I don’t know about you, but when I hear the word “detox” I think of laxatives, green smoothies, and lots of tea. What if I told you there is an essential nutrient that acts as an integral part of our own internal detoxification system? Well, guess what? Vitamin B12 does just that!
How does vitamin B12 work in the detox process?
Vitamin B12 plays an integral role in a metabolic reaction important for our health. In this reaction, vitamin B12 is needed to convert homocysteine to methionine. This is commonly known as part of methylation. As you can see below, methionine, the byproduct of homocysteine breakdown, is needed for DNA synthesis, as well as for the production of SAM, which is needed for methylation. There are many downstream effects that can occur from these reactions being hindered. These manifest as symptoms of vitamin B12 deficiency.
Pictured below, you can see the intricacies of the detox mechanism of vitamin B12.
What is homocysteine and why does it matter?
Homocysteine (Hcy) is an amino acid produced by the human body, and is usually present in relatively small amounts (1). It is synthesized by transmethylation of the amino acid methionine, which we obtain from our diet.
- Elevated homocysteine alone is considered an independent risk factor for heart disease (2).
- In mouse models, elevated homocysteine led to increases in oxidative stress. (3, 4)
- Elevated homocysteine has been identified as a risk factor for heart attack. In a prospective case-control study of 14,916 male physicians, those in the highest 5% of homocysteine levels had a 3.1x greater risk of heart attack compared with those in the bottom 90%. (5)
- Hyperhomocysteinemia has also been identified as a risk factor for Alzheimer’s disease and dementia. In a subset of the Framingham Heart Study, there was a 1.4x increased relative risk of dementia for every standard deviation increase in plasma Hcy. In this same study, the relative risk of Alzheimer’s disease was 80% higher at baseline for each standard deviation increase in plasma Hcy. (6)
As you can see, elevated homocysteine can have detrimental effects on the body. We can prevent this from happening by ensuring we get enough vitamin B12 into our bodies, through both diet and supplementation, since vitamin B12 is essential for the breakdown of homocysteine into methionine.
Should you be concerned?
The following groups of people are at an elevated risk of vitamin B12 deficiency, and should consider supplementation to prevent elevated homocysteine levels.
- Vegetarians and vegans.
- Those with low stomach acid.
- Those with malabsorptive disorders or digestive disorders, i.e., Celiac disease, Crohn’s disease, etc.
- Those who have had bariatric surgery.
- Those with depression. (7)
- Those with frequent migraines. (8)
- Long-term users of proton pump inhibitors or antacids. (9)
- Those using selected medications including: metformin, inhalant or systemic corticosteroids, antibiotic medications, phenobarbital, birth control pills, bile acid-sequestrants, uricosuric agents, or histamine antagonists. (10)
If you fall into any of these categories, you should consider supplementing with vitamin B12. The best form, which is used to treat deficiency in clinical settings, is hydroxocobalamin. Hydroxocobalamin is an activated form of vitamin B12, which bypasses the need for stomach acid and intrinsic factor for absorption (common factors in B12 malabsorption). We recommend starting with 2,000 mcg per day, which can be found in one lozenge of our supplement Rise Well.
While vitamin B12 might not be the first thing on your mind when you think of improving your longevity, optimizing your vitamin B12 status can help to detoxify your body of excess homocysteine. Doing so will reduce your risk for several diseases related to elevated homocysteine, such as heart disease, heart attack, Alzheimer's, and dementia. Set yourself up for success. And read our other blogs to learn more about vitamin B12!
- Shiel, Jr., W. C. Medical definition of homocysteine. MedicineNet. Accessed 29 November 2020.
- Škovierová, H., et al. 2016. The molecular and cellular effect of homocysteine metabolism imbalance on human health. International Journal of Molecular Sciences 17(10):1733. Doi: 10.3390/ijms17101733.
- Dayal, S., et al. 2004. Cerebral vascular dysfunction mediated by superoxide in hyperhomocysteinemic mice. Stroke 35(8):1957-1962. Doi: 10.1161/01.STR.0000131749.81508.18.
- Timkova, V., et al. 2016. Effects of mild hyperhomocysteinemia on electron transport chain complexes, oxidative stress, and protein expression in rat cardiac mitochondria. Molecular and Cellular Biochemistry 411(1-2):261-270. Doi: 10.1007/s11010-015-2588-7.
- Stampfer, M. J., et al. 1992. A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 268(7):877–881.
- Seshadri, S., et al. 2002. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. New England Journal of Medicine 346(7):476-483. Doi: 10.1056/NEJMoa011613.
- Penninx, B. W., et al. 2000. Vitamin B(12) deficiency and depression in physically disabled older women: Epidemiologic evidence from the Women’s Health and Aging Study. The American Journal of Psychiatry 157(5):715–721. Doi: 10.1176/appi.ajp.157.5.715.
- Togha, M., et al. 2019. Serum vitamin B12 and methylmalonic acid status in migraineurs: A case-control study. Headache The Journal of Head and Face Pain 59(9):1492–1503. Doi: 10.1111/head.13618.
- Termanini, B., et al. 1998. Effect of long-term gastric acid suppressive therapy on serum vitamin B12 levels in patients with Zollinger-Ellison syndrome. The American Journal of Medicine 104(5):422–430. Doi: 10.1016/S0002-9343(98)00087-4.
- A.D.A.M. Drugs that deplete: Vitamin B12 (cobalamin). A.D.A.M. SmartEngage Health Education Library website. Accessed 29 November 2020.