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How to avoid dangerous sulfites that can cause Alzheimer’s

The relationship between chronic heavy drinking and low thiamine status has been known for decades and is now well-established.

This association is so well-known that when heavy drinkers are found with neurological problems, they are invariably diagnosed with Korsakoff syndrome — a thiamine deficiency disease. 

Korsakoff syndrome is one of only three thiamine deficiency diseases, along with Wernicke encephalopathy and beriberi, highlighting the importance of this vitamin.

Thiamine deficiency is so debilitating that it acquired three names before their respective causes were universally recognized, and found to be the same.

And beer and wine are so notorious for inducing thiamine deficiency that various mechanisms have been proposed to account for it, such as “reduced absorption” and the like. 

Yet such mechanisms aren’t very convincing.

For instance: they cannot explain why thiamine, of all things, is absorbed with reduced efficiency.

This idea becomes even more unconvincing when considering that ethanol generally INCREASES the absorption of practically all molecular types, and especially the lipophilic ones like thiamine.

‘Chronic alcohol consumption can cause thiamine deficiency and thus reduced enzyme activity through several mechanisms, including inadequate dietary intake, malabsorption of thiamine from the gastrointestinal tract, and impaired utilization of thiamine in the cells.’ ―Martin

Yet they always miss one, which I maintain is the most realistic…

Sulfites have been known for nearly a century to physically, directly, and irreversibly destroy thiamine (Williams, 1935).

This most certainly occurs in vivo, as suggested by the finding that thiamine-sufficient diets increase sulfite tolerance (LD₅₀) sixfold in rats (Wilmes, 1967).

Yet most of the proof has been printed in German, never having been translated into English for the mostly-monolingual American physicians.

‘Toxicity was in part attributed to the well-known destructive action of sulfite on thiamine. It has been suggested that the ingestion of SO₂ in a beverage June effectively reduces the level of thiamine in the rest of the diet.’ ―Guido

The English-speaking world seems completely oblivious to this, and instead shifted all the focus away from beer’s impurities towards ethanol itself.

Fusel oils, methanol, and sulfites are much more toxic than ethanol. Many of us already intuitively know this, as hangovers are very mild-to-nonexistent after high quality vodka or London dry gin. 

On account of sulfites being only added to wine and beer, most distilled forms of alcohol are exonerated from this effect.

Brandy however, as a distillate of wine, would be expected to have at least residual sulfites (SO₃²⁻).

Yet since these are in equilibrium with sulfur dioxide (SO₂) gas, it’s not unreasonable to suppose they could have become concentrated through distillation.

‘Beer, ale, stout, porter and malt liquor are exempt from the requirement to declare food allergen, gluten or added sulfites unless a list of ingredients is shown on the product’s label in a statement entitled ‘Contains’. Any list of ingredients that is voluntarily provided must be complete…’ ―Guido

Yet this isn’t necessarily an issue for even the most dedicated beer drinkers, as the effects of sulfite can be largely circumvented through supplementation.

A one-month supply of thiamine can now be bought online, shipping included, for roughly the price of a 12-pack of beer.

Alternatively and/or additionally, the supplementation of molybdenum can be initiated to increase the activity of hepatic sulfite oxidase.

This enzyme transforms ingested sulfites (SO₃²⁻) into the harmless sulfate ion (SO₄²⁻), and it is strictly dependent upon a molybdenum cofactor.

Low activity of sulfite oxidase is what best explains sulfite sensitivity. This enzyme is of such importance that it’s deficiency is fatal (Mudd, 1967). 

It now seems likely that all cerebral changes in long-term alcoholics is simply thiamine deficiency, a condition not caused by alcohol per se, and instead a consequence of chronic sulfite intake.

You can make a very good case for both points being true, and although these suspicions aren’t universally held they are shared by some others:

The author presents evidence that Korsakoff syndrome is synonymous with “alcoholic dementia,” differing only in extent of thiamine deficiency.

Nobody denies that Korsakoff syndrome is chronic alcohol-induced thiamine deficiency, but “alcoholic dementia” is a separate DSM category that is assumed thiamine-independent.

The author summarizes contemporaneous research showing that most long-term alcoholics are thiamine deficient, not simply those officially diagnosed with Wernicke-Korsakoff syndrome.

Both Korsakoff and non-Korsakoff chronic drinkers are invariably found having the same types of cerebral changes when either biochemically or physiologically compared.

‘The clinical presentation of brain damaged alcoholics is heterogenous and includes minimal cognitive impairment, amnesia and dementia. Whichever neurobiological technique is used, the evidence suggests that thiamine malnutrition is the mechanism which can best account for all clinical forms.’ ―Joyce

Although magnesium is usually found a bit lower in heavy drinkers as well — a result of increased urination and slightly reduced renal reuptake — the effects of thiamine depletion outshadow all others in importance.

And even though liver problems are often blamed on alcohol, which can induce dementia through hyperammonemia, this is actually caused by the concomitant intake of certain fatty acids. 

Fatty liver almost  always precedes cirrhosis, and BOTH of these conditions are quite common in non-drinkers (Farrell, 2006) — even Mormons.

‘Nonalcoholic fatty liver disease (NAFLD) is now present in 17% to 33% of Americans, has a worldwide distribution, and parallels the frequency of central adiposity, obesity, insulin resistance, metabolic syndrome and type 2 diabetes. Nonalcoholic steatohepatitis could be present in one third of NAFLD cases. Age, activity of steatohepatitis, and established fibrosis predispose to cirrhosis, which has a 7- to 10-year liver-related mortality of 12% to 25%. Many cases of cryptogenic cirrhosis are likely endstage NASH.’  ―Farrell

Alcohol only increases the absorption of fatty acids, and isn’t necessary nor sufficient to induce steatohepatitis all by itself.

Fatty liver would be unlikely to occur without the nutritional support from potato chips, peanuts, french fries, chicken wings, and various other forms of PUFA-fried bar foods.

A report published just one year after Joyce’s article supports his contention, suggesting that thiamine deficiency is a universal property of chronic drinking.

Although it doesn’t implicate sulfite directly, it doesn’t exclude it from being the prime cause:

This study was done on long term drinkers that weren’t officially diagnosed as having Korsakoff’s syndrome, Wernicke’s encephalopathy, or even beriberi.

They had all died from a separate cause, hepatic coma: This is often a result of the injudicious combining of ethanol and polyunsaturated fatty acids. 

They had found reductions of all three primary thiamine dependent enzymes in the brain, as compared with age-matched controls:

Since this non-Korsakoff group had a relatively mild deficiency of thiamine, we can probably assume they were drinking mostly vodka, gin, rum, and/or whiskey.

Nonetheless, this data provides support of the universality of this effect.

This suggests that vitamin B₁ should be an indispensable component of any serious drinker’s cupboard.

‘That Wernicke’s encephalopathy is the consequence of thiamine deficiency rather than a direct neurotoxic effect of ethanol is well established.’ ―Lavoie

A lack of thiamine would be expected to cause neurological problems in at least three ways:

(1) It would lower the activity of pyruvate dehydrogenase and hence its two products, CO₂ and acetyl-CoA, one of which is a direct precursor of acetylcholine.

(2) The lack of vitamin B₁ would also lead to a general reduction in metabolic rate through lowering the activity of transketolase, the enzyme needed to to synthesize NADPH.

This is the prime energy transferring molecule, so the metabolic rate is proportional to its electron-rich forms (e.g. NADPH, NADH).

(3) And thiamine deficiency would also reduce DNA synthesis through lowering ribose production, the other product of transketolase.

Low thiamine status is also found in Alzheimer’s disease, a form of “non-alcoholic dementia.”

This vitamin is so central to cognition that it’s viewed as a nootropic by some, and classic studies on school children prove they gain an edge through it (Harrell, 1945)

Thiamine studies of all types demonstrate its prime importance, and many have been conducted with the express intent of examining its known ability to enhance acetylcholine (Eder, 1980).

Newer studies show reductions of thiamine itself in the serum of heavy drinkers (Mancinelli, 2002).

As the one cited had been conducted in Italy, the subjects were likely drinking the sulfite-rich wine.

Others have correlated low thiamine concentrations to reduced transketolase activity (Baines, 1988), supporting the theoretical expectation of their strong relationship.

Old German studies show that sulfites destroy thiamine in vivo just as they do in vitro. 

Even when the two are mixed together in distilled water, at neutral pH and room temperature, practically all of the thiamine is destroyed in under an hour.

As being products of yeast fermentation, beer and wine would otherwise be decent sources of vitamin B₁ were it not for the added sulfites destroying it.

Sulfites also bind-to disulfides — e.g. cystine, α-lipoic acid, glutathione disulfide — and also induce oxidative damage through readily becoming the sulfite radical (ṠO₃⁻).

Sulfite can catalyze lipid peroxidation directly. This process is enhanced by its ability to bind glutathione, tying-up the molecule most responsible for preventing it. 

And on account of its tendency to bind the α-lipoic acid, sulfites would be expected to inhibit acetylcholine synthesis in more than one way.

Alpha-lipoic acid is classically known as a coenzyme and prosthetic group in the enzyme pyruvate dehydrogenase, which makes acetyl-CoA.

There’s also indication that it’s needed for full choline acetyltransferase activity (Haugaard, 2000).

Yet the negative effects of sulfite can largely be overcome simply through taking additional thiamine and molybdenum, the transition metal needed in sulfite oxidase. 

Inhibiting this enzyme with tungsten, which specifically displaces molybdenum, has been shown to decrease survival time in rats exposed to sulfur dioxide or metabisulfite (Cohen, 1973):

These two supplements, along with some magnesium and PUFA avoidance, should prevent the serious pathological outcomes that can come from massive intakes of beer and wine.

Because ethanol, really, is somewhat of a kitten. Many scientists have obtained funding trying to directly implicate it in many problems, somewhere in the body, with little to show for it.

The best they can do is show ethanol’s subtle effects on the glycine and GABA_A receptors, and then frame their language in ways that make its anxiolytic effects appear somehow pathological.

—-Important Message—-

Beware this toxic poison for men — it’s hiding in your bathroom

Most men don’t know it… but every time they enter the bathroom, they are exposing themselves to a toxic poison…

A toxic poison that drains men of their testosterone, swells up the prostate, and can even lead to cancer.

Shockingly, almost nobody is warning men about this toxic poison.

So do me a favor and check this out — it could save your manhood…

———-

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Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.