Lead and Your French Fries?

David Quig, PhD | March 10, 2021

There are some overlapping mechanistic concerns with respect to past exposure to lead, the current obesity epidemic, and a looming increase in incidence of Cardiometabolic syndrome. Widespread environmental exposures to lead (Pb) have been greatly ameliorated in the U.S. and overall blood Pb levels for children have progressively diminished in recent decades. However past Pb exposure appears to be associated with persistent adverse effects with respect to cardiovascular disease (CVD) in adults, and Pb may exacerbate some of the metabolic disruptions that are associated with Cardiometabolic syndrome.

Environmental Pb exposure has been associated with hypertension, and compromised renal and neurological functions, but exposure to Pb has been largely overlooked as a direct risk factor for CVD. A recent systematic review and meta-analysis of epidemiological studies found that non-occupational exposure appears to be associated with a near-linear increase for risk of CVD. That association was independent of exposures to arsenic, cadmium, and copper. A prospective 20 year follow-up study of adults > 20 years of age (NHANES-III, n= 14,289) revealed that blood lead levels (BLLs) below 5 μg/dL at baseline contributed statistically CVD and ischemic heart disease mortalities. The data analysis adjusted for an extensive array of potential confounders. Similar to findings regarding BLLs and IQ scores for children, the steepest increase in CVD risk for adults was found across the lower BLLs.

The aforementioned epidemiological efforts would likely have been more revealing had life-long retention of Pb been estimated via K x-ray fluorescence. It is well established that Pb accumulates in bone even in children, and the half time for Pb in bone is very long. It is also acknowledged that bone Pb is slowly released back into blood, and that rate of “endogenous re-exposure” increases with enhanced bone resorption that occurs with aging and changes in hormonal status. Accelerated bone demineralization is also affected by sedentary lifestyle and positive caloric balance, which is also associated with excessive visceral adiposity and cardiometabolic disorders.

Excessive visceral adiposity (VAT) is causally associated with cardiometabolic disorders and chronic low-grade inflammation, and recent evidence indicates that Pb may also contribute to inflammation in the body. Aggregation of immune cells in VAT, and Pb ions both effectuate increased proinflammatory cytokines and reactive oxygen/nitrogen species (ROS/RNS) that may be associated with endothelial cell dysfunction, oxidation of LDL, and platelet activation. Excessive formation of the ROS radical superoxide may decrease the local availability of nitric oxide (NO), which is the vascular endothelium-derived relaxation factor that plays a key role in the local regulation of blood flow, blood pressure, and thrombus formation. The interaction of superoxide with NO produces peroxynitrite, which can perpetuate the production of excess ROS and proinflammatory cytokines via activation of NFkB. Those effects are likely enhanced in the presence of excessive VAT because VAT is associated with hypoadiponectinemia, and adiponectin imparts anti-inflammatory, anti-oxidative, antidiabetic, and vascular protective effects.

Exposure to Pb may exacerbate inflammation and oxidative damage that is associated with Cardiometabolic syndrome. Clinical consideration of past exposure to Pb and accelerated bone demineralization may be warranted for some patients who may be caught up in the current surge of excessive adiposity.


Chowdhury R et al. Environmental toxic metal contaminants and risk of cardiovascular disease: systematic review and meta-analysis. BMJ (2018)362:k3310 http://dx.doi.org/10.1136/bmj.k3310

Lanphear B et al. Low-level lead exposure. Lancet (2018) http://dx.doi.org/10.1016/S2468-2667(18)30025-2

Bhattarai HK et al. Vitamin D, calcium, parathyroid hormone, and sex steroids in bone health and effects of aging. J Osteoporosis (2020) https://doi.org/10.1155/2020/9324505

Metryka E et al. Lead (Pb) exposure enhances expression of factors associated with inflammation. Int J Mol. Sci (2018)19: 1813 https://doi.org/10.3390/ijms19061813

Radi R. Oxygen radicals, nitric oxide, and peroxynitrite: Redox pathways in molecular medicine. PNAS (2018)115: 5839-48 https://doi.org/10.1073/pnas.1804932115

Hallaway N and Strauts Z. Turning Lead into Gold. New Star Books;1995. ISBN-10:0921586515

Wellness Wednesday Webinar

Neurotransmitter Primer

Fiona Campbell, ND

April 7, 2021 at 9 AM and 12 PM Pacific

Each session is approximately 60 minutes in length with Q&A

Review the anatomy and physiology of neurotransmitter (NT) secretion and function

Exam the role of individual NTs and how imbalances present clinically

Learn to incorporate NT evaluation and treatment in your hormone balancing practice

Obtain treatment considerations for addressing neurotransmitter imbalances, without prescription medications

Beyond Adrenal Fatigue: Reframing our Understanding of Stress and the HPA Axis

Tom Guilliams PhD

April 21, 2021 | 12-1 PM Pacific

For too long, complex stress-related changes to HPA axis function have been labeled as "adrenal fatigue." This outdated and incorrect nomenclature has often prevented clinicians from properly understanding how the HPA axis adapts to stressors and why simplistic solutions (i.e., adrenal support) are inadequate for most patients. Our knowledge of the stress response system, HPA axis maladaptation, and the factors that influence glucocorticoid signaling have greatly advanced in just the past decade, though much of this knowledge is not well leveraged in most clinical practices. This webinar will reframe our orientation of stress in a way that focuses on the brain (rather than the adrenal gland), and shows that the stress response is not as linear as it is often perceived. While navigating through one of the premier resources to help clinicians understand the functional medicine approach to stress and the HPA axis, this lecture will also help re-frame the stress response within the larger (non-stress) functions performed by the HPA axis


Disclaimer: All information given about health conditions, treatment, products, and dosages are for educational purposes only and do not constitute medical advice.



800.323.2784 (US and Canada)

+1.630.377.8139 (Global)