Don’t Forget the Beer
Environmental Contributors to Heart Disease
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A recent statement from the American College of Cardiology, the American Heart Association, the European Society of Cardiology and the World Health Organization attributes at least 20% of worldwide cardiovascular disease (CVD) deaths to environmental risk factors. (1)
These risk factors include noise/light pollution, climate change including extreme heat, and chemical, soil, air and water pollution. This combination of factors over one’s lifetime is referred to as one’s “exposome”. Air pollution is the largest contributor to CVD, especially in lower income societies where indoor cooking and home heating often depend on polluting heat sources. (2) Airborne particles from air pollution not only affect the lungs, but can enter the bloodstream through the alveoli and affect other organ systems. (1)
I discussed on Substack on November 13, 2024 that micro plastics have been found in human atherosclerotic tissue and may contribute to the development of atherosclerosis.
An article in the New England Journal of Medicine (NEJM) discussed the link between environmental metals including lead, mercury, arsenic, and cadmium and CVD. (2) Lead is a known hypertension risk factor, but also appears to increase coronary artery disease (CAD), even at low levels. Mercury enters the environment from gold mining and burning coal. Mercury from burning coal precipitates into water, is consumed by fish, and enters the fish-to-woman food chain. Arsenic is usually obtained from drinking water from international “hot spots” including the southwest US and northern New England. Arsenic in New England enters the water from the granite bedrock. Many New England residents are unaware of the arsenic in New England, but you should remember it when you buy your next vacation home in northern New England. Cadmium pollution comes from tobacco smoke and work exposure, as well as green leafy and tuberous vegetables grown in contaminated soil.
We wrote a review on chelation (3), partly to convince one of my patients that his chelation therapy was a waste of money. To my amazement, there was a large, well-done study that demonstrated that chelation using EDTA reduced the composite endpoint of total mortality, myocardial infarction, coronary revascularization, stroke, and hospitalization by 18% (95% CI, 1–31%, P <.04) with a larger effect in patients with diabetes. A subsequent NIH-funded study (4) did not find any benefit from chelation therapy, but the authors of the NEJM review (2) wondered if chelation therapy might be beneficial by removing such toxic metals as cadmium.
Both the NEJM review of metals and the recent multiple-society position statement “forgot the beer.” Let me explain this:
I was a medical student in the early 1970s, and not far removed from my fraternity-house, undergraduate days when a lecturer mentioned that in 1965–6, there had been an outbreak of heart failure linked to beer in Quebec, Canada. (5) I woke up immediately. A brewery in Quebec had added cobalt to their beer to stabilize the beer’s foam “head”. The cobalt was determined to be the cause of the cardiomyopathy.
The cobalt cardiomyopathy was associated with elevated hemoglobin levels and pericardial effusions. A total of 48 habitual beer drinkers were affected in Quebec with a mortality rate of 46%. Similar epidemics related to beer consumption were subsequently reported from Omaha, NE; Minneapolis, MN; and Belgium. The dose of cobalt was not large and was below the dose of cobalt used at the time to treat anemia. (I never knew cobalt was used to treat anemia!) This led to the hypothesis that it was the combination of the cobalt and the alcohol that lead to the cardiomyopathy.
Concern about cobalt heart disease re-appeared with evidence that some patients developed heart failure from cobalt leakage from failed hip replacements. (5) This concern has abated, but not totally disappeared. There is also concern about exposure in individuals who work with cobalt.
According to OpenEvidence, an AI platform for physicians:
Cobalt – chromium alloys are widely used in joint prostheses.
About 20 million North Americans have such a prosthesis.
There is some concern (and some reports of cardiomyopathy) with these prostheses especially in metal-on-metal hip replacements because their corrosion can release cobalt into the systemic circulation.
Excess cobalt blood levels can be identified by blood cobalt assays.
I am not suggesting that cobalt hip replacements are a rampant cause of cardiomyopathy. But, we should at least think about it and get a cobalt blood level in someone with an unexplained cardiomyopathy, a failed metal-on-metal joint prosthesis, and an alcohol issue, especially if their hematocrit is high.
I like these historical stories, and they sometimes (rarely) are useful. Nevertheless, I propose changing, “Those who forget the past are doomed to repeat it” to “Those who forget the past are doomed to miss the present.” Catchy, no?
According to OpenEvidence, large registries have not identified a cobalt problem with hip replacement, but how many patients have failed metal-on-metal prostheses and drink too much? Maybe these registries found no association because they, too, “forgot the beer.”
References:
1. Anderer S. Cardiology Societies Urge Action on Environmental Risk Factors. JAMA. 2026;335(10):838-839.
2. Rajagopalan S, Landrigan PJ. Pollution and the Heart. N Engl J Med. 2021 Nov 11;385(20):1881–1892. PMID: 34758254
3. Ibad A, Khalid R, Thompson PD. Chelation therapy in the treatment of cardiovascular diseases. J Clin Lipidol. 2016 Jan-Feb;10(1):58-62. PMID: 26892121
4. Lamas GA, et.al. Edetate Disodium-Based Chelation for Patients With a Previous Myocardial Infarction and Diabetes: TACT2 Randomized Clinical Trial. JAMA. 2024 Sep 10;332(10):794-803. PMID: 39141385. Metal-on-Metal Total Hip Resurfacing Arthroplasty: An Evidence-Based Analysis. Medical Advisory Secretariat. Ont Health Technol Assess Ser. 2006;6(4):1–57. Epub 2006 Feb
5. Bradberry SM, Wilkinson JM, Ferner RE. Systemic toxicity related to metal hip prostheses. Clin Toxicol (Phila). 2014 Sep-Oct;52(8):837–47.
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