluoride after sampling will not help if alcohol has already been produced. The concentrations of alcohol measured in urine, VH or CSF should not be routinely translated into the coexisting BAC owing to the wide individual variations in body fluidlblood ratios of alcohol. The principle of the QED® analysis involves enzymatic oxidation of ethanol by alcohol dehydrogenase (ADH) and the coenzyme NAD+.
Also, the much larger absorption surface area available in the upper part of the small intestine facilitates rapid absorption of alcohol, which requires no prior digestion.
Although heart blood is occasionally used as a specimen for postmortem alcohol analysis, this is not recommended owing to the risk of contamination with alcohol diffusing from the stomach or upper airways. The lungs, cardiac blood and abdominal spaces might also be contaminated with alcohol if the deceased aspirated vomit when high concentrations of alcohol remained in the stomach. Finding a negative concentration of alcohol in VH and an elevated BAC strongly suggests that alcohol has been produced in the blood after death. None of the bloods from living subjects showed increases in the concentration of alcohol and the rate of alcohol loss did not depend on the BAC present initially. Whenever large quantities of alcohol remain unabsorbed in the stomach, postmortem diffusion needs to be considered when analytical results are interpreted. Finding a postmortem BAC of 200 mg 100 ml” 1 or more suggests that some alcohol at least was ingested prior to death even if the body was appreciably decomposed.
The case history and the circumstances of the death including tracing important events by interviewing friends or relatives of the victim or by reading police records can sometimes provide useful hints about what to expect from the toxicological alcohol analysis.
Long-term abuse of alcohol eventually leads to malfunctioning of body organs and tissue necrosis. Making these allowances for water-content have been advocated and applied by forensic pathologists in Germany when results of postmortem alcohol analysis are interpreted. The concentrations of these other primary alcohols are usually much less than that of ethanol. Furthermore, aspiration of vomit or gastroesophageal reflux of stomach contents still containing a high concentration of alcohol will promote diffusion of alcohol into the upper airways and lungs.
A very small fraction of the alcohol ingested is converted by the liver into ethyl glucuronide and this water-soluble minor metabolite can be measured in urine specimens to confirm that a person had actually taken alcohol. The mode of transport, storage and overall security of the materials sent for analysis often needs to be documented in medicolegal casework whenever the results of alcohol analysis are challenged in court. However, there are so many other uncertainties when interpreting results of postmortem alcohol analysis that making a correction for water content might not be so important. The length of the blue stain in the capillary tube is proportional to the concentration of alcohol in the sample analyzed. This mode of death is well documented in teenagers and young people unaccustomed to heavy drinking and for whatever reason have engaged in forced consumption of alcohol, such as occurs during drinking competitions. Table 8 gives examples of various strategies available for judging whether alcohol determined in postmortem blood was produced after death by microbial activity. Dairy products, especially milk, are so laden with toxic bacteria that the FDA allows dozens of antibiotics to be used directly in milkAlcoholAlcohol use in excess kills off friendly bacteria, increases toxic overload of the liver, and allow candida overgrowth dysbiosis.
Add to this dilemma the fact that alcohol is actually a yeast by-product and you can see the potential problems.
People with extreme CO can have high blood alcohol levels and literally be drunk, just from eating sugar.
The alcoholic by–products it creates can actually serve as a fertilizer to help it grow further. This explains why various researchers have indicated that everyone who drinks alcohol regularly (daily or a few times weekly) is likely harboring Candida Overgrowth.



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