Welcome to the new year, the year of the revival of sugar and the vindication of fructose. Wishful thinking?
If you’ve already made it – or for those of you still lingering somewhere over in last year – here are some tips in relation to alcohol consumption.
Fructose or sucrose are known to accelerate the metabolism of alcohol, so it might be helpful to mix your drinks with orange juice or a sweet soda or soft drink. Or you can just add cane sugar like they have done in many countries, for many many years.
“Oral administration of fructose was found to exert the most pronounced effect. It increased the rate of blood alcohol clearance by about 100%.”
“Oral administration of fructose or sucrose would result in blood alcohol levels returning to ‘sober levels’ in a considerably shorter time interval, reducing the time of sobering up by 3 to 4 hours.”
“…sugar can attenuate alcohol intoxication in fasting humans without altering blood alcohol levels significantly.”
Although it is not an antidote against the effects of alcohol, there are a number of reasons why sugar, when consumed in sufficient quantities, might help protect against some of the negative consequences of excessive alcohol consumption.
Polyunsaturated fat (PUFA) and alcohol is not a great combination. The breakdown products of PUFA have been shown to play a major role in the progression of damage done by excessive alcohol consumption.
“Dietary fat plays an important role in alcoholic liver disease pathogenesis… a combination of ethanol and a diet rich in linoleic acid (LA) leads to the increased production of oxidized LA metabolites…which contribute to a hepatic proinflammatory response exacerbating liver injury.”
“The generation of hepatic liver peroxidation by free radicals has been proposed as a mechanism for ethanol induced hepatotoxicity…The proportion of 18:2(9,11) linoleic acid in hepatic lipids correlated significantly with inflammatory histological features and inversely with hepatic glutathione.”
Sugar is fuel for metabolism, and as such helps to keep stress at bay. The ability to meet stress with an appropriate energy supply, limits the release of stored PUFA into circulation.
Sugar is important for proper liver function, and a well functioning liver helps to keep stress low, as well as allowing for alcohol to be metabolized more effectively.
A well fueled metabolism promotes effective digestion and helps to keep intestinal barrier function high. Both of these factors protect against excessive levels of endotoxin getting to the liver and into the main system, potentially helping to reduce damage from alcohol.
“…intestinal permeability is indeed increased during the early stages of experimental alcoholic liver injury and…LPS [endotoxin] aggravates alcoholic liver injury…”
“…we found an increase in the levels of LPS…with excessive drinkers….levels are correlated with the quantity as well as timing of recent alcohol consumption and declined upon abstinence.”
“Dietary fat is an important cofactor in alcohol-associated liver injury…USF (corn oil/linoleic acid) by itself results in dysregulation of intestinal TJ integrity leading to increased gut permeability, and alcohol further exacerbates these alterations….elevated blood endotoxin levels in response to USF and alcohol…combine to cause hepatic injury in ALD.”
“When animals were injected with LPS…there was a 5-fold rise in ALT levels in the ethanol-fed group…”
Metabolic stress has been shown to be a promoter of different kinds of addiction, and there is evidence that oxidative stress and inflammation (from the breakdown of PUFA), exacerbates alcohol addiction and increases the severity of withdrawal symptoms.
“…results demonstrate that stress alters the neural and behavioral responses to alcohol through a neuroendocrine signal that shifts inhibitory GABA transmission toward excitation.”
” MDA [malondialdehyde, a breakdown product of PUFA] was the only variable significantly correlated with the average and highest CIWA-Ar-C [Clinical Institute Withdrawal Assessment for Alcohol Scale] scores at the first day of detoxification…serum MDA levels were significantly elevated…in alcoholic patients.”
“Alcoholic hepatitis is associated with high short-term mortality. Although not included in prognostic scores, lipid peroxidation plays an outstanding role in its pathogenesis.”
In stark contrast to the combined effects of PUFA and alcohol on the liver, saturated fats have been shown to protect the liver from – and even potentially reverse – alcoholic liver injury. Excess sugar which is unable to be immediately used or stored as glycogen, is converted largely to saturated fat, further protecting against damage from PUFA and alcohol.
“A diet enriched in saturated fatty acids effectively reverses alcohol-induced necrosis, inflammation, and fibrosis despite continued alcohol consumption.”
“A diet enriched in saturated but not unsaturated fatty acids reversed alcoholic liver injury. This effect may be explained by down-regulation of lipid peroxidation.”
Sugar helps with cholesterol production, and with the conversion of cholesterol into the protective hormones, including pregnenolone and progesterone. Low cholesterol has been associated with addiction, and pregnenolone has been shown to help with chronic alcohol abuse, as well as possibly helping repair some of the damage from excessive alcohol consumption.
“Cholesterol could be associated with the cognitive aspect of craving and may be a potential marker to predict risk of drug relapse.”
“…study showed an association between a low total cholesterol level and relapse rates in detoxified cocaine addicts.”
“…pregnenolone may be a novel therapeutic for reducing chronic ethanol drinking…pregnenolone serum levels…were positively correlated with cognitive improvements…significant given that cognitive deficits are common in alcohol dependent individuals and may interfere with effective therapy.”
Exposure to PUFA and endotoxin can also impact upon levels of vitamin D, nitric oxide, estrogen and serotonin and all of these have been associated with alcohol damage and addiction.
“…the preference for alcohol, which was induced by behavioral stress, could be altered [reduced] by lowering serotonin levels in the brain.”
“…high rates of vitamin D deficiency in alcohol treatment sample and shows a positive association between vitamin D deficiency and severity of alcohol-use disorders.”
The stress lowering effects of sugar (combined with some other nutritious pro-metabolic foods) can help to keep the substances of stress at bay, whilst promoting thyroid metabolism and the production of all things protective.
“…attenuation of GR [glucocorticoid receptor] function…reduces compulsive-like alcohol intake…and reduces both excessive drinking and alcohol craving in recently abstinent alcoholics — in addition to improving liver-function markers in subjects with a history of heavy drinking — without any major adverse effects.”
Some other things which might provide some protection against the negative effects of alcohol include niacinamide, aspirin, cyproheptadine, activated charcoal, raw carrot fiber, certain antibiotics (like minocycline), thiamine (B1) and coconut oil.
If you do decide to drink, an evening with some tequila or vodka with fresh lemon and lime, fresh sweet ripe fruits and juices, cane sugar, honey and a platter of mixed cheeses is a reasonable approach to celebrating the end of the old year, and the beginning of a new era of tolerance towards sugar, in its many disguises.
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Increased rate of alcohol removal from blood with oral fructose and sucrose.
Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration.
Dietary saturated fatty acids: a novel treatment for alcoholic liver disease.
Overexpression of the Steroidogenic Enzyme Cytochrome P450 Side Chain Cleavage in the Ventral Tegmental Area Increases 3α,5α-THP and Reduces Long-Term Operant Ethanol Self-Administration
Malondialdehyde as a Prognostic Factor in Alcoholic Hepatitis.
Effect of sucrose consumption on alcohol-induced impairment in male social drinkers.
Honey reduces blood alcohol concentration but not affects the level of serum MDA and GSH-Px activity in intoxicated male mice models.
Effects of fructose and other substances on ethanol and acetaldehyde metabolism in man.
Effects of fructose and glucose on ethanol-induced metabolic changes and on the intensity of alcohol intoxication and hangover.
[Thiamine (vitamin B1) treatment in patients with alcohol dependence].
The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease.
Dietary saturated fatty acids down-regulate cyclooxygenase-2 and tumor necrosis factor alfa and reverse fibrosis in alcohol-induced liver disease in the rat.
Oxidative status in patients with alcohol dependence: a clinical study in Taiwan.
Decreased tumor necrosis factor-alpha and interleukin-1alpha production from intrahepatic mononuclear cells in chronic ethanol consumption and upregulation by endotoxin.
Effect of Alcohol Consumption on Oxidative Stress Markers and its Role in the Pathogenesis and Progression of Liver Cirrhosis
Medium chain triglycerides dose-dependently prevent liver pathology in a rat model of non-alcoholic fatty liver disease.
Saturated and Unsaturated Dietary Fats Differentially Modulate Ethanol-Induced Changes in Gut Microbiome and Metabolome in a Mouse Model of Alcoholic Liver Disease.
Beneficial effects of nicotinamide on alcohol-induced liver injury in senescence-accelerated mice.
The efficacy of (+)-Naltrexone on alcohol preference and seeking behaviour is dependent on light-cycle.
Effects of chronic ethanol intake on aromatization of androgens and concentration of estrogen and androgen receptors in rat liver.
Aspirin attenuation of alcohol-induced flushing and intoxication in Oriental and Occidental subjects.
Glucocorticoid receptor antagonism decreases alcohol seeking in alcohol-dependent individuals.
Ethanol-induced reductions in testicular steroidogenesis: major differences between in vitro and in vitro approaches.
Dietary Linoleic Acid and Its Oxidized Metabolites Exacerbate Liver Injury Caused by Ethanol via Induction of Hepatic Proinflammatory Response in Mice.
Effects of ethanol on conjugated gonadal hormones in plasma of men.
Minocycline Reduces Ethanol Drinking
Stress Increases Ethanol Self-Administration via a Shift toward Excitatory GABA Signaling in the Ventral Tegmental Area
Pregnenolone and ganaxolone reduce operant ethanol self-administration in alcohol-preferring P rats
Aspirin reduces alcohol-induced prenatal mortality and malformations in mice.
Vitamin D deficiency in alcohol-use disorders and its relationship to comorbid major depression: a cross-sectional study of inpatients in Nepal.
Lipid peroxidation and hepatic antioxidants in alcoholic liver disease.
Alcohol-induced generation of lipid peroxidation products in humans
Evaluation of effect of minocycline on rewarding potential and alcohol relapse in place preference model in mice.
Reduced ethanol consumption during cyproheptadine administration in rats from a long-term alcohol-treated colony.
Association between cholesterol plasma levels and craving among heroin users.
Exacerbation of alcoholic liver injury by enteral endotoxin in rats.
The correlation between early alcohol withdrawal severity and oxidative stress in patients with alcohol dependence.
Alcoholic Liver Disease: Update on the Role of Dietary Fat
HPA axis dysregulation in men with hypersexual disorder.
Alcohol preference in the rat: reduction following depletion of brain serotonin.
Effects of Serotonin Depletion on the Volitional Alcohol Intake of Rats During a Condition of Psychological Stress
Quantity of alcohol drinking positively correlates with serum levels of endotoxin and markers of monocyte activation
Association between low plasma levels of cholesterol and relapse in cocaine addicts.
Is vitamin D deficiency a confounder in alcoholic skeletal muscle myopathy?
Potential effects of L-NAME on alcohol-induced oxidative stress