(503) 419-7505 ben@modernvital.com
Zinc and The Metabolism of Alcohol

Zinc and The Metabolism of Alcohol

It’s well known that vitamin C, B complex vitamins, glutathione, and N-acetyl Cysteine (NAC) play a large role in alcohol metabolism, but zinc is rarely mentioned. However, zinc is actually a requisite cofactor in the metabolism of alcohol. (1) Zinc has not been studied extensively as a treatment for alcoholism, though alcoholics are usually zinc deficient and suffer from conditions which may benefit from zinc supplementation, such as low sperm counts and rosacea.

The body’s main enzyme for alcohol metabolism, alcohol dehydrogenase (ADH), actually contains zinc at its catalytic site. Zinc is now considered a novel therapeutic approach to alcohol liver disease (ALD). (2) ADH exists in decreased amounts in women, which contributes to less “first-pass metabolism,” and may in part explain why women are more susceptible to alcohol intoxication.

Zinc, an essential trace element, goes hand-in-hand with protein intake; in other words, poor protein intake correlates with poor zinc status. (3) Some symptoms of zinc deficiency include poor growth, infertility, skin disease, and impaired immune function.

The Epidemic of Chronic Alcoholism

Did you know that 50% of the world’s population drinks alcohol, and 5% to 10% have chronic alcoholism? In fact, over 3% of all deaths worldwide are due to alcohol. (4)

Ethanol

Ethanol is the natural product of sugar fermentation by yeasts. According to the USDA, one standard drink contains about half an ounce of ethanol. This is the equivalent of a light 12 oz beer, a 5 oz pour of wine, or 1.5 oz of an 80-proof distilled liquor. Ethanol is found in many household products, such as mouthwash, perfume, and cooking extracts.

The Metabolism of Alcohol

Alcohol is biotransformed to acetaldehyde by three main enzyme systems in the liver. (5)

  1. The first and main system lies in the cytosol of hepatocytes, where alcohol dehydrogenase (ADH) transforms ethanol to acetaldehyde. As mentioned, the ADHs are actually are actually a class of zinc enzymes!
  2. The second involves CYPs which oxidize ethanol in the microsomes of cells, known as the microsomal ethanol-oxidizing system (MEOS). Microsomes are basically fragments of hepatocellular endoplasmic reticulum.
  3. The third involves catalase in the peroxisomes, which acts upon hydrogen peroxide as substrate, metabolizing no more than 5% of all liver ethanol.

Ethanol crosses cell membranes, about 80% of its absorption occurring in the duodenum and 20% in the stomach itself. Peak blood ethanol levels are reached approximately 30 to 90 minutes after a meal. (6) Once ethanol reaches the blood, its taken up mainly by hepatocytes replete with ample quantities of ADH. ADH, however, is also available in the mucosa of the gut.

Zinc Status as a Biomarker of Chronic Alcoholism

Studies looking at evidence of the association of zinc metabolism and alcohol-associated disorders, such as those involving the liver, brain, lung, gut, and even fetal alcohol syndrome, suggest that zinc status should be used as a biomarker for alcohol abuse. (7,8) While it has been confirmed that alcohol induces autophagy in mice, a recent animal study found that adequate zinc intake is required for autophagy. (9)

Conclusion

Given that the body’s main enzyme system responsible for metabolizing alcohol in the liver is zinc-based, there appears to be enough evidence to warrant further studies in zinc supplementation for alcohol-induced diseases.

Resources

  1. Alcohol dehydrogenase. Egyptian Journal of Medical Human Genetics.
  2. Kharbanda K, Ronis M, Shearn C, et al. Role of Nutrition in Alcoholic Liver Disease: Summary of the Symposium at the ESBRA 2017 CongressBiomolecules. 2018;8(2):16. doi:10.3390/biom8020016.
  3. Gibson RS. A Historical Review of Progress in the Assessment of Dietary Zinc Intake as an Indicator of Population Zinc StatusAdvances in Nutrition. 2012;3(6):772-782. doi:10.3945/an.112.002287.
  4. Alcohol. World Health Organization. http://www.who.int/substance_abuse/facts/alcohol/en/. Published May 12, 2014. Accessed July 17, 2018.
  5. Alcohol Metabolism: An Update. National Institute on Alcohol Abuse and Alcoholism. https://pubs.niaaa.nih.gov/publications/aa72/aa72.htm. Accessed July 17, 2018.
  6. Mitchell MC, Teigen EL, Ramchandani VA. Absorption and Peak Blood Alcohol Concentration After Drinking Beer, Wine, or SpiritsAlcoholism: Clinical and Experimental Research. 2014;38(5):1200-1204. doi:10.1111/acer.12355.
  7. McClain CJ, Su LC. Zinc deficiency in the alcoholic: a review. Alcohol Clin Exp Res 1983;7:5-10.
  8. Skalny AV, Skalnaya MG, Grabeklis AR, Skalnaya AA, Tinkov AA. Zinc deficiency as a mediator of toxic effects of alcohol abuseEuropean Journal of Nutrition. 2017. doi:10.1007/s00394-017-1584-y.
  9. Liuzzi JP, Narayanan V, Doan H, Yoo C. Effect of zinc intake on hepatic autophagy during acute alcohol intoxicationBioMetals. 2018;31(2):217-232. doi:10.1007/s10534-018-0077-7.
The Myth of GERD: It’s Not the Acid, Stupid!

The Myth of GERD: It’s Not the Acid, Stupid!

There is a myth that GERD, popularly known as heartburn, is due to having too much stomach acid, a condition known as hyperchlorhydria. But there is ample research (1,2,3,4) demonstrating the opposite is true, that is, that GERD is most likely due to not having enough stomach acid.

How It Works

Lower esophageal sphincter (LES) tone is reduced and so the LES relaxes when there is not enough acid in the stomach, a condition known as hypochlorhydria. Hence, the sphincter does not close properly and acidic contents are much more likely to reflux upward from the upper GI into the esophagus. Interestingly, the hypochlorhydria theory of GERD, proponents of which include Jonathan Wright, M.D., author of Why Stomach Acid is Good for You (2001), has been called an alternative medicine theory, when it’s actually grounded in basic med school physiology.

Turn Off the Symptom Rather than Treat the Cause

To treat GERD, modern medicine prescribes drugs first-line in the on-average 7-minute visit: antacids like Tums which neutralize stomach acid; and H2 blockers like Tagamet and proton pump inhibitors (PPI’s) like Prilosec, that temporarily turn off our stomach’s ability to produce stomach acid. But turning off stomach acid in response to gastric reflux is the equivalent of an auto mechanic pulling the automotive fuse for your sudden dashboard engine warning light, or worse yet, simply cutting the wiring which carries the signal, because it is bothersome and annoying, rather than troubleshooting to find the underlying cause.

Common sense tells us there will be downstream consequences for the life of any car (in medicine, these are known as sequelae) if any engine light warning goes unheeded for long enough. Stomach pH varies from roughly 1.5 (more acidic: normal fasting) to 3.5 (less acidic: with food), and proper pH is essential to breaking down proteins as well as a healthy microbiome (5).

Our Addiction to GERD Drugs Causing More Chronic Disease

Our use of drugs to treat GERD is supposed to be short-lived (for example, an initial course of PPI’s is supposed to last no more than 8 weeks), but millions of people end up dependent on these drugs for years, and even decades. And weaning off these drugs, particularly PPI’s, can be challenging. There is an ample body of research now linking chronic PPI use to osteoporosis, increased infection risk, magnesium deficiency, and depression and dementia. But PPI’s are blockbuster drugs, as the market is projected to generate $4.34 billion by 2025.

On a yearly basis:

  • More than 80 million experience GERD symptoms in the U.S. alone.
  • 25 million suffer from heartburn daily in the U.S. alone.
  • 60 million suffer from heartburn monthly in the U.S. alone.

Also, there is evidence that the body upregulates stomach acid production when it is blocked, because the body is smart enough to know that without proper stomach acid it will essentially starve.

Too Much Stomach Acid Actually A Rare Condition

Having too much stomach acid, a condition known as hyperchlorhydria, is actually rare, seen in cases such as Zollinger-Ellison Syndrome (ZES), where tumors in your pancreas produce excessive amounts of gastrin, which leads to excessive stomach acid and thereby causes stomach ulcers. HCl production declines significantly with age, and GERD onset presents on average at age 50, another fact suggesting that GERD is due to hypochlohydria. Though GERD can be due to a number of causes, such as stress, hiatal hernia, or ZES, it is most likely that it is due to not having enough stomach acid.

Treat the Whole Person, Treat the Underlying Cause, and Stimulate the Vital Force, to Help Improve GERD

In naturopathic medicine, we treat the whole person and usually that begins with diet and lifestyle, but people need to be met where they are at. The innate healing mechanism of the body needs to be stimulated and obstacles to cure need to be eliminated for symptoms to improve.

For people who have symptoms of GERD, it is important to determine if they are hypochlorhydric and if so, then to stimulate the production of stomach acid, so that not only can the lower esophageal sphincter maintain proper tone so that it remains closed when it’s supposed to, but so that healthy flora are maintained in the gut and digestion and absorption is optimized. Of course  a person must consult their doctor before engaging in any medical treatment.

Four natural ways to stimulate the production of stomach acid include:

  • Apple cider vinegar (ACV)
  • Digestive bitters
  • Betaine HCl
  • Deglycerrhizinated licorice (DGL).

What do you think? I’d love to hear your thoughts!

Also, here are three excellent articles I greatly appreciated on GERD and hypochlorhydria:

Sources:

  1. Ayazi S, Leers, JM, Oezcelik A, Abate E, et al. Measurement of gastric pH in ambulatory esophageal pH monitoring. Surg Endosc. 2009 Sep;23(9):1968-73.
  2. Giles GR, Humphries C, Mason C, Clark G, et al. Effect of pH changes on the cardiac sphincter. Gut 1969;10:852-856.
  3. Kaye MD. On the relationship between gastric pH and pressure in the normal human lower oesophageal sphincter. Gut 1979;20:59-63.
  4. Giles GR, Mason MC, Humphries C, and Clark CG. Action of gastrin on the lower oesophageal sphincter in man. Gut 1969;10:730-734.
  5.     Shreiner AB, Kao JY, and Young BV. The gut microbiome in health and disease. Curr Opin Gastroenterol. 2015 Jan;31(1):69-75.