Here’s To A Sweet Ripe New Year!
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 concerning alcohol consumption.
Fructose or sucrose are known to accelerate the metabolism of alcohol, so mix your drinks with orange juice or a sweet soda or soft drink. Or you can add cane sugar like they have done in many countries for 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%.’ (Rawat AK. 1977)
‘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.’ (J Soterakis, F L Iber, 1975)
‘…sugar can attenuate alcohol intoxication in fasting humans without altering blood alcohol levels significantly.’ (Zacchia C, et al., 1991)
Although it is not an antidote against the effects of alcohol, there are several reasons why sugar, when consumed in sufficient quantities, might help protect against some of the negative consequences of excessive alcohol consumption.
Polyunsaturated fats (PUFAs) and alcohol are not a great combination. And the breakdown products of PUFAs get shown to play a significant 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.’ (Warner DR, et al., 2017)
‘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.’ (Situnayake RD, et al., 1990)
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 PUFAs into circulation.
Sugar is vital for proper liver function, and a well-functioning liver helps keep stress low and allows alcohol to get 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 primary 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…’ (Mathurin P, et al., 2000)
‘…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.’ (Liangpunsakul, S., et al., 2017)
‘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.’ (Kirpich IA, et al., 2012)
‘When animals were injected with LPS…there was a 5-fold rise in ALT levels in the ethanol-fed group…’ (Batey R, et al., 1998)
Metabolic stress is a promoter of all kinds of addiction. For example, there is evidence that oxidative stress and inflammation (from the breakdown of PUFAs) exacerbate alcohol addiction and increase 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.’ (Ostroumov A, et al., 2016)
‘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.’ (Huang MC, et al., 2009)
‘Alcoholic hepatitis is associated with high short-term mortality. Although not included in prognostic scores, lipid peroxidation plays an outstanding role in its pathogenesis.’ (Pérez-Hernández O, et al., 2017)
In stark contrast to the combined effects of PUFAs and alcohol on the liver, saturated fats get shown to protect the liver from – and even potentially reverse – alcoholic liver injury. In addition, excess sugar, which cannot be immediately used or stored as glycogen, is converted mainly to saturated fat, further protecting against damage from PUFAs and alcohol.
‘A diet enriched in saturated fatty acids effectively reverses alcohol-induced necrosis, inflammation, and fibrosis despite continued alcohol consumption.’ (Nanji AA, et al., 2001)
‘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.’ (Nanji AA, et al., 1995)
Sugar helps with cholesterol production and converts cholesterol into protective hormones, including pregnenolone and progesterone. Low cholesterol gets associated with addiction, and pregnenolone helps 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.’ (Lin SH, et al., 2012)
‘…study showed an association between a low total cholesterol level and relapse rates in detoxified cocaine addicts.’ (Buydens-Branchey L, Branchey M. 2003)
‘…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.’ (Besheer J, et al., 2010)
Exposure to PUFAs and endotoxin can also impact vitamin D, nitric oxide, estrogen, and serotonin levels, which are 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.’ (Myers, R.D., Cicero, T.J. 1969)
‘…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.’ (Neupane SP, et al., 2013)
The stress-lowering effects of sugar (combined with other nutritious pro-metabolic foods) can help keep the stress substances 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.’ (Vendruscolo LF, et al., 2015)
I’m not a doctor or nutritionist; none of this is health advice. Still, things that protect against the harmful effects of alcohol include niacinamide, aspirin, Periactin and activated charcoal. And raw carrot fibre, specific antibiotics (like minocycline), thiamine (B1) and coconut oil.
If you decide to drink, an evening with some tequila or vodka with fresh lemon and lime, 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.
Copyright 2021, by Dan M @ CowsEatGrass. All rights reserved (except for quotations and images having their own protected copyrights). This copyright protects author-publisher Dan M’s right to future publication of his work in any manner, in any and all media — utilizing technology now known or hereafter devised — throughout the world in perpetuity. Everything described in this publication is for information purposes only. The author-publisher, Dan M, is not directly or indirectly presenting or recommending any part of this publication’s data as a diagnosis or prescription for any ailment of any reader. If anyone uses this information without the advice of their professional health adviser, they are prescribing for themselves, and the author- publisher assumes no responsibility or liability. Persons using any of this data do so at their own risk and must take personal responsibility for what they don’t know as well as for what they do know.
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