Dr. Eric Berg DC · 2026-06-26 · Eric Berg (host), Steve, Tashia, Edward, Amy

The Dr. Berg Show LIVE - June 26, 2026

39 research-tied claims examined: 2 contradicted 10 overstated 3 context 16 supported 8 unverified

2

Contradicted by research

0:53:33Eric Berg (host)contradictedhigh

Estrogen replacement therapy that is not paired with progesterone increases the risk of stroke and heart attack.

"There is data that shows uh and I've read this that um like estrogen replacement therapy um that's not paired with progesterone could increase your risk of stroke and heart attack." (said at 0:53:33)

Progestogen is added to estrogen therapy exclusively to prevent endometrial hyperplasia and uterine cancer in women with an intact uterus, not to mitigate cardiovascular risks. Large randomized controlled trial evidence from the Women's Health Initiative (WHI) shows that oral estrogen-alone therapy does increase the risk of ischemic stroke (similar to combined therapy), but it does not increase the risk of coronary heart disease or heart attack (hazard ratio 0.94, 95% CI 0.78–1.14). In fact, adding a progestin (combined hormone therapy) was associated with an early elevation in coronary heart disease risk, rather than offering protection against heart attacks.

1:01:13Eric Berg (host)contradictedhigh

Cyanocobalamin does not break down or become active in individuals with methylation issues, resulting in toxic buildup in the body.

"the type they put it in or the type that they have is called cyanocobalamin and that's the one that um is not good for you because it doesn't it has to go through these processes to break down and become active. And so it if you have also a problem with that methylation thing, it it never really breaks down. So you you create a buildup in the body, it becomes toxic." (said at 1:01:13)

The host's claim that cyanocobalamin requires methylation to break down—and that methylation defects prevent its breakdown, causing toxic accumulation—is contradicted by established biochemical literature. Cobalamin (vitamin B12) serves as a coenzyme in human physiology for two primary reactions: the conversion of L-methylmalonyl-CoA to succinyl-CoA and the methylation of homocysteine to methionine (PMID: 39376196). Methylation defects, such as methylene tetrahydrofolate reductase (MTHFR) deficiency, impair folate-dependent remethylation pathways, but they are distinct from cobalamin processing and intracellular trafficking and do not prevent cyanocobalamin breakdown or cause it to build up toxically in the body (PMID: 30761552).

Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.