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 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 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.”
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 (PUFAs) and alcohol is not a great combination. The breakdown products of PUFAs 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 PUFAs 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.
“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.”
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 PUFAs), exacerbates alcohol addiction and increases the severity of withdrawal symptoms.
” 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.”
In stark contrast to the combined effects of PUFAs 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 PUFAs and alcohol.
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.
“…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 PUFAs 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 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.
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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