Mike Lustgarten has published a lot about Luteolin - I recommend you review it:
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I use pipingrock.com just because they ship cheaply to where I live.
Based on the Rick Johnson’s episode, I also try to ensure I’m drinking enough water when I eat fruits or salt. Psyllium husk is not a fructokinase inhibitor but perhaps it reduces the speed of uptake of fructose as well.
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Yeah but I thought he said in the interview that fruits also have alot of vitamins and minerals that help protect against fructose issues that would arise in comparison to dried fruits or fruit concentrate juice. In fact he says he doesnt tell people to not eat fruits, he just says not to overdue it
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Interestingly, back in the day, fructose was considered the “good” sugar as opposed to cane and beet sugars.
"This was promoted by: Adelle Davis (25 February 1904 – 31 May 1974) was an American author and nutritionist, considered “the most famous nutritionist in the early to mid-20th century.”[1]: 150 She was an advocate for improved health through better nutrition. "
Adelle Davis - Wikipedia(25%20February%201904,improved%20health%20through%20better%20nutrition.
She was not promoting sugar as anything but bad, but if you use sugar, use fructose.
The thinking was because it came from “healthy” fruits it must be better.
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I believe a lot of one’s microbiome uses fructose as a fuel, so it’s worth having a little bit, just not a lot.
Fantastic new paper on Cana and it’s similar effects to 17AE, Rapa and ACA when it comes to MTOR activities and anti-aging.
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Interesting. Perhaps the thinking was insulin. No insulin effect from fructose. In sports performance the idea is fructose and glucose use separate uptake pathways so you can consume more per hour (during exercise) using both.
Yes - full paper and info already posted here: Canagliflozin shares common mTOR and MAPK signaling mechanisms with other lifespan extension treatments
My apologies, I don’t mean to duplicate efforts. I should have looked.
No problem. There are a ton of posts and most people don’t have time to read them all.
A new paper from Richard Miller’s lab on Canagliflozin:
Hypothalamic Sex-Specific Metabolic Shift by Canagliflozin during Aging
Hashan S.M Jayarathne, Ryan Sullivan, Luke Stilgenbauer, Lucas Kniess Debarba, Artur Kuchumov, Lisa Koshko, Sydney Scofield, Wanqing Liu, Brett C Ginsburg, Richard A Miller and Marianna Sadagurski
The hypothalamus undergoes significant changes with aging and plays crucial roles in age-related metabolic alterations. Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are anti-diabetic agents that promote glucose excretion, and promote metabolic homeostasis. Recent studies have shown that SGLT2i, Canagliflozin (Cana), can extend the median survival of genetically heterogeneous UM-HET3 male mice and improve central metabolic control via increases in hypothalamic insulin responsiveness in aged males, as well as reduced age-associated hypothalamic inflammation. We studied the long- and short-term effects of Cana on hypothalamic metabolic control in UM-HET3 mice. We show that Cana treatment reduced body weight and fat mass in male mice that was associated with enhanced glucose tolerance and insulin sensitivity observed by 12 months. Indirect calorimetry showed that short-term Cana treatment (5 months) increased energy expenditure in male, but not female mice, at 12 months of age. Long-term Cana treatment (18 months) increased metabolic rates in both sexes, and markedly increasing formation of both orexigenic and anorexigenic projections to the paraventricular nucleus of the hypothalamus (PVH) mostly in females by 25 months. Hypothalamic RNA-sequencing analysis revealed sex-specific genes and signaling pathways related to insulin signaling, glycogen catabolic pathway, neuropeptide signaling, and mitochondrial function upregulated by Cana, with males showing a more pronounced and sustained effect on metabolic pathways at both age groups. Overall, our data provide critical evidence for sex-specific mechanisms that are impacted by Cana during aging suggesting key targets of hypothalamic Cana-induced neuroprotection for metabolic control.
bioRxiv. posted 23 March 2024, 10.1101/2024.03.21.586115
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Cana is actually both SGLT1i and 2i.
My understanding is that it hence actually does also act via lowering glucose effects at the intestine level. See eg below. Does that make sense?
SGLT1 is involved in glucose absorption by the intestinal absorptive epithelial cells, and it regulates glucose-dependent incretin secretion from enteroendocrine cells such as GLP-1-secreting L cells and GIP-secreting K cells [10].
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But is that sglt1 inhibition in the intestine by canagliflozin clinically significant enough to have a real world effect on glucose absorption?
For Cana my understanding is yes (though perhaps not so for Empa and Dapa and others).
@Davin8r Is your understanding different re Cana?
My bad, sorry, yes, you’re right – I’d always thought the sglt1 inhibition was clinically insignificant because it doesn’t cause flatulence/diarrhea in the way acarbose does, but that’s because cana just slows down (but doesn’t block) absorption in the small intestine.
Unfortunately, I can’t edit my original post from 3 years ago😬
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This is encouraging. I have moderately elevated lp(a) and haven’t wanted to take a statin because they can elevate it, so bempedoic acid has been on my research list. Yet bempedoic acid can increase uric acid, so I have been on the fence. Maybe SGLT2 inhibitors are the answer to the serum uric acid side effect.
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PCSK9i often lower Lp(a) in a meaningful way if that is something you could access.
phloridzin from apple is a potent SGLT2 inhibitor… Actually dual one
That’s a good thought and if insurance would cover it I might try finding a really aggressive cardiologist to prescribe it, but my cholesterol is otherwise pretty decent without drugs (apoB fluctuates between 52-62, triglycerides below 35, LDL 44+, HDL not horrible at 52). NMR Lipoprofile looks great.
lp(a) is “only” 100, probably elevated because of pushing my triglycerides so low.
I haven’t even bothered trying to find a doctor because I don’t come anywhere close to any standard treatment thresholds. Still, the lp(a) elevates my risk so I’d like to knock LDL down a bit more.
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