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DavidPerlmutterMD · 2024-05-06 · David Perlmutter (host), Jeffrey Bland

A Closer Look At Immune Health & Himalayan Tartary Buckwheat | Dr. Jeffrey Bland

28 research-tied claims examined: 4 contradicted 3 contradicted online 2 overstated 5 context 8 supported 6 unverified

8

Supported by research

0:24:07Jeffrey Blandsupportedmoderate

2-hydroxybenzylamine (2-HOBA), a compound studied for treating hypertension via immune-vascular signaling, is found in only one food: Tartary buckwheat.

"And the compound that they were studying that causes that effect on the immune system was called 2-hydroxybenzylamine. 2-hydroxybenzylamine, when I read the fine print in the paper it turns out this is it says this is found in only one food, Himalayan tartary buckwheat or I I think it said tartary buckwheat." (said at 0:24:07)

Published preclinical studies demonstrate that 2-hydroxybenzylamine (2-HOBA), a selective scavenger of reactive lipid dicarbonyls (isoketals/isolevuglandins), prevents immune cell activation (dendritic cells and T cells), vascular inflammation, aortic stiffening, and hypertension in vascular oxidative stress models. Literature describing the natural origins of 2-HOBA identifies buckwheat (particularly Tartary buckwheat, *Fagopyrum tataricum*) as its primary dietary plant source.

0:13:19David Perlmutter (host)supportedmoderate

Glyphosate alters the soil microbiome by damaging the shikimate pathway.

"what is that information signal we're getting uh based upon the alteration of the influence of the soil microbiome when it's been so radically changed through this uh damaging of the shikimate pathway via glyphosate" (said at 0:13:19)

Glyphosate acts by inhibiting 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), a key enzyme in the shikimate pathway required for the biosynthesis of essential aromatic amino acids in plants, fungi, and many bacteria. Because many soil and plant-associated microorganisms possess glyphosate-sensitive Class I EPSPS enzymes, glyphosate exposure can disrupt microbial metabolism, inhibit susceptible taxa, select for resistant or degrading strains, and alter microbial community composition and diversity in soil and root environments.

0:33:15David Perlmutter (host)supportedhigh

Certain pharmaceutical drugs produce their effects by downregulating complex I of oxidative phosphorylation.

"there are drugs as you mentioned that actually work via down regulating complex I of uh oxidative phosphorylation." (said at 0:33:15)

Several pharmaceutical drugs exert their primary or secondary therapeutic actions through the inhibition or downregulation of complex I (NADH:ubiquinone oxidoreductase) of the mitochondrial electron transport chain in oxidative phosphorylation. The most prominent and widely prescribed example is the biguanide class of drugs, particularly metformin and phenformin, which inhibit complex I activity to modulate cellular energy metabolism, activate AMPK, and reduce hepatic gluconeogenesis. Other pharmaceutical agents and investigational oncology drugs (such as IACS-010759) have also been specifically developed to target complex I.

0:38:16Jeffrey Blandsupportedlow

Sprouting Himalayan Tartary Buckwheat increases its polyphenol levels by approximately threefold within the first four days.

"that particular plant when it sprouts, just as you suggested, increases the level of polyphenols by about threefold in that first four days of sprouting." (said at 0:38:16)

Published agricultural and food chemistry literature supports the claim that germination and sprouting of Tartary buckwheat (Fagopyrum tataricum) triggers substantial de novo synthesis and accumulation of polyphenols and flavonoids (principally rutin, quercetin, and related phenolic acids) over the early days of sprouting, typically resulting in multi-fold increases compared to ungerminated grains. Because these findings are derived from laboratory food science and botanical assays rather than clinical studies, the certainty of evidence is graded as low.

0:41:34David Perlmutter (host)supportedhigh

Microglial cells clear beta-amyloid from the brain.

"the idea that it's nurturing neurons, it's clearing the brain of beta-amyloid, that it is regulating its own metabolism based upon the conditions in which it sees itself" (said at 0:41:34)

Extensive neurobiological research confirms that microglial cells, the resident immune cells and phagocytes of the central nervous system, are responsible for engulfing and clearing amyloid-beta (Aβ) peptides and protein aggregates from the brain. While their phagocytic efficiency can become impaired or dysregulated during the chronic neuroinflammatory progression of Alzheimer's disease, microglial uptake and degradation of beta-amyloid remains a well-established physiological mechanism of brain clearance.

0:45:07Jeffrey Blandsupportedhigh

The innate immune system is concentrated primarily in barrier tissues like the gut mucosa and the pulmonary system.

"the innate immune system which resides by by the way, as you'd expect, mostly on the barrier tissues that are exposed to the outside world. So the innate immune system is very rich in the gut mucosa. It's very rich in the lungs, in the pulmonary system" (said at 0:45:07)

Established immunological consensus demonstrates that mucosal and barrier tissues exposed to the external environment (such as the gastrointestinal tract and pulmonary system) are major sites of innate immune system concentration and activity. These tissues are densely populated by innate immune effectors, including innate lymphoid cells (ILCs), mucosal-associated invariant T (MAIT) cells, tissue-resident macrophages, and epithelial sentinel mechanisms designed to provide frontline host defense and barrier maintenance.

0:48:14David Perlmutter (host)supportedmoderate

Beta-amyloid and phosphorylated tau bind to RAGE (receptor for advanced glycation end products) on microglial cell surfaces.

"there are receptors on these immune cells that respond to beta-amyloid and phosphorylated tau, those chemicals misfolded proteins rather that accumulate in the brain that are associated with neurodegeneration, things like Alzheimer's, of course. But where these bind on the cell surface of these immune cells, the microglial cells, are receptors called RAGE receptors." (said at 0:48:14)

Published literature confirms that the receptor for advanced glycation end products (RAGE) is expressed on microglial cell surfaces and functions as a cell-surface receptor binding amyloid-beta (Aβ), triggering microglial activation and proinflammatory signaling in Alzheimer's disease models. RAGE also interacts with both Aβ and tau proteins in the pathogenesis of dementia and neurodegeneration.

0:48:44David Perlmutter (host)supportedmoderate

RAGE receptors on microglial cells respond to advanced glycation end products resulting from chronically elevated blood sugar.

"it's the receptor for advanced glycation end products. And that's important because that's a receptor that is responsive to the situation in which blood sugar has been elevated over a period of time, i.e. a metabolic derangement." (said at 0:48:44)

Published literature confirms that the receptor for advanced glycation end products (RAGE) binds to advanced glycation end products (AGEs) that accumulate during chronic hyperglycemia and metabolic derangement. In the central nervous system, RAGE activation on microglial cells and other neural tissue mediates downstream neuroinflammatory pathways associated with diabetes-related cognitive impairment and neurovascular pathology.

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.