Sulforaphane research findings have commonalities with a super informative presentation by the lead researcher of clinical trial Reversal of aging and immunosenescent trends. I did a PubMed search of sulforaphane and each presentation topic, and used a 1/1/2015 publication date cutoff.
Presentation topics through the first 13 minutes were:
Thymus – no recent sulforaphane studies
Treatments
- Cellular Stress and AMPK Activation as a Common Mechanism of Action Linking the Effects of Metformin and Diverse Compounds That Alleviate Accelerated Aging Defects in Hutchinson-Gilford Progeria Syndrome “Metformin significantly reducing the mRNA and protein levels of both SRSF1 and progerin, activating AMPK, and alleviating pathological defects in HGPS cells. Metformin has also recently been shown to beneficially alter gene splicing in normal humans. Interestingly, several chemically distinct compounds, including rapamycin, methylene blue, all-trans retinoic acid, MG132, 1α,25-dihydroxyvitamin D3, sulforaphane, and oltipraz have each been shown to alleviate accelerated aging defects in patient-derived HGPS cells. Each of these compounds has also been independently shown to induce AMPK activation. Because these compounds improve accelerated aging defects in HGPS cells either by enhancing mitochondrial functionality, increasing Nrf2 activity, inducing autophagy, or by altering gene splicing and because AMPK activation beneficially modulates each of the aforementioned processes, it is our hypothesis that cellular stress-induced AMPK activation represents an indirect yet common mechanism of action linking such chemically diverse compounds with the beneficial effects of those compounds observed in HGPS cells. As normal humans also produce progerin at much lower levels through a similar mechanism, compounds that safely induce AMPK activation may have wide-ranging implications for both normal and pathological aging.“
- Untargeted Metabolomic Screen Reveals Changes in Human Plasma Metabolite Profiles Following Consumption of Fresh Broccoli Sprouts “Levels of several plasma metabolites are significantly different before and after sprout intake, including fatty acids, glutathione, glutamine, cysteine, dehydroepiandrosterone [DHEA], and deoxyuridine monophosphate.”
- The Prevention of a High Dose of Vitamin D or Its Combination With Sulforaphane on Intestinal Inflammation and Tumorigenesis in Apc 1638N Mice Fed a High-Fat Diet [the presenter didn’t mention Vitamin D although used] “VD [Vitamin D] administration decreased tumor incidence and size, and the co-administration with SFN (HFDS) magnified the effects. Inflammation and Wnt-signaling are suppressed by VD. The addition of SFN decreased the activity of histone deacetylase (HDAC) and increased autophagy.”
- Combination of Broccoli Sprout Extract and Zinc Provides Better Protection Against Intermittent Hypoxia-Induced Cardiomyopathy Than Monotherapy in Mice [the presenter didn’t mention zinc although used] “The effects of the combined treatment with BSE and zinc were always greater than those of single treatments.”
- Hgh – no recent studies
PSA
- Phytotherapeutic Interventions in the Management of Biochemically Recurrent Prostate Cancer: A Systematic Review of Randomised Trials “All studies found serum PSA levels to stabilise, decrease or rise more slowly in a significant number of men, and three studies reported stabilising or lengthening of PSA-doubling time.”
C-reactive protein and IL-6
- Effects of Long-Term Consumption of Broccoli Sprouts on Inflammatory Markers in Overweight Subjects [our model clinical trial] “IL-6 levels significantly decreased with 70 days of broccoli consumption and during control phase the inflammatory levels were maintained at low grade. C-reactive protein significantly decreased as well.”
Bone marrow fat – no recent studies
T cells
- Sulforaphane Inhibits Inflammatory Responses of Primary Human T-Cells by Increasing ROS and Depleting Glutathione “SFN significantly inhibited the activation of untransformed human T-cells derived from healthy donors or RA patients, and downregulated the expression of the transcription factor RORγt, and the TH17-related cytokines IL-17A, IL-17F, and IL-22, which play a major role within the pathophysiology of many chronic inflammatory/autoimmune diseases.”
PD-1 / PD-L1
- Modulating glioma-mediated myeloid-derived suppressor cell development with sulforaphane “Sulforaphane inhibits the formation of mMDSCs in vitro when monocytes are exposed to glioma conditioned media, decreases their expression of immunosuppressive PD-L1, and drives them towards a mature dendritic cell phenotype which promotes T-cell proliferation.”
Treatment cost
I estimate the annual cost of the non-prescription treatments of the clinical trial to be $100. The estimated annual cost of eating broccoli sprouts every day is < $500 for the broccoli seeds.
The above image isn’t an endorsement although it’s what I’ve used. It’s buzzword marketing to put “sprouts” and “sulforaphane” but not “seeds” on the label of a broccoli seeds package. For another thing, broccoli sprouts don’t “abound with phytochemical sulforaphane.”
Repeating a point from Estimating daily consumption of broccoli sprout compounds, broccoli seeds and sprouts contain little or no sulforaphane. They have glucoraphanin and myrosinase enzyme which are structurally separated. Disturbing their cells mixes the two, and the enzyme hydrolyzes glucoraphanin and other glucosinolates into sulforaphane and other healthy compounds.
Continue presentation topic commonalities with sulforaphane research at A pair of broccoli sprout studies and Part 2 of Reversal of aging and immunosenescent trends with sulforaphane.
How many grams of sprouts pr. day would be needed to achieve any clinical relevant results? Also, I suppose that just chewing the sprouts would be enough to form sulforaphane?
Good questions! What did you think about A pair of broccoli sprout studies?